Chagas disease frequently causes megacolon. We investigated the enteric nervous systems in patients with chagasic megacolon compared to idiopathic megacolon and controls. Surgical specimens were obtained from 12 patients with chagasic megacolon (1 woman, 11 men, age range 41 to 72 y) and 9 patients with idiopathic megacolon (3 women, 6 men, age range 39 to 68 y), undergoing surgery for intractable constipation. A control group of 10 patients (9 women, 1 man, age range 43 to 75 y) undergoing left hemicolectomy for nonobstructing colorectal cancer was also studied. Colonic sections were investigated by conventional and immunohistochemical methods, also taking into consideration the presence of lymphocytes. Compared to controls, the 2 megacolon groups showed a decrease of enteric neurons (not due to increased apoptosis) and of enteric glial cells (all more important in chagasic patients). The interstitial cells of Cajal subtypes were decreased but not absent in megacolons, although an increase of the intramuscular subtype was found, suggesting a possible compensative mechanism. An increased amount of fibrosis was found in the smooth muscle and the myenteric plexus of chagasic patients compared to the idiopathic megacolon and the control group. A mild lymphocytic infiltration of the enteric plexuses (more evident in Chagas disease) was also found in megacolons but not in controls. Patients with chagasic megacolon display important abnormalities of several components of the enteric nervous system. Similar alterations, although of lesser severity, may be found in patients with idiopathic megacolon.
Background:
Pouchitis has been suggested to be a recurrence of ulcerative colitis in a colon‐like mucosa. Topical steroids are a valid therapeutic alternative for distal forms of ulcerative colitis.
Aim:
To investigate the efficacy and tolerability of budesonide enema in the treatment of pouchitis compared with oral metronidazole.
Materials and methods:
Twenty‐six patients with an active episode of pouchitis (defined as a pouchitis disease activity index score ≥ 7) and no treatment during the previous month were randomized to receive either budesonide enema (2 mg/100 mL at bedtime) plus placebo tablets or oral metronidazole (0.5 g b.d.) plus placebo enema in a prospective, double‐blind, double‐dummy, 6‐week, controlled trial.
Results:
Based on the intention‐to‐treat principle, we detected a significant improvement in disease activity at the end of the first week with both drugs (P < 0.01). After that, improvement was moderated until stabilization at 4 weeks in both treatments. The per protocol analysis showed that both drugs had similar efficacy in terms of disease activity, clinical and endoscopic findings. Fifty‐eight per cent and 50% of patients improved (decrease in pouchitis disease activity index ≥ 3) with budesonide enema and metronidazole, respectively (odds ratio, 1.4; confidence interval, 0.2–8.9). Adverse effects were observed in 57% of patients given metronidazole and in 25% of patients given budesonide.
Conclusions:
Budesonide enemas are an alternative treatment for active pouchitis, with similar efficacy but better tolerability than oral metronidazole.
Increased sucrose permeability is a sensitive marker for advanced celiac disease. Moreover, it decreases rapidly in response to a gluten-free diet and therefore is potentially useful to follow response to therapy.
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