Microscopic colitis may be defined as a clinical syndrome, of unknown etiology, consisting of chronic watery
diarrhea, with no alterations in the large bowel at the endoscopic and radiologic evaluation. Therefore, a definitive diagnosis is only possible by histological analysis. The epidemiological impact of this disease has become increasingly clear in the last years, with most data coming from Western countries.
Microscopic colitis includes two histological subtypes [
collagenous colitis (CC) and
lymphocytic colitis (LC)] with no differences in clinical presentation and management.
Collagenous colitis is characterized by a thickening of the subepithelial
collagen layer that is absent in LC. The main feature of LC is an increase of the density of intra-epithelial lymphocytes in the surface epithelium. A number of pathogenetic theories have been proposed over the years, involving the role of
luminal agents, autoimmunity, eosinophils, genetics (human leukocyte
antigen), biliary
acids,
infections, alterations of pericryptal fibroblasts, and
drug intake; drugs like
ticlopidine,
carbamazepine or
ranitidine are especially associated with the development of LC, while CC is more frequently linked to
cimetidine, non-steroidal antiinflammatory drugs and
lansoprazole.
Microscopic colitis typically presents as chronic or intermittent watery
diarrhea, that may be accompanied by symptoms such as
abdominal pain,
weight loss and incontinence. Recent evidence has added new pharmacological options for the treatment of
microscopic colitis: the role of steroidal
therapy, especially oral
budesonide, has gained relevance, as well as
immunosuppressive agents such as
azathioprine and
6-mercaptopurine. The use of anti-
tumor necrosis factor-α agents,
infliximab and
adalimumab, constitutes a new, interesting tool for the treatment of
microscopic colitis, but larger, adequately designed studies are needed to confirm existing data.