Endothelial cell autoantibodies are a marker of disease susceptibility in inflammatory bowel disease but apparently not linked to persistent measles virus infection.

Intestinal vasculitis caused by persistent measles virus infection of intestinal endothelial cells was described in Crohn's disease. Furthermore, endothelial cell autoantibodies have been demonstrated in inflammatory bowel disease (IBD). Autoantibodies against intestinal endothelial cells were visualized by indirect immunofluorescence in patients with IBD, in their healthy first-degree relatives, in patients with infectious enterocolitis, and in healthy, unrelated controls. In intestinal tissue specimens of 22 antibody-positive IBD patients a search for the measles virus genome was performed. Endothelial cell autoantibodies were significantly more frequent in patients with IBD, in both groups of first-degree relatives, and in patients with infectious enterocolitis than in the healthy controls (P = 0.0002 or less). The measles virus genome was found in none of the intestinal biopsies. Endothelial cell autoantibodies are not a genetic but rather an epigenetic (infectious) marker of disease susceptibility. The expression of these autoantibodies is unlikely to be triggered by a persistent measles virus infection.

Antineutrophil and pancreatic autoantibodies in first-degree relatives of patients with inflammatory bowel disease.

BACKGROUND: Perinuclear antineutrophil antibodies (P-ANCA) are found in ulcerative colitis, and autoantibodies against exocrine pancreas (PAB) in Crohn's disease. Their potential role as genetic or pathophysiologic factors is unclear. METHODS: In 61 patients with ulcerative colitis, 76 patients with Crohn's disease, 101 first-degree relatives of patients with ulcerative colitis, 105 first-degree relatives of Crohn's disease patients, and 56 healthy unrelated controls autoantibodies were detected by indirect immunofluorescence. RESULTS: Forty-six per cent of patients with ulcerative colitis (28 of 61) and 38% of patients with Crohn's disease (29 of 76) were P-ANCA- and PAB-positive, respectively. In relatives of patients with ulcerative colitis P-ANCA were found in 3% (3 of 101), and in relatives of Crohn's disease patients PAB were detected in 4% (4 of 105), which is not significantly different from the occurrence in the healthy controls. CONCLUSIONS: The frequency of P-ANCA and PAB does not suggest a role as genetic markers for inflammatory bowel disease.

Antinuclear autoantibodies in patients with inflammatory bowel disease. High prevalence in first-degree relatives.

Crohn's disease and ulcerative colitis show a familial aggregation. The role of antinuclear autoantibodies, which occur in both diseases, remains to be defined. In 76 patients with Crohn's disease, 61 patients with ulcerative colitis, 105 first-degree relatives of patients with Crohn's disease, 101 first-degree relatives of patients with ulcerative colitis, and 40 healthy unrelated controls antinuclear autoantibodies were detected by indirect immunofluorescence. Existence of autoantibodies was correlated with clinical features. Eighteen percent of patients with Crohn's disease (14/76), 43% of patients with ulcerative colitis (26/61), 13% of relatives of patients with Crohn's disease (14/105), 24% of relatives of ulcerative colitis patients (24/101), and 2% of the healthy controls (1/40) were positive for antinuclear autoantibodies. The difference between controls and patients and the first-degree relatives of patients with ulcerative colitis, respectively, was statistically significant (P < or = 0.0144). In ulcerative colitis, the existence of antinuclear autoantibodies was negatively correlated with immunosuppressive therapy or extraintestinal manifestations (P = 0.0004 and 0.0273, respectively). Antinuclear autoantibodies may represent a factor disposing to the development of ulcerative colitis.

Goblet cell autoantibodies in patients with inflammatory bowel disease and their first-degree relatives.

BACKGROUND & AIMS: Crohn's disease and ulcerative colitis show a familial aggregation. In both diseases, anti-goblet cell autoantibodies (GABs) have been described. The aim of this study was to define the role of GABs in the pathogenesis of inflammatory bowel disease. METHODS: The study population comprised 61 patients with ulcerative colitis, 76 patients with Crohn's disease, 101 first-degree relatives of patients with ulcerative colitis, and 105 first-degree relatives of patients with Crohn's disease. Thirty-five patients with infectious enterocolitis and 56 healthy unrelated subjects served as controls. Autoantibodies were detected by indirect immunofluorescence. RESULTS: Thirty-nine percent of patients with ulcerative colitis (24 of 61) and 30% of patients with Crohn's disease (23 of 76) were positive for GABs. GABs were detected in 21% (21 of 101) of first-degree relatives of patients with ulcerative colitis and in 19% (20 of 105) of first-degree relatives of patients with Crohn's disease. In patients with infectious enterocolitis and in healthy controls, GABs were seen in 3% (1 of 35) and 2% (1 of 56), respectively. The differences between control groups and both groups of patients or their first-degree relatives were significant. CONCLUSIONS: The high prevalence in first-degree relatives suggests that GABs may represent a marker characterizing susceptibility to inflammatory bowel disease.

[Effects of various prokinetic drugs on gastrointestinal transit times in patients with progressive systemic scleroderma]. / Einfluss verschiedener Prokinetika auf gastrointestinale Transitzeiten bei Patienten mit progressiv-systemischer Sklerodermie.

The intestine is involved in about half of the cases with progressive-systemic sclerosis. Intestinal transit disturbances which are caused by neuropathy of the enteric nerve system occur frequently. However, upto-date only few studies which determined the effect of prokinetic drugs exist. Patients with intestinal involvement caused by progressive-systemic sclerosis were treated with the prokinetic drugs cisapride (20 mg, TID; n = 9), erythromycin (250 mg, TID; n = 7) and octreotide (50 micrograms s. c., at night time; n = 5) over a period of four weeks. At study entry and after each treatment period the transit times through the stomach, small and large intestine were evaluated by use of the metal-detector test. Gastric emptying was only accelerated by erythromycin (42 +/- 3 min vs. 54 +/- 6 min; p = 0.0422), whereas treatment with cisapride and octreotide did not result in significant changes (48 +/- 4 min; p = 0.3743 and 44 +/- 4 min; p = 0.1975; resp.). Small intestinal transit times were not altered significantly by cisapride (108 +/- 15 min vs. 108 +/- 9 min; p = 0.2733), crythromycin (92 +/- 8 min; p = 0.0707) or octreotide (106 +/- 12 min; p = 0.8927). Furthermore colonic transit was not fastened by none of the prokinetic agents (study entry: 68 +/- 12 h; cisapride: 88 +/- 12 h; p = 0.0569; erythromycin 77 +/- 14 h; p = 0.7349; octreotide 107 +/- 14 h; p = 0.8927). Four patients were withdrawn from the study because of diarrhea. Prokinetic drugs do not seem to have a major impact on intestinal transit times in patients with progressive-systemic sclerosis. The use of these drugs is limited because of frequent side effects.