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Biomedical subjects

M Ligumsky

Publications and source records attributed to M Ligumsky.

At least 37 records · Page 2Linked to original sources
PubMed1990

Enhanced gastric and duodenal platelet-activating factor and leukotriene generation in duodenal ulcer patients.

Platelet-activating factor (PAF), leukotriene B4 (LTB4), and leukotriene C4 (LTC4) generation by gastroduodenal mucosa was assessed in duodenal ulcer patients and in normal subjects, to elucidate their possible role in the pathogenesis of peptic ulcer disease. Endoscopic fundic, antral, and duodenal biopsy specimens were obtained from 35 duodenal ulcer patients on the day the diagnosis was established and from 42 normal controls. In duodenal ulcer patients PAF generation, determined by platelet aggregation, was two- to three-fold higher than its respective generation by normal subjects. LTB4 and LTC4 synthesis by cultured antral and duodenal mucosa obtained from duodenal ulcer patients was twofold higher than their synthesis by normal subjects. Fundic LTB4 and LTC4 generation was similar in ulcer patients and controls. In 11 patients PAF, LTB4, and LTC4 generation was also assessed after 4 weeks of treatment resulting in ulcer healing and found to be significantly reduced when compared with their synthesis when the ulcer was active. These results thus suggest that PAF, LTB4, and LTC4 may have a role in the pathogenesis of duodenal ulcer, and therefore their modulation may have therapeutic benefits.

Adult↗
PubMed1990

Rectal administration of nonsteroidal antiinflammatory drugs. Effect on rat gastric ulcerogenicity and prostaglandin E2 synthesis.

Oral administration of nonsteroidal antiinflammatory drugs induces gastroduodenal mucosal damage in experimental animals as well as in humans. The aim of the present study was to evaluate the effect of rectally administered nonsteroidal antiinflammatory drugs on gastric mucosal damage, as well as on mucosal prostaglandin E2 synthesis. Fasting male rats were treated intrarectally with 0.5 ml 1% NaHCO3 solution containing several concentrations of either indomethacin, aspirin, ibuprofen, diclofenac, ketoprofen, or sulindac and concomitantly received 1 ml of 150 mM HCL intragastrically. Control rats received intrarectally the vehicle only. After 4 h, lesions in the secretory part of the stomach were scored and mucosal prostaglandin E2 synthesis was determined by the ex vivo prostaglandin generation technique. Dose-dependent mucosal damage was observed in indomethacin- and diclofenac-treated rats. Ketoprofen damage did not show dose dependency. In sulindac- and aspirin-treated rats, as well as in controls, no damage was detected. All drugs induced a significant and comparable degree of inhibition of prostaglandin E2 synthesis. There was no correlation between the severity of the mucosal damage and the inhibition of prostaglandin E2 synthesis. The ulcerogenicity of rectally administered nonsteroidal antiinflammatory drugs is therefore not directly related to the degree of inhibition of prostaglandin E2 synthesis and is probably related to the specific chemical and pharmacokinetic properties of each individual drug.

Administration, Rectal↗
PubMed1989

Effect of sucralfate on experimental colitis in the rat.

The therapeutic effect of sucralfate on ulcerated gastric and duodenal mucosa is well known. There is, however, almost no information about its activity in colitis. Experimental colitis was produced in rats by rectal instillation of 1 ml of 10 percent acetic acid, and 1.5 ml of a 20 percent suspension of sucralfate was then administered every 12 hours for various lengths of time. Study animals and appropriate controls were killed after 3, 7, 10, or 14 days. The distal colons were studied macroscopically and histologically. Colonic prostaglandin E2 levels were measured in animals killed after 3, 7, 10, or 14 days. The macroscopic score was significantly improved 10 and 14 days after induction of colitis, although the histologic appearance was unchanged. Acetic acid administration increased and sucralfate treatment reduced prostaglandin E2 levels in colitic animals on days 3 and 7, but not later. The present study supports a role for sucralfate in the treatment of colitis, but further studies on the mechanism of its effect and on its clinical activity are indicated.

Animals↗
PubMed1989

Indomethacin-induced gastroduodenal damage is not affected by cotreatment with ranitidine.

A randomized, double-blind, placebo-controlled study was conducted to determine whether concomitant administration of ranitidine reduces gastroduodenal mucosal damage associated with 1 week of indomethacin treatment. One hundred ten subjects with acute musculoskeletal conditions and who received indomethacin 150 mg/day completed the trial: 55 were treated with ranitidine 150 mg b.i.d. and 51 subjects received placebo b.i.d. Endoscopic gastric and duodenal injury were assessed before and after one week of treatment. There was no statistically significant difference in the percentage of patients with gastroduodenal damage or in the severity of the lesions in both treatment groups. Ranitidine did not ameliorate indomethacin-induced gastrointestinal symptoms and there was no correlation between upper gastrointestinal symptoms and endoscopic findings.

Adolescent↗
PubMed1988

No correlation between indomethacin-induced gastroduodenal damage and inhibition of gastric prostanoid synthesis.

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.

Adolescent↗
PubMed1988

Cimetidine decreases indomethacin induced duodenal mucosal damage in patients with acute musculoskeletal disorders.

The effect of two doses of cimetidine, 400 mg at night and 400 mg bd, on the protection of indomethacin (50 mg tid) induced mucosal damage was evaluated in a double blind study in patients with acute musculoskeletal disorders. Endoscopic mucosal lesions were scored before and after five to seven days of treatment. One hundred and ninety one patients were endoscoped before the trial, 34 (17.8%) had greater than one erosion and were not recruited. Forty patients were excluded for non-compliance, or lost to follow up. At the second endoscopy, oesophageal, and fundic damage was negligible. Gastric and duodenal lesion score in patients treated with cimetidine 400 mg bd: 2.7 (0.5) (SE); n = 42) was significantly lower (p less than 0.0122) than in placebo treated patients: 6.1 (0.9) (n = 50) or in patients treated with cimetidine 400 mg at night 7.1 (0.8) (n = 21). Cimetidine 400 mg bd provided significant protection for the duodenum, but its protection of antral mucosa did not reach statistical significance. There was no correlation between upper gastrointestinal symptoms and endoscopic findings.

Adolescent↗
PubMed1988

Sucralfate is protective against indomethacin-induced intestinal ulceration in the rat.

The therapeutic effects of sucralfate on ulcerated gastric and duodenal mucosa is well known. There is, however, very little information about its effect on the mucosa of the small intestine. We studied the possible protective effect of sucralfate against indomethacin-induced intestinal ulceration in the rat. Sucralfate was found to possess a marked protective effect on the intestinal mucosa (ulcer index 23.16 +/- 6.58 vs. 225 +/- 36.37; p less than 0.001). Sucralfate elevated basal mucosal prostaglandin E2 generation (p less than 0.001), and partially overcame the inhibition of prostaglandin E2 synthesis caused by indomethacin (p less than 0.03), but had no effect on mucosal cAMP level. The effect of sucralfate on prostaglandin E2 content might partially explain its protective effect on the intestinal mucosa.

Animals↗
PubMed1988

Somatostatin release by human gastric mucosa. Studies in peptic ulcer disease and pernicious anemia.

Somatostation has been postulated to have a paracrine modulating role in gastrin and gastric acid secretion. We applied the organ culture technique to examine somatostatin release by explants of human gastric mucosa taken from patients with active duodenal ulcer, from control subjects, and from patients with pernicious anemia. Somatostatin was found to be released at a constant rate by antral explants during 3 h of incubation. In active duodenal ulcer antral and fundic 2-h somatostatin release (18.7 +/- 2.6 pg/mg tissue (means + SE), n = 75; and 27 +/- 3 pg/mg tissue, n = 94, respectively) was significantly lower than release by control antral and fundic mucosa (83 +/- 17 pg/mg tissue, n = 39, and 72 +/- 16 pg/mg tissue, n = 42, respectively) (P less than 0.01). Somatostatin release by antral and fundic mucosa of patients with pernicious anemia was also significantly decreased (20 +/- 8 pg/mg tissue, n = 12, and 7.6 +/- 2 pg/mg tissue, n = 12, respectively) (P less than 0.05). These results imply possible impairments of the paracrine release of somatostatin in peptic ulcer disease and in pernicious anemia.

Anemia, Pernicious↗
PubMed1988

Comparison of misoprostol and ranitidine in the treatment of duodenal ulcer.

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.

Adult↗
PubMed1987

Cytoprotective doses of arbacet with minimal antisecretory properties are not effective in duodenal ulcer healing.

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.

Adolescent↗
PubMed1987

Pentagastrin protects the proximal small intestine against indomethacin-induced ulcers in the rat.

The possible protective effects of pentagastrin on indomethacin-induced small intestinal ulceration were investigated in rats. Ulcers were induced by subcutaneous injection of 30 mg/kg indomethacin, 30 min after refeeding rats fasted for 24 h. Administration of pentagastrin at a dose of 250 or 400 micrograms/kg i.p., 3 h prior to refeeding, reduced total ulcer area from 27.6 +/- 6.5 to 7.2 +/- 1.97 mm2 (mean +/- SEM; p less than 0.02) in the proximal small intestine only. Cyclic adenosine monophasphate, but not prostaglandin E2 levels were significantly raised by 250 micrograms/kg pentagastrin (0.15 +/- 0.05 vs. 0.38 +/- 0.07 pmol/mg protein; mean +/- SEM; p less than 0.02) in the same intestinal segment.

Animals↗
PubMed1987

Human gastric mucosal mast cells are chondroitin sulphate E-containing mast cells.

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.

Chemical Phenomena↗
PubMed1987

Drug-induced bleeding of gastric leiomyoma.

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.

Adult↗
PubMed1987

Nodular regenerative hyperplasia with portal hypertension in a patient with myasthenia gravis.

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.

Esophageal and Gastric Varices↗
PubMed1986

Role of endogenous gastric prostanoids in the pathogenesis and therapy of duodenal ulcer.

Synthesis of prostaglandin E2 and 6-keto prostaglandin F1 alpha by cultured antral and fundic gastric mucosa obtained from 86 patients with active duodenal ulcer who were not receiving medication was 50% lower (p less than 0.01) than their respective synthesis by cultured gastric mucosa in normal subjects. Antral and fundic prostanoid synthesis in patients receiving chronic therapy with nonsteroidal antiinflammatory drugs was almost completely inhibited. The decreased synthesis of antral and fundic prostaglandin E2 and 6-keto prostaglandin F1 alpha in duodenal ulcer patients was not affected following ulcer healing achieved after 4 wk of therapy with placebo, arbacet, misoprostol, sucralfate, and pirenzepine. In contrast, following 4 wk of therapy with ranitidine, both antral and fundic prostaglandin E2 synthesis were significantly increased when compared with their respective synthesis before therapy. These results confirm that gastric prostanoid synthesis is decreased in patients with active duodenal ulcer and in subjects treated with nonsteroidal antiinflammatory drugs, suggesting that decreased endogenous prostanoid synthesis may contribute to the pathogenesis of mucosal damage. The induction of endogenous prostanoids by ranitidine may contribute to its therapeutic effect.

6-Ketoprostaglandin F1 alpha↗