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Biomedical subjects

R Eliakim

Publications and source records attributed to R Eliakim.

At least 55 records · Page 3Linked to original sources
PubMed1999

Lymphocytic colitis: a clue to an infectious trigger.

We present a 19-year-old patient who was admitted for evaluation of prolonged watery diarrhea. Previous study showed one stool culture positive for Campylobacter jejuni, which was treated with appropriate antibiotics with no response. She underwent colonoscopy with multiple biopsies, which led to a diagnosis of lymphocytic colitis. We believe that the patient's disease was due to the infectious process, which triggered an autoimmune response and caused the lymphocytic colitis.

Adult↗
PubMed1999

Rectal ulcers: a rare gastrointestinal manifestation of systemic lupus erythematosus.

A patient with systemic lupus erythematosus (SLE) developed a rectal ulcer and sepsis from colonic bacteria. At that time she had no other clinical manifestations of SLE. Histopathologic examination of the biopsies taken from the ulcer found evidence of vasculitis. Treatment with high-dose systemic steroids healed the ulcer clinically and endoscopically, but symptoms recurred when steroids were tapered. The patient was referred for surgery. This is a rare but dangerous complication of SLE and can be the only clinical manifestation of the disease.

Adult↗
PubMed1999

Sulphydryl blocker-induced rat colitis is ameliorated by intravenous injection of antibody to colonic surfactant-like particle.

A rat model of experimental colitis and jejunitis induced by iodoacetamide (IA), a sulphydryl blocker is accompanied by increased leukotriene, prostaglandin E2 (PGE2) generation, and nitric oxide synthase (NOS) activity. Rat small intestinal and colonic surfactant-like particles (SLP) that accumulate on the apical surface of mucosal cells have been identified and specific antibodies to them have been produced. The aim of this study was to evaluate a possible role of SLP in IA-induced colitis and jejunitis. Inflammation was induced in Sprague-Dawley rats either by intracolonic administration of 3% IA (0.1 ml) or by intrajejunal administration of 2% IA (0.1 ml). Antisera raised against either colonic SLP, pulmonary SP-A (a major protein associated with colonic SLP), or small intestinal SLP were injected into the tail vein of rats 48 h before, simultaneous with, or 24 h after IA administration. Rats were killed 2 or 10 days after IA was given, their colon or small intestine was isolated and rinsed, and a segment of colon (10 cm) or small bowel (30 cm) was weighed and processed for microscopy, NOS and myeloperoxidase (MPO) activities, and PGE2 generation. Intracolonic or jejunal IA resulted after 48 h in extensive macroscopic and microscopic damage, accompanied by increased segmental weight, MPO and NOS activity, and PGE2 generation. Colonic SLP antibody administration, either 48 h before or at the time of damage induction, significantly decreased macroscopic as well as microscopic damage, segmental weight, MPO activity, and PGE2 generation, but had no effect on NOS activity. Neither control sera nor antisera against SP-A had any protective effect, nor did injection of anti-colonic SLP antisera given 24 h after IA. Small bowel SLP antibody offered no protection against IA jejunitis. IA-induced colitis but not jejunitis is ameliorated by intravenous injection of SLP antibody by a mechanism yet to be determined. These data provide further evidence of a physiologic role for gastrointestinal SLP.

Animals↗
PubMed1998

Budesonide versus prednisone in the treatment of active Crohn's disease. The Israeli Budesonide Study Group.

BACKGROUND & AIMS: Budesonide (BUD) is a potent steroid that undergoes extensive first-pass metabolism. BUD incorporated in a pH-dependent formulation has been proposed as an alternative treatment for Crohn's disease (CD). The aim of this study was to compare the efficacy and safety of BUD and prednisone (PRED) in the treatment of active CD involving the terminal ileum and/or the colon. METHODS: Patients with mild to moderately active CD were included in a randomized, double-blind, double-dummy controlled trial. Patients received either 9 mg BUD once daily for 8 weeks or 40 mg PRED once daily for the first 2 weeks tapered gradually to 5 mg/day by the end of the study. Disease activity, quality of life, and laboratory parameters were recorded. RESULTS: One hundred patients received BUD, and 101 patients received PRED. By intention-to-treat analysis, treatment efficacy defined as Crohn's Disease Activity Index of <150 at completion was 51% and 52.5% for the BUD and PRED groups, respectively. Twice as many responded to treatment with no side effects in the BUD compared with the PRED group (30% vs. 14%) (P = 0.006). Most of the decrease in CDAI scores occurred during the first 2 weeks. CONCLUSIONS: BUD is as effective as PRED in the treatment of CD involving the terminal ileum and right colon. BUD has significantly fewer steroid-related adverse reactions.

Adult↗
PubMed1998

Direct determination of colonic nitric oxide level--a sensitive marker of disease activity in ulcerative colitis.

OBJECTIVE: In active ulcerative colitis, colonic nitric oxide (NO) generation is enhanced and probably has an important role in its pathogenesis. We tested the reliability of an NO electrode in monitoring colonic NO levels in ulcerative colitis patients and control subjects and its possible usage as a marker of disease activity. METHODS: Colonic NO level was determined by the NO detection system model NO-501 (InterMedical, Nagoya, Japan). The working electrode was inserted into a 7-mm diameter polyvinyl tube and introduced at a distance 6 cm from the anus. In each subject sigmoidoscopy was performed and mucosal biopsies were obtained. NO synthase (NOS) activity was determined by monitoring the conversion of 3H-arginine to citrulline. RESULTS: Colonic NO level is significantly increased in patients with active ulcerative or Crohn's colitis--more than 2-fold higher than in control subjects. There was good correlation between colonic NO level and NOS activity and the clinical and endoscopic indices of disease activity. CONCLUSION: Direct determination of colonic NO level is convenient, and reliable, and may help to monitor disease activity in ulcerative colitis.

Adult↗
PubMed1998

Femoral neck osteopenia in patients with inflammatory bowel disease.

OBJECTIVE: The mechanism of bone loss in patients with inflammatory bowel disease (IBD) is not completely understood. The aim of this study was to assess indices of bone turnover and bone mineral density (BMD) in the lumbar spine and femoral neck in IBD patients. METHODS: Sixty-three patients with Crohn's disease and 41 with ulcerative colitis were studied. Serum bone-specific alkaline phosphatase (B-ALP), osteocalcin, parathyroid hormone (PTH), 25 hydroxyvitamin D, interleukin-6 (IL-6), and urinary N-telopeptide cross linked type 1 collagen (NTX) were determined. BMD of the lumbar spine and femoral neck was determined by dual x-ray absorptiometry in 59 patients. RESULTS: In the femoral neck 42% of the patients had osteopenia (-2.5 SD < BMD T score < -1 SD) and another 41% had osteoporosis (BMD T score < -2.5). In the spine 34% of the patients had osteopenia and additional 42% had osteoporosis. BMD T scores were lower in the femoral neck compared to the spine. Reduced BMD was unrelated to gender, disease type, lifetime corticosteroid dose, but inversely correlated with disease duration (r = -0.36, p < 0.05). Serum IL-6 was higher in IBD patients compared to controls. A reduced level of osteocalcin, a marker of bone formation, was present in 7% of patients and an increase in NTX, a marker of bone resorption, in 25% of them. Osteoporotic IBD patients (spine or hip BMD T score < -2.5) had increased serum IL-6, osteocalcin and PTH level compared to nonosteoporotic patients. CONCLUSIONS: There is a high prevalence of reduced BMD at the spine and femoral neck in IBD patients, which is more severe in the hip. Bone turnover in osteoporotic IBD patients is associated with an increase in osteocalcin, PTH and IL-6. IL-6 may play a role in the pathogenesis of bone loss in IBD.

Adult↗
PubMed1998

Effect of chronic nicotine administration on trinitrobenzene sulphonic acid-induced colitis.

BACKGROUND: Smoking, probably due to nicotine, has a bivalent effect on inflammatory bowel disease, ameliorating disease activity in ulcerative colitis and with a deleterious effect on Crohn's disease. The effect of nicotine patches in ulcerative colitis is controversial. AIM: To investigate the effect of chronic nicotine use in a rat model of colitis. METHODS: Colitis was induced in Sprague-Dawley rats by rectal administration of 30 mg trinitrobenzene sulphonic acid (TNBS) in 50% ethanol. Nicotine was dissolved in drinking water (2.5, 12.5, 25 and 250 microg/ml), with rats drinking ad libitum. Nicotine administration started 10 days prior to damage induction and had no effect on weight gain or daily food intake of rats. Rats were sacrificed 1 and 5 days after TNBS administration, their colons resected, rinsed, weighed, damage assessed macroscopically (mm2) and microscopically and tissue processed for myeloperoxidase (MPO) and nitric oxide synthase (NOS) activities, leukotriene B4 (LTB4), prostaglandin E2 (PGE2) generation and interleukin-1 (IL-1) serum levels. RESULTS: Nicotine, by itself, caused no damage to the colon. Nicotine had a dose-dependent bivalent effect on colitis, significantly reducing macroscopic damage from 983 +/- 10 mm2 on TNBS alone to 429 +/- 118 mm2 on TNBS plus 12.5 microg/ml of nicotine, and escalating to 1086 +/- 262 mm2 on 250 microg/ml of nicotine. Segmental weight declined significantly (from 2.4 +/- 0.2 to 1.65 +/- 0.20 g/10 cm), on 12.5 microg/ml nicotine, as did MPO activity (from 3.2 +/- 0.4 to 0.7 +/- 0.1 units/g). All these parameters returned to the levels of TNBS alone when the dose of nicotine was increased to 250 microg/ml. Nicotine had no effect on NOS activity, PGE2 generation and serum IL-1 levels, but increased LTB4 generation. CONCLUSIONS: Nicotine has a dose-dependent bivalent effect on TNBS-induced colitis which is not due to reduction in IL-1 serum levels or PGE2 generation, and is not NOS-mediated.

Animals↗
PubMed1997

[Cyclosporin for severe ulcerative colitis].

In recent years there have been numerous reports of successful treatment of resistant ulcerative colitis with cyclosporin. A series of 9 patients with moderate to severe active ulcerative colitis was treated with cyclosporin between September 1993 and October 1994. All 9 had failed to respond to conventional therapy, including salazopyrine and intravenous corticosteroids. They underwent colonoscopy and after contraindications to therapy were ruled out, received intravenous cyclosporin, 4 mg/kg/day for 7-10 days. They were discharged on oral cyclosporin with average serum levels maintained at 200 ng/ml. Response was assessed using the clinical score system of Schroeder et al. 2 out of 9 patients (22%) responded with full clinical remissions lasting more than 6 months. 6 patients had partial responses to the intravenous therapy, but symptoms resumed shortly after its cessation. Factors predicting favorable response to cyclosporin therapy were a shorter duration of disease with a fulminant clinical course. The success rate was less than that reported in the literature, possibly because of comparatively low serum cyclosporin levels. Potential complications of therapy and high cost preclude the routine use of cyclosporin in ulcerative colitis. Larger controlled studies are required to assess its efficacy and safety. Until such studies are available, cyclosporin may be tried in poor surgical risks or those not yet ready psychologically for total colectomy.

Administration, Oral↗
PubMed1997

A more liberal approach to the surgical treatment of Crohn's disease.

BACKGROUND: Surgery for Crohn's disease is not intended for cure, but rather to relieve symptoms and treat complications. Perioperative morbidity, the fear of creating short bowel syndrome, and the tendency of the disease to recur convinced many physicians to refer their Crohn's patients for surgery only when life-threatening complications occur. METHODS: This is a retrospective analysis of 47 patients operated on for Crohn's disease between 1989 and 1994. Twenty-six patients were operated on for "classic" indications ("classic" group) and the other 21 were operated on to improve their quality of life ("quality" group). RESULTS: There was no operative or postoperative mortality during a mean follow-up period of 50 (27 to 84) months. All major postoperative complications occurred only in patients operated on for the classic indications (four abscesses, two fistulas, one wound dehiscence, and two small bowel obstructions). During the follow-up period, a total of 13 patients (50%) in the classic group and only 5 patients (24%) in the quality group required reintroduction of medical therapy or additional operations for exacerbations and complications of Crohn's disease. CONCLUSIONS: Our data suggest that surgical intervention intended to improve the quality of life for Crohn's disease patients is safe and effective for carefully selected patients. It does improve quality of life, may prevent life-threatening complications, and offers a lower recurrence rate following surgery.

Adolescent↗
PubMed1997

Anti-thyroid drugs decrease mucosal damage in a rat model of experimental colitis.

BACKGROUND: Methimazole, an anti-thyroid drug, was recently found to be useful in the treatment of systemic lupus erythematosus and other autoimmune diseases. Moreover, decreased thyroid hormone production is associated with a variety of immunological manifestations, such as reduced activation of CD4+ cells, increased CD8+ cell activity and reduced soluble IL-2 receptors. In the present study we examined the effects of methimazole and propylthiouracil on a rat model of experimental colitis. METHODS: Colitis was induced by intracolonic administration of 30 mg trinitrobenzene sulphonic acid (TNB). Two weeks prior to induction of colitis, rats were treated by either methimaziole (0.04%) or propylthiouracil (0.01%) in drinking water after a week of free access to water. Rats were sacrificed 48 h or 7 days after induction of colitis. The colon was isolated, rinsed with ice-cold water and weighed. Damage was assessed both macroscopically and microscopically and myeloperoxidase (MPO) activity determined. RESULTS: All treated rats were hypothyroid as manifested by a significant elevation of thyroid stimulating hormone (TSH), by comparison with the control groups (mean -1.82 +/- 0.40 versus 0.11 +/- 0.02 mmol/L, respectively). The inflammatory response elicited by TNB resulted in severe mucosal damage 48 h after damage induction, which persisted for 7 days. Pre-treatment with either methimazole 0.04% or propylthiouracil 0.01% significantly decreased mucosal damage macroscopically (lesion area, lesion score and segmental weight) microscopically and also significantly decreased MPO level at both time points (P < 0.01). CONCLUSIONS: Methimazole and propylthiouracil significantly reduce mucosal damage and colonic weight in a rat model of colitis. The mode by which they do so remains to be studied.

Animals↗
PubMed1997

Brucellosis and the gastrointestinal tract. The odd couple.

Though pathogenetically qualifying as an enteric fever, the gastroenterological manifestations of Brucella in humans are relatively uncommon. We present a typical case of Brucellosis with gastrointestinal symptoms and review these by organ involvement, ranging from the mild nonspecific, such as diarrhea and abdominal pain, to the pathologically distinct hepatic lesions, and to the rare colonic, pancreatic, and peritoneal involvement. The limited indications for diagnostic procedures, such as endoscopy and liver biopsy are discussed.

Abdominal Pain↗
PubMed1997

Assessing disease activity in Crohn's disease--are we there yet?

Many attempts have been made over recent years to assess accurately disease activity in Crohn's disease. We review some of these attempts, giving particular emphasis to the combination of serum levels of proinflammatory cytokines (interleukin-6, tumour necrosis factor alpha, recombinant interleukin-2 and acid alpha-1-glycoprotein).

Biomarkers↗
PubMed1997

Isolation and characterization of surfactant-like particles in rat and human colon.

The source of a phospholipid-rich layer recovered from the surface of the mammalian colon has been obscure. This report describes the isolation of a low-density membrane from the surface of rat and human colons (d = 1.07-1.08 g/ml), with a low cholesterol-to-phospholipid ratio and phosphatidylcholine as its major phospholipid. Electron microscopy shows unilamellar and partially coiled membranes. Compared with microvillous membranes isolated from underlying mucosa, this extracellular membrane is enriched for tissue-unspecific alkaline phosphatase and surfactant protein A. It does not contain small intestinal marker proteins (intestinal alkaline phosphatase and sucrase-isomaltase). The human membrane contains only traces of the colonic microvillous membrane marker, carcinoembryonic antigen. Antiserum against the rat colonic membrane does not recognize colonic microvillous membrane or small intestinal surfactant-like particle proteins. Antiserum against human colonic membrane identifies one protein in the surfactant-like particle from the adjacent small intestine and two proteins in the colonic microvillous membrane. These data show that the colonocyte microvillous membrane is covered by another membrane with a different protein composition. Enrichment for surfactant protein A suggests that this colonic membrane is another example of a surfactant-like particle sharing proteins with pulmonary surfactant.

Alkaline Phosphatase↗