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  • 101.
    Holme, Ingar
    et al.
    Ullevaal University Hospital.
    E Strandberg, Timo
    University of Oulu.
    Faergeman, Ole
    Arhus University Hospital.
    Kastelein, John J P
    University of Amsterdam.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Tikkanen, Matti J
    University of Helsinki.
    Lytken Larsen, Mogens
    Arhus University Hospital.
    Lindahl, Christina
    Pfizer Sweden.
    Pedersen, Terje R
    Ullevaal University Hospital.
    Congestive heart failure is associated with lipoprotein components in statin-treated patients with coronary heart disease Insights from the Incremental Decrease in End points Through Aggressive Lipid Lowering Trial (IDEAL)2009Inngår i: ATHEROSCLEROSIS, ISSN 0021-9150, Vol. 205, nr 2, s. 522-527Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Very few, if any, studies have assessed the ability of apolipoproteins to predict new-onset of congestive heart failure (HF) in statin-treated patients with coronary heart disease (CHD). Aims: To employ the Incremental Decrease in End points Through Aggressive Lipid Lowering Trial (IDEAL) study database to assess the association of on-treatment lipoprotein components with prediction of HF events and to compare their predictive value with that of established risk factors such as hypertension and diabetes. Methods: We used Cox regression models to study the relationships between on-treatment levels of apolipoproteins A1 and B to subsequent HE Chi square information value from the log likelihood was used to compare the predictive value of lipoprotein components with established risk factors of HF. Findings: In the IDEAL study, on-treatment apolipoproteins proved to be associated with the occurrence of new-onset HE Variables related to low-density lipoprotein cholesterol (LDL-C) carried less predictive information than those related to high-density lipoprotein cholesterol (HDL-C), and apoA-1 was the single variable most strongly associated with HF. LDL-C was less predictive than both non-HDL-C (total cholesterol minus HDL-C) and apoB. The ratio of apoB to apoA-1 was most strongly related to HF after adjustment for potential confounders, among which diabetes had a stronger correlation with HF than did hypertension. ApoB/apoA-1 carried approximately 2.2 times more of the statistical information value than that of diabetes. Calculation of the net reclassification improvement index revealed that about 3.7% of the patients had to be reclassified into more correct categories of risk once apoB/apoA-1 was added to the adjustment factors. The reduction in risk by intensive lipid-lowering treatment as compared to usual-dose simvastatin was well predicted by the difference in apoB/apoA-1 on-treatment levels. Interpretation: The on-treatment ratio of apoB/apoA-1 was the strongest predictor of HF in CHD patients of both IDEAL treatment arms combined, mostly driven by the strong association with apoA-1, whereas LDL-C and non-HDL-C were less able to predict HF outcome. The predictive information value contained within apoB/apoA-1 was about 2.2 times more than that of diabetes. Between-treatment group differences in HF were to a significant extent explained by on-treatment differences in apoB/apoA-1, mostly through the changes in apoB. We argue therefore, on-treatment lipoprotein components contribute to the overall future risk of HF in statin-treated patients with CHD.

  • 102.
    Holme, Ingar
    et al.
    Oslo University Hospital.
    Szarek, Michael
    Cater, Nilo B
    Pfizer Inc.
    Faergeman, Ole
    Pfizer Inc.
    Kastelein, John J P
    University of Amsterdam.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Tikkanen, Matti J
    Helsinki University Hospital.
    Lytken Larsen, Mogens
    Arhus University Hospital.
    Lindahl, Christina
    Pfizer Sweden.
    Pedersen, Terje R
    Oslo University Hospital.
    Adherence-adjusted efficacy with intensive versus standard statin therapy in patients with acute myocardial infarction in the IDEAL study2009Inngår i: EUROPEAN JOURNAL OF CARDIOVASCULAR PREVENTION and REHABILITATION, ISSN 1741-8267, Vol. 16, nr 3, s. 315-320Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background The Incremental Decrease in End Points through Aggressive Lipid Lowering trial showed that the primary endpoint major coronary event was reduced by 11% (0.78-1.01) using atorvastatin 80 mg versus simvastatin 20-40 mg in patients with coronary heart disease (P=0.07). Adherence was high in both treatment groups but significantly higher in patients treated with simvastatin. Design The Incremental Decrease in End Points through Aggressive Lipid Lowering was a prescription trial with a prospective randomized open label endpoint evaluation. Methods and results Adherence was calculated as exposure time on prescribed drugs divided by total follow-up time until death or end of follow-up and was a potential confounder. Adjusting for categorical adherence below or above 80% by two methods revealed that the relative risk reduction of the primary endpoint was more in the region of 15% (P=0.02) than 11% as found unadjusted. Censoring at the first occurrence of a cardiovascular event rather than at death increased this estimate to 17% (P=0.02). Noncardiovascular mortality was reduced on atorvastatin treatment by 21% (1-37%) after adjustment for adherence, whereas such reduction was not observed for cardiovascular mortality. Conclusion This study found that the difference in adherence between treatment groups may have underestimated the true effect of the treatment differential. Usage of prospective randomized open label endpoint evaluation design should be carefully considered when well-known treatments are compared with rather new ones and especially in segments where patients could be more vulnerable, as in the elderly. Nonadherers in a clinical trial may be at especially high risk of fatal and nonfatal endpoints from various diseases and should be carefully monitored.

  • 103.
    Holmer, Helene
    et al.
    Centralsjukhuset, Kristianstad.
    Ekman, Bertil
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Björk, Jonas
    Lund University Hospital.
    Nordström, Carl-Henrik
    Lund University Hospital.
    Popovic, Vera
    Centralsjukhuset, Kristianstad.
    Siversson, AnnBritt
    Centralsjukhuset, Kristianstad.
    Hypothalamic involvement predicts cardiovascular risk in adults with childhood onset craniopharyngioma on long-term GH therapy.2009Inngår i: European Journal of Endocrinology, ISSN 0804-4643, E-ISSN 1479-683X, Vol. 16, s. 671-679Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Context: Craniopharyngioma patients without GH therapy are at an increased cardiovascular disease (CVD) risk and particularly concerning women. No previous study on long-term GH therapy in adults with childhood onset (CO) craniopharyngioma was identified.

    Objective: To investigate CVD risk in adults with CO craniopharyngioma on complete hormone replacement, including long-term GH therapy, and to investigate the impact of disease-related factors on CVD risk.

    Design and participants: In a cross-sectional study of operated CO craniopharyngiomas (1958–2000) from a defined area of Sweden (2.5 million), we enrolled 42 patients (20 women) with a median age of 28 years (range 17–57) and assessed CVD risk of 20 (4–40) years after first operation. Comparisons were made with matched controls and between patients with tumor growth into the third ventricle (TGTV) versus non-TGTV. GH therapy was 10–12 years in women and men.

    Results: In comparison with controls, both male and female patients had increased body mass index, fat mass, insulin, and leptin levels. Overall, while not significantly increased in male patients, 55–60% of female patients had a medium–high CVD risk, compared with 10–20% in controls. An increased CVD risk (all P<0.05) and higher levels of fat mass and insulin were recorded in the TGTV group versus the non-TGTV group. Late puberty induction and lack of androgens were shown in female patients.

    Conclusions: Adult patients with CO craniopharyngioma, especially those with TGTV, have persistently increased CVD risk. Conventional hormone substitution, including GH, is insufficient to normalize CVD risk, suggesting an important role for irreversible hypothalamic dysfunction.

  • 104.
    Holmer, Helene
    et al.
    Central Hospital, Kristianstad, Sweden.
    Pozarek, Gabriella
    Lund-Malmö University Hospital, Lund, Sweden.
    Wirfält, Elisabet
    Lund University, Sweden.
    Popovic, Vera
    University Clinical Center, Belgrade, Serbia.
    Ekman, Bertil
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Björk, Jonas
    Lund University Hospital, Sweden.
    Erfurth, Eva-Marie
    Lund-Malmö University Hospital, Lund, Sweden.
    Reduced Energy Expenditure and Impaired Feeding-Related Signals But Not High Energy Intake Reinforces Hypothalamic Obesity in Adults with Childhood Onset Craniopharyngioma2010Inngår i: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 95, nr 12, s. 5395-5402Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Context: Obesity is a frequent manifestation of hypothalamic damage from a craniopharyngioma (CP). It is not yet clarified whether the obesity is due to alterations in energy expenditure, i.e. basal metabolic rate (BMR) and physical activity, or to increased energy intake (EI). Objective: The aim was to investigate whether energy expenditure and EI differed between childhood onset CP patients and matched population controls and whether these measures were related to hypothalamic damage, as tumor growth into the third ventricle (TGTV). Design and Methods: Forty-two CP patients (20 women) aged 28 yr (range, 17-57 yr) operated between 1958 and 2000 in the South Medical Region of Sweden (population, 2.5 million) were studied. Body composition, satiety hormones, BMR (indirect calorimetry), physical activity, EI, and attitudes toward eating were assessed. Comparisons were made with matched controls and between patients with (n = 25) and without (n = 17) TGTV. Results: After adjustment, patients had lower BMR compared to controls (-90 kcal/24 h; P = 0.02) and also had lower EI (1778 vs. 2094 kcal/24h; P = 0.008), and the EI/BMR ratio was significantly lower in TGTV patients. Similar dietary macronutrient composition was found, and only significantly higher scales in restricting food intake were recorded in patients. Ghrelin levels were significantly lower in patients, whereas serum insulin and leptin levels were higher (P less than 0.001), and both ghrelin and insulin correlated significantly to tumor growth. Lower levels of physical activity (P less than 0.01) were recorded in patients. Conclusions: The major mechanisms that reinforced obesity were hypothalamic damage causing disrupted or impaired sensitivity to feeding-related signals for leptin, insulin, and ghrelin, and reductions in both BMR and physical activity.

  • 105.
    Holmer, Helene
    et al.
    Centralsjukhuset, Kristianstad, Sweden.
    Svensson, Johan
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Rylander, Lars
    Lund University, Sweden.
    Johansson, Gudmundur
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Rosén, Thord
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Bengtsson, Bengt Åke
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Thorén, Marja
    Karolinska University Hospital Solna, Stockholm, Sweden .
    Höybye, Charlotte
    Karolinska University Hospital Solna, Stockholm, Sweden.
    Degerblad, Marie
    Karolinska University Hospital Solna, Stockholm, Sweden.
    Bramnert, Margareta
    University Hospital, Malmö, Sweden.
    Hägg, Erik
    University Hospital, Umeå, Sweden.
    Edén Engström, Britt
    Uppsala University Hospital, Sweden.
    Ekman, Bertil
    Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Norrving, Bo
    Lund University Hospital, Sweden.
    Hagmar, Lars
    Lund University, Sweden.
    Erfurth, Eva-Marie
    Lund University Hospital, Sweden.
    Nonfatal stroke, cardiac disease, and diabetes mellitus in hypopituitary patients on hormone replacement including growth hormone2007Inngår i: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 92, nr 9, s. 3560-3567Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Context: The impact of long-term GH replacement on cerebrovascular and cardiovascular diseases and diabetes mellitus in hypopituitary patients is unknown. Objective: The incidence of nonfatal stroke and cardiac events, and prevalence of type 2 diabetes mellitus (T2D) and cardioprotective medication were compared between cohorts of GH-deficient (GHD) patients and population controls. Design and Participants: The incidence of nonfatal stroke and cardiac events was estimated retrospectively from questionnaires in 750 GHD patients and 2314 matched population controls. A prevalence of T2D and cardioprotective medication was recorded at the distribution of questionnaires. Time since first pituitary deficiency to start of GH therapy was 4 and 2 yr, and time on GH therapy was 6 yr for GHD women and men, respectively. Results: Lifelong incidence of nonfatal stroke was tripled in GHD women and doubled in GHD men, but a decline was seen in both genders during periods after first pituitary hormone deficiency and GHD, during which most patients had GH therapy. The lifelong incidence of nonfatal cardiac events declined in GHD men during first pituitary hormone deficiency and GHD periods. GHD women had a higher prevalence of T2D and lipid-lowering medication, whereas GHD men had a higher prevalence of antihypertensive medication. Conclusions: The declined risks of nonfatal stroke in both genders and of nonfatal cardiac events in GHD men during periods on GH replacement may be caused by prescription of cardioprotective drugs and 6-yr GH replacement. GHD women had an increased prevalence of T2D, partly attributed to higher body mass index and lower physical activity. Copyright © 2007 by The Endocrine Society.

  • 106.
    Holmer, Helene
    et al.
    Centralsjukhuset, Kristianstad, Sweden.
    Svensson, Johan
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Rylander, Lars
    Lund University, Sweden.
    Johansson, Gudmundur
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Rosén, Thord
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Bengtsson, Bengt-Åke
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Thorén, Marja
    Karolinska University Hospital Solna, Stockholm, Sweden .
    Höybye, Charlotte
    Karolinska University Hospital Solna, Stockholm, Sweden .
    Degerblad, Marie
    Karolinska University Hospital Solna, Stockholm, Sweden .
    Bramnert, Margareta
    University Hospital, Malmö, Sweden.
    Hägg, Erik
    University Hospital, Umeå, Sweden.
    Engström, Britt Edén
    Uppsala University Hospital, Sweden.
    Ekman, Bertil
    Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Thorngren, Karl-Göran
    University Hospital, Lund, Sweden.
    Hagmar, Lars
    Lund University, Sweden.
    Erfurth, Eva-Marie
    Lund University Hospital, Sweden.
    Fracture incidence in GH-deficient patients on complete hormone replacement including GH2007Inngår i: Journal of Bone and Mineral Research, ISSN 0884-0431, E-ISSN 1523-4681, Vol. 22, nr 12, s. 1842-1850Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Fracture risk in GHD patients is not definitely established. Studying fracture incidence in 832 patients on GH therapy and 2581 matched population controls, we recorded a doubled fracture risk in CO GHD women, but a significantly lower fracture risk in AO GHD men. Introduction: The objective of this study was to evaluate fracture incidence in patients wilh confirmed growth hormone deficiency (GHD) on replacement therapy (including growth hormone [GH]) compared with population controls, while also taking potential confounders and effect modifiers into account. Materials and Methods: Eight hundred thirty-two patients with GHD and 2581 matched population controls answered a questionnaire about fractures and other background information. Incidence rate ratio (IRR) and 95% CI for first fracture were estimated. The median time on GH therapy for childhood onset (CO) GHD men and women was 15 and 12 yr, respectively, and 6 and 5 yr for adult onset (AO) GHD men and women, respectively. Results: A more than doubled risk (IRR, 2.29, 95% CI, 1.23-4.28) for nonosteoporotic fractures was recorded in women with CO GHD, whereas no risk increase was observed among CO GHD men (IRR. 0.61) and AO GHD women (IRR, 1.08). A significantly decreased incidence of fractures (IRR, 0.54, 95% CI 0.34-0.86) was recorded in AO GHD men. Conclusions: Increased fracture risk in CO GHD women can most likely be explained by interaction between oral estrogen and the GH-IGF-I axis. The adequate substitution rate of testosterone (90%) and GH (94%) may have resulted in significantly lower fracture risk in AO GHD men.

  • 107.
    Janke, J
    et al.
    Franz Volhard Clinic.
    Schupp, M
    n/a.
    Engeli, S
    n/a.
    Gorzelniak, K
    n/a.
    Boschmann, M
    n/a.
    Sauma, Lilian
    Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Nystrom, Fredrik H
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Jordan, J
    n/a.
    Luft, FC
    n/a.
    Sharma, AM
    n/a.
    Angiotensin type 1 receptor antagonists induce human in-vitro adipogenesis through peroxisome prolifertor-activated receptor-gamma activation2006Inngår i: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 24, nr 9, s. 1809-1816Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVE: In clonal animal cells, certain angiotensin receptor blockers (ARB) activate the peroxisome proliferator-activated receptor-gamma (PPARgamma). The aim of this work was to validate that observation in human cells and humans. METHODS: We investigated the induction of in-vitro adipogenesis and the activation of PPARgamma-target genes, adiponectin and lipoprotein lipase, by ARB in human preadipocytes. We also studied PPARgamma response-element-driven luciferase reporter gene activation in human adipocytes. Finally, we treated 14 obese men for 10 days with placebo crossed over with 150 mg/day irbesartan. Subcutaneous fat was analyzed for mRNA expression of adiponectin and lipoprotein lipase. RESULTS: Telmisartan and irbesartan, and to a lesser degree losartan, induced adipogenesis and activated PPARgamma-target genes. This stimulation of PPARgamma-target genes was prevented by the PPARgamma antagonist GW9662. Eprosartan had no effect. Paradoxically, all ARB activated the luciferase reporter gene. PPARgamma activity increased approximately two-fold with pioglitazone and 1.5-fold with the ARB in all assays. In the cross-over clinical study, irbesartan lowered blood pressure but had no effect on adiponectin or lipoprotein lipase mRNA expression. CONCLUSIONS: Our data are the first to show that ARB induce adipogenesis and PPARgamma-target gene expression in human adipocytes. Pharmacokinetic differences may contribute to the heterogeneous effects on metabolism and preadipocyte differentiation. In humans, larger doses of ARB, longer treatments, or both may be required to activate PPARgamma in adipose cells.

  • 108. Jardine, AG
    et al.
    Fellstrom, B
    Logan, JO
    Cole, E
    Nyberg, G
    Gronhagen-Riska, C
    Madsen, S
    Neumayer, HH
    Maes, B
    Ambuhl, P
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Pedersen, T
    Holdaas, H
    Cardiovascular risk and renal transplantation: Post hoc analyses of the Assessment of Lescol in Renal Transplantation (ALERT) study2005Inngår i: American Journal of Kidney Diseases, ISSN 0272-6386, E-ISSN 1523-6838, Vol. 46, nr 3, s. 529-536Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background Renal transplantation is associated with an increased risk for premature cardiovascular disease. We analyzed the data in the placebo arm of Assessment of Lescol in Renal Transplantation (ALERT) to improve our understanding of the relationship between cardiovascular risk factors and outcomes in this unique population. Methods: We performed Cox survival analysis for myocardial infarction, cardiac death, and noncardiac death in 1,052 patients recruited to the placebo arm of ALERT. These subjects were aged 30 to 75 years, had stable graft function at least 6 months after transplantation, had a serum total cholesterol level between 155 and 348 mg/dL (4 and 9 mmol/L), and were receiving cyclosporine-based immunosuppression. Results: The results confirm previous studies. In multivarlate analysis, preexisting coronary heart disease (hazard ratio [HR], 3.69, P < 0.001), total cholesterol level (HR, 1.55 per 50 mg/dL, P = 0.0045), and prior acute rejection (HR, 2.36, P = 0.0023) were independent risk factors. Conversely, independent risk factors for cardiac death were age (HR, 1.58 per decade, P = 0.0033), diabetes (HR, 3.35, P = 0.0002), ST-T changes on the ECG (HR, 3.17, P = 0.0004), and serum creatinine level (HR, 2.65 per milligram per deciliter, P < 0.0001). Conclusion: This analysis confirms that renal transplant recipients share risk factors for myocardial infarction and cardiac death with the general population. However, the pattern of risk factors and their relationship with outcomes is atypical, highlighting the unique nature of cardiovascular risk in transplant recipients.

  • 109.
    Jennersjo, P E
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet.
    Wiréhn, Ann-Britt
    Linköpings universitet, Institutionen för medicin och hälsa, Hälsa och samhälle. Linköpings universitet, Filosofiska fakulteten.
    Länne, Toste
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärtcentrum, Thorax-kärlkliniken.
    Engvall, Jan
    Linköpings universitet, Institutionen för medicin och hälsa, Klinisk fysiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärtcentrum, Fysiologiska kliniken.
    Nyström, Fredrik
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Östgren, Carl Johan
    Linköpings universitet, Institutionen för medicin och hälsa, Allmänmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Närsjukvården i västra Östergötland, Primärvården i västra länsdelen.
    Circadian blood pressure variation in patients with type 2 diabetes - relationship between dipper status and early cardiovascular organ damage2009Inngår i: in DIABETOLOGIA, vol 52, 2009, Vol. 52, s. S430-S430Konferansepaper (Fagfellevurdert)
    Abstract [en]

    n/a

  • 110.
    Jerotskaja, Jana
    et al.
    Department of Biomedical Engineering, Technomedicum, Tallinn University of Technology, Tallinn, Estonia.
    Uhlin, Fredrik
    Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Lauri, Kai
    Department of Biomedical Engineering, Technomedicum, Tallinn University of Technology, Tallinn, Estonia.
    Tanner, Risto
    Department of Biomedical Engineering, Technomedicum, Tallinn University of Technology, Tallinn, Estonia.
    Luman, Merike
    Department of Dialysis and Nephrology, North-Estonian Regional Hospital, Tallinn, Estonia.
    Fridolin, Ivo
    Department of Biomedical Engineering, Technomedicum, Tallinn University of Technology, Tallinn, Estonia.
    A multicentre study of an enhanced optical method for measuring concentration of uric acid removed during dialysis.2009Inngår i: Annual International Conference of the IEEE Engineering in Medicine and Biology Society, 2009. EMBC 2009, 2009, nr 1, s. 1477-1480Konferansepaper (Fagfellevurdert)
    Abstract [en]

    The aim of this study was to compare concentration measurements of uric acid (UA) removed during dialysis by two algorithms based on UV-absorbance and the 1st derivate of UV absorbance. Ten uremic patients from Tallinn and ten from Linköping, during 30+40 haemodialysis treatments, were followed at the Departments of Dialysis and Nephrology at North-Estonian Medical Centre and at Linköping University Hospital. The dialysate samples were taken and analyzed by means of UA concentration at the chemical laboratory and with a double-beam spectrophotometer. UV absorbance and derivate of UV absorbance was transformed into UA concentration in the spent dialysate using the regression models from the calibration set of material, noted as UV-absorbance (UV_A) and the 1st derivate of UV absorbance (UV_D) method. These models were tested on validation set of material and concentrations of UA from the two methods were compared regarding mean values and SD. Mean concentration of UA were 52.7 +/- 25.0 micromol/l measured at the chemical laboratory (UA_Lab), 54.9 +/- 23.8 micromol/l determined by UV_A and 52.9 +/- 23.0 micromol/l determined by UV_D. The results of mean concentrations were not significantly different (p >/= 0.54). The systematic errors were -7.8 % and -3.3% and random errors were 15.8 % and 10.4 % using UV_A and UV_D respectively. The systematic and random errors were significantly different (p < 0.05) indicating that the new algorithm enables more accurate UA estimation.

  • 111.
    Johannsson, G
    et al.
    Sahlgrens University Hospital.
    Nilsson, A G
    Sahlgrens University Hospital.
    Bergthorsdottir, R
    Sahlgrens University Hospital.
    Burman, P A
    Malmo University Hospital.
    Eden Engstrom, B
    Uppsala University Hospital.
    Ekman, Bertil
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Dahlqvist, P
    Umea University Hospital.
    Ryberg, M
    Umea University Hospital.
    Ragnarsson, O
    Sahlgrens University Hospital.
    Wahlberg Topp, Jeanette
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Lennernas, H
    Uppsala University.
    Skrtic, S
    Sahlgrens University Hospital.
    Improved Quality of Life in Patients with Primary Adrenal Insufficiency by Using a Novel Once-Daily Dual Release Hydrocortisone Tablet: A Randomised Controlled, Cross-Over Trial. in ENDOCRINE REVIEWS, vol 31, issue 3, pp2010Inngår i: ENDOCRINE REVIEWS, Endocrine Society , 2010, Vol. 31, nr 3Konferansepaper (Fagfellevurdert)
    Abstract [en]

    n/a

  • 112.
    Johansson, Git S
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Arnqvist, Hans J
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Insulin and IGF-I action on insulin receptors, IGF-I receptors, and hybrid insulin/IGF-I receptors in vascular smooth muscle cells2006Inngår i: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 291, nr 5, s. 1124-1130Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Insulin and insulin-like growth factor I (IGF-I) are known to affect cardiovascular disease. We have investigated ligand binding and the dose-response relationship for insulin and IGF-I on vascular smooth muscle cells (VSMCs) at the receptor level. VSMCs from rat thoracic aorta were serum starved, stimulated with IGF-I or insulin, lysed, immunoprecipitated, and analyzed by Western blot. D-[U-14C]Glucose accumulation and [6-3H]thymidine incorporation into DNA were also measured. Specific binding of both insulin and IGF-I was demonstrated, being higher for IGF-I. Both IGF-I receptor (IGF-IR) and insulin receptor (IR) β-subunits were detected and coprecipitated after immunoprecipitation (IP) against either of the two. No coprecipitation was found after reduction of disulphide bonds with dithiotreitol before IP. After stimulation with 10–10–10–9 M IGF-I, IP of the IGF-IR, or IR β-subunit and immunoblot with anti-phosphotyrosine antibody, we found two distinct bands indicating phosphorylation of both the IGF-IR and the IR β-subunit. Stimulation with 10–10–10–9 M insulin and IP against the IGF-IR did not show phosphorylation of either β-subunit, whereas after IP of the IR we found phosphorylation of the IR β-subunit. [14C]Glucose accumulation and [3H]thymidine incorporation were elevated in cells stimulated with IGF-I at 10–10–10–7 M, reaching maximum by 10–9 M. Insulin stimulation showed measurable effects only at supraphysiological concentrations, 10–8–10–7 M. In conclusion, coprecipitation of both the IGF-IR and the IR β-subunit indicates the presence of hybrid insulin/IGF-I receptors in VSMC. At a physiological concentration, insulin activates the IR but does not affect either glucose metabolism or DNA synthesis, whereas IGF-I both activates the receptor and elicits biological effect.

  • 113.
    Johansson, Git
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Simona Chisalita, Ioana
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Närsjukvården i centrala Östergötland, Akutkliniken.
    Arnqvist, Hans
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Human microvascular endothelial cells are sensitive to IGF-I but resistant to insulin at the receptor level2008Inngår i: Molecular and Cellular Endocrinology, ISSN 0303-7207, E-ISSN 1872-8057, Vol. 296, nr 1-2, s. 58-63Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Human microvascular endothelial cells (HMVEC) are sensitive to IGF-I but insulin resistant and express several times more IGF-I receptors (IGF-IR) than insulin receptors (IR). Our aim was to investigate the mechanism of this insulin resistance in cultured HMVEC by studying receptor activation and signal propagation downstream.

    propagation downstream. The IGF-IR β-subunit and the IR β-subunitwere detected and found to co-precipitate. IRAwas themajor IR isoformexpressed in HMVEC. IGF-I 10−9 to 10−8M phosphorylated its cognate receptor β-subunit. IGF- I also phosphorylated the IR β-subunit at 10−9 M. Phosphorylation of insulin receptor substrate 1 was obtained by IGF-I 10−9 to 10−8 M. Akt was phosphorylated by IGF-I at 10−8 to 10−7M and by insulin 10−7M. IGF-I at 10−8 to 10−6M significantly increased DNA-synthesis. We conclude that microvascular endothelial cells are sensitive to IGF-I but resistant to insulin due to a preponderance of IGF-I receptors and sequestration of insulin receptors into insulin/IGF-I hybrid receptors.

  • 114.
    Johansson, Git
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Svedjeholm, Rolf
    Linköpings universitet, Institutionen för medicin och hälsa, Thoraxkirurgi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärtcentrum, Thorax-kärlkliniken.
    Arnqvist, Hans
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    High expression of IGF-I receptors compared to insulin receptors in human mammary arteryManuskript (Annet vitenskapelig)
    Abstract [en]

    Aims/hypothesis: Cultured endothelial and vascular smooth muscle cells from different vascular beds express several fold more IGF-I receptors (IGF-IR) than insulin receptors (IR). The aim of this study was to investigate the gene expression of IR and IGF-IR in tissue samples from the left internal mammary artery (LIMA) to see if there is a higher gene expression of IGF-IR compared to IR in arterial tissue in vivo.

    Methods: Samples from LIMA (n=16) were obtained at coronary bypass surgery, immediately frozen in liquid nitrogen and stored at -70°C until analysis. The samples were thawed, placed on ice and dissected free from surrounding connective tissue and fat, homogenized and total RNA was extracted. Receptor mRNA was analyzed by quantitative real time RT-PCR and comparison of CT-values.

    Results: LIMA samples were obtained from 16 patients, 10 non-diabetic and 6 diabetic patients. Gene expression of IGF-IR was detected in all LIMA samples, however, the insulin receptor mRNA was under the detection limit in 4 samples. Compared to IR the gene expression of IGF-IR was 36 fold higher (n=12. p <0.0001). The relative gene expression of IGF-IR to IR in LIMA from non-diabetic patients (n=9) and diabetic patients (n=3) was similar, 39 and 32 fold, respectively.

    Conclusions/interpretation: Our results in mammary artery samples indicate that IGF-IR are more expressed than IR in arterial tissue in vivo.

  • 115. Johansson, Unn-Britt
    et al.
    Amsberg, Susanne
    Hannerz, Lena
    Wredling, Regina
    Adamson, Ulf
    Arnqvist, Hans
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för medicinsk cellbiologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Lins, Per-Eric
    Impaired absorption of insulin aspart from lipohypertrophic injection sites2005Inngår i: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 28, nr 8, s. 2025-2027Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    [No abstract available]

  • 116. Jonasson, L
    et al.
    Linderfalk, C
    Hoeglandssjukhuset, Eksjoe, Sweden Univ Coll Hlth Sci, Jonkoping, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Wikby, A
    Hoeglandssjukhuset, Eksjoe, Sweden Univ Coll Hlth Sci, Jonkoping, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    T lymphocyte activation in stable angina pectoris: The influence of statin treatment.2000Inngår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 102, nr 18, s. 1990-Konferansepaper (Annet vitenskapelig)
  • 117.
    Jonasson, Lena
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Wikby, A.
    Dept. of Nat. Sci. and Biomedicine, School of Health Sciences, Jönköping University, Jönköping, Sweden.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Low serum ß-carotene reflects immune activation in patients with coronary artery disease2003Inngår i: NMCD. Nutrition Metabolism and Cardiovascular Diseases, ISSN 0939-4753, E-ISSN 1590-3729, Vol. 13, nr 3, s. 120-125Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background and Aim: Low serum levels of antioxidant vitamins are associated with coronary artery disease (CAD). An immunomodulatory effect of antioxidants has been proposed. The aim of the study was to investigate whether an increased immune response in CAD patients was associated with suppressed circulating levels of antioxidant vitamins. Methods and Results: Forty-four men with stable angina and angiographically verified CAD were included as well as 69 healthy controls. T cell subsets in peripheral blood were quantified by 3-colour flow cytometry. C-reactive protein (CRP), soluble interleukin-2 receptor (sIL-2R) and the lipophilic antioxidants a-tocopherol, ß-carotene and lycopene were determined in serum. Compared with controls, patients had signs of an enhanced inflammatory activity assessed by significantly increased levels of CRP, sIL-2R and CD4+CD25+T cell subsets. Patients also had significantly lower ß-carotene and lycopene levels whereas a-tocopherol levels did not differ. The increased inflammatory/immune parameters in patients showed a significant inverse relationship to serum ß-carotene but not to lycopene or a-tocopherol. Conclusions: Low serum ß-carotene in CAD patients reflects activation of the immune system. Inflammation should be considered as an important confounding factor when analysing data on ß-carotene and CAD. © 2003, Medikal Press.

  • 118.
    Jormeus, Anders
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Hälsouniversitetet.
    Karlsson, Samuel
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Hälsouniversitetet.
    Dahlgren, Christina
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Hälsouniversitetet.
    Lindström, Torbjörn
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Nyström, Fredrik
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Doubling of Water Intake Increases Daytime Blood Pressure and Reduces Vertigo in Healthy Subjects2010Inngår i: CLINICAL AND EXPERIMENTAL HYPERTENSION, ISSN 1064-1963, Vol. 32, nr 7, s. 439-443Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    We studied the effect of increased water intake on ambulatory blood pressure (BP) in healthy individuals. Blood pressure was recorded after 2 weeks of either regular (RWI) or extra water intake (EWI, an additional 30 ml water/kg body weight per day) in 20 healthy subjects (10 males, 10 females). The extra water intake (RWI: 1.7 +/- 0.59 l, EWI: 3.7 +/- 0.84 l, respectively, p andlt; 0.0001, i.e., an increase of 2 liters) induced an increase in mean arterial daytime BP from 89.0 +/- 5.5 mmHg during RWI to 91.4 +/- 6.4 mmHg during the EWI phase (p = 0.005), while night-time BP was unchanged by the intervention. The visual-analogue-scale (VAS, maximum score of 10) score corresponding to the statement "I often experience vertigo" was 3.1 +/- 2.6 during RWI and decreased to 2.1 +/- 2. 1 during EWI phase (p = 0.008). In conclusion, two liters of extra water intake for 2 weeks significantly increased daytime blood pressure and reduced a sense of vertigo in healthy individuals.

  • 119.
    Järnerot, Gunnar
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi.
    Hertervig, Erik
    Friis-Liby, Ingalill
    Blomquist, Lars
    Karlén, Per
    Grännö, Christer
    Vilien, Mogens
    Ström, Magnus
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Danielsson, Åke
    Verbaan, Hans
    Hellström, Per M
    Magnuson, Anders
    Curman, Bengt
    Infliximab as rescue therapy in severe to moderately severe ulcerative colitis: A randomized, placebo-controlled study2005Inngår i: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 128, nr 7, s. 1805-1811Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background & Aims: Despite treatment with corticosteroids, severe to moderately severe attacks of ulcerative colitis have a high colectomy rate. We intended to find a rescue therapy other than cyclosporin A, which imposes a high risk of side effects and cyclosporine-related mortality. Methods: This was a randomized double-blind trial of infliximab or placebo in severe to moderately severe ulcerative colitis not responding to conventional treatment. Patients were randomized to infliximab/placebo either on day 4 after the initiation of corticosteroid treatment if they fulfilled the index criteria for fulminant ulcerative colitis on day 3 or on day 6-8 if they fulfilled index criteria on day 5-7 for a severe or moderately severe acute attack of ulcerative colitis. Results were analyzed according to the intention-to-treat principle. The primary end point was colectomy or death 3 months after randomization. Secondary end points were clinical and endoscopic remission at that time in patients who did not undergo operation. Results: Forty-five patients were included (24 infliximab and 21 placebo). No patient died. Seven patients in the infliximab group and 14 in the placebo group had a colectomy (P =. 017, odds ratio, 4.9, 95% confidence interval, 1.4-17) within 3 months after randomization. No serious side effects occurred. Three patients in the placebo group required operation for septic complications. Conclusions: Infliximab 4-5 mg/kg is an effective and safe rescue therapy in patients experiencing an acute severe or moderately severe attack of ulcerative colitis not responding to conventional treatment. © 2005 by the American Gastroenterological Association.

  • 120.
    Kald, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Kirurgiska kliniken i Östergötland med verksamhet i Linköping, Norrköping och Motala.
    Juul, Kristian N.
    Coloplast A/S, Clinical Development Global RD, Humlebaek, Denmark.
    Hjortswang, Henrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Sjödahl, Rune
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Kirurgiska kliniken i Östergötland med verksamhet i Linköping, Norrköping och Motala.
    Quality of life is impaired in patients with peristomal bulging of a sigmoid colostomy2008Inngår i: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 43, nr 5, s. 627-633Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective. Peristomal bulging caused by hernia or prolapse is common in patients with a sigmoidostomy. It is not known whether and to what extent peristomal bulging influences various daily activities. The purpose of this study was to evaluate the effects of bulging by using a general and disease-specific health scale (Short Health Scale, SHS) and a stoma-specific quality of life (Stoma-QoL) questionnaire in patients with and without peristomal bulging. Material and methods. Seventy patients with sigmoidostomies were examined to identify peristomal bulging. The mean (SD) age was 71.7 (13.7) years and the patients had had their sigmoidostomies for a mean of 8.1 (7.9) years. Bulging was noticed in 46 patients (66%) while 24 had no bulging. Results. It was found that patients with bulging were at a disadvantage. In the SHS, patients with bulging reported significantly impaired QoL in 3 out of 4 scales regarding symptom load, worry and general sense of well-being. Also, in the Stoma-QoL questionnaire there was a significant difference between patients with and those without bulging. Conclusions. QoL evaluated with a general and disease-specific instrument (SHS) was significantly impaired in patients with bulging around a sigmoidostomy. The Stoma-QoL questionnaire showed a small but statistically significant difference between patients with and those without bulging but the clinical significance is uncertain. Further studies are required to evaluate the role of some of the individual items in the Stoma-QoL questionnaire. © 2008 Taylor & Francis.

  • 121.
    Karling, Pontus
    et al.
    Umeå University Hospital.
    Abrahamsson, Hasse
    Sahlgrens University Hospital.
    Dolk, Anders
    Karolinska University.
    Hallböök, Olof
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Kirurgi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Kirurgiska kliniken i Östergötland med verksamhet i Linköping, Norrköping och Motala.
    Hellstrom, Per M
    Karolinska University.
    Knowles, Charles H
    St Bartholomews & Royal London School of Med & Dent,.
    Kjellstrom, Lars
    Ersta Hospital.
    Lindberg, Greger
    Karolinska University.
    Lindfors, Per-Johan
    Ersta Hospital.
    Nyhlin, Henry
    Ersta Hospital.
    Ohlsson, Bodil
    Malmo University Hospital.
    Schmidt, Peter T
    Karolinska University.
    Sjolund, Kristina
    Trelleborg Hospital.
    Sjovall, Henrik
    Sahlgrens University Hospital.
    Walter, Susanna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Gastroenterologi och hepatologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Function and dysfunction of the colon and anorectum in adults: Working team report of the Swedish Motility Group (SMoG)2009Inngår i: SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, ISSN 0036-5521, Vol. 44, nr 6, s. 646-660Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Symptoms of fecal incontinence and constipation are common in the general population. These can, however, be unreliably reported and are poorly discriminatory for underlying pathophysiology. Furthermore, both symptoms may coexist. In the elderly, fecal impaction always must be excluded. For patients with constipation, colon transit studies, anorectal manometry and defecography may help to identify patients with slow-transit constipation and/or pelvic floor dysfunction. The best documented medical treatments for constipation are the macrogols, lactulose and isphagula. Evolving drugs include lubiprostone, which enhances colonic secretion by activating chloride channels. Surgery is restricted for a highly selected group of patients with severe slow-transit constipation and for those with large rectoceles that demonstrably cause rectal evacuatory impairment. For patients with fecal incontinence that does not resolve on antidiarrheal treatment, functional and structural evaluation with anorectal manometry and endoanal ultrasound or magnetic resonance (MR) of the anal canal may help to guide management. Sacral nerve stimulation is a rapidly evolving alternative when other treatments such as biofeedback and direct sphincter repair have failed. Advances in understanding the pathophysiology as a guide to treatment of patients with constipation and fecal incontinence is a continuing important goal for translational research. The content of this article is a summary of presentations given by the authors at the Fourth Meeting of the Swedish Motility Group, held in Gothenburg in April 2007.

  • 122. Karlsson, J
    et al.
    Lind, L
    Hallberg, P
    Michaelsson, K
    Kurland, L
    Kahan, T
    Malmqvist, K
    Ohman, KP
    Nyström, Fredrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Melhus, H
    Beta1-adrenergic receptor gene polymorphisms and response to beta1-adrenergic receptor blockade in patients with essential hypertension2004Inngår i: Clinical Cardiology, ISSN 0160-9289, E-ISSN 1932-8737, Vol. 27, nr 6 SUPPL. 3, s. 347-350Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Studies suggest that the Ser49Gly and Arg389Gly polymorphisms in the β1-adrenergic receptor might be of functional importance for the cardiovascular system. Both have been associated with altered receptor activity in vitro, and with hypertension and cardiac failure in vivo. Hypothesis: The aim of this study was to test whether these polymorphisms were associated with the change in heart rate or blood pressure in patients with essential hypertension and left ventricular (LV) hypertrophy treated with the β1-adrenergic receptor blocker atenolol. Methods: Blood pressure and heart rate were measured in 101 hypertensive patients with echocardiographically verified LV hypertrophy, randomized in a double-blind study to treatment with either the β1-adrenergic receptor blocker atenolol or the angiotensin II type I receptor antagonist irbesartan. Changes in blood pressure and heart rate were evaluated after 12 weeks. Beta1-adrenergic receptor genotyping was performed using polymerase chain reaction and restriction fragment length polymorphism. Results: We found no significant associations between the changes in the measured variables and either of the two polymorphisms. However, carriers of the 49Gly allele showed a tendency toward a greater reduction in heart rate compared with patients with the Ser/Ser49 genotype (p = 0.06). Conclusions: The Ser49Gly and Arg389Gly β1-adrenergic receptor polymorphisms do not seem to exert a major effect on the changes in heart rate and blood pressure during 12 weeks of treatment with atenolol in patients with essential hypertension and LV hypertrophy.

  • 123.
    Kastelein, John J. P.
    et al.
    Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1100 DD Amsterdam, Netherlands.
    van der Steeg, Wim A.
    Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1100 DD Amsterdam, Netherlands.
    Holme, Ingar
    Ullevaal Univ Hosp, Ctr Prevent Med, Oslo, Norway.
    Gaffney, Michael
    Pfizer Inc, New York, NY USA.
    Cater, Nilo B.
    Pfizer Inc, New York, NY USA.
    Barter, Philip
    Heart Res Inst, Sydney, NSW, Australia.
    Deedwania, Prakash
    Vet Affairs Cent Calif Healthcare Syst, San Francisco, CA USA.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Boekholdt, S. Matthijs
    Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1100 DD Amsterdam, Netherlands.
    Demicco, David A.
    Pfizer Inc, New York, NY USA.
    Szarek, Michael
    Pfizer Inc, New York, NY USA.
    LaRosa, John C.
    SUNY Hlth Sci Ctr, Brooklyn, NY 11203 USA.
    Pedersen, Terje R.
    Ullevaal Univ Hosp, Ctr Prevent Med, Oslo, Norway.
    Grundy, S
    Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
    Lipids, apolipoproteins, and their ratios in relation to cardiovascular events with statin treatment2008Inngår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 117, nr 23, s. 3002-3009Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background - Low-density lipoprotein (LDL)cholesterol is the principal target of lipid-lowering therapy, but recent evidence has suggested more appropriate targets. We compared the relationships of on-treatment levels of LDL cholesterol, non-high-density lipoprotein (HDL) cholesterol, and apolipoprotein B, as well as ratios of total/HDL cholesterol, LDL/HDL cholesterol, and apolipoprotein B/A-I, with the occurrence of cardiovascular events in patients receiving statin therapy. Methods and Results - A post hoc analysis was performed that combined data from 2 prospective, randomized clinical trials in which 10 001 ("Treating to New Targets") and 8888 ("Incremental Decrease in End Points through Aggressive Lipid Lowering") patients with established coronary heart disease were assigned to usual-dose or high-dose statin treatment. In models with LDL cholesterol, non-HDL cholesterol and apolipoprotein B were positively associated with cardiovascular outcome, whereas a positive relationship with LDL cholesterol was lost. In a model that contained non-HDL cholesterol and apolipoprotein B, neither was significant owing to collinearity. Total/HDL cholesterol ratio and the apolipoprotein B/A-I ratio in particular were each more closely associated with outcome than any of the individual proatherogenic lipoprotein parameters. Conclusions - In patients receiving statin therapy, on-treatment levels of non-HDL cholesterol and apolipoprotein B were more closely associated with cardiovascular outcome than levels of LDL cholesterol. Inclusion of measurements of the antiatherogenic lipoprotein fraction further strengthened the relationships. These data support the use of non-HDL cholesterol or apolipoprotein B as novel treatment targets for statin therapy. Given the absence of interventions that have been proven to consistently reduce cardiovascular disease risk through raising plasma levels of HDL cholesterol or apolipoprotein A-I, it seems premature to consider the ratio variables as clinically useful.

  • 124.
    Kechagias, Stergios
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Ernersson, Åsa
    Linköpings universitet, Institutionen för medicin och hälsa, Omvårdnad. Linköpings universitet, Hälsouniversitetet.
    Dahlqvist Leinhard, Olof
    Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Institutionen för medicin och hälsa, Medicinsk radiofysik. Linköpings universitet, Hälsouniversitetet.
    Lundberg, Peter
    Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Radiofysikavdelningen.
    Lindström, Torbjörn
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Nyström, Fredrik
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Länne, Toste
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    Fast-food-based hyper-alimentation can induce rapid and profound elevation of serum alanine aminotransferase in healthy subjects2008Inngår i: Gut, ISSN 0017-5749, E-ISSN 1468-3288, Vol. 57, nr 5, s. 649-654Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

     Objective: To study the effect of fast-food-based hyperalimentation on liver enzymes and hepatic triglyceride content (HTGC).

    Design: Prospective interventional study with parallel control group.

    Setting: University Hospital of Linko¨ping, Sweden.

    Participants: 12 healthy men and six healthy women with a mean (SD) age of 26 (6.6) years and a matched control group.

    Intervention: Subjects in the intervention group aimed for a body weight increase of 5–15% by eating at least two fast-food-based meals a day with the goal to double the regular caloric intake in combination with adoption of a sedentary lifestyle for 4 weeks.

    Main outcome measures: Weekly changes of serum aminotransferases and HTGC measured by proton nuclear magnetic resonance spectroscopy at baseline and after the intervention.

    Results: Subjects in the intervention group increased from 67.6 (9.1) kg to 74.0 (11) kg in weight (p,0.001). Serum ALT increased from 22.1 (11.4) U/l at study start to an individual mean maximum level of 97 (103) U/l (range 19.4–447 U/l). Eleven of the 18 subjectspersistently showed ALT above reference limits (women .19 U/l, men .30 U/l) during the intervention. Sugar (mono- and disaccharides) intake during week 3 correlated with the maximal ALT/baseline ALT ratio(r=0.62, p=0.006). HTGC increased from 1.1 (1.9)% to 2.8 (4.8)%, although this was not related to the increase in ALT levels. ALT levels were unchanged in controls.

    Conclusion: Hyper-alimentation per se can induce profound ALT elevations in less than 4 weeks. Our study clearly shows that in the evaluation of subjects with elevated ALT the medical history should include not only questions about alcohol intake but also explore whetherrecent excessive food intake has occurred.

  • 125. Kinlay, S
    et al.
    Libby, P
    Ganz, P
    Schwartz, GG
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Leslie, SJ
    Sasiela, WJ
    Szarek, M
    Early intervention with atorvastatin modulates Th1/Th2 imbalance in patients with acute coronary syndrome: From bedside to bench - Response2004Inngår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 109, nr 18, s. E213-E214Annet (Annet vitenskapelig)
  • 126. Kinlay, S
    et al.
    Schwartz, G
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Rifai, N
    Sasiela, W
    Szarek, M
    Ganz, P
    Libby, P
    Effect of atorvastatin on risk of recurrent cardiovascular events after an acute coronary syndrome associated with high soluble CD40 ligand in the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study2004Inngår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 110, nr 4, s. 386-391Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background - Patients with acute coronary syndromes have elevated plasma levels of the proinflammatory, prothrombotic cytokine CD40 ligand (sCD40L). Statins inhibit CD40L signaling in vitro, but there are no prospective studies of statins and sCD40L in acute coronary syndromes. Methods and Results - We measured sCD40L in subjects with an acute coronary syndrome enrolled in the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study. Subjects were randomized in this double-blind trial to atorvastatin 80 mg/d or placebo for 16 weeks. Plasma CD40L was measured from 2908 (94%) of 3086 subjects at baseline and 2352 (76%) at 16 weeks. Odds ratios (Ors) and 95% Cis from logistic regression models assessed the risk of recurrent cardiovascular events over 16 weeks (death, nonfatal myocardial infarction, cardiac arrest, and worsening angina requiring rehospitalization) in the placebo group from baseline sCD40L and the effect of atorvastatin on the risk associated with CD40L in all subjects. The effects of atorvastatin on plasma concentrations of CD40L were assessed by Wilcoxon tests. There was a threshold effect, with only high sCD40L (>90th centile) being a risk factor for a recurrent cardiovascular event (OR 1.86, 95% CI 1.25 to 2.77). This risk was abolished by atorvastatin (OR 1.09, 95% CI 0.69 to 1.76), which reduced the risk by 48%. Atorvastatin had only a modest effect on sCD40L (P=0-08). Conclusions - In patients with acute coronary syndromes, atorvastatin abrogated the risk of recurrent cardiovascular events associated with high sCD40L. Early statin therapy after acute coronary syndromes counters the risk associated with elevated sCD40L.

  • 127.
    Kristenson, Margareta
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för hälsa och samhälle, Socialmedicin och folkhälsovetenskap. Östergötlands Läns Landsting, Folkhälsovetenskapligt centrum, Folkhälsovetenskapligt centrum.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Kucinskiene, Zita
    Vilnius University, Lithuania.
    Good self-rated health is related to psychosocial resources and a strong cortisol response to acute stress: The LiVicordia study of middle-aged men2005Inngår i: International Journal of Behavioral Medicine, ISSN 1070-5503, E-ISSN 1532-7558, Vol. 12, nr 3, s. 153-160Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Self-rated health (SRH) is a strong predictor for disease and death. The relations among SRH, psychosocial factors, and cortisol dynamics were tested using pooled data from the LiVicordia study of 50-year-old men in Lithuania (n = 94) and Sweden (n = 89), controlling for effect of residence. SRH was assessed by " How would you assess your own health?" A standardized laboratory stress test included measures of cortisol in serum and saliva. Good SRH related to high scale scores of decision latitude, social support at work, coping, self-esteem, and sense of coherence, to low scores of overcommitment (all p < .01) and vital exhaustion (r = -0.40, p < 0.001), to low concentrations of saliva baseline cortisol (r = -.26, p = .001), and to a strong cortisol response to stress (r = .27, p = .001). Findings that good SRH related to favorable psychosocial characteristics and to a dynamic cortisol stress response indicate a possible explanation for observed lower risk for disease and death in this state. Copyright © 2005 by Lawrence Erlbaum Associates, Inc.

  • 128.
    Krusinska, Eva
    et al.
    Univesity of Wroclaw Polen.
    Babic, Ankica
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik.
    Mathiesen, Ulrik
    Oskarshamn Hospital .
    Wigertz, Ove
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik.
    Bodemar, Göran
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Statistical decision support in patients with elevated routine laboratory liver tests1992Inngår i: Theoretical surgery, ISSN 0179-8669, Vol. 7, nr 3, s. 153-153Artikkel i tidsskrift (Fagfellevurdert)
  • 129.
    Krusinska, Ewa
    et al.
    University of Wroclaw .
    Babic, Ankica
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik.
    Chowdhury, Shamsul
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik.
    Wigertz, Ove
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik.
    Bodemar, Göran
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Integrated approach for designing medical decision support systems with knowledge extracted from clinical databases by statistical methods1991Inngår i: SCAMC,1991, MCGRAWHILL, Inc , 1991, s. 353-Konferansepaper (Fagfellevurdert)
  • 130.
    Krusinska, Ewa
    et al.
    Dept of Mathemtics and iInformatics Paris.
    Babic, Ankica
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik.
    Mathiesen, Ulrik
    Oskarshamns hospital .
    Chowdhury, Shamsul
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik.
    Wigertz, Ove
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik.
    Bodemar, Göran
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Franzén, Lennart
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Patologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk patologi och klinisk genetik.
    A statistically rule-based decision support system for the management of patients with suspected liver disease1993Inngår i: Vol. 18, nr 2, s. 113-130Artikkel i tidsskrift (Fagfellevurdert)
  • 131.
    Krusinska, Ewa
    et al.
    University of Wroclaw Poland.
    Babic, Ankica
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik.
    Mathiesen, Ulrik
    Oskarshamn Hospital .
    Franzén, Lennart
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Patologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk patologi och klinisk genetik.
    Foberg, Ulla
    Dept of Infectious diseases Linköping.
    Frydén, Aril
    Linköpings universitet, Institutionen för molekylär och klinisk medicin.
    Bodemar, Göran
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Wigertz, Ove
    Linköpings universitet, Tekniska högskolan. Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik.
    Empirical modelling versus commonly applied data analysis techniques as used for decision support in liver diseases1992Inngår i: MEDINFO92,1992, Amsterdam: Elsevier Science Publ , 1992, s. 949-Konferansepaper (Fagfellevurdert)
  • 132.
    Kurland, L
    et al.
    Univ Uppsala Hosp, Dept Internal Med, S-75185 Uppsala, Sweden Karolinska Inst, Danderyd, Sweden Fac Hlth Sci Linkoping, Dept Med & Care, Linkoping, Sweden.
    Melhus, H
    Univ Uppsala Hosp, Dept Internal Med, S-75185 Uppsala, Sweden Karolinska Inst, Danderyd, Sweden Fac Hlth Sci Linkoping, Dept Med & Care, Linkoping, Sweden.
    Kahan, T
    Univ Uppsala Hosp, Dept Internal Med, S-75185 Uppsala, Sweden Karolinska Inst, Danderyd, Sweden Fac Hlth Sci Linkoping, Dept Med & Care, Linkoping, Sweden.
    Malmquist, K
    Univ Uppsala Hosp, Dept Internal Med, S-75185 Uppsala, Sweden Karolinska Inst, Danderyd, Sweden Fac Hlth Sci Linkoping, Dept Med & Care, Linkoping, Sweden.
    Ohman, KP
    Univ Uppsala Hosp, Dept Internal Med, S-75185 Uppsala, Sweden Karolinska Inst, Danderyd, Sweden Fac Hlth Sci Linkoping, Dept Med & Care, Linkoping, Sweden.
    Nyström, Fredrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Hagg, A
    Univ Uppsala Hosp, Dept Internal Med, S-75185 Uppsala, Sweden Karolinska Inst, Danderyd, Sweden Fac Hlth Sci Linkoping, Dept Med & Care, Linkoping, Sweden.
    Lind, L
    ACE-gene polymorphism predicts blood pressure response to AT1-receptor antagonist treatment in hypertensive patients2000Inngår i: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 18, s. S165-S165Konferansepaper (Annet vitenskapelig)
  • 133.
    Kurland, L.
    et al.
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden, Department of Internal Medicine, Uppsala University Hospital, SE-751 85, Uppsala, Sweden.
    Melhus, H.
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Karlsson, J.
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Kahan, T.
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital.
    Malmqvist, K.
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital.
    Ohman, K.P.
    Nyström, Fredrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Hagg, A.
    Hägg, A., Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Lind, L.
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Angiotensin converting enzyme gene polymorphism predicts blood pressure response to angiotensin II receptor type 1 antagonist treatment in hypertensive patients2001Inngår i: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 19, nr 10, s. 1783-1787Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objectives To determine whether polymorphisms in the renin-angiotensin system can predict blood pressure-lowering response to antihypertensive treatment, more specifically, in response to treatment with irbesartan or atenolol. Design and methods Eighty-six patients with hypertension were randomized to double-blind treatment with either the angiotensin II type 1 receptor antagonist irbesartan or the ß1 adrenergic receptor blocker atenolol and followed for 3 months. We analysed angiotensinogen T174M and M235T, angiotensin converting enzyme (ACE) I/D and angiotensin II type 1 receptor A1166C polymorphisms and related them to blood pressure reduction. Results The mean reductions in blood pressure were similar for both treatments. In the irbesartan group, individuals homozygous for the ACE gene I allele showed a greater reduction in diastolic blood pressure, exceeding those with the D allele (-18±11 SD versus -7±10 mmHg, P=0.0096). This was not the case during treatment with atenolol, and the interaction term between type of treatment and ACE II genotype was significant (P=0.0176). The angiotensinogen and angiotensin II type 1 receptor polymorhisms were not related to the response to treatment Conclusions ACE genotyping predicted the blood pressure-lowering response to antihypertensive treatment with irbesartan but not atenolol. Thus, specific genotypes might predict the response to specific antihypertensive treatment. © 2001 Lippincott Williams & Wilkins.

  • 134.
    Kurland, L.
    et al.
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden, Department of Internal Medicine, Uppsala University Hospital, SE-751 85 Uppsala, Sweden.
    Melhus, H.akan
    Melhus, H.åkan, Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Karlsson, J.
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Kahan, T.
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital, Danderyd, Sweden.
    Malmqvist, K.
    Division of Internal Medicine, Karolinska Institute, Danderyd Hospital, Danderyd, Sweden.
    Öhman, P.
    Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi. Linköpings universitet, Hälsouniversitetet.
    Nyström, Fredrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Hagg, A.
    Hägg, A., Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Lind, L.
    Department of Internal Medicine, Uppsala University Hospital, Uppsala, Sweden.
    Aldosterone synthase (CYP11B2) -344 C/T polymorphism is related to antihypertensive response: Results from the Swedish Irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA) trial2002Inngår i: American Journal of Hypertension, ISSN 0895-7061, E-ISSN 1941-7225, Vol. 15, nr 5, s. 389-393Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Our aim was to determine whether the aldosterone synthase (CYP11B2) -344 C/T polymorphism was associated with the blood pressure (BP)-lowering response to antihypertensive treatment. Methods: Patients with mild-to-moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind study to receive treatment with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan (n = 43), or the ß1-adrenergic receptor blocker atenolol (n = 43). The aldosterone synthase (CYP11B2) -344 C/T polymorphism was analyzed using solid-phase minisequencing and related to BP reduction after 3 months treatment. Serum aldosterone levels were measured. Results: After 3 months treatment the mean reductions in BP were similar for both treatment groups. When assessing the systolic BP reduction in the irbesartan group, patients with the TT variant had a more pronounced reduction (-21 ± 19 SD mm Hg, n = 17) than both the TC (-14 ± 18 mm Hg, n = 18) and CC (0 ± 17 mm Hg, n = 8) genotypes (P = .04). There was no association between this polymorphism and the diastolic BP response. The -344 C/T polymorphism was not associated with the BP response to atenolol. Nor was it related to the baseline serum aldosterone level. Conclusions: The aldosterone synthase -344 C/T polymorphism was related to the BP-lowering response in hypertensive patients treated with the AT1-receptor antagonist irbesartan. © 2002 American Journal of Hypertension, Ltd.

  • 135.
    L Ohsfeldt, R
    et al.
    Department Hlth Policy and Management, College Stn, USA.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Jensen, M M
    AstraZeneca.
    Gandhi, S K
    AstraZeneca.
    Paulsson, T
    AstraZeneca.
    The cost-effectiveness of rosuvastatin 20 mg for the prevention of cardiovascular morbidity and mortality - a swedish economic evaluation of the JUPITER trial in EUROPEAN HEART JOURNAL, vol 31, issue , pp 225-2252010Inngår i: EUROPEAN HEART JOURNAL, Oxford University Press , 2010, Vol. 31, s. 225-225Konferansepaper (Fagfellevurdert)
    Abstract [en]

    n/a

  • 136.
    Ladenson, Paul W
    et al.
    Johns Hopkins University.
    Kristensen, Jens D
    Karo Bio.
    Ridgway, E Chester
    University of Colorado.
    Olsson, Anders
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Carlsson, Bo
    Karo Bio.
    Klein, Irwin
    N Shore University Hospital.
    Baxter, John D
    Methodist Hospital.
    Angelin, Bo
    Karolinska University Hospital.
    Use of the Thyroid Hormone Analogue Eprotirome in Statin-Treated Dyslipidemia2010Inngår i: NEW ENGLAND JOURNAL OF MEDICINE, ISSN 0028-4793, Vol. 362, nr 10, s. 906-916Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND Dyslipidemia increases the risk of atherosclerotic cardiovascular disease and is incompletely reversed by statin therapy alone in many patients. Thyroid hormone lowers levels of serum low-density lipoprotein (LDL) cholesterol and has other potentially favorable actions on lipoprotein metabolism. Consequently, thyromimetic drugs hold promise as lipid-lowering agents if adverse effects can be avoided. METHODS We performed a randomized, placebo-controlled, double-blind, multicenter trial to assess the safety and efficacy of the thyromimetic compound eprotirome (KB2115) in lowering the level of serum LDL cholesterol in patients with hypercholesterolemia who were already receiving simvastatin or atorvastatin. In addition to statin treatment, patients received either eprotirome (at a dose of 25, 50, or 100 mu g per day) or placebo. Secondary outcomes were changes in levels of serum apolipoprotein B, triglycerides, and Lp(a) lipoprotein. Patients were monitored for potential adverse thyromimetic effects on the heart, bone, and pituitary. RESULTS The addition of placebo or eprotirome at a dose of 25, 50, or 100 mu g daily to statin treatment for 12 weeks reduced the mean level of serum LDL cholesterol from 141 mg per deciliter (3.6 mmol per liter) to 127, 113, 99, and 94 mg per deciliter (3.3, 2.9, 2.6, and 2.4 mmol per liter), respectively, (mean reduction from baseline, 7%, 22%, 28%, and 32%). Similar reductions were seen in levels of serum apolipoprotein B, triglycerides, and Lp(a) lipoprotein. Eprotirome therapy was not associated with adverse effects on the heart or bone. No change in levels of serum thyrotropin or triiodothyronine was detected, although the thyroxine level decreased in patients receiving eprotirome. CONCLUSIONS In this 12-week trial, the thyroid hormone analogue eprotirome was associated with decreases in levels of atherogenic lipoproteins in patients receiving treatment with statins.

  • 137.
    Ladenson, Paul W
    et al.
    Johns Hopkins University.
    Kristensen, Jens D
    Karo Bio AB.
    Ridgway, E Chester
    University of Colorado.
    Olsson, Anders G
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Carlsson, Bo
    Klein, Irwin
    Baxter, John D
    Angelin, Bo
    Karolinska Institutet.
    Use of the Thyroid Hormone Analogue Eprotirome in Statin-Treated Dyslipidemia2010Inngår i: Obstetrical and Gynecological Survey, ISSN 0029-7828, E-ISSN 1533-9866, Vol. 65, nr 8, s. 512-513Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    Statins effectively reduce levels of serum cholesterol and lower the risk of cardiovascular disease, but have limited effectiveness if stringent goals for serum low-density lipoprotein (LDL) cholesterol levels are not met or adverse effects develop, requiring a dose reduction or drug discontinuation. Previous studies have shown that thyroid hormone and some of its metabolites reduce levels of serum LDL cholesterol and have potentially favorable actions on other lipoproteins. The studies were discontinued because of reports of adverse effects on heart and bone, and possible deaths. In a recent report, eprotirome, a thyromimetic compound with minimal uptake in nonhepatic-tissues, was shown to reduce levels of serum total and LDL cholesterol and apolipoprotein B without apparent side effects in patients not receiving statin therapy. This randomized, placebo-controlled, double-blind, multicenter trial investigated the safety and efficacy of eprotirome in lowering the level of serum LDL cholesterol in patients with hypercholesterolemia who already were receiving simvastatin or atorvastatin. The aim of the study was to determine whether adding eprotirome to statin therapy would provide additional lipid-lowering actions without producing adverse extrahepatic thyromimetic effects. Patients were randomly assigned to receive daily oral doses of 25, 50, or 100 mcg of eprotirome or a placebo for 12 weeks. The primary study outcome was changes in serum LDL cholesterol. The potential adverse thyromimetic effects on the heart, bone, and pituitary were examined. Treatment of patients for 12 weeks already receiving statins with either placebo or eprotirome at a dose of 25, 50, or 100 mu g reduced the mean level of serum LDL cholesterol from 141 mg per deciliter (3.6 mmol per liter) at baseline to 127, 113, 99, and 94 mg per deciliter (3.3, 2.9, 2.6, and 2.4 mmol per liter), respectively; this represented a mean reduction from baseline of 7%, 22%, 28%, and 32%, respectively. Similar reductions were found in the secondary study outcomes, which included serum levels of apolipoprotein B, triglycerides, and Lp(a) lipoprotein. No evidence of adverse effects of eprotirome on the heart, bone, or pituitary was noted. Although reductions in serum levels of thyroxine occurred in some patients who received eprotirome, there were no changes in levels of thyrotropin or triiodothyronine. These findings demonstrate that the addition of eprotirome to statin therapy produces substantial further reductions in serum LDL cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B. The drug appears to have an excellent safety profile.

  • 138.
    Leinhard, Olof Dahlqvist
    et al.
    Linköpings universitet, Institutionen för medicin och vård, Radiofysik. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Hälsouniversitetet.
    Johansson, Andreas
    Linköpings universitet, Institutionen för medicin och hälsa, Medicinsk radiofysik. Linköpings universitet, Hälsouniversitetet.
    Rydell, Joakim
    Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik. Linköpings universitet, Tekniska högskolan. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV.
    Smedby, Örjan
    Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Institutionen för medicin och hälsa, Medicinsk radiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Bildmedicinskt centrum, Röntgenkliniken i Linköping.
    Nystöm, Fredrik
    Linköpings universitet, Institutionen för medicin och hälsa, Internmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Lundberg, Peter
    Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Institutionen för medicin och hälsa, Medicinsk radiofysik. Linköpings universitet, Institutionen för medicin och hälsa, Medicinsk radiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Radiofysikavdelningen. Östergötlands Läns Landsting, Bildmedicinskt centrum, Röntgenkliniken i Linköping.
    Borga, Magnus
    Linköpings universitet, Institutionen för medicinsk teknik, Medicinsk informatik. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Tekniska högskolan.
    Quantitative Abdominal Fat Estimation Using MRI2008Inngår i: Proceedings - International Conference on Pattern Recognition, IEEE Computer Society, 2008, s. 1-4Konferansepaper (Fagfellevurdert)
    Abstract [en]

    This paper introduces a new method for automaticquantification of subcutaneous, visceral and nonvisceralinternal fat from MR-images acquired usingthe two point Dixon technique in the abdominal region.The method includes (1) a three dimensionalphase unwrapping to provide water and fat images, (2)an image intensity inhomogeneity correction, and (3) amorphon based registration and segmentation of thetissue. This is followed by an integration of the correctedfat images within the different fat compartmentsthat avoids the partial volume effects associated withtraditional fat segmentation methods. The method wastested on 18 subjects before and after a period of fastfoodhyper-alimentation showing high stability andperformance in all analysis steps.

  • 139.
    Lesage, S
    et al.
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Chamaillard, M
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Colombel, JF
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Belaiche, J
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Cizard, JP
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Tysk, C
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Almer, Sven
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Gassull, MA
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Binder, V
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Zouali, H
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Thomas, G
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Hugot, JP
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Protective effect of CYP2D6*4 allele in ulcerative colitis disease.2000Inngår i: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 118, nr 4, s. 1805-Konferansepaper (Annet vitenskapelig)
  • 140.
    Li, Wei
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Patologi.
    Hellsten, Anna
    Linköpings universitet, Institutionen för biomedicin och kirurgi.
    Jacobsson, Leif
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Farmakologi.
    Blomqvist, Henrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Yuan, Xi Ming
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Patologi.
    Alpha-tocopherol and astaxanthin decrease macrophage infiltration, apoptosis and vulnerability in atheroma of hyperlipidaemic rabbits2004Inngår i: Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, E-ISSN 1095-8584, Vol. 37, nr 5, s. 969-978Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The composition of atherosclerotic plaques, not just macroscopical lesion size, has been implicated in their susceptibility to rupture and the risk of thrombus formation. By focusing on the quality of lipids, macrophages, apoptosis, collagen, metalloproteinase expression and plaque integrity, we evaluated the possible anti-atherosclerotic effect of the antioxidants α-tocopherol and astaxanthin in Watanabe heritable hyperlipidemic (WHHL) rabbits. Thirty-one WHHL rabbits were divided into three groups and were fed a standard diet, as controls (N =10), or a standard diet with the addition of 500 mg α-tocopherol per kg feed (N =11) or 100 mg astaxanthin per kg feed (N =10) for 24 weeks. We found that both antioxidants, particularly astaxanthin, significantly decreased macrophage infiltration in the plaques although they did not affect lipid accumulation. All lesions in the astaxanthin-treated rabbits were classified as early plaques according to the distribution of collagen and smooth muscle cells. Both antioxidants also improved plaque stability and significantly diminished apoptosis, which mainly occurred in macrophages, matrix metalloproteinase three expressions and plaque ruptures. Although neither antioxidant altered the positive correlations between the lesion size and lipid accumulation, the lesion size and apoptosis were only positively correlated in the control group. Astaxanthin and α-tocopherol may improve plaque stability by decreasing macrophage infiltration and apoptosis in this atherosclerotic setting. Apoptosis reduction by α-tocopherol and astaxanthin may be a new anti-atherogenic property of these antioxidants. © 2004 Elsevier Ltd. All rights reserved.

  • 141.
    Liefvendahl, Ellinor
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin.
    Arnqvist, Hans
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Mitogenic effect of the insulin analogue glargine in malignant cells in comparison with insulin and IGF-I2008Inngår i: Hormone and Metabolic Research, ISSN 0018-5043, E-ISSN 1439-4286, Vol. 40, nr 6, s. 369-374Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aim of the study was to investigate if the insulin analogue glargine, with an increased affinity for the IGF-I receptor (ICF-IR), affects the cell growth to a larger extent than human insulin in malignant cells expressing IGF-IRs. The breast cancer cell lines MCF-7 and SKBR-3, and the osteosarcoma cell line SaOS-2 were used. Gene expression was determined by real-time RT-PCR and receptor protein quantified by ELISAs. Receptor phosphorylation was assessed by immuno-precipitation and Western blot. Mitogenic effect was determined as 3H-thymidine incorporation into DNA. The gene expression of insulin receptor (IR) varied between 4.3-7.5-10-3 and the expression of IGF-IR between 7.7-147.7 10-3 in relation to GAPDH (glyceraldehyde-3-phosphate dehydrogenase). Insulin receptor and IGF-IR protein varied between 2.0-4.1 ng/mg protein and 2.0-40.4 ng/mg protein, respectively. The IGF-IR was phosphorylated by IGF-I at a concentration of 10 -10-10-10M. All three polypeptides stimulated DNA synthesis in MCF-7, SKBR-3, and SaOS-2 cells. SaOS-2 cells were more sensitive to IGF-I than to insulin and glargine. MCF-7 cells were more sensitive to des(l-3)IGF-I than to IGF-I. In SKBR-3 and SaOS-2 cells, glargine tended to be more potent than human insulin to stimulate DNA synthesis. Our results suggest that glargine, compared to human insulin, has little or no increased mitogenic effect in malignant cells expressing IGF-IRs. © Georg Thieme Verlag KG Stuttgart · New York.

  • 142. Lind, S
    et al.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Eriksson, M
    Rudling, M
    Eggertsen, G
    Angelin, B
    Autosomal recessive hypercholesterolaemia: Normalization of plasma LDL cholesterol by ezetimibe in combination with statin treatment2004Inngår i: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 256, nr 5, s. 406-412Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background. Severe hereditary hypercholesterolaemia is most frequently due to familial hypercholesterolaemia (FH), caused by mutations in the LDL receptor (LDLR) gene. However, a phenotype very similar to FH may also be caused by defects in other genes like the genes for apolipoprotein (apo) B-100 or autosomal recessive hypercholesterolaemia (ARH). Subject. An 8-year-old male of Lebanese origin was diagnosed with severe hypercholesterolaemia and extensive cutaneous and tendon xanthomas. Plasma LDL cholesterol before treatment was 17 mmol L-1, whilst parents and both siblings had normal levels. Diagnosis. Degradation of 125I-labelled LDL in blood lymphocytes was reduced, but not abolished. Sequencing analysis of the LDLR and apoB-100 genes were negative, whilst a splice acceptor mutation in intron 1 (IVS 1 - 1G>C) was detected in the ARH gene. The patient was homozygous for the mutation, whilst the parents were heterozygous. These findings were in agreement with a diagnosis of ARH. Treatment and clinical course. Monthly LDL apheresis and atorvastatin 120 mg daily reduced LDL cholesterol preapheresis level to 4.8 mmol L-1. When ezetimibe was given 10 mg day-1 in combination with rosuvastatin 80 mg day-1, LDL cholesterol was further lowered to 1.6 mmol L-1, which made apheresis unnecessary. Cutaneous and tendon xanthomas disappeared completely and the intima-media thickness of the common carotid arteries decreased. At age 23 he developed a small myocardial infarction. Conclusion. ARH should be considered in cases of severe hypercholesterolaemia with a pattern of recessive inheritance. Combination therapy with high-dose statin and ezetimibe seems to be the treatment of choice in ARH and may reduce or eliminate the need for LDL apheresis treatment.

  • 143.
    Lindgren, Peter
    et al.
    Stockholm.
    Graff, Jennifer
    Nw York.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Pedersen, Terje J
    Ullevål, Oslo.
    Jönsson, Bengt
    Stockholm.
    Cost-effectiveness of high-dose atorvastatin compared with regular dose simvastatin2007Inngår i: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 28, nr 12, s. 1448-1453Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Aims: The aim of the study was to evaluate the long-term cost-effectiveness of high-dose atorvastatin when compared with generic simvastatin for secondary prevention in Denmark, Finland, Norway, and Sweden based on the recently completed IDEAL trial. Methods and results: The IDEAL trial showed that high-dose treatment with atorvastatin was associated with fewer non-fatal myocardial infarctions (MI) or coronary heart disease death (RR 0.89, 95% CI 0.78-1.01) and major cardiovascular events by (RR 0.87, 95% CI 0.77-0.98) or any coronary event (RR 0.84, 95% CI 0.76-0.91) than simvastatin with no significant difference in the number of serious adverse events. Costs during the trial period was estimated based on the trial data and a Markov model was constructed where the risk of MIs and revascularization procedures and the long-term costs, quality of life, and mortality associated with these events was simulated. Costs were based on resource consumptions recorded in the trial multiplied with recent unit costs from each country. Both direct health care costs and indirect costs (costs from lost production due to work absence) were included. Intervention lasted for the duration of the trial (4.8 years) while health-effects and costs are predicted for the lifespan of the patient. The main outcome was quality adjusted life-years (QALY) gained. High-dose treatment was predicted to lead to a mean increase in survival of 0.049 years per patient and 0.033 QALYs gained. The cost to gain one QALY was predicted to 47 197€ (Denmark), 62 639€ (Finland), 35 210€ (Norway), and 43 667€ (Sweden), with cost-effectiveness ratio decreasing with higher risk. Conclusion: In the prevention of cardiovascular events among patients with a previous MI, high-dose atorvastatin appears to be a cost-effective strategy when compared with generic simvastatin 20-40 mg in Denmark, Norway, and Sweden. In Finland, it is cost-effective in high-risk patients. The key driver of the cost-effectiveness is the price-difference between 80 mg atorvastatin and generic simvastatin. © The European Society of Cardiology 2007. All rights reserved.

  • 144.
    Lindgren, Stefan
    et al.
    University Hospital MAS.
    Glaumann, Hans
    Karolinska University Hospital.
    Almer, Sven
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Gastroenterologi och hepatologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Bergquist, Annika
    Karolinska University Hospital.
    Bjornsson, Einar
    Sahlgrenska University Hospital.
    Broome, Ulrika
    Karolinska University Hospital.
    Danielsson, Ake
    Umea University Hospital.
    Lebrun, Barbro
    Karolinska University Hospital.
    Prytz, Hanne
    Lund University Hospital.
    Olsson, Rolf
    Sahlgrenska University Hospital.
    Transitions between variant forms of primary biliary cirrhosis during long-term follow-up2009Inngår i: EUROPEAN JOURNAL OF INTERNAL MEDICINE, ISSN 0953-6205, Vol. 20, nr 4, s. 398-402Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Conditions exhibiting features of two different autoimmune liver diseases are designated overlap syndromes. Variant forms display some, but not all, characteristics of a distinct autoimmune liver disease. We describe transitions over time between variant forms of PBC, i.e. AMA-negative PBC, autoimmune hepatitis (AIH)-PBC overlap and autoimmune cholangitis (AIC) in a large cohort of PBC patients in Sweden. Methods: We retrieved all patients with variant forms of PBC in six university hospitals in Sweden, covering 60% of the Swedish population. The diagnosis of PBC and its variants was based on laboratory findings and compatible histological features. The revised autoimmune hepatitis scoring system proposed by the International Autoimmune Hepatitis Group was used to establish the diagnosis of AIH. Results: In a population of 800 patients with PBC, we identified 35 (5%) variant forms; 25 patients with AIH-PBC overlap, 8 with AIC and 2 with AMA-negative PBC at the time of our study. The initial diagnoses were PBC (3 patients), AIH (3), AIH-PBC overlap (16), AIC (8) and AMA-negative PBC with (1) or without (4) concomitant AIH. The median follow-up was 125 (41-360) months. Immunosuppression and ursodeoxycholic acid induced a complete or good regression of increased aminotransferases in about half of the patients who were given one or both of these treatments. Conclusions: Variant forms of PBC are seen in approximately 5% of PBC patients in Sweden. Transition between different forms may occur, emphasizing the value of repeat biopsies, but established overlapping AIH-PBC seems to be stable over time.

  • 145.
    Lindqvist Appell, Malin
    et al.
    Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi. Linköpings universitet, Hälsouniversitetet.
    Haglund, Sofie
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Linköpings universitet, Hälsouniversitetet.
    Almer, Sven
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Peterson, Curt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk farmakologi.
    Taipalensuu, Jan
    Division of Research and Development in Laboratory Medicine, Ryhov County Hospital, Jönköping.
    Hertervig, Erik
    dDepartment of Medicine, Lund University Hospital, Lund.
    Lyrenäs, Ebbe
    Department of Medicine, Blekinge County Hospital, Karlskrona.
    Söderkvist, Peter
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för medicinsk cellbiologi.
    Identification of two novel sequence variants affecting thiopurine methyltransferase enzyme activity2004Inngår i: Pharmacogenetics, ISSN 0960-314X, E-ISSN 1473-561X, Vol. 14, nr 4, s. 261-265Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The polymorphic enzyme thiopurine methyltransferase (TPMT) is involved in the methylation of thiopurines. On comparing the phenotype with the genotype in Swedish patients with inflammatory bowel disease and healthy individuals, we found two discordant cases with low TPMT enzyme activity (0.3 and 0.4 U/ml packed red blood cells (pRBC). Genotyping by pyrosequencing revealed that they carried the nucleotide substitutions 460G>A and 719A>G, giving two possible genotypes (TPMT*1/*3A or TPMT*3B/ *3C). DNA sequencing of exon III to X was performed in the patients and their parents. We identified an A>G transition in the start codon (exon III, 1A>G, Met>Val, TPMT*14) in one of the patients and her father (6.3 U/ml pRBC). The mother in this family carried the 460G>A and 719A>G nucleotide substitutions (TPMT*3A, 5.0 U/ml pRBC). In the second family, sequencing revealed a G>A transition in the acceptor splice site in intron VII/exon VIII (IVS7 - 1G>A, TPMT*15) in the patient and his mother (6.9 U/ml pRBC). His father was genotyped as TPMT*1/*3A (6.0 U/ml pRBC). Hence, we report the identification of two novel sequence variants, present in highly conserved nucleotide positions of the human TPMT gene, resulting in a loss of enzyme activity.

  • 146.
    Lindqvist Appell, Malin
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi.
    Hindorf, U
    Almer, Sven
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Söderkvist, Peter
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för medicinsk cellbiologi.
    Ström, Magnus
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Hjortswang, Henrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Peterson, Curt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk farmakologi.
    No induction of thiopurine methyltransferase during thiopurine treatment in inflammatory bowel disease2006Inngår i: Nucleosides, Nucleotides & Nucleic Acids, ISSN 1525-7770, E-ISSN 1532-2335, Vol. 25, nr 9-11, s. 1033-1037Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The aim of this study was to follow, during standardized initiation of thiopurine treatment, thiopurine methyltransferase (TPMT) gene expression and enzyme activity and thiopurine metabolite concentrations, and to study the role of TPMT and ITPA 94C > A polymorphisms for the development of adverse drug reactions. Sixty patients with ulcerative colitis or Crohn's disease were included in this open and prospective multi-center study. Thiopurine naïve patients were prescribed azathioprine (AZA), patients previously intolerant to AZA received 6-mercaptopurine (6-MP). The patients followed a predetermined dose escalation schedule, reaching target dose at Week 3, 2.5 and 1.25 mg/kg body weight for AZA and 6-MP, respectively. The patients were followed every week during Weeks 1-8 from baseline and then every 4 weeks until 20 weeks. TPMT activity and thiopurine metabolites were determined in erythrocytes, TPMT and ITPA genotypes, and TPMT gene expression were determined in whole blood. One homozygous TPMT-deficient patient was excluded. Five non compliant patients were withdrawn during the first weeks. Twenty-seven patients completed the study per protocol, 27 patients were withdrawn because of adverse events. Sixty-seven percent of the withdrawn patients tolerated thiopurines at a lower dose at Week 20. There was no difference in baseline TPMT enzyme activity between individuals completing the study and those withdrawn for adverse events (p = 0.45). A significant decrease in TPMT gene expression (TPMT/huCYC ratio, p = 0.02) was found, however TPMT enzyme activity did not change. TPMT heterozygous individuals had a lower probability of remaining in the study on the predetermined dose (p = 0.039). The ITPA 94C > A polymorphism was not predictive of adverse events (p = 0.35). Copyright © Taylor & Francis Group, LLC.

  • 147.
    Lindqvist Appell, Malin
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi.
    Hindorf, Ulf
    Lund.
    Almer, Sven
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Peterson, Curt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk farmakologi.
    Thiopurines in inflammatory bowel disease - The role of pharmacogenetics and therapeutic drug monitoring2006Inngår i: Current Pharmacogenomics, ISSN 1570-1603, Vol. 4, nr 4, s. 285-300Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Pharmacogenetics represents the study of variability in drug response due to genetic variations. Inflammatory bowel disease (IBD, i.e. primarily Crohn's disease and ulcerative colitis) is characterized by a chronic or relapsing inflammation of the digestive tract. The thiopurines 6-mercaptopurine (6-MP) and azathioprine (AZA), an imidazol derivative and pro-drug of 6-MP, are widely used in IBD, particularly in Crohn's disease. The metabolism of thiopurines is complex and individually variable. Thiopurine methyltransferase (TPMT) is a key enzyme in this metabolism and exhibits a genetic variability due to a number of variant alleles coding for a defective enzyme. The formation of biologically active thioguanine nucleotides (TGN) and methylated metabolites may vary considerably due to the TPMT activity. Patients with decreased TPMT activity are at increased risk of developing severe side effects if treated with conventional thiopurine doses, due to the accumulation of toxic metabolites. Determination of the TPMT phenotype or genotype is often used to identify individuals with increased risk for adverse events. Twenty-one variant TPMT alleles have been described, of which three are more common than the others. An association between inosine triphosphate pyrophosphatase polymorphisms and adverse events during thiopurine treatment has also been proposed. In this review, the clinical value of TPMT status determination and pharmacological monitoring of thiopurine metabolites are discussed as well as the increased interest in the use of 6-thioguanine, a thiopurine with a less complex metabolism, as an alternative for patients who do not tolerate AZA or 6-MP. It can be concluded that TPMT determination before start of thiopurine therapy is of value to identify individuals with increased risk for adverse reactions due to genetic enzyme deficiency. However, large prospective studies are still needed to evaluate the true benefit of monitoring thiopurine metabolites during thiopurine treatment. © 2006 Bentham Science Publishers Ltd.

  • 148.
    Lindqvist Appell, Malin
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi.
    Hindorf, Ulf
    Lund.
    Almer, Sven
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Söderkvist, Peter
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för medicinsk cellbiologi.
    Ström, Magnus
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Hjortswang, Henrik
    Linköpings universitet, Institutionen för molekylär och klinisk medicin.
    Peterson, Curt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk farmakologi.
    No induction of thiopurine methyltransferase (TPMT) during thiopurine treatment in IBD2005Inngår i: 10th Symposium European Society for the Study of Purine and Pyrimidine Metabolism in Man,2005, 2005Konferansepaper (Fagfellevurdert)
  • 149.
    Lindqvist Appell, Malin
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi.
    Hindorf, Ulf
    Lund.
    Almer, Sven
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Söderkvist, Peter
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för medicinsk cellbiologi.
    Ström, Magnus
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Hjortswang, Henrik
    Linköpings universitet, Institutionen för molekylär och klinisk medicin.
    Peterson, Curt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk farmakologi.
    No induction of thiopurine methyltransferase (TPMT) during thiopurine treatment in IBD2005Inngår i: 13th United European Gastroenterology week,2005, Stuttgart: Georg Thieme Verlag KG , 2005, s. A173-Konferansepaper (Fagfellevurdert)
  • 150.
    Lindqvist Appell, Malin
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi.
    Skoglund, Karin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi.
    Karlgren, Anna
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Klinisk farmakologi.
    Peterson, Curt
    Linköpings universitet, Institutionen för medicin och hälsa, Klinisk farmakologi. Linköpings universitet, Hälsouniversitetet.
    Söderkvist, Peter
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Avdelningen för medicinsk cellbiologi.
    Kidhall, Irene
    Danderyds sjukhus.
    Almer, Sven
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Gastroenterologi och hepatologi. Östergötlands Läns Landsting, Medicincentrum, Endokrin- och magtarmmedicinska kliniken US.
    Explaining TPMT genotype/phenotype discrepancy by haplotyping of TPMT*3A and identification of a novel sequence variant, TPMT*232007Inngår i: Pharmacogenetics and Genomics, ISSN 1744-6872, Vol. 17, nr 10, s. 891-895Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Thiopurine methyltransferase (TPMT) is a polymorphic enzyme involved in the metabolism of thiopurine drugs. Owing to polymorphisms in the TPMT gene (TPMT*2-*22), the enzyme activity varies interindividually. Patients with reduced TPMT activity may develop adverse reactions when treated with standard doses of thiopurines. This work focuses on a TPMT genotype/phenotype discrepancy found in a patient during routine testing. The patient displayed very low TPMT enzyme activity and she was genotyped by pyrosequencing as being heterozygous for the 460G>A and 719A>G polymorphisms (TPMT*3A). Complete sequencing in combination with haplotyping of the TPMT gene revealed a novel sequence variant, 500C>G, on one allele and TPMT*3A on the other allele, giving rise to the novel genotype TPMT*3A/*23. When investigating the patient's relatives, they too had the TPMT*3A/*23 genotype in combination with low enzyme activity. We conclude that this novel variant allele affects enzyme activity, as the individuals carrying it had almost undetectable TPMT activity. © 2007 Lippincott Williams & Wilkins, Inc.

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