Diplopia and diarrhea: ileal carcinoid metastatic to the central nervous system.

The case of a patient with metastatic ileal carcinoid is reported. The peculiarities of this case were as follows: 1) The patient presented with symptoms attributable to a mass lesion in the brain which was proven to be a carcinoid tumor by biopsy. 2) The patient had symptoms attributable to carcinoid syndrome without radiologic evidence of hepatic metastasis. 3) No bony or pulmonary metastasis was evident, which suggests that the metastatic spread from the ileum occurred through the spinous venous plexus of Batson. The patient's symptoms were managed with cyproheptadine with good effect. A review of the carcinoid syndrome and the determinants of its metastatic spread is presented.

Nonsteroidal anti-inflammatory gastropathy: from theory to practice.

The success of nonsteroidal anti-inflammatory drugs in managing joint inflammation and pain has come at the cost of impressive side effects, particularly in the gastrointestinal tract. This manuscript reviews the magnitude of the problem, the risk factors, and presentation of nonsteroidal gastropathy. It also presents some points in the prevention and management of the disorder.

Gastric contents retained in rat stomach following mild irritant exposure contribute to adaptive cytoprotection.

Fluid retained in the gastric lumen immediately preceding the administration of a damaging product will dilute that product and decrease its injurious capacity. In an attempt to explain the phenomenon of adaptive cytoprotection, we studied the effect of mild irritant exposure on the volume of fluid retained in the gastric lumen. Rats treated with 0.2 N-0.4 N HCl had a larger volume of gastric fluid retained as compared to animals treated with 0.4 N NaCl. Additionally, a mixture of gastric juice derived from rats exposed to 0.4 N HCl with 2 ml ethanol was significantly less damaging to the gastric mucosa than a similar mixture containing an equal volume of gastric juice derived from 0.4 N NaCl-exposed rats. We conclude from our observations that in mild irritant-exposed stomachs, the gastric juice is a main contributor to the protection against ethanol injury.

Diethylcarbamazine decreases ethanol-injury to the gastric mucosa of the rat.

Exposure of the rat stomach to ethanol stimulates the generation of leukotrienes. Leukotrienes are potent mediators of tissue inflammation and injury. In this work we show that pretreatment with diethylcarbamazine, a lipoxygenase enzyme inhibitor, significantly decreases ethanol injury to the rat gastric mucosa. At a dose of 250 mg/kg the compound significantly reduced the ETOH-stimulated mucosal LTC4 generation by 40% and PGE2 generation by 79%. We conclude that diethylcarbamazine is an inhibitor of the cyclooxygenase and lipoxygenase enzymes in the gastric mucosa. That inhibition of leukotriene synthesis decreases the extent of ethanol-stimulated suggests that leukotrienes play a key role in mediating ethanol-injury to that tissue.

Colonic filiform polyposis and a malignant adenomatous polyp.

We have reported a case of pseudopolyposis in the unusual form of filiform polyps in the transverse colon with an adenomatous polyp in the sigmoid colon that had a focus of malignant degeneration. The patient did not have any significant past history of inflammatory bowel disease.

Release of protective products, different from prostaglandins, by rat stomachs exposed to mild irritant.

The factors responsible for the mediation of mild irritant-induced (adaptive) cytoprotection to the rat stomach are not fully understood. The existence of cytoprotective products that are released by the gastric mucosa in response to its exposure to a mild irritant is assessed in this work. Gastric contents of rats exposed to a mild irritant (0.3 N HCl) or to 0.3 N NaCl (control) were collected, titrated to neutrality, and administered orally to prefasted animals followed by 100% ethanol. Ethanol-induced gross hemorrhagic injury in rats pretreated with the 0.3 N HCl gastric contents were significantly less than in control treated rats (P less than 0.01). Pretreating the donor or recipient rats with indomethacin did not interfere with the generation or protective action of the 0.3 N HCl gastric contents. These findings demonstrate that the exposure of the gastric mucosa to a mild irritant causes the release of protective products, which are different from prostaglandins, into the gastric lumen.

Prostaglandin synthesis by enterocyte microsomes of rabbit small intestine.

We studied the prostaglandin (PG) synthetic capacity of microsomes of a relatively pure population of rabbit enterocytes and determined ideal conditions for product synthesis. The epithelial cells were freed from the basement membrane by a combination of calcium chelation and mechanical vibration, and 100,000 X g microsomes were prepared. These microsomes were found to synthesize PG from exogenously added arachidonic acid. The ideal conditions for the reaction were a microsomal protein concentration of 1.0 mg/ml, an arachidonic acid concentration of 33 uM, a reaction mixture pH of 8.0-9.5 and with epinephrine 1.5 mM added as a cofactor. The product yields increased linearly with time up to 30 min. of incubation and were inhibited by 100 uM indomethacin. Under the above ideal conditions enterocyte microsomes yielded the following products expressed as pmole/mg protein/20 min. incubation: PGF2 alpha 98 +/- 7, PGE2 48 +/- 9, PGD2 28 +/- 7, TxB2 40 +/- 5, 6 Keto PGF1 alpha 15 +/- 6.