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Biomedical subjects

R Eliakim

Publications and source records attributed to R Eliakim.

At least 19 recordsLinked to original sources
PubMed1996

Methotrexate in chronic active ulcerative colitis: a double-blind, randomized, Israeli multicenter trial.

BACKGROUND & AIMS: Uncontrolled studies have suggested that methotrexate may be effective in patients with active ulcerative colitis. The aim of this study was to evaluate the effectiveness of oral methotrexate in chronic steroid-dependent ulcerative colitis in a randomized, double-blind multicenter trial. METHODS: Patients with active ulcerative colitis who have received steroids and/or immunosuppressives for at least 4 months during the preceding 12 months with a current Mayo Clinic score of > or = 7 were included in the study. Methotrexate (12.5 mg) or placebo was added to their treatment once weekly for 9 months. RESULTS: Sixty-seven patients were included (methotrexate, 30 patients, placebo, 37 patients). The proportion of patients entering first remission (methotrexate, 46.7%; placebo, 48.6%), the time to reach first remission (methotrexate, 4.1 +/- 1.9 months; placebo, 3.4 +/- 1.7 months), as well as the proportions of patients having a relapse after first remission (methotrexate, 64.3%; placebo, 44.4%) were not significantly different between the two groups. The mean Mayo Clinic score, the mean monthly steroid dose, and the proportion of abnormal laboratory results during the study were also similar. CONCLUSIONS: Methotrexate at a weekly oral dose of 12.5 mg was not found to be better than placebo in the induction or maintenance of remission in patients with chronic active ulcerative colitis.

Administration, Oral↗
PubMed1996

The Jerusalem 70 year olds longitudinal study: gastrointestinal findings.

The objective of this part of the first cross-section of the longitudinal study of a cohort of 70 year olds in Jerusalem was to survey the gastrointestinal symptoms and signs of this heterogeneous population and thus contribute to the knowledge of the development of gastrointestinal diseases in this age group. A total of 605 persons replied to a home-visit questionnaire gathering data on socioeconomic and migration variables. Later on, 463 of these attended an examination at the Geriatric Research Institute where an in-depth anamnesis and physical examination were conducted. A battery of biochemical and hematologic blood tests were performed as well as urine analysis, ECG, and pulmonary function tests. At 3 year follow-up, the interviewed subjects, subjects examined in the hospital, and the control group consisting of 70 year olds who were not examined, were compared. By the measures of disease-specific mortality and hospital morbidity, the three groups were found to be similar, demonstrating that the sample population does represent the total Jerusalem 70-year-old population. This paper describes the symptoms, signs and laboratory results of the gastrointestinal part of this study. Up to a third of the subjects complained of upper gastrointestinal symptoms, most prominent of which was heartburn. Almost 10% of subjects complained of abdominal pain occurring at least once a week, but less than 1% noted left lower quadrant pain. There was a direct association between upper abdominal pain and symptoms of ischemic heart disease. The second part of this study, which began in 1996, will provide additional information regarding the natural history of these complaints.

Aged↗
PubMed1996

Role of small bowel biopsy in the endoscopic evaluation of adults with iron deficiency anemia.

OBJECTIVES: The recommended evaluation of adult patients presenting with iron deficiency anemia (IDA) includes the performance of colonoscopy and esophagogastroduodenoscopy. IDA is a common feature in patients with celiac disease and, in several, may be the only presenting sign. The performance of small bowel biopsy (SBB) for the evaluation of celiac disease as the cause of IDA is not routinely recommended. The aim of the present study was to determine the yield of SBB performed during routine endoscopy of adults with IDA. METHODS: We prospectively studied 93 patients with IDA. Three control groups were included: 23 patients with steatorrhea, 37 patients with idiopathic diarrhea, and 9 patients in whom SBB was performed for miscellaneous indications. RESULTS: Eleven patients with IDA and two patients with steatorrhea had SBB findings compatible with celiac disease. None of the patients from the other two groups had similar findings. Two patients with IDA, who were later diagnosed to suffer from celiac disease, presented: one with occult blood in the stool and the other with rectal bleeding. Subgroup analysis of patients with IDA revealed that patients with celiac disease were younger, had significantly more episodes of diarrhea, lower mean hemoglobin level, and longer duration of anemia than those without celiac disease. Other mucosal abnormalities were found in a substantial number of patients with celiac disease: esophagitis, gastritis, duodenitis, hemorrhoids, and colitis. CONCLUSIONS: A substantial number of adult Israeli patients who present with IDA are found, on SBB, to have mucosal abnormalities compatible with the diagnosis of celiac disease. The presence of esophagitis, gastritis, or duodenitis on esophagogastroduodenoscopy, or other abnormalities on colonoscopy, do not exclude the coexistence of celiac disease. Celiac disease should be included and routinely looked for in the differential diagnosis of adult patients with IDA.

Adult↗
PubMed1995

Ketotifen and nitroxides decrease capsaicin-augmented ethanol-induced gastric damage in rats.

Systemic administration of capsaicin aggravates ethanol-induced injury of rat gastric mucosa. We evaluated the effect of subcutaneous administration of capsaicin on the gastric mucosa and on inflammatory mediators in saline- and ethanol-treated rats. Functional ablation of primary afferent C-fibers by capsaicin (total 100 mg/kg subcutaneous) tripled ethanol-induced damage. Pretreatment with ketotifen, a mast cell stabilizer (1 mg/kg) protected rat gastric mucosa from the amplified injury induced by capsaicin and ethanol. Tempol, a selective nontoxic cell-permeable nitroxide, completely prevented the amplified gastric ulceration induced by capsaicin and ethanol. This was accompanied by a significant decrease in leukotriene B4 and C4 generation. It is therefore suggested that mast cells and free radicals contribute to the amplified injury observed in rats pretreated with capsaicin and ethanol and that the pharmacological modulation of mast cell release and scavenging of free radicals may be of therapeutic efficacy in the prevention of gastric injury.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Ketotifen ameliorates capsaicin-augmented acetic acid-induced colitis.

Capsaicin-sensitive afferent neurons are involved in maintaining the integrity of the gastrointestinal mucosa. These neurons are closely apposed to mast cells and could, therefore, lead to their activation. In the present study, the role of capsaicin-sensitive neurons in the pathogenesis of experimental colitis and the possible involvement of mast cells and nitric oxide were evaluated. Rats were treated with capsaicin subcutaneously, 20, 30, and 50 mg/kg, on three consecutive days, a regimen shown to ablate primary afferent neurons. Colitis was induced two weeks later by flushing 2 ml 5% acetic acid into the proximal colon. Control rats received saline, acetic acid, or capsaicin alone. Another group of rats received ketotifen (100 micrograms/100 g body wt x 2/day) intragastrically 48 hr prior to damage induction and thereafter. Rats were sacrificed 24 hr after damage induction, the colon isolated, damage assessed, explants were organ-cultured for 24 hr for determination of nitric oxide generation, and mucosa extracted for determination of leukotriene B4 generation and nitric oxide synthase activity. Significant increases in colonic weight, nitric oxide synthase activity, and nitric oxide and leukotriene B4 generation accompanied the near tripling of acetic acid-induced damage in capsaicin-pretreated rats. Ketotifen pretreatment significantly decreased the macroscopic damage and the increase in colonic weight. The protection provided by ketotifen was accompanied by a significant decrease in leukotriene B4 generation and nitric oxide synthase activity (80%).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1995

Conventional dose of omeprazole alters gastric flora.

Quantitative cultures were carried out on samples from gastric juice obtained from 12 ambulatory patients with esophagitis before and one month after omeprazole therapy. An increase in the number of patients in whom gastric juice was culture-positive, as well as an increment in the bacterial counts were noted. The spectrum of microorganisms isolated from gastric juice was identical to the normal flora of the oral cavity, mainly alpha-hemolytic streptococci, corynebacteria, and Candida species. Thus, the counts of organisms within gastric contents are simply a reflection of swallowed oral microflora that were able to survive due to the less acidic environment.

Antacids↗
PubMed1995

A stable nitroxide radical effectively decreases mucosal damage in experimental colitis.

TEMPOL, a cyclic nitroxide stable radical blocks biological damage by breaking chain reactions through termination reaction with free radicals, and by inhibiting the catalytic effect of transition metals. This study tested its protective effect on two models of experimental colitis as free radicals play an important part in their pathogenesis. TEMPOL was given intragastrically immediately after induction of colitis with acetic acid or trinitrobenzene sulphonic acid (TNB) and mucosal damage was assessed one, three, or seven days later. Cellular partition of TEMPOL was determined by electron paramagnetic resonance spectroscopy. In vitro experiments showed that TEMPOL immediately penetrates colonic mucosa and, following its intragastric administration, it persists in both gastric and colonic mucosa for several hours. Intragastric administration of TEMPOL, 0.5 g/kg/bw, immediately after intracaecal administration of 5% acetic acid significantly decreased mucosal lesion area, myeloperoxidase activity, and leukotriene B4 and C4 generation when assessed 24 hours after damage induction. Intragastric administration of TEMPOL, 0.5 g/kg/bw, immediately after intracolonic administration of 30 mg TNB in 0.25 ml 50% ethanol, and once daily thereafter, significantly decreased mucosal lesion area assessed after one, three, and seven days, having no effect on LTC4 generation and affecting colonic weight, myeloperoxidase activity, and LTB4 generation only sporadically. In conclusion, TNB and acetic acid induced colitis can be pharmacologically manipulated by TEMPOL. TEMPOL may be beneficial in the treatment or prevention of inflammatory bowel disease.

Acetates↗
PubMed1995

Isolated iron deficiency: an atypical manifestation of celiac disease.

A 38-year-old woman presented with iron-deficiency anemia in 1983. Eight years later, she developed classic symptoms of celiac disease, ie, diarrhea, weight loss, and diminished appetite. New noninvasive blood tests and the ease with which small bowel biopsies can be achieved are having an impact on the clinical pattern of the disease. This report includes a discussion of anemia as the presenting sign of celiac disease and a review of the literature.

Adult↗
PubMed1994

Somatostatin effectively prevents ethanol- and NSAID-induced gastric mucosal damage in rats.

The interrelationship between somatostatin and its synthetic analog, sandostatin, with neuropeptides and inflammatory mediators, as well as their protection of gastric mucosal damage, were tested in rats. Rats were treated intragastrically with 1.0 ml of 96% ethanol with or without intravenous or intraperitoneal coadministration of somatostatin (1.0 microM/kg). Mucosal damage was also induced by the administration of either indomethacin (30 mg/kg subcutaneously) with or without intravenous sandostatin (10 micrograms/rat), given 30 min prior to damage induction. Somatostatin levels in ethanol-damaged gastric mucosa were significantly lower than in control rats. Substance P and vasoactive intestinal peptide (VIP) levels were significantly higher in the damaged mucosa in rats treated with ethanol, as was the mucosal generation of leukotriene B4 (LTB4) and cysteinyl-containing leukotrienes. The coadministration of somatostatin with ethanol significantly reduced gastric mucosal injury induced by ethanol alone. The protection of the mucosa was accompanied by reduction of mucosal substance P and VIP levels, as well as the generation of leukotrienes, an effect that was reversed by intraperitoneal or intravenous coadministration of somatostatin antagonist, cyclo-(7-aminoheptanoyl-PH-E-D-Trp-Lys-THR), 1.0 microM/100 g, with somatostatin (1.0 microM/kg) and ethanol. When given by itself somatostatin significantly reduced mucosal leukotriene generation compared with their generation in saline-treated rats. Sandostatin completely abolished gastric mucosal damage induced by indomethacin administration. In rats treated with somatostatin and indomethacin, this effect was accompanied by reduction of mucosal leukotriene generation. Administration of sandostatin to pylorus-ligated rats significantly reduced gastric acid output.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Dermatomyositis associated with Crohn's disease.

A 29-year-old woman with quiescent Crohn's disease developed severe myositis. Serum creatine phosphokinase was markedly elevated, and muscle biopsy showed typical findings of dermatomyositis. The muscular symptoms promptly responded to combined treatment with corticosteroids and azathioprine. The association between inflammatory bowel disease and inflammatory myopathies is very rare. We review the clinical, pathological, and pathophysiological aspects of this association.

Adult↗
PubMed1994

Enhanced gastric nitric oxide synthase activity in duodenal ulcer patients.

Nitric oxide, the product of nitric oxide synthase in inflammatory cells, may have a role in tissue injury through its oxidative metabolism. Nitric oxide may have a role in the pathogenesis of duodenal ulcer and may be one of the mechanisms responsible for the association between gastric infection with Helicobacter pylori and peptic disease. In this study, calcium independent nitric oxide synthase activity was detected in human gastric mucosa suggesting expression of the inducible isoform. In 17 duodenal ulcer patients gastric antral and fundic nitric oxide synthase activity was found to be two and 1.5-fold respectively higher than its activity in the antrum and fundus of 14 normal subjects (p < 0.05). H pylori was detected in the antrum of 15 of 17 duodenal ulcer patients and only in 7 of 14 of the control subjects. Antral nitric oxide synthase activity in H pylori positive duodenal ulcer patients was twofold higher than in H pylori positive normal subjects (p < 0.05). In duodenal ulcer patients antral and fundic nitric oxide synthase activity resumed normal values after induction of ulcer healing with ranitidine. Eradication of H pylori did not further affect gastric nitric oxide synthase activity. These findings suggest that in duodenal ulcer patients stimulated gastric mucosal nitric oxide synthase activity, though independent of the H pylori state, may contribute to the pathogenesis of the disease.

Acute Disease↗
PubMed1994

A possible role for rat intestinal surfactant-like particles in transepithelial triacylglycerol transport.

To further examine whether surfactant-like particles (DeSchryver-Kecskemeti, K., R. Eliakim, S. Carroll, W. F. Stenson, M. A. Moxley, and D. H. Alpers. 1989. J. Clin. Invest. 84:1355-1361) were involved in the transepithelial transport of lipid, alkaline phosphatase activity and surfactant-like particle content were measured in apical mucosal scrapings, enterocytes, lamina propria, and serum after inhibition of chylomicron transport. Serum triacylglycerol levels were decreased 60-76% by Pluronic L-81, fenfluramine, and choline deficiency compared with fat-fed controls. 5 h after triacylglycerol feed, alkaline phosphatase activity in all three experimental groups was decreased compared with controls by 52-69% in mucosal scrapings and by 33-72% in serum. A parallel decline (60%) in alkaline phosphatase activity occurred in the lamina propria of Pluronic-treated animals. Total particle content (measured by an ELISA using antiserum against purified particle) after Pluronic treatment was decreased in mucosal scrapings, lamina propria, and serum by 16, 22, and 29% at 3 h and by 33, 40, and 8%, respectively, at 5 h after fat feeding. In contrast, particle content was increased in enterocytes by 29% 3 h and by 8% 5 h after fat feeding. By electron microscopy, enterocytes from Pluronic- and fenfluramine-treated animals exhibited a two- to threefold increase in large intracellular cytoplasmic lipid globules and the appearance of lamellae in apposition, with a marked decrease in the number of surfactant-like particles overlying the brush border. These changes, produced by inhibition of chylomicron transport, in the distribution of surfactant-like particles and particle-bound alkaline phosphatase are consistent with a role for these particles in transepithelial triacylglycerol transport across and out of the enterocyte.

Animals↗
PubMed1994

The effect of nizatidine on duodenal ulcer healing and on mucosal inflammatory mediators.

The aim of this double-blind, randomized, placebo-controlled trial was to evaluate the effect of nizatidine on duodenal ulcer healing and generation of mucosal prostaglandin estradiol and inflammatory mediators. Fifty-five patients with endoscopically proven active duodenal ulcer received either nizatidine 300 mg or placebo, once nightly, for 4 weeks, when a second endoscopy was performed. Healing was defined as complete epithelialization of the ulcer crater. At both endoscopies mucosal biopsies were obtained for determination of prostanoids and inflammatory mediators. Nizatidine and placebo induced ulcer healing in 76% and 60.9% of the patients, respectively, but the difference did not reach statistical significance. Nizatidine treatment did not significantly affect mucosal leukotriene B4, leukotriene C4 or platelet activating factor generation. It is concluded, therefore, that the antisecretory effect is probably the main mechanism responsible for nizatidine's therapeutic effects in peptic ulcer disease.

Adult↗