The role of dietary supplements in inflammatory bowel disease: a systematic review.

Inflammatory bowel diseases (IBD) are chronic immune disorders of unclear aetiology. Dietary deficiencies may be a potential pathogenic factor in their development. Patients often take food supplements without knowledge of any evidence base. We have therefore assessed the evidence for food supplementation in the management of IBD. A PubMed search was performed for the terms Inflammatory bowel disease; nutritional deficiencies; dietary supplements; curcumin; green tea; vitamin D/other vitamins; folic acid; iron; zinc; probiotics; andrographis paniculata; and boswellia serrate. PubMed was used to search for all relevant articles published between January 1975 and September 2015. Curcumin supplementation has been reported to be effective in reducing the symptoms and the inflammatory indices in IBD patients. Similar results have been observed for green tea; however, pertinent studies are limited. Vitamin D supplementation may help to increase bone mineral density in IBD patients and to reduce disease activity. IBD patients with ileal resections higher than 20 cm may develop vitamin B12 deficiency that requires parenteral supplementation. There is no current evidence to support fat-soluble vitamin supplementation in IBD patients. Zinc and iron should be supplemented in selected cases. Probiotics (VSL#3) may reduce disease activity in IBD patients with pouchitis. Complementary and alternative medicines are used by IBD patients and some studies have shown promising results. In summary, attention to dietary factors such as curcumin, green tea and vitamins, including vitamins D and B12, appears to be beneficial and, if necessary, supplementation may be appropriate.

Does the severity of primary sclerosing cholangitis influence the clinical course of associated ulcerative colitis?

BACKGROUND AND AIMS: Ulcerative colitis (UC) associated with primary sclerosing cholangitis (PSC) is usually clinically mild. The aim of the study was to assess whether there is an association between severity of PSC and activity of UC, comparing the course of UC in patients with PSC not needing liver transplantation (LT) and those eventually transplanted. METHODS: Between 1990 and 2009, 96 consecutive patients with PSC/UC were seen in the authors' institution. Data were evaluated from a database regarding UC activity (median follow-up 144 months). Follow-up was censored at time of LT or last clinical review. RESULTS: Patients with PSC/UC were divided into two groups: 46 did not need LT (no-LT) and 50 were transplanted (LT). There were no significant differences concerning duration of UC or PSC and extent of UC. The LT group had significantly (p=0.002) more clinically quiescent UC compared with the no-LT group. The LT group had fewer UC flare-ups (p=0.04) and required fewer steroid courses (p=0.025) with shorter duration (p=0.022) and less use of azathioprine (p=0.003). There was an increased need for surgery in the no-LT group (p=0.006). Colon carcinoma and high grade dysplasia were more frequent in the no-LT group (p=0.004). The no-LT group had increased inflammation in the colonic mucosa at histology (p=0.011), but without visual difference at colonoscopy. CONCLUSIONS: Clinically progressive PSC requiring LT is associated with a milder course of UC (reduced disease activity and less use of steroids, azathioprine and surgery). This is paralleled by less histological activity and reduced incidence of dysplasia and colon carcinoma.

Decrease of intragastric acidity in healthy subjects dosed with ranitidine 75 mg, cimetidine 200 mg, or placebo.

This study assessed the duration of action of single doses of ranitidine (75 mg), cimetidine (200 mg), or placebo on intragastric acidity in healthy subjects. When dosed with placebo, mean daytime intragastric acidity (0-10 hr after dose) was 37.62 mmol/liter, decreasing to 17.21 mmol/liter (mean decrease 59%; P < 0.001 vs placebo) and 25.06 mmol/liter (mean decrease 35%; P < 0.001 vs placebo) when treated with ranitidine and cimetidine, respectively. Ranitidine inhibited intragastric acidity to a greater degree than cimetidine (P < 0.001). Mean nighttime (10-20 hr after-dose) intragastric acidity when dosed with placebo was 34.37 mmol/liter, decreasing to 29.06 mmol/liter (mean decrease 18%; P = 0.027 vs placebo) when dosed with ranitidine and remaining virtually unchanged at 33.85 mmol/liter (mean decrease 2%; NS vs. placebo) when dosed with cimetidine. Ranitidine inhibited acidity to a greater degree than cimetidine (P = 0.043). The inhibitory effect of ranitidine, 75 mg, on intragastric acidity can be detected from 0-15 hr after an oral dose. Cimetidine 200 mg has little inhibitory effect beyond 10 hr.