Biomedical subjects
Publications and source records attributed to R Eliakim.
Diffuse intramural pseudodiverticulosis of the esophagus is a rare cause of dysphagia. A 19-year-old patient with a long history of recurrent episodes of food impaction was diagnosed with diffuse intramural pseudodiverticulosis. The clue to diagnosis is a critical and thorough review of the barium swallow. Treatment is aimed toward dilatation of strictures and treatment of inflammation.
Platelet-activating factor is released from inflammatory cells. It activates neutrophils, releases secondary messengers, and mediates mucosal ulceration and ischemia in the rat. We assessed its possible role in the pathogenesis of ulcerative colitis. Colonic biopsy specimens from patients with active ulcerative colitis and controls were incubated for 4 h in Tyrode's buffer in the presence or absence of 0.2 microM calcium ionophore (A23187) or 50 microliter of antihuman immunoglobulin E. Platelet-activating factor was determined in the tissue by aggregation assay after extraction with 80% ethanol and was confirmed by thin-layer chromatography and its inactivation by phospholipases. Platelet-activating factor was not detected in normal mucosa. Only A23187 and antihuman immunoglobulin E stimulated its activity: mean +/- SE, 43.2 +/- 8.6 and 33.0 +/- 6.1 pg/10 mg wet wt, respectively. In active ulcerative colitis basal platelet-activating factor activity was 8.9 +/- 3.5 pg/10 mg wet wt. A23187 and antihuman immunoglobulin E induced significantly higher stimulation of platelet-activating factor synthesis when compared with their effects on normal mucosa: 200 +/- 28 and 70 +/- 8.3 pg/10 mg wet wt, respectively. The enhanced stimulation induced by A23187 was dose-dependently inhibited by salazopyrine, 5-amino-salicylic acid, and prednisolone, but not by sulfapyridine. It is thus suggested that platelet-activating factor may be involved in the pathogenesis of the inflammatory response in ulcerative colitis and that its inhibition by steroids, 5-aminosalicylic acid, and salazopyrine may be an additional mechanism to explain their therapeutic effects.
Invitations to participate in a screening program for fecal occult blood were sent or given directly to 20,251 people in Israel aged 40 years or above. We received 11,985 requests for stool testing kits, and ultimately we received 7,096 stool specimens (35% response). The highest response was from subjects using their own initiative to participate in the program (62%), followed by members of 23 communal farms, where 59% of subjects submitted specimens. The lowest response came from a low-middle class urban neighborhood (10%), and an intermediate response from an upper middle-class neighborhood (17%). Subsequent to the mail campaigns, a series of local newspaper articles yielded 6,519 specimens. Over all, 59% of subjects requesting kits returned specimens. Among the 7,096 specimens submitted, 145 (2%) were positive for occult blood. One hundred and twelve subjects were evaluated colonoscopically. Sixteen malignancies (14%) and 34 benign growths (30%) were found and resected. The prevalence of benign and malignant large bowel lesions was 7.0 and 7.2 per 1000 specimens in the screened urban and farm communities, respectively. In communities with limited resources for early cancer detection programs, efforts should be directed toward subgroups at risk who are most likely to respond.
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The effect of 1 week of treatment with indomethacin 150 mg/day on human gastric prostanoid synthesis was correlated with its effect on gastric and duodenal mucosa. Before and following 1 week of treatment, endoscopic appearance of the mucosa was evaluated and scored. Following 1 week of treatment with indomethacin, antral PGE2 and 6-keto-PGF1 alpha were significantly lower than in normal subjects, but similar in patients with significant or with no mucosal damage. Co-treatment with ranitidine 150 mg b.d. or with cimetidine 400 mg b.d. reduced the mean mucosal damage score but did not affect gastric prostanoid synthesis, which was similar irrespective of the presence or absence of mucosal damage. It is therefore suggested that there is no correlation between indomethacin-induced inhibition of gastric prostanoid synthesis and its induction of mucosal damage.
The efficacy of misoprostol (a synthetic analogue of prostaglandin E1) and ranitidine in the treatment of duodenal ulcer was evaluated. Seventy-one patients with endoscopically proven duodenal ulcer were randomized in a double-blind manner in one of two groups that received two daily doses of 400 micrograms misoprostol or 150 mg ranitidine. Ulcer healing was assessed endoscopically after 4 weeks of treatment; in subjects who had not healed treatment was continued and endoscopy was repeated after another 4 weeks. The mean age, sex distribution and tobacco, alcohol and caffein consumption were similar in both groups. In the misoprostol-treated group, healing of the ulcer was observed in 74.8% of patients at 4 weeks and in 86.5% at 8 weeks; in the ranitidine group (n = 34), the healing rate was 91.2 and 100%, respectively. The differences between healing rates in the two groups were not statistically significant. In the misoprostol group (n = 37), 27% of patients experienced diarrhea; of these, two were withdrawn from the trial due to this side effect. These results, which are part of a multicenter international study, suggest that misoprostol at a daily dose of 800 micrograms is as effective as 300 mg/day ranitidine in the treatment of duodenal ulcer.
The pathophysiological changes occurring with increasing grade of encephalopathy were examined in 93 consecutive episodes in 44 patients with liver cirrhosis (37 posthepatic). The incidence of gastrointestinal bleeding and leukocytosis increased significantly when the grade advanced from 1 to 5. The following variables showed a trend for change that did not reach statistical significance: rising serum bilirubin, SGOT, and BUN levels; decreasing serum sodium and chloride levels; and increased incidence of infection. The mean values of the following variables were significantly different in 25 fatal episodes and 68 survivors, implicating a bad prognosis: high serum bilirubin, alkaline phosphatase, and BUN levels; low serum albumin, sodium, and chloride levels; and a higher incidence of severe infections (sepsis, infected ascitic fluid). Because increasing grade of encephalopathy is the most important factor in determining the prognosis of hepatic encephalopathy (mortality 0, 10, 5, 19, and 85 percent in grades 1 to 5, respectively), more efforts should be made to understand and prevent the pathophysiological changes associated with advancing grades of encephalopathy.
Eight patients with pemphigus vulgaris were examined endoscopically for esophageal involvement. Most of them (seven of eight) had gastrointestinal symptoms of various types. Four of the patients had microscopical evidence of pemphigus vulgaris involving the esophagus. Three patients were found to have other diseases in their upper gastrointestinal tract accounting for their symptoms. There was no correlation between patients symptoms and macroscopic and microscopic findings. In patients with pemphigus vulgaris, endoscopy should be performed whenever gastrointestinal complaints appear, because the approaches to therapy could differ, according to the endoscopic findings.
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The efficacy of arbacet (a synthetic analog of prostaglandin E2) in definite cytoprotective but minimal antisecretory dose was evaluated in the treatment of duodenal ulcer. One hundred five patients with endoscopically proven duodenal ulcer were randomized in a double-blind manner to receive four times daily either arbacet 25 micrograms or placebo. Ulcer healing was assessed endoscopically after two and four weeks of treatment. The mean age, sex distribution, and tobacco and alcohol consumption were similar in the two treatment groups. The ulcers of 16 patients in both the placebo and the arbacet-treated group healed after 14 days of treatment. At the end of the study, healing of the ulcer was observed in 69.2% of the arbacet-treated patients and in 60.4% of patients in the placebo treated group. (Difference was not statistically significant). We conclude that cytoprotective doses of arbacet with minimal antisecretory properties are not effective in duodenal ulcer healing.
The effect of nonsteroidal antiinflammatory drugs (NSAIDs) on duodenal mucosa was assessed both retrospectively and prospectively. In 444 patients with duodenal ulcer, the incidence of upper gastrointestinal bleeding was five times higher in 56 patients who were treated with NSAIDs than in those who did not receive NSAIDs. Indomethacin and naproxen had the most potent damaging effects. In a control group of patients with gastric ulcer, nine out of 134 had taken NSAIDs. The incidence of bleeding in these patients was three times higher than in those who were not on NSAIDs. The effect of indomethacin, 150 mg/day, on the upper gastrointestinal tract was examined in a prospective study of 75 patients with acute musculoskeletal disorders. Endoscopy after 1 week of therapy showed that 45% had mucosal damage in the duodenum, and this was as frequent and as severe as the gastric mucosal damage. In most instances, the duodenal damage was erosive duodenitis.
Two patients with pernicious anemia developed gastric carcinoid, one 20 years and the other 1 year after diagnosis of pernicious anemia. One of the patients underwent successful resection of the tumor, while the second, with diffuse gastric carcinoid, was managed conservatively. She is well and asymptomatic 32 months after the diagnosis. We discuss the dilemma in management of gastric carcinoid associated with pernicious anemia.
Pancreatitis due to Crohn's disease of the duodenum is very rare. It is the result of either reflux of duodenal content into the pancreatic duct or stenosis due to direct involvement of the ampullary region with Crohn's disease. The patient described had isolated Crohn's disease of the duodenum; pancreatitis was the result of persimmon bezoar's constricting the ampullary region.
Our recent identification of chondroitin sulphate E-containing mast cells (E-MC) in the human colonic mucosa is extended here to the human gastric mucosa by using a combination of both biochemical and immunochemical approaches. Most of the mast cells in human gastric biopsies, which were located mainly around small blood vessels in the submucosa, showed various degrees of degranulation and were granular when stained by monoclonal antibody against chondroitin sulphate proteoglycan. The human gastric mucosa biopsies incorporated (35S)-sulphate into proteoglycans. Cells in the tissues which were histamine-positive also incorporated (35S). The 35S proteoglycans, which were either left associated with the tissue or released into the medium, were found not to be heparin but chondroitin sulphate E. Incubation of the human gastric mucosa biopsies in the presence of anti-human IgE revealed significant enhancement in the release of both (35S)-chondroitin sulphate E proteoglycan and histamine.
Gastrointestinal bleeding is a major sign by which smooth muscle tumors are brought to medical attention. Bleeding usually occurs from an ulceration on the mucosal surface of the tumor. Agents such as nonsteroidal antiinflammatory drugs and steroids may damage the gastric mucosa, thus becoming predisposed to bleeding. Three patients presenting with ulcerated or bleeding leiomyomas while on either nonsteroidal antiinflammatory drugs or steroid therapy are herein reported.
Nodular regenerative hyperplasia of the liver is a rare cause of portal hypertension and bleeding esophageal varices, occurring mainly in association with collagen vascular diseases. The patient described herein had both myasthenia gravis and nodular regenerative hyperplasia. To the best of our knowledge, this is the first report of this association.