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Sundqvist, Tommy
Publications (10 of 83) Show all publications
Tjellstrom, B., Högberg, L., Stenhammar, L., Magnusson, K.-E., Midtvedt, T., Norin, E. & Sundqvist, T. (2016). Letter: A Role for Bacteria in Celiac Disease? in DIGESTIVE DISEASES AND SCIENCES, vol 61, issue 7, pp 2140-2140 [Letter to the editor]. Digestive Diseases and Sciences, 61(7), 2140-2140
Open this publication in new window or tab >>Letter: A Role for Bacteria in Celiac Disease? in DIGESTIVE DISEASES AND SCIENCES, vol 61, issue 7, pp 2140-2140
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2016 (English)In: Digestive Diseases and Sciences, ISSN 0163-2116, E-ISSN 1573-2568, Vol. 61, no 7, p. 2140-2140Article in journal, Letter (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
SPRINGER, 2016
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-130728 (URN)10.1007/s10620-016-4131-4 (DOI)000379013300046 ()27017223 (PubMedID)
Available from: 2016-08-22 Created: 2016-08-22 Last updated: 2017-11-28
Tjellström, B., Stenhammar, L., Magnusson, K.-E., Midtvedt, T., Norin, E., Sundqvist, T. & Högberg, L. (2015). Letter: Exclusive Enteral Nutrition Does Not Normalize Gut Microflora Function in Pediatric Perianal Crohn Disease in JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION, vol 61, issue 1, pp E4-E4 [Letter to the editor]. Journal of Pediatric Gastroenterology and Nutrition - JPGN, 61(1), E4-E4
Open this publication in new window or tab >>Letter: Exclusive Enteral Nutrition Does Not Normalize Gut Microflora Function in Pediatric Perianal Crohn Disease in JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION, vol 61, issue 1, pp E4-E4
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2015 (English)In: Journal of Pediatric Gastroenterology and Nutrition - JPGN, ISSN 0277-2116, E-ISSN 1536-4801, Vol. 61, no 1, p. E4-E4Article in journal, Letter (Other academic) Published
Abstract [en]

n/a

Place, publisher, year, edition, pages
Lippincott, Williams andamp; Wilkins, 2015
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-120654 (URN)10.1097/MPG.0000000000000831 (DOI)000358168800001 ()25905542 (PubMedID)
Available from: 2015-08-20 Created: 2015-08-20 Last updated: 2017-12-04
Björnsson, B., Bojmar, L., Olsson, H., Sundqvist, T. & Sandström, P. (2015). Nitrite, a novel method to decrease ischemia/reperfusion injury in the rat liver. World Journal of Gastroenterology, 21(6), 1775-1783
Open this publication in new window or tab >>Nitrite, a novel method to decrease ischemia/reperfusion injury in the rat liver
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2015 (English)In: World Journal of Gastroenterology, ISSN 1007-9327, E-ISSN 2219-2840, Vol. 21, no 6, p. 1775-1783Article in journal (Refereed) Published
Abstract [en]

AIM: To investigate whether nitrite administered prior to ischemia/reperfusion (I/R) reduces liver injury.

METHODS: Thirty-six male Sprague-Dawley rats were randomized to 3 groups, including sham operated (n = 8), 45-min segmental ischemia of the left liver lobe (IR, n = 14) and ischemia/reperfusion (I/R) preceded by the administration of 480 nmol of nitrite (n = 14). Serum transaminases were measured after 4 h of reperfusion. Liver microdialysate (MD) was sampled in 30-min intervals and analyzed for glucose, lactate, pyruvate and glycerol as well as the total nitrite and nitrate (NOx). The NOx was measured in serum.

RESULTS: Aspartate aminotransferase (AST) at the end of reperfusion was higher in the IR group than in the nitrite group (40 ± 6.8 μkat/L vs 22 ± 2.6 μkat/L, P = 0.022). Similarly, alanine aminotransferase (ALT) was also higher in the I/R group than in the nitrite group (34 ± 6 μkat vs 14 ± 1.5 μkat, P = 0.0045). The NOx in MD was significantly higher in the nitrite group than in the I/R group (10.1 ± 2.9 μM vs 3.2 ± 0.9 μM, P = 0.031) after the administration of nitrite. During ischemia, the levels decreased in both groups and then increased again during reperfusion. At the end of reperfusion, there was a tendency towards a higher NOx in the I/R group than in the nitrite group (11.6 ± 0.7 μM vs 9.2 ± 1.1 μM, P = 0.067). Lactate in MD was significantly higher in the IR group than in the nitrite group (3.37 ± 0.18 mM vs 2.8 ± 0.12 mM, P = 0.01) during ischemia and the first 30 min of reperfusion. During the same period, glycerol was also higher in the IRI group than in the nitrite group (464 ± 38 μM vs 367 ± 31 μM, P = 0.049). With respect to histology, there were more signs of tissue damage in the I/R group than in the nitrite group, and 29% of the animals in the I/R group exhibited necrosis compared with none in the nitrite group. Inducible nitric oxide synthase (iNOS) transcription increased between early ischemia (t = 15) and the end of reperfusion in both groups.

CONCLUSION: Nitrite administered before liver ischemia in the rat liver reduces anaerobic metabolism and cell necrosis, which could be important in the clinical setting.

Place, publisher, year, edition, pages
Baishideng Publishing Group Co. Limited, 2015
Keywords
Ischemia-reperfusion injury; Nitrite; Liver ischemia; Liver surgery; Microdialysis; Nitric oxide; Inducible nitric oxide synthase
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:liu:diva-110262 (URN)10.3748/wjg.v21.i6.1775 (DOI)000349666300010 ()25684942 (PubMedID)
Available from: 2014-09-05 Created: 2014-09-05 Last updated: 2017-12-05Bibliographically approved
Andersson, H., Björnström-Karlsson, K., Eintrei, C. & Sundqvist, T. (2015). Orexin A Phosphorylates the gamma-Aminobutyric Acid Type A Receptor beta(2) Subunit on a Serine Residue and Changes the Surface Expression of the Receptor in SH-SY5Y Cells Exposed to Propofol. Journal of Neuroscience Research, 93(11), 1748-1755
Open this publication in new window or tab >>Orexin A Phosphorylates the gamma-Aminobutyric Acid Type A Receptor beta(2) Subunit on a Serine Residue and Changes the Surface Expression of the Receptor in SH-SY5Y Cells Exposed to Propofol
2015 (English)In: Journal of Neuroscience Research, ISSN 0360-4012, E-ISSN 1097-4547, Vol. 93, no 11, p. 1748-1755Article in journal (Refereed) Published
Abstract [en]

Propofol activates the gamma-aminobutyric acid type A receptor (GABA(A)R) and causes a reversible neurite retraction, leaving a thin, thread-like structure behind; it also reverses the transport of vesicles in rat cortical neurons. The awakening peptide orexin A (OA) inhibits this retraction via phospholipase D (PLD) and protein kinase CE (PKCE). The human SH-SY5Y cells express both GABA(A)Rs and orexin 1 and 2 receptors. These cells are used to examine the interaction between OA and the GABAAR. The effects of OA are studied with flow cytometry and immunoblotting. This study shows that OA stimulates phosphorylation on the serine residues of the GABA(A)R beta(2) subunit and that the phosphorylation is caused by the activation of PLD and PKCE. OA administration followed by propofol reduces the cell surface expression of the GABA(A)R, whereas propofol stimulation before OA increases the surface expression. The GABA(A)R beta(2) subunit is important for receptor recirculation, and the effect of OA on propofol-stimulated cells may be due to a disturbed recirculation of the GABA(A)R. (C) 2015 Wiley Periodicals, Inc.

Place, publisher, year, edition, pages
WILEY-BLACKWELL, 2015
Keywords
orexin; propofol; GABAAR; cell signaling; AB_10675844; AB_1269637; AB_10712311; AB_2247467; AB_307187; AB_307184; AB_1566589
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-122517 (URN)10.1002/jnr.23631 (DOI)000362831800013 ()26283475 (PubMedID)
Note

Funding Agencies|County Council of Ostergotland ALF Grants; Linkoping University Hospital; Ella and Henry Stahl Research Foundation

Available from: 2015-11-09 Created: 2015-11-06 Last updated: 2018-01-10
Björnsson, B., Winbladh, A., Bojmar, L., Sundqvist, T., Gullstrand, P. & Sandström, P. (2014). Conventional, but not remote ischemic preconditioning, reduces iNOS transcription in liver ischemia/reperfusion. World Journal of Gastroenterology, 20(28), 9506-9512
Open this publication in new window or tab >>Conventional, but not remote ischemic preconditioning, reduces iNOS transcription in liver ischemia/reperfusion
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2014 (English)In: World Journal of Gastroenterology, ISSN 1007-9327, E-ISSN 2219-2840, Vol. 20, no 28, p. 9506-9512Article in journal (Refereed) Published
Abstract [en]

AIM: To study the effects of preconditioning on inducible nitric oxide synthase (iNOS) and interleukin 1 (IL-1) receptor transcription in rat liver ischemia/reperfusion injury (IRI). METHODS: Seventy-two male rats were randomized into 3 groups: the one-hour segmental ischemia (IRI, n = 24) group, the ischemic preconditioning (IPC, n = 24) group or the remote ischemic preconditioning (R-IPC, n = 24) group. The IPC and R-IPC were performed as 10 min of ischemia and 10 min of reperfusion. The iNOS and the IL-1 receptor mRNA in the liver tissue was analyzed with real time PCR. The total Nitrite and Nitrate (NOx) in continuously sampled microdialysate (MD) from the liver was analyzed. In addition, the NOx levels in the serum were analyzed. RESULTS: After 4 h of reperfusion, the iNOS mRNA was significantly higher in the R-IPC (Delta Ct: 3.44 +/- 0.57) group than in the IPC (Delta Ct: 5.86 +/- 0.82) group (P = 0.025). The IL-1 receptor transcription activity was reduced in the IPC group (Delta Ct: 1.88 +/- 0.53 to 4.81 +/- 0.21), but not in the R-IPC group, during reperfusion (P = 0.027). In the MD, a significant drop in the NOx levels was noted in the R-IPC group (12.3 +/- 2.2 to 4.7 +/- 1.2 mu mol/L) at the end of ischemia compared with the levels in early ischemia (P = 0.008). A similar trend was observed in the IPC group (11.8 +/- 2.1 to 6.4 +/- 1.5 mu mol/L), although this difference was not statistically significant. The levels of NOx rose quickly during reperfusion in both groups. CONCLUSION: IPC, but not R-IPC, reduces iNOS and IL-1 receptor transcription during early reperfusion, indicating a lower inflammatory reaction. NOx is consumed in the ischemic liver lobe.

Place, publisher, year, edition, pages
Baishideng Publishing Group Co. Limited, 2014
Keywords
Ischemia-reperfusion injury; Preconditioning; Remote preconditioning; Liver ischemia; Liver surgery; Microdialysis; Nitric oxide; inducible nitric oxide synthase; interleukin-1 receptor
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:liu:diva-109589 (URN)10.3748/wjg.v20.i28.9506 (DOI)000339389800032 ()25071345 (PubMedID)
Available from: 2014-08-21 Created: 2014-08-21 Last updated: 2017-12-05
Björnström-Karlsson, K., Turina, D., Strid, T., Sundqvist, T. & Eintrei, C. (2014). Orexin A Inhibits Propofol-Induced Neurite Retraction by a Phospholipase D/Protein Kinase C-epsilon-Dependent Mechanism in Neurons. PLoS ONE, 9(5), e0097129
Open this publication in new window or tab >>Orexin A Inhibits Propofol-Induced Neurite Retraction by a Phospholipase D/Protein Kinase C-epsilon-Dependent Mechanism in Neurons
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2014 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, no 5, p. e0097129-Article in journal (Refereed) Published
Abstract [en]

Background: The intravenous anaesthetic propofol retracts neurites and reverses the transport of vesicles in rat cortical neurons. Orexin A (OA) is an endogenous neuropeptide regulating wakefulness and may counterbalance anaesthesia. We aim to investigate if OA interacts with anaesthetics by inhibition of the propofol-induced neurite retraction. Methods: In primary cortical cell cultures from newborn rats brains, live cell light microscopy was used to measure neurite retraction after propofol (2 mu M) treatment with or without OA (10 nM) application. The intracellular signalling involved was tested using a protein kinase C (PKC) activator [phorbol 12-myristate 13-acetate (PMA)] and inhibitors of Rho-kinase (HA-1077), phospholipase D (PLD) [5-fluoro-2-indolyl des-chlorohalopemide (FIPI)], PKC (staurosporine), and a PKC epsilon translocation inhibitor peptide. Changes in PKC epsilon Ser(729) phosphorylation were detected with Western blot. Results: The neurite retraction induced by propofol is blocked by Rho-kinase and PMA. OA blocks neurite retraction induced by propofol, and this inhibitory effect could be prevented by FIPI, staurosporine and PKC epsilon translocation inhibitor peptide. OA increases via PLD and propofol decreases PKC epsilon Ser(729) phosphorylation, a crucial step in the activation of PKC epsilon. Conclusions: Rho-kinase is essential for propofol-induced neurite retraction in cortical neuronal cells. Activation of PKC inhibits neurite retraction caused by propofol. OA blocks propofol-induced neurite retraction by a PLD/PKC epsilon-mediated pathway, and PKC epsilon maybe the key enzyme where the wakefulness and anaesthesia signal pathways converge.

Place, publisher, year, edition, pages
Public Library of Science, 2014
National Category
Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:liu:diva-108807 (URN)10.1371/journal.pone.0097129 (DOI)000336857400058 ()
Available from: 2014-07-07 Created: 2014-07-06 Last updated: 2017-12-05
Tjellstrom, B., Stenhammar, L., Sundqvist, T., Fälth-Magnusson, K., Hollén, E., Magnusson, K.-E., . . . Högberg, L. (2014). The effects of oats on the function of gut microflora in children with coeliac disease. Alimentary Pharmacology and Therapeutics, 39(10), 1156-1160
Open this publication in new window or tab >>The effects of oats on the function of gut microflora in children with coeliac disease
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2014 (English)In: Alimentary Pharmacology and Therapeutics, ISSN 0269-2813, E-ISSN 1365-2036, Vol. 39, no 10, p. 1156-1160Article in journal (Refereed) Published
Abstract [en]

Background Faecal short chain fatty acids (SCFAs) are produced by the gut microflora. We have previously reported high faecal SCFA levels in children with coeliac disease (CD), indicating alteration in gut microfloral metabolism. Data accumulated over recent decades by us and others suggest that wheat-free oats can safely be included in a gluten-free diet (GFD). However, concerns have been raised with respect to the safety of oats in a subset of coeliacs. Aim To describe faecal SCFA patterns in children with newly diagnosed CD treated for 1year with a GFD with or without oats. Methods This report is part of a randomised, double-blind study on the effect of a GFD containing oats (GFD-oats) vs. a standard GFD (GFD-std). Faecal samples were received from 34 children in the GFD-oats group and 37 in the GFD-std group at initial diagnosis and/or after 1year on a GFD. Faecal SCFAs were analysed. Results The GFD-std group had a significantly lower total faecal SCFA concentration at 12months compared with 0months (Pless than0.05). In contrast, total SCFA in the GFD-oats group remained high after 1year on the GFD. The children in the GFD-oats group had significantly higher acetic acid (Pless than0.05), n-butyric acid (Pless than0.05) and total SCFA concentration (Pless than0.01) after 1-year diet treatment compared to the GFD-std group. Conclusions Our results indicate that oats do affect the gut microflora function, and that some coeliac children receiving oats may develop gut mucosal inflammation, that may present a risk for future complications.

Place, publisher, year, edition, pages
Wiley, 2014
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-106829 (URN)10.1111/apt.12707 (DOI)000334304200013 ()
Available from: 2014-05-28 Created: 2014-05-23 Last updated: 2017-12-05
Tapsas, D., Fälth-Magnusson, K., Högberg, L., Forslund, T., Sundqvist, T. & Hollén, E. (2014). Urinary nitric oxide metabolites in children with celiac disease after long-term consumption of oats-containing gluten-free diet. Scandinavian Journal of Gastroenterology, 49(11), 1311-1317
Open this publication in new window or tab >>Urinary nitric oxide metabolites in children with celiac disease after long-term consumption of oats-containing gluten-free diet
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2014 (English)In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 49, no 11, p. 1311-1317Article in journal (Refereed) Published
Abstract [en]

Objective. Oats are accepted in the gluten-free diet (GFD) for children with celiac disease (CD). Some reports have indicated, however, that not all celiac patients tolerate oats. We have previously shown that some children still have high levels of urinary nitric oxide (NO) metabolites as markers of intestinal inflammation after 1 year on GFD with oats. In this study, we measured urinary NO metabolites in CD children who had been consuming oats-containing GFD for an extended, 2-6-year period, also taking into consideration ordinary consumption of nitrite/nitrate-rich foods close to the urine sampling. Materials and Methods. Morning urinary nitrite/nitrate concentrations were measured in 188 pediatric CD patients. A questionnaire was used to elucidate factors possibly affecting the urinary levels, for example, dietary factors, asthma, or urinary tract infection. Results. Oats were consumed by 89.4% of the patients for a median time of 3 years. The median nitrite/nitrate level was 980 mu M. The majority (70.2%) who consumed oats had low levels of urinary nitrite/nitrate, that is, less than 1400 mu M, while 29.8% demonstrated high levels, that is, greater than 1400 mu M. Nitrite/nitrate-rich foods did not significantly influence the urinary concentrations. Conclusion. The urinary levels of NO metabolites revealed two subpopulations, one with high and one with low levels. The high levels could be possibly due to poor adherence to the GFD, sensitivity to oats, or some unknown factor(s). Nitrate-rich foods, asthma, or urinary tract infection did not affect the result. The elevated levels of NO metabolites could indicate mucosal inflammation and pinpoint the need of careful follow-up of children on oats-containing GFD.

Place, publisher, year, edition, pages
Informa Healthcare, 2014
Keywords
celiac disease; gluten-free diet; oats; urinary nitrite/nitrate
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-113064 (URN)10.3109/00365521.2014.946081 (DOI)000345603400006 ()25263796 (PubMedID)
Note

Funding Agencies|Medical Research Council of Southeast Sweden; County Council of Ostergotland; Swedish Research Council

Available from: 2015-01-09 Created: 2015-01-08 Last updated: 2017-12-05
Tjellström, B., Högberg, L., Stenhammar, L., Fälth-Magnusson, K., Magnusson, K.-E., Norin, E., . . . Midtvedt, T. (2013). Faecal short-chain fatty acid pattern in childhood coeliac disease is normalised after more than one year's gluten-free diet. Microbiological Ecology in Health and Disease, 24
Open this publication in new window or tab >>Faecal short-chain fatty acid pattern in childhood coeliac disease is normalised after more than one year's gluten-free diet
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2013 (English)In: Microbiological Ecology in Health and Disease, ISSN 0891-060X, E-ISSN 1651-2235, Vol. 24Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: Recent work indicates that the gut microflora is altered in patients with coeliac disease (CD). Faecal short-chain fatty acids (SCFAs) are produced by the gut microflora. We have previously reported a high SCFA output in children with symptomatic and asymptomatic CD at presentation, as well as in CD children on a gluten-free diet (GFD) for less than 1 year, indicating deviant gut microfloral function. In this report, we focus on faecal SCFA production in coeliacs on GFD for more than 1 year.

MATERIALS AND METHODS: Faecal samples were collected from 53 children with CD at presentation, 74 coeliac children on GFD for less than 1 year, and 25 individuals diagnosed with CD in childhood and on GFD for more than 1 year. The control group comprised 54 healthy children (HC). The faecal samples were analysed to show the SCFA pattern taken as a marker of gut microflora function. We applied a new fermentation index, reflecting the inflammatory activity of the SCFAs (amount of acetic acid minus propionic acid and n-butyric acid, together divided by the total amount of SCFAs).

RESULTS: In coeliacs on GFD for more than 1 year, the individual SCFAs, total SCFA, and fermentation index did not differ significantly from the findings in controls. In contrast, the faecal SCFA level was clearly higher in coeliacs treated with GFD for less than 1 year compared to those more than 1 year.

CONCLUSIONS: This is the first study on SCFA patterns in faecal samples from individuals with CD on GFD for more than 1 year. Our study indicates that the disturbed gut microflora function in children with CD at presentation and after less than 1 year of GFD, previously demonstrated by us, is normalised on GFD for more than 1 year.

Place, publisher, year, edition, pages
Järfälla, Sweden: Co-Action Publishing, 2013
Keywords
children; coeliac disease; gluten free diet; faecal short chain fatty acids; gut microflora
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-107042 (URN)10.3402/mehd.v24i0.20905 (DOI)24082880 (PubMedID)
Available from: 2014-06-04 Created: 2014-06-04 Last updated: 2017-12-05Bibliographically approved
Tjellstrom, B., Högberg, L., Stenhammar, L., Magnusson, K.-E., Midtvedt, T., Norin, E. & Sundqvist, T. (2012). Effect of exclusive enteral nutrition on gut microflora function in children with Crohns disease. Scandinavian Journal of Gastroenterology, 47(12), 1454-1459
Open this publication in new window or tab >>Effect of exclusive enteral nutrition on gut microflora function in children with Crohns disease
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2012 (English)In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 47, no 12, p. 1454-1459Article in journal (Refereed) Published
Abstract [en]

Objective. Exclusive enteral nutrition (EEN) is a first-line treatment in children with active Crohns disease (CD) but is seldom used in adults with active disease. The mode of action of EEN in suppressing mucosa] inflammation is not fully understood, but modulation of intestinal microflora activity is one possible explanation. The aim of this study was to investigate the effect of 6-week EEN in children with active CD, with special reference to intestinal microflora function. Materials and methods. Fecal samples from 18 children (11 boys, 7 girls; median age 13.5 years) with active CD (13 children with small bowel/colonic and 5 with perianal disease) were analyzed for short chain fatty acid (SCFA) pattern as marker of gut microflora function. The children were studied before and after EEN treatment. Results from 12 healthy teenagers were used for comparison. Results. Eleven (79%) of the children with small bowel/colonic CD responded clinically positively to EEN treatment showing decreased levels of pro-inflammatory acetic acid as well as increased concentrations of anti-inflammatory butyric acids and also of valeric acids, similar to the levels in healthy age-matched children. In children with active perianal CD, however, EEN had no positive effect on clinical status or inflammatory parameters. Conclusions. The authors present new data supporting the hypothesis that the well-documented anti-inflammatory effect of EEN in children with active small bowel/colonic CD is brought about by modulation of gut microflora activity, resulting in an anti-inflammatory SCFA pattern. By contrast, none of the children with perianal disease showed clinical or biochemical improvement after EEN treatment.

Place, publisher, year, edition, pages
Informa Healthcare, 2012
Keywords
children, Crohns disease, exclusive enteral nutrition, fecal short chain fatty acids, gut microflora
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-87463 (URN)10.3109/00365521.2012.703234 (DOI)000312427800007 ()
Note

Funding Agencies|Swedish Research Council|2007-3483, 2008-4051 and 2009-6649|Research Council of Southeast Sweden (FORSS)||

Available from: 2013-01-18 Created: 2013-01-18 Last updated: 2017-12-06
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