Apoptosis: one of the mechanisms that maintains unresponsiveness of the intestinal mucosal immune system.

Intestinal mucosa is constantly exposed to environmental AGS: Activation of lamina propria (LP) T cells by luminal Ags may lead to the production of inflammatory cytokines and subsequent mucosal inflammation and tissue damage. However, in normal circumstances, LP T cells do not respond to antigenic stimulation. The mechanisms of this unresponsiveness in healthy subjects are not fully understood. In this study, we found by in vivo analysis that, except for T cells in lymph nodules of the mucosa, 15% of LP T cells underwent apoptosis in normal individuals. In contrast, there was a marked reduction in apoptosis of LP T cells in patients with inflammatory bowel disease (Crohn's disease and ulcerative colitis) and those with specific colitis. Our findings suggest that apoptosis might be a mechanism that turns off mucosal T cell responses to environmental Ags in healthy subjects, and resistance to apoptosis could be an important cause of mucosal immune dysregulation and tissue inflammation in colitis.

Evaluation and revision of a vasopressin/nitroglycerin protocol for use in variceal bleeding.

BACKGROUND: Continuous infusion of IV vasopressin have been widely used to lower portal pressure and reduce bleeding from esophageal varices. Recently, the combination of vasopressin and nitroglycerin has been noted to be superior to vasopressin alone. This is due to the ability of nitroglycerin to reduce the detrimental effects of vasopressin while preserving its beneficial effects. In September 1989 the authors initiated a protocol in the medical intensive care unit of a large university teaching center that directed caregivers in the simultaneous use of vasopressin and nitroglycerin for use in variceal bleeding. OBJECTIVE: To determine whether the protocol was being used correctly and whether the addition of nitroglycerin produced the desired cardiovascular effects. METHOD: Nineteen patients (25 separate episodes) assigned to the vasopressin/nitroglycerin protocol were monitored retrospectively over a 20-month period for a total of 1068 hours of vasopressin/nitroglycerin infusion. Twenty-four patients received nitroglycerin at 10 to 50 micrograms per minute, 13 at 50 to 100 micrograms per minute and 6 at 100 to 400 micrograms per minute. RESULTS: Nitroglycerin dosage was not advanced appropriately in 78% of episodes despite evidence of bradycardia, hypertension and peripheral vasoconstriction. CONCLUSIONS: Revision of the protocol, giving additional guidance to clinicians on assessment and nitroglycerin advancement, was necessary and was accomplished.

Pepsin fibrinolysis of artificial clots made from fibrinogen concentrate and bovine thrombin: the effect of pH and epsilon aminocaproic acid.

Artificial clots made from fibrin glue with and without an inhibitor of fibrinolysis can be used to treat gastrointestinal bleeding. We have been unable to find descriptions of the effects of acid and pepsin upon such artificial clots. Therefore, 10(-2) mol/l epsilon aminocaproic acid was added to fibrin glue in vitro at acid concentrations of pH 1.0 and pH 5.5. Pepsin was added at 9000 U/50 ml, the expected value for fasting human subjects. There was a highly significant reduction in clot survival at pH 1.0. At pH 5.5, clot weight was also significantly decreased with pepsin, compared to control. Thus pepsin and acidity greatly affect survival of artificial clots, but the addition of epsilon aminocaproic acid did not affect clot survival.

Solitary hamartomatous polyp of the duodenum in the absence of familial polyposis.

A large hamartomatous polyp of the Peutz-Jegher type was discovered in the distal duodenum by endoscopy in a patient with occult gastrointestinal bleeding. There were no other polyps in the gastrointestinal tract and the patient lacked any stigmata associated with the familial polyposis syndromes. This is the second well-documented case of an isolated hamartomatous polyp of the Peutz-Jegher type in the small intestine occurring in the absence of familial polyposis.

Adult respiratory distress syndrome due to malignant histiocytosis.

While a 23-year-old man was being evaluated for a two-month history of night sweats, fever, and weight loss, he had the typical clinical, radiologic, and laboratory findings of adult respiratory distress syndrome (ARDS). After a diagnosis of malignant histiocytosis (MH) was established by lymph node biopsy, review of an earlier lung biopsy initially interpreted as nonspecific revealed malignant histiocytes. He failed to respond to combination chemotherapy and died as a result of progressive respiratory failure.