Long-term results of endoscopic balloon dilatation for gastric outlet obstruction.

Endoscopic balloon dilatation has been used for more than 10 years for the treatment of peptic gastric outlet obstruction. Long-term outcomes in series from tertiary centers have shown a high rate of failure in several studies. We reviewed a series of patients treated with balloon dilatation in a community hospital to evaluate the effectiveness in this procedure and factors that would affect success rate. Forty consecutive patients who had successful initial balloon dilatation for benign gastric outlet obstruction were followed for at least two years or until death or surgical therapy occurred. Data were obtained from the gastrointestinal laboratory log book, hospital, and office records. Patients were also interviewed by telephone. Twelve patients had relief of obstruction by initial dilatation. The remaining 28 patients developed recurrent symptoms and 12 in this group eventually required surgery. Factors predicting referral for surgery included younger age, need for multiple procedures, technical failure of dilatation in four patients, and long duration of treatment course. Eradication of Helicobacter pylori was associated with successful relief of obstruction without surgery, whereas continued use of nonsteroidal antiinflammatory drugs was associated with recurrent obstruction. In the community hospital, endoscopic treatment is safe and is usually successful in relieving benign gastric outlet obstruction. Repeat dilation is often needed and long-term success will be improved by elimination of H. pylori infection and nonsteroidal antiinflammatory use.

Bleeding from polypoid colonic arteriovenous malformations.

The endoscopic appearance of vascular ectasias has been well characterized. We present two cases of bleeding polypoid colonic arteriovenous malformations.

Fistulous degeneration of a giant esophageal ulcer in a patient with acquired immune deficiency syndrome.

Esophageal involvement in human immunodeficiency virus (HIV) disease can take many forms, including the recently described giant solitary ulcerations thought to be due to cytomegalovirus or, more recently, Mycobacterium species. Current experience suggests that steroids may provide symptom relief and healing in selected patients. We report a case of fistulous change in one such ulcer, with documented endoscopic, radiologic, and pathologic findings. No organism was identified by culture or pathologic staining, leading to a postulated role for the persistent irritation of medications.

Primary aortoduodenal fistula following radiotherapy.

Primary aortoduodenal fistula is a rare condition. Common causes include atherosclerosis, leading to formation of an aortic aneurysm (most common); syphilis; carcinoma of the pancreas; trauma; tuberculosis, and myocosis. Presented herein is the recognition and successful treatment of what appears to be the first patient with a primary aortoduodenal fistula following paraaortic radiotherapy. Once suspected, immediate surgical treatment is mandatory. Primary aortic control (closure or resection), along with resection of the diseased intestinal segment, would appear to be the safest and most acceptable treatment.

Excretion of chlordecone by the gastrointestinal tract: evidence for a nonbiliary mechanism.

Workers exposed to chlordecone (Kepone), a toxic organochlorine pesticide, excreted larger amounts of chlordecone in bile than in stool, suggesting that it may undergo enterohepatic recirculation. We found in a single subject that equal amounts of chlordecone and of its reduced metabolite, chlordecone alcohol, were excreted in bile at a rate four times as great as in stool. When biliary contents were diverted from the intestine through a T tube, fecal excretion of chlordecone alcohol was abolished, presumably due to interruption of its passage via bile to intestine. This change was not accompanied by disappearance of chlordecone from the stool. The amount of chlordecone in stool when bile was diverted was increased six- to tenfold over that when diverted bile was continuously infused into the duodenum. Analogous experiments with [14C]-chlordecone-treated rats in which bile flow was exteriorized through a plastic cannula showed that the excretion of radioactivity in feces was in the same range when bile was reinfused in the duodenum or was totally diverted. Moreover, in rats with bile diverted, cholestyramine, an anion-exchange resin which binds chlordecone in vitro, doubled the excretion of radioactivity in stool. A similar effect was observed in intact animals. We conclude that chlordecone enters the intestinal lumen from a nonbiliary source, probably the gut, and that net excretion of chlordecone from this source can be augmented by cholestyramine.

Cholestyramine: use as a new therapeutic approach for chlordecone (kepone) poisoning.

In rats, as reported in humans, chlordecone (Kepone) is excreted predominantly in the feces. Cholestyramine, an anion exchange resin, binds chlordecone in rat intestine, increases its excretion into the feces, and decreases its content in the tissues. The resin appears to offer a practical method for treating chronic poisoning with this and possibly with other lipophilic toxins.

Treatment of chlordecone (Kepone) toxicity with cholestyramine. Results of a controlled clinical trial.

Industrial workers exposed to the organochlorine pesticide, chlordecone (Kepone), had signs of toxicity in several organs. The extent of toxicity was proportional to the levels of this chemical in the tissues. In 22 patients, chlordecone was eliminated slowly from blood (half time of 165 +/- 27 days--mean +/- S.E.M.) and fat (half time of 125 days, with a range of 97 to 177), chiefly in the stool. Output of chlordecone in bile was 10 to 20 times greater than in stool, suggesting that chlordecone is reabsorbed in the "ntestine. Cholestyramine, an anion-exchange resin that binds chlordecone, increased its fecal excretion by seven times. In a five-month trial, cholestyramine significantly accelerated elimination of chlordecone from blood, with a half life of 80 +/- 4 days (S.E.M.) (P less than 0.005) and fat (half life of 64 days, with a range of 52 to 85) (P less than 0.05). Cholestyramine offers a practical means for detoxification of persons exposed to chlordecone and possibly to other lipophilic toxins.