Enteric neuropathology of the terminal ileum in patients with intractable slow-transit constipation.

Slow-transit constipation is usually considered a colonic motor disorder. However, there is some evidence that abnormalities may be present in locations other than the colon. In particular, several studies have reported abnormal motor activity of the small bowel in these patients. We evaluated the neuropathological aspects of the terminal ileum in patients with slow-transit constipation to see whether abnormalities are present that may explain an abnormal motility of the small intestine. Specimens of the terminal ileum were obtained from 16 female patients (age range, 42-76 years) with slow-transit constipation undergoing surgery for intractable symptoms. Fifteen age- and sex-matched controls were used for comparison. Histologic and immunohistochemical evaluation of the myenteric plexus and the smooth muscle of the proximal ileal resection margin was carried out by means of hematoxylin and eosin, trichrome and periodic acid-Schiff stain, neuron-specific enolase, S-100, CD117, CD34, anti-alpha-actin, desmin, and vimentin antibodies. The patient group displayed a significantly reduced number of glial cells, compared with controls, in both the submucosal and the myenteric plexus. Only 1 of the 3 populations of interstitial cells of Cajal (that associated with the deep muscular plexus) was decreased in patients. No differences were found between patients and controls concerning ganglia neurons, fibroblast-like cells, enteric neurons, apoptotic phenomena, and smooth muscle. Patients with slow-transit constipation display neuropathological abnormalities of the terminal ileum to a lesser extent than those we previously found in the colon, which might explain the abnormal motor aspects sometimes found in these patients.

Gastrointestinal stromal tumors: usefulness of immunohistochemistry, flow cytometry and fluorescence in situ hybridization.

BACKGROUND AND AIMS: Gastrointestinal stromal tumors (GIST) constitute a group of primary mesenchymal tumors of the gastrointestinal tract, known for their diversity in clinical behavior and the difficulties in determining malignancy and prognosis. This retrospective study evaluated a series of GIST by means of immunohistochemical techniques, flow cytometry and fluorescence in situ hybridization (FISH). METHODS: Nine patients with GIST were analyzed for tumor size, mitotic count and CD117, CD34, MIB-1 with immunohistochemistry. In addition, the GIST were tested with FISH for chromosomes 8 and 17 and DNA index was evaluated by flow cytometry. RESULTS: The findings confirmed the usefulness of CD117 and CD34 in diagnosing GIST and the prognostic role of MIB-1, but do not support a correlation between aneuploidy in flow cytometry and poor outcome. The FISH results suggest close follow-up for patients with benign GIST with a numerical alteration of chromosome 8. The technique could select patients with tumors at high-risk with aneusomy of chromosome 17. CONCLUSION: This study shows the possible application of FISH to the evaluation of patients with GIST, in addition to analysis of morphological features.

Apoptotic phenomena are not a major cause of enteric neuronal loss in constipated patients with dementia.

Chronic constipation is a frequent symptom in patients with dementia, especially in those institutionalized. However, few data are available on the neuropathological aspects of the colon in such patients. We investigated the enteric neuropathology of the colon in two patients with longstanding dementia and intractable constipation, requiring surgery to alleviate symptoms. The results were compared to those obtained in 10 controls. No abnormalities were found at conventional histological examination, except for the presence of melanosis coli. Immunohistochemical evaluation revealed no important difference between patients and controls, except for a decreased number of enteric neurons in patients. However, this neuronal decrease was not associated to apoptotic phenomena, as observed in patients with severe idiopathic constipation. We concluded that in severely constipated patients with dementia the neuropathological abnormalities might be reconducted to a physiological neuronal decrease as a result of aging, and that the pathophysiological aspects of constipation in these subjects differ from those found in idiopathic constipation.