Misdiagnosed amoebic colitis leading to severe dysentery and necrotizing colitis--report of a case and review of the literature.

We present a case of amoebic colitis, misdiagnosed as inflammatory bowel disease and treated with corticosteroids, leading to severe necrotizing enterocolitis. We review the literature on the epidemiology, pathogenesis, diagnosis, and treatment of amoebic dysentery, with special emphasis on the association between immunosuppressive treatment and the development of severe invasive amoebiasis.

The association between soluble CD163, disease severity, and ursodiol treatment in patients with primary biliary cholangitis.

INTRODUCTION: The macrophage activation marker soluble (s)CD163 is associated with disease severity and prognosis in patients with primary biliary cholangitis (PBC). Ursodeoxycholic acid (UDCA) treatment attenuates fibrosis progression in PBC patients, but its effect on macrophage activation is unclear. We examined the effect of UDCA on macrophage activation, as determined by sCD163 levels. METHODS: We included 2 cohorts of PBC patients; 1 cohort with prevalent PBC patients, and 1 cohort of incident PBC patients before start of UDCA treatment and with follow-up after 4 weeks and 6 months. We measured sCD163 and liver stiffness in both cohorts. Further, we measured sCD163 and TNF-α shedding in vitro in monocyte-derived macrophages after UDCA and lipopolysaccharide incubation. RESULTS: We included 100 patients with prevalent PBC [93% women, median age 63 y (interquartile range: 51-70)] and 47 patients with incident PBC [77% women, median age 60 y (49-67)]. Prevalent PBC patients had a lower median sCD163 of 3.54 mg/L (2.77-4.72) than incident PBC patients with a median sCD163 of 4.33 mg/L (2.83-5.99) at inclusion. Patients with an incomplete response to UDCA and patients with cirrhosis had higher sCD163 than responders to UDCA and noncirrhosis patients. After 4 weeks and 6 months of UDCA treatment median sCD163 decreased by 4.6% and 9.0%, respectively. In in vitro experiments, UDCA attenuated shedding of TNF-α, but not sCD163, from monocyte-derived macrophages. CONCLUSION: In PBC patients, sCD163 levels correlated with liver disease severity and treatment response to UDCA. Further, after 6 months of UDCA treatment, we observed a decrease in sCD163, which may be related to the treatment.

The insulin-like growth factor (IGF)-system in active ulcerative colitis and Crohn's disease: relations to disease activity and corticosteroid treatment.

BACKGROUND: Metabolic bone disease (MBD) and muscle wasting (MW) are serious complications in adults suffering from inflammatory bowel disease (IBD). The inflammatory process and corticosteroid treatment may lead to changes in the IGF-system associated with MBD and MW. AIM: To assess changes in the IGF-system and clinical and biochemical markers in ulcerative colitis (UC) and Crohn's disease (CD). METHODS: We studied 37 IBD patients with severe clinical exacerbation (20 with UC, 17 with CD) before and during high dose corticosteroid treatment and tapering (8-12 weeks). RESULTS: Total IGF-I was reduced in CD (36% p<0.01) and UC (41% p<0.001) before treatment and normalized completely. Free IGF-I baseline levels were unchanged compared to controls. In UC, free IGF-I levels increased significantly at week 1 and week 4 (p<0.01, respectively). In CD, no changes in free IGF-I levels were observed. IGFBP-2 baseline levels were increased by a factor 2.3 in UC and CD compared to controls (p<0.01 respectively) and normalized during treatment. IGFBP-3 was reduced by 38% (p<0.01) in CD and 32% (p<0.01) in UC with only partial normalization. Harvey-Bradshaw index, C - reactive protein and albumin normalized during treatment. CONCLUSIONS: Significant changes in total and free IGF-I and IGFBP-2 and IGFBP-3 were demonstrated in CD and UC patients in exacerbation with only partial normalization during high dose corticosteroid treatment and tapering without differences between UC and CD. These changes may be part of MBD and MW in active IBD.

Impact of enteral supplements enriched with omega-3 fatty acids and/or omega-6 fatty acids, arginine and ribonucleic acid compounds on leptin levels and nutritional status in active Crohn's disease treated with prednisolone.

BACKGROUND: Patients with Crohn's disease (CD) often develop malnutrition due to disease activity. We aimed to assess the effect of two different enteral supplements of Impact(R) Powder (IP; Novartis, Switzerland) on leptin levels and nutritional status in active CD patients during prednisolone treatment and tapering. METHODS: Thirty-one CD patients were randomized to IP Extra (group 1) or IP Standard (group 2). Leptin levels, nutritional, clinical and biochemical markers were studied at inclusion, after 5 and after 9 weeks of the study. RESULTS: Leptin levels, body mass index (BMI) and total cholesterol increased significantly within both groups at week 5 compared to inclusion. Leptin levels correlated with BMI in both groups at inclusion and in group 2 at week 9. In group 1, triglyceride levels remained unchanged, while levels in group 2 increased significantly at week 5 compared to inclusion. Clinical and biochemical markers improved during the study compared to inclusion. CONCLUSIONS: Increased leptin levels during the study progress were transient, decreasing due to prednisolone withdrawal at the end of the study. Both formulas used as adjuvant therapy to prednisolone treatment were able to improve nutritional status in CD patients.

Diagnosis and treatment of unexplained anemia with iron deficiency without overt bleeding.

A general overview is given of the causes of anemia with iron deficiency as well as the pathogenesis of anemia and the para-clinical diagnosis of anemia. Anemia with iron deficiency but without overt GI bleeding is associated with a risk of malignant disease of the gastrointestinal tract; upper gastrointestinal cancer is 1/7 as common as colon cancer. Benign gastrointestinal causes of anemia are iron malabsorption (atrophic gastritis, celiac disease, chronic inflammation, and bariatric surgery) and chronic blood loss due to gastrointestinal ulcerations. The following diagnostic strategy is recommended for unexplained anemia with iron deficiency: conduct serological celiac disease screening with transglutaminase antibody (IgA type) and IgA testing and perform bidirectional endoscopy (gastroscopy and colonoscopy). Bidirectional endoscopy is not required in premenopausal women < 40 years of age. Small intestine investigation (capsule endoscopy, CT, or MRI enterography) is not recommended routinely after negative bidirectional endoscopy but should be conducted if there are red flags indicating malignant or inflammatory small bowel disease (e.g., involuntary weight loss, abdominal pain or increased CRP). Targeted treatment of any cause of anemia with iron deficiency found on diagnostic assessment should be initiated. In addition, iron supplementation should be administered, with the goal of normalizing hemoglobin levels and replenishing iron stores. Oral treatment with a 100-200 mg daily dose of elemental iron is recommended (lower dose if side effects), but 3-6 months of oral iron therapy is often required to achieve therapeutic goals. Intravenous iron therapy is used if oral treatment lacks efficacy or causes side effects or in the presence of intestinal malabsorption or prolonged inflammation. Three algorithms are given for the following conditions: a) the paraclinical diagnosis of anemia with iron deficiency; b) the diagnostic work-up for unexplained anemia with iron deficiency without overt bleeding; and c) how to proceed after negative bidirectional endoscopy of the gastrointestinal tract.

[Nonalcoholic steatohepatitis. Three case reports]. / Nonalkoholisk steatohepatitis. Tre sygehistorier.

Non-alcoholic steatohepatitis (NASH) may develop in a subset of patients with non-alcoholic fatty liver disease (NAFLD). NASH is strongly associated to the metabolic syndrome with insulin resistance and obesity. NASH can progress to liver fibrosis, cirrhosis and chronic hepatic failure and eventual need for a liver transplantation. Three case stories are presented with characteristic clinical and histopathological changes.

[Nonalcoholic steatohepatitis--a "new" hepatic disease]. / Nonalkoholisk steatohepatitis--en "ny" sygdom i hepatologien.

Non-alcoholic fatty liver disease (NAFLD) is one of the most common hepatic disorders in the Western world. Non-alcoholic steatohepatitis (NASH) may occur in a subset of NAFLD patients and is an increasingly recognised clinicopathologial hepatic disorder. NASH may have significant impact on the healthcare system as it is associated with the metabolic syndrome comprising insulin resistance, obesity, hypertension, and type 2 diabetes mellitus. NASH can progress to liver fibrosis, cirrhosis and chronic hepatic failure and eventually to the need for a liver transplantation. The present review deals with the epidemiological features of NASH, describes a two-step pathogenesis with hepatic lipid accumulation (NAFLD) followed by the development of steatohepatitis (NASH). A strategy for establishing a diagnosis of NASH is presented including the indication for liver biopsy. The treatment of NASH may comprise different modalities from diet, weight loss, and exercise to pharmacological treatment to improve insulin resistance and drugs with antioxidant effects.

The insulin-like growth factor (IGF) system and its relation to infliximab treatment in adult patients with Crohn's disease.

OBJECTIVE: Metabolic bone disease (MBD) and muscle wasting (MW) are serious complications in adult patients suffering from inflammatory bowel disease. These complications may be caused by alterations in the insulin-like growth factor (IGF) system. The aim of the present study was to assess changes in the IGF system in patients with active Crohn's disease (CD) before and during infliximab treatment. MATERIAL AND METHODS: We studied 13 patients with therapy refractory CD, treated with infliximab (5 mg/kg body-weight) at baseline and after 2 weeks. The IGF system and markers of inflammation were examined at baseline, on days 2-5 and after 1, 4, and 8 weeks. Ten healthy age- and gender-matched persons served as controls. RESULTS: Total IGF-I and IGF binding protein (IGFBP)-3 levels were reduced by 36% (p<0.05) and 27% (p<0.001), respectively, compared with those of controls, and normalized during the study period. Free IGF-I levels were reduced by 46% (p<0.05) compared with those of controls and remained suppressed. IGFBP-2 levels were increased at baseline by a factor 2.3 compared to controls (p<0.01) with partial normalization at the end of the study period. The Crohn's disease Activity Index, the Harvey Bradshaw Index, C-reactive protein, orosomucoid and albumin reached normal levels during infliximab treatment. CONCLUSIONS: Treatment with infliximab normalized circulating levels of total IGF-I and IGFBP-3, and partially normalized IGFBP-2, whereas free IGF-I remained suppressed. We suggest that the changes in the IGF system may be part of the catabolic state in active CD and may have an association with MBD and MW.

Insulin-like growth factors (IGFs) and IGF binding proteins in active Crohn's disease treated with omega-3 or omega-6 fatty acids and corticosteroids.

OBJECTIVE: Catabolism and growth impairment are well-known complications of inflammatory bowel disease (IBD). This may be caused by the disease activity itself and/or the medical treatment, and both may lead to changes in the growth hormone (GH)/insulin-like growth factor I (IGF-I) axis. The aim of the present study was to examine the effects of enteral nutrition, Impact Powder, as adjuvant therapy to corticosteroid treatment on changes in the GH/IGF-I axis in patients with Crohn's disease (CD). MATERIAL AND METHODS: The patients were randomized to 3-IP (omega-3-fatty acid (FA), 3 g/day) or 6-IP (omega-6-FA, 9 g/day). Changes in total IGF-I (tIGF-I) and total IGF-II (tIGF-II), free IGF-I (fIGF-I), IGF binding proteins (IGFBP-1 and IGFBP-3), IGFBP-3 protease activity and insulin levels were examined in 31 patients with active CD (CDAI: 186-603) during treatment with prednisolone (40 mg for 1 week) and tapering the dose by 5 mg/week. Clinical and biochemical markers of inflammation were studied at day 0, and after 5 and 9 weeks. RESULTS: There were no differences at baseline between the two groups. During the treatment period, tIGF-I, fIGF-I and IGFBP-3 increased significantly in both groups compared to baseline (p<0.05) without differences between the groups. Insulin and IGFBP-1 showed no significant changes throughout the treatment period. CONCLUSIONS: There was no difference between 3-IP and 6-IP as adjuvant enteral nutrition on the GH/IGF-I axis. The changes observed in the GH/IGF-I axis are in line with previously published studies and may be explained by corticosteroid treatment; however, we cannot exclude an additional effect of omega3-/omega6 FA as adjuvant enteral nutrition.