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  • 1. Hallberg, P
    et al.
    Karlsson, J
    Kurland, L
    Lind, L
    Kahan, T
    Malmqvist, K
    Ohman, KP
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin.
    Nyström, Fredrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Melhus, H
    The CYP2C9 genotype predicts the blood pressure response to irbesartan: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial2002Inngår i: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 10, s. 2089-2093Artikkel i tidsskrift (Fagfellevurdert)
  • 2.
    Hollman, Gunilla
    et al.
    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, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Ek, Anna-Christina
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Omvårdnad. Östergötlands Läns Landsting, Närsjukvården i centrala Östergötland, Akutkliniken.
    Quality of life in non affected family members of familial hypercholesterolemia families2002Inngår i: Konferens Familjefokuserad omvårdnad, Kalmar,2002, 2002Konferansepaper (Fagfellevurdert)
  • 3. Kullberg, C
    et al.
    Abrahamsson, M
    Arnqvist, Hans
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Cellbiologi. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Finnström, Kerstin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Oftalmologi. Östergötlands Läns Landsting, Rekonstruktionscentrum, Ögonkliniken US/LiM.
    Ludvigsson, Johnny
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Pediatrik. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn.
    Prevalence of retinopathy differs with age at onset of diabetes in a population of patients with Type 1 diabetes2002Inngår i: Diabetic Medicine, ISSN 0742-3071, E-ISSN 1464-5491, Vol. 19, nr 11, s. 924-931Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Aim. The VISS study (Vascular complications in South-east Sweden) investigates prevalence and incidence of vascular complications in a population with Type 1 diabetes, from a well-defined geographical area and followed from diag-nosis with HbA1c measurement. Method. The study population comprised all 440 patients with Type 1 diabetes onset before the age of 36 years, onset during 1983-1987, and at the time of onset living within the counties of J÷nk÷ping, Kalmar or ╓sterg÷tland. Retinopathy was examined with fundus photography 1994-1995, and classified according to a modified Airlie House protocol. Results. Fundus photographs from 390 patients were evaluated. In 277 (71%) patients no retinopathy was seen. The prevalence of retinopathy increased from 11% among patients < 5 years old at diabetes onset, to 48% among those 15-19 years old at diabetes onset, and then decreased to 30% for patients 30-35 years old at diabetes onset (P for ?2 for linear trend for all ages 0.017, for age at onset 0-19 yearsP = 0.0003), without corresponding differences in duration or HbA1c between patients with different onset age. Patients with HbA1c in the highest quartile (> 8.3% HbA1c) had a relative risk of 2.4 (95% confidence) interval (CI) 1.7-3.2) of having any retinopathy compared with patients with lower HbA1c, and a relative risk of 7.1 (95% CI 3.0-16.7) of having other forms of retinopathy than microaneurysms. Conclusion. In patients with diabetes duration of 6-13 years, the prevalence of retinopathy is clearly related to glycaemic control. Furthermore, the risk of retinopathy varies with different age at onset, independently of differences in duration or glycaemic control.

  • 4.
    Kurland, Lisa
    et al.
    Internmedicin Uppsala.
    Melhus, Håkan
    Internmedicin Uppsala.
    Karlsson, Julia
    Internmedicin Uppsala.
    Kahan, Thomas
    Internmedicin Danderyd.
    Malmqvist, Karin
    Internmedicin Danderyd.
    Öhman, Peter
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin.
    Nyström, Fredrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Hägg, Anders
    Internmedicin Uppsala.
    Lind, Lars
    Internmedicin Uppsala.
    Polymorphisms in the angiotensinogen and angiotensin II type 1 receptor gene are related to change in left ventricular mass during antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial2002Inngår i: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 20, s. 657-663Artikkel i tidsskrift (Fagfellevurdert)
  • 5.
    Malmqvist, Karin
    et al.
    Internmedicin Danderyd Stockholm.
    Öhman, P
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin.
    Lind, L
    Nyström, Fredrik
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Kahan, T
    Relationships between left ventricular mass and the renin-angiotensin system, catecholamines, insulin and leptin.2002Inngår i: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 252, s. 430-439Artikkel i tidsskrift (Fagfellevurdert)
  • 6.
    Nyström, Fredrik
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Malmqvist, Karin
    Öhman, Peter
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin.
    Kahan, Thomas
    Nurse-recorded and ambulatory blood pressure predicts treatment-induced reduction of left ventricular hypertrophy equally well in hypertension: Results from the Swedish irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA) study2002Inngår i: Journal of Hypertension, ISSN 0263-6352, E-ISSN 1473-5598, Vol. 20, nr 8, s. 1527-1533Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: To compare the relationships of treatment-induced reductions of left ventricular hypertrophy to the changes in clinic and ambulatory blood pressure (BP). Design: Double-blind and randomized treatment with irbesartan or atenolol for 48 weeks. Patients: Patients with hypertension and left ventricular hypertrophy (n = 66) with a seated diastolic BP 90-115 mmHg (average of three measurements one minute apart by nurses). Main outcome measures: Registrations of echocardiographic left ventricular (LV) mass. Clinic and ambulatory BP. Results: In the total material, nurse-measured BP was reduced by 23 +/- 15/16 +/- 7.7 mmHg and 24-h ambulatory BP fell 20 +/- 15/14 +/- 8.5 mmHg by treatment. The correlation between the change in nurse-measured BP and LV mass index (LVMI) induced by treatment was r = 0.35, P = 0.004 for systolic BP and r = 0.26, P = 0.03 for diastolic BP. Corresponding values for 24-h ambulatory BP were r = 0.29, P = 0.02 and r = 0.35, P = 0.004, respectively, with similar correlations for day- and night-time ambulatory BP. The nurse-recorded BP was slightly higher than ambulatory BP (systolic clinic - systolic 24-h ambulatory BP = 5 mmHg). Using 130/80 mmHg as a cut-off value for normal 24-h ambulatory BP, eight subjects had normal diastolic or systolic ambulatory BP, or both. Interestingly, these patients also experienced LVMI regression following treatment (low/normal ABP, -13 +/- 21 g/m2, remaining patients, -18 +/- 22 g/m2, P > 0.5). Conclusions: In patients with hypertension and left ventricular hypertrophy, ambulatory BP is not superior to carefully standardized nurse-recorded seated BP in terms of associations with treatment-induced changes in LV mass.

  • 7.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Nya rön talar mot statinbehandling vid akut kranskärlssjukdom. Men vanskligt att bedöma behandlingseffekt utifrån observationella studier.2002Inngår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 99, s. 4348-4349Artikkel i tidsskrift (Annet (populærvitenskap, debatt, mm))
  • 8.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Eriksson, M
    Johnson, O
    Kjellström, T
    Lanke, J
    Lytken Larsen, M
    Pedersen, T
    Tikkanen, MJ
    Wiklund, O
    A 52-week, multicenter, randomized, parallel-group, double-blind, double-dummy study to assess the efficacy of atorvastatin and simvastatin in reaching low-density lipoprotein cholesterol and triglyceride targets: The Treat-to-Target (3T) Study2003Inngår i: Clinical Therapeutics, ISSN 0149-2918, E-ISSN 1879-114X, Vol. 25, nr 1, s. 119-138Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Guidelines for the prevention of coronary heart disease call for low-density lipoprotein cholesterol (LDL-C) reduction as the primary target of treatment and reduction of triglycerides (TG) as an additional target. Objective: The purpose of this study was to investigate the ability of atorvastatin and simvastatin to reduce LDL-C and TG concentrations and to meet 3 target lipid levels: LDL-C =2.6 mmol/L, TG =1.5 mmol/L, and both LDL-C =2.6 mmol/L and TG =1.5 mmol/L. Methods: The Treat-to-Target (3T) Study was a 52-week, multicenter, randomized, parallel-group study. Using the double-blind, double-dummy technique, adult patients aged 35 to 75 years with cardiovascular disease and dyslipidemia, defined as LDL-C concentration =4.0 mmol/L (=155 mg/dL), were randomized in a 1:1 ratio to receive once-daily oral treatment with 20 mg atorvastatin or 20 mg simvastatin. Fasting (12-hour) blood samples for the estimation of lipid levels and clinical laboratory values were collected after 4, 8, 12, 26, and 52 weeks. The dose was doubled after 12 weeks if the target National Cholesterol Education Program level of LDL-C (=2.6 mmol/L [100 mg/dL]) was not reached at 8 weeks. Results: The intent-to-treat analysis included 552 patients (418 men, 134 women) randomized to receive atorvastatin and 535 (404 men, 131 women) randomized to receive simvastatin. The number of patients enrolled in the study allowed the evaluation of the drugs' effects on YG. Patient demographic characteristics were similar for the 2 treatment groups, and there were no differences in baseline lipid values. Compared with simvastatin, atorvastatin produced significantly greater reductions in LDL-C (8 weeks: -46% vs -40%, P < 0.001, 52 weeks: -49% vs -44%, P < 0.001) and in YG (8 weeks: -23% vs -14%, P < 0.001, 52 weeks: -24% vs -16%, P < 0.001). Compared with simvastatin-treated patients, a significantly greater number of atorvastatin-treated patients reached the LDL-C target after 8 weeks (45% vs 24%, P < 0.001). Fewer atorvastatin patients needed to have their dose doubled, nevertheless more atorvastatin patients reached the LDL-C target after 52 weeks (61% vs 41%, P < 0.001). Both statins were well tolerated. Muscular symptoms occurred in 12 patients (2.2%) in the atorvastatin group and in 13 patients (2.4%) in the simvastatin group. Conclusions: Atorvastatin 20 or 40 mg/d for up to 1 year of treatment was significantly more effective than simvastatin 20 or 40 mg/d m reducing LDL-C and YG levels and at achieving recommended lipid targets in this selected patient population with cardiovascular disease and dyslipidemia. Both statins were well tolerated.

  • 9.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Istad, Helge
    Luurila, Olavi
    Ose, Leiv
    Stender, Steen
    Tuomilehto, Jaakko
    Wiklund, Olov
    Southworth, Harry
    Pears, John
    Wilpshaar, J W
    Effects of rosuvastatin and atorvastatin compared over 52 weeks of treatment in patients with hypercholesterolemia2002Inngår i: American Heart Journal, ISSN 0002-8703, E-ISSN 1097-6744, Vol. 144, nr 6, s. 1044-1051Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Despite the demonstrated benefits of low-density lipoprotein cholesterol (LDL-C) reduction in reducing the risk of coronary heart disease, many patients receiving lipid-lowering therapy fail to achieve LDL-C goals. We compared the effects of rosuvastatin and atorvastatin in reducing LDL-C and achieving LDL-C goals in patients with primary hypercholesterolemia. Methods and Results: In this 52-week, randomized, double-blind, multicenter trial (4522IL/0026), 412 patients with LDL-C 160 to <250 mg/dL received a 5-mg dose of rosuvastatin (n = 138), a 10-mg dose of rosuvastatin (n = 134), or a 10-mg dose of atorvastatin (n = 140) for 12 weeks, during the following 40 weeks, dosages could be sequentially doubled up to 80 mg if National Cholesterol Education Program Adult Treatment Panel II (ATP-II) LDL-C goals were not achieved. At 12 weeks, 5- and 10-mg doses of rosuvastatin were associated with significantly greater LDL-C reductions than 10-mg doses of atorvastatin (46% and 50% vs 39%, both P < .001). At 12 weeks, both rosuvastatin dosages brought more patients to within ATP-II and European LDL-C goals than atorvastatin (86% and 89% vs 73% and 75%, and 86% vs 55%, respectively). At 52 weeks, compared with atorvastatin, both initial rosuvastatin treatment groups significantly reduced LDL-C (47% and 53% vs 44%, P < .05 and P < .001). Overall, more patients in the initial rosuvastatin 10-mg group achieved their ATP-II LDL-C goal than those in the initial atorvastatin 10-mg group (98% vs 87%), with 82% of patients treated with rosuvastatin achieving their goal at the 10-mg starting dosage without the need for titration, compared with 59% of patients treated with atorvastatin. Both treatments were well tolerated over 52 weeks. Conclusion: Compared with atorvastatin, rosuvastatin produced greater reductions in LDL-C, which may offer advantages in LDL-C goal attainment over existing lipid-lowering therapies.

  • 10.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Packard, C
    Glasgow, Scotland.
    New global standards in lipid lowering: a review of emerging evidence and concepts.2002Inngår i: Int J Clin Practice,2002, 2002Konferansepaper (Fagfellevurdert)
  • 11.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Schwartz, G G
    Jonasson, Lena
    Linderfalk, C
    Are early clinical effects of cholesterol lowering mediated through effects on inflammation?2002Inngår i: Acta Physiologica Scandinavica, ISSN 0001-6772, E-ISSN 1365-201X, Vol. 176, nr 2, s. 147-150Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    In a randomized, double-blind trial in 3086 patients with unstable angina pectoris or non-Q wave myocardial infarction we investigated if 80 mg of atorvastatin daily could improve outcome of cardiovascular events during a short period of time (16 weeks) compared with placebo. Baseline LDL cholesterol was 3.2 mmol L-1 (124 mg dL-1) and decreased by 40% to 1.9 mmol L-1 (72 mg dL-1) during atorvastatin treatment. The primary endpoint, which was a composite of death, non-fatal acute myocardial infarction, cardiac arrest with resuscitation or recurrent symptomatic myocardial ischaemia with objective evidence and requiring emergency rehospitalization occurred in 228 patients (14.8%) in the atorvastatin group and 269 patients (17.4%) in the placebo group. The relative risk was 0.84 and 95% confidence interval was 0.70-1.00 (P = 0.048). Thus for patients with acute coronary syndromes, lipid-lowering therapy with high dose atorvastatin reduces recurrent ischaemic events in the short-term. A possible mechanism behind this rapid clinical effect induced by statin treatment is on inflammatory processes. Recent studies strongly suggest that acute T-cell activation is involved in the pathogenesis of unstable angina. In another study we investigated whether circulating T cells showed signs of activation in patients with stable angina pectoris (SA). Systemic venous blood samples were taken from 38 men with SA and 42 healthy controls. The T-cell receptor expression was assessed by three-colour flow cytometry using monoclonal antibodies against CD3, CD4, CD8, CD25 and human leucocyte antigen (HLA)-DR. Soluble interleukin-2 receptor (sIL-2R) was measured as the circulating form in serum. Levels of circulating CD3+ and CD4+ T cells tended to be higher in patients compared with controls. Patients were also shown to have a significant increase in CD4+ T cells expressing the activation markers CD25 (P < 0.05) and HLA-DR (P < 0.01). Furthermore, serum levels of sIL-2R were significantly higher (P < 0.001) in patients than in controls. We also observed that the T-cell response was more pronounced in patients without simvastatin treatment (n = 18) compared with simvastatin-treated patients (n = 20). In conclusion, our findings indicate that a continuous immune system activation takes place in patients with chronic angina pectoris, predominantly involving proliferation of CD4+ T cells. Statin treatment seems to be able to decrease this inflammatory response.

  • 12.
    Olsson, Anders
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Schwartz, GG
    Early initiation of treatment with statins in acute coronary syndromes2002Inngår i: Annals of Medicine, ISSN 0785-3890, E-ISSN 1365-2060, Vol. 34, nr 1, s. 37-41Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Statins may act rapidly to reverse abnormalities of the arterial wall that may predispose to recurrent ischemic events after acute coronary syndromes. Such abnormalities are endothelial dysfunction, a local inflammatory response, and an exaggerated thrombogenic tendency. In one study almost 20 000 patients with first myocardial infarction were studied with regard to statin treatment (28%) or not. Baseline characteristics were adjusted using multivariate regression analysis including propensity analysis. One year mortality was 3.7/5.0% in statin/not statin groups, respectively, P = 0.001, relative risk 0.75. In another study of more than 20 000 patients, 18% were prescribed statin after an acute coronary syndrome and followed for six months. Propensity analysis was performed in this study as well. Deaths in statin/not statin groups were 1.7/3.5%, P < 0.0001, relative risk 0.48. In the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL), a double-blind randomized, placebo-controlled intervention study, 3086 patient with acute non-Q-wave coronary syndromes were allocated immediately in hospital to receive atorvastatin 80 mg daily or placebo for four months. No lower limit for plasma LDL cholesterol was used. Primary endpoint was time to first occurrence of death, non-fatal myocardial infarction, cardiac arrest, and worsening angina with objective evidence of ischemia. This was significantly reduced compared to the placebo group by 2.4% (14.8 versus 17.2%, relative risk 0.84, P = 0.048). Atorvastatin also reduced significantly fatal or non-fatal strokes. Possible mechanisms behind these acute beneficial effects are discussed. The studies highlight the importance of treatment with a statin in the early management of acute coronary syndromes and the need to incorporate this therapeutic strategy in national guidelines and treatment recommendations.

  • 13. Olsson, PO
    et al.
    Lindström, Torbjörn
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Combination-therapy with bedtime NPH insulin and sulphonylureas gives similar glycaemic control but lower weight gain than insulin twice daily in patients with type 2 diabetes2002Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: To study the effect on body weight and glycaemic control of two insulin treatment regimens in patients with Type 2 diabetes and moderate failure to oral hypoglycaemic agents. Methods: Sixteen patients treated with oral hypoglycaemic agents (6 men and 10 women) were included in this open-label, randomized, parallel group study. Their age was 62 ▒ 2 (mean ▒ SEM) years (range 44-79 years), body weight 71.3 ▒ 2.9 kg, body mass index (BMI) 24.6 ▒ 0.8 kg/m2. The patients were switched to insulin treatment with bedtime NPH insulin combined with daytime sulphonylurea (combination group) or twice daily injections of a premixed combination of regular human and NPH insulin (insulin twice daily group) with measurements as given below before and after 12 and 24 weeks of treatment. Results: HbA1c was lowered from 8.3 ▒ 0.3% to 7.0 ▒ 0.2% in the insulin twice daily group (p < 0.05) and from 8.3 ▒ 0.3% to 6.8 ▒ 0.5% in the combination group (p < 0.03, ns between treatment groups). Body weight increased from 71.7 ▒ 4.0 kg to 77.6 ▒ 4.4 kg in the insulin twice daily group (p < 0.001) and from 70.8 ▒ 4.6 kg to 72.7 ▒ 5.1 kg in the combination group (ns, p < 0.02 between groups). The dose of insulin at 24 weeks in the insulin twice daily group was 45.8 ▒ 4.2 U and 29.4 ▒ 5.4 U in the combination group (p = 0.03). Combination treatment reduced fasting and stimulated C-peptide levels. Conclusions: Both treatments improved glycaemic control to the same extent but the combination of bedtime NPH insulin and daytime sulphonylurea gave a very small increase of body weight over a 6 months period. We conclude that combination therapy is an attractive alternative when starting insulin treatment in patients with Type 2 diabetes as this is a critical period for weight gain in such patients.

  • 14. Schwartz, GG
    et al.
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Lipid lowering in acute coronary syndromes: New evidence, new questions2002Inngår i: Current Atherosclerosis Reports, ISSN 1523-3804, E-ISSN 1534-6242, Vol. 4Artikkel i tidsskrift (Fagfellevurdert)
  • 15.
    Vrethem, Magnus
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för nervsystem och rörelseorgan. Östergötlands Läns Landsting, Närsjukvården i centrala Östergötland, Neurologiska kliniken.
    Boivie, Jörgen
    Östergötlands Läns Landsting, Närsjukvården i centrala Östergötland, Neurologiska kliniken.
    Arnqvist, Hans
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för biomedicin och kirurgi, Cellbiologi.
    Holmgren, Helen
    Östergötlands Läns Landsting, Närsjukvården i centrala Östergötland, Neurologiska kliniken.
    Lindström, Torbjörn
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Painful polyneuropathy in patients with and without diabetes: Clinical, neurophysiologic, and quantitative sensory characteristics2002Inngår i: The Clinical Journal of Pain, ISSN 0749-8047, E-ISSN 1536-5409, Vol. 18, nr 2, s. 122-127Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objectives: To study pain characteristics and peripheral nerve involvement in patients with painful diabetic and nondiabetic polyneuropathy in comparison with patients with nonpainful polyneuropathy. Patients and Methods: Fifty-five patients with polyneuropathy (37 with painful polyneuropathy, of whom 19 had diabetes and 18 had no diabetes, and 18 with painless polyneuropathy of different etiologies) were examined clinically using quantitative sensory tests and neurophysiology. Pain intensity and characteristics were analyzed by daily ratings on a 10-step verbal scale and by a questionnaire. Results: Most patients experienced pain of more than one character. There was no clear difference in character or duration of pain between patients with and without diabetes. The mean value of the daily rating of pain intensity showed that pain was more severe in the evenings than in the mornings and that diabetic patients reported worse pain than nondiabetic patients. Thirty-two of the 37 patients with pain had paresthesias and/or dysesthesias, whereas only 7 of 18 patients without pain had paresthesias. Pain was always located in the feet, and, in most patients, also in the lower part of the legs. Some patients also experienced pain in the hands. Tactile sensibility, measured by quantitative tests, was more affected in both diabetic and nondiabetic patients with painful polyneuropathy compared with patients without pain (p = 0.02). Temperature, pain, and vibratory sensibility were equally affected in all patient groups. Nerve conduction velocity, amplitudes, and distal latency were equally affected in the pain group as compared with the control group, indicating that both thin and thick nerve afferents are affected in patients with painful as well as nonpainful polyneuropathy and that etiology has no clear impact on nerve involvement. Conclusions: Neuropathy pain was always located in the feet and more severe in diabetic patients compared with patients with neuropathy pain of other etiologies. The authors also found evidence for a greater tactile sensibility involvement in patients with neuropathy pain, irrespective of etiology, whereas other quantitative sensibility and neurography parameters were equally affected in all patient groups.

  • 16. Waters, DD
    et al.
    Schwartz, GG
    Olsson, Anders
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Zeiher, A
    Oliver, MF
    Ganz, P
    Ezekowitz, M
    Chaitman, BR
    Leslie, SJ
    Stern, T
    Effects of atorvastatin on stroke in patients with unstable angina or non-Q-wave myocardial infarction: A myocardial ischemia reduction with aggressive cholesterol lowering (MIRACL) substudy2002Inngår i: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 106, nr 13, s. 1690-1695Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background - This report describes the effect of intensive cholesterol lowering with atorvastatin on the incidence of nonfatal stroke, a secondary end point, in a randomized, placebo-controlled trial of patients with unstable angina or non-Q-wave myocardial infarction. The primary end point, a composite of death, nonfatal myocardial infarction, resuscitated cardiac arrest, or recurrent symptomatic myocardial ischemia with objective evidence requiring emergency rehospitalization, was reduced from 17.4% in the placebo group to 14.8% in the atorvastatin group over the 16 weeks of the trial (P=0.048). Methods and Results - Strokes were adjudicated by a blinded end-point committee using standard clinical and imaging criteria. The outcomes of nonfatal stroke and fatal plus nonfatal stroke were analyzed by time to first occurrence during the 16-week trial. Of 38 events (in 36 patients) adjudicated as fatal or nonfatal strokes, 3 were classified as hemorrhagic, one as embolic, and 29 as thrombotic or embolic, 5 could not be categorized. Nonfatal stroke occurred in 9 patients in the atorvastatin group and 22 in the placebo group (relative risk, 0.40, 95% confidence intervals, 0.19 to 0.88, P=0.02). Fatal or nonfatal stroke occurred in 12 atorvastatin patients and 24 placebo patients (relative risk, 0.49, 95% confidence intervals, 0.24 to 0.98, P=0.04). All 3 hemorrhagic strokes occurred in the placebo group. Conclusion - Intensive cholesterol lowering with atorvastatin over 16 weeks in patients with acute coronary syndromes reduced the overall stroke rate by half and did not cause hemorrhagic stroke. These findings need to be confirmed in future trials.

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