Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Desensitization to sulfasalazine was successful in 40/47 (85%) patients with IBD who previously had hypersensitivity reactions. The desensitization with sulfasalazine was well-tolerated with no serious complications in short- or long-term follow-up. The course of IBD was subsequently favorable in 35/40 (87%) for extended periods including 17/17 (100%) with ulcerative colitis. Desensitization should be attempted in patients who have had typical hypersensitivity reactions to sulfasalazine.
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PMID:Desensitization to sulfasalazine after hypersensitivity reactions in patients with inflammatory bowel disease. 614 67

Convalescent serum given to 1-day-old poults delayed clinical signs of turkey coryza by several days and reduced mortality on infected farms. Turkey breeders immunized with cell-culture-adapted infectious bursal disease virus (IBDV) or turkey infectious bursal disease virus (TIBDV) had a marked increase in virus-neutralization (VN) antibody titers. The VN antibody titer was significantly higher in progeny poults than in poults from unimmunized breeders. Clinical turkey coryza and mortality was considerably less in poults from IBD- or TIBD-vaccinated breeders than in control poults. They also responded more favorably to hemorrhagic enteritis and fowl cholera vaccination.
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PMID:Field studies with convalescent serum and infectious bursal disease vaccine to control turkey coryza. 625 90

The experiment involved 392,955 broilers from breeders vaccinated with a commercially available killed infectious bursal disease (KIBD) virus vaccine (Treatments 1 and 2) and 373,371 broilers from breeders not vaccinated with a KIBD virus vaccine (Treatment 2). The broilers from the KIBD-vaccinated breeders were divided into two treatment groups: Treatment 1 consisted of 209,457 broilers and Treatment 2 consisted of 183,498 broilers. Treatment 2 broilers were vaccinated at 10 days of age intraocularly with a commercially available modified liver infectious bursal disease virus (IBD-MLV) vaccine. Broilers in all three treatments were raised on commercially contracted farms serviced by the same company representative. Broiler performance was based on mortality, body weight, feed efficiency, condemnations, and how each farm ranked with respect to contract settlements. Compared with birds in Treatments 2 and 3 respectively, Treatment 1 broilers had 1.65% and 0.89% less mortality; 0.22 lbs. and 0.09 lbs. increased weight per bird; 0.03 and 0.03 increased feed efficiency; 0.09% and 0.32% fewer air sacculitis condemnations; and 0.57% and 0.83% fewer total condemnations. Treatment 1 broilers ranked in the top 37%; Treatment 2 ranked in the bottom 36%; and Treatment 3 ranked in the lower 57% of contract settlements for all broilers processed. The results clearly showed that Treatment 1 broilers outperformed Treatment 2 amd 3 birds and that the IBD-MLV vaccine had a detrimental effect on Treatment 2 broilers.
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PMID:The detrimental effect of vaccinating parentally immune broilers with a modified liver virus vaccine for infectious bursal disease. 626 38

Inactivated Newcastle disease (NDV), infectious bursal disease (IBDV), and viral arthritis/tenosynovitis (VA) viruses were incorporated into water-in-oil emulsion vaccines either alone, in bivalent combinations, or in a trivalent vaccine. Twenty-week-old broiler breeder chickens with no previous exposure to NDV, IBDV, or VA live virus vaccines were injected intramuscularly with the monovalent, bivalent, or trivalent vaccines. The antibody responses to NDV in all three vaccines were poor, and NDV-hemagglutination-inhibition (HI) geometric mean titers (GMTs) never rose above 20 during the 40-week trial. The antibody response to IBDV showed a strong primary response 4 weeks after vaccination, but IBD-VN geometric mean titers declined steadily to less than 100 by 4 months after vaccination. The antibody GMTs to IBDV continued to decline for the remainder of the trial. The antibody response to VA virus was biphasic, with peak VA-virus neutralization (VN) geometric mean titers occurring at 3 months and 6 months postvaccination. The amplitude of the response to the monovalent, bivalent, and trivalent vaccines was inversely proportional to the number of antigens incorporated into each vaccine. Maternal antibody titers in the progeny against each of the three antigens reflected those of the parents. In no case were maternal antibody titers detectable beyond 14 days of age.
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PMID:Multivalent inactivated virus oil emulsion vaccines in broiler breeder chickens. II. Trivalent vaccines in breeders not previously vaccinated with live Newcastle disease, infectious bursal disease, and tenosynovitis vaccines. 631 8

Since recently adding Intralipid (IL) to our standard total parenteral nutrition (TPN) regimen for children with inflammatory bowel (IBD) disease, two children undergoing major intestinal resections have developed acute pancreatitis in the early postoperative period. Herein, we present the clinical summaries of these two patients, discuss the multifactoral etiologies of acute pancreatitis, and review the role of emulsified fat solutions in TPN in children with IBD.
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PMID:Pancreatitis and intravenous fat: an association in patients with inflammatory bowel disease. 641 38

Treatment programs for digestive diseases should be evaluated by randomized clinical trials. Under most circumstances, the best design for such trials requires placebo controls. For example, clinical trials should include groups of placebo-treated patients when there is no commonly accepted standard patients when there is no commonly accepted standard therapy for the disease under study, when standard therapy is of doubtful efficacy, or when standard therapy is unacceptably toxic. Moreover, illnesses--including peptic ulcer and IBD--may have sufficiently high response rates to placebo therapy as to favor placebo-controlled study designs. Placebo treatment is also free of substantial risk, at least compared to active drug treatment, when the disease process is very mild or when the study period is very short. Acceptable alternatives to placebo control include direct comparisons of new agents to standard therapy and addition of either new agents or placebo to a continuing baseline of standard therapy. Similarly, both placebo and active-treatment groups can sometimes be permitted access to standard therapy on a p.r.n. basis, with utilization thereof serving as one of the criteria of therapeutic response. Placebo-controlled trials are therefore generally feasible and desirable methods for testing the safety and efficacy of various proposed treatments for gastrointestinal diseases. High ethical standards in clinical medicine depend on high scientific standards in clinical research.
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PMID:Placebo-controlled clinical trials in gastroenterology. A position paper of the American College of Gastroenterology. 650 16

It has been shown that genetic factors within the HLA region are involved in the etiology of several diseases. For some of these, the existence of another genetic factor has been suggested, although not proven. A possible way to give evidence for another locus (G) is to show that the disease and an unlinked HLA-marker locus (M) do not segregate independently. The usual lod-score method, which assumes monogenic inheritance, is inappropriate for this test. We propose a correction of this method for performing a linkage analysis between the G and M loci, taking into account the role of HLA. A very simple way of using the HLA information is by modifying, for each individual of a pedigree, the penetrance values at the G locus according to the number of HLA haplotypes shared with the index case. These penetrance values are inferred from the observed IBD (identity-by-descent) distribution of HLA haplotypes in a sample of affected sib-pairs. The advantage of using this empirical distribution is that it is not based on any assumptions concerning the mode of inheritance at the HLA-linked locus. This correction method was established using a two-locus model with restrictive assumptions. Its value is discussed for various sets of parameters in more general and realistic two-locus models using simulations.
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PMID:HLA-associated diseases: a new method for performing linkage analysis with other markers than HLA. 659 41

As in any operation for IBD, colectomy and ileorectal anastomosis should be performed only after every effort has been made to control the disease medically. Only in uncontrolled disease should early proctectomy be advised on the grounds of lack of normal physical development and sexual immaturity. Ileorectal anastomosis should not be performed upon every patient requiring surgical treatment any more than proctocolectomy and ileostomy should be performed upon every patient. Unless there is severe persistent disease of the rectum or destruction of the anal sphincter, the rectum should be preserved because severe ulcerative proctitis may heal or improve postoperatively with further medical treatment. If further surgical treatment is necessary, conversion to an ileostomy can be undertaken, and there are now other alternatives, such as the continent ileostomy and the ileoanal anastomosis, with or without a pelvic pouch.
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PMID:Ileorectal anastomosis for inflammatory bowel disease in children and adolescents. 664 77

An infectious etiology has been suggested for the inflammatory bowel diseases, Crohn's disease and ulcerative colitis, and an association of cell wall-defective variants of Pseudomonas maltophilia and Pseudomonas-like group Va bacteria with Crohn's disease has been reported by Parent and Mitchell. Seven of the Parent-Mitchell isolates were compared by using DNA hybridization and six were identical and similar, but not identical, to a type strain of P. maltophilia. The seventh isolate showed extensive homology with VARC, a reference strain of group Va organism, but not with P. maltophilia. Pseudomonas DNAs were radiolabeled by nick translation and used as probes for homologous DNA in hybridization experiments involving 48 different tissues. The presence of DNA with sequences homologous to those of P. maltophilia was detected in three of 23 Crohn's disease samples, two of 10 ulcerative colitis samples, and none of 15 control samples. There was no hybridization with VARC or Pseudomonas aeruginosa probes. We were unable to culture cell wall-defective organisms from patients' tissues but have detected pleomorphic organisms in hypertonic cultures of 14 of 53 Crohn's disease specimens, none of six ulcerative colitis specimens, and none of 11 control specimens. None reverted to normal bacteria. These results do not support an exclusive association of P. maltophilia with Crohn's disease but rather suggest a possible association of P. maltophilia with IBD. Technical limitations currently preclude definitive conclusions regarding the significance of this association. Although we demonstrated the presence of DNA sequences with homology to P. maltophilia DNA in tissues of some patients with IBD, the role, if any, of these bacteria in the pathogenesis of IBD has yet to be established.
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PMID:DNA hybridization studies of the association of Pseudomonas maltophilia with inflammatory bowel diseases. 685 28

In a 4-year period 45 patients were admitted to our gastroenterological u nit with acute infective colitis. The endemic pathogens responsible for the colitis were Yersinia enterocolitica (46%), Campylobacter fetus jejuni (20%), common Salmonellae (13%), less virulent strains of Shigella (9%), Entamoeba hystolytica (7%) and Cytomegalovirus (4%). These microorganisms caused very severe disease in 18% of the patients, who were mostly predisposed. While Salmonella- and amoebic colitis always mimicked ulcerative colitis by the presence of diffuse lesions, the other pathogens caused focal colitis, thus necessitating differential diagnosis vis a vis Crohn's colitis. Two patients (4%) died of complications, while 93% of the patients were cured by proper antimicrobial therapy. In the same period 12 patients were admitted with an acute attack of inflammatory bowel disease due to an intercurrent infection with the same pathogens. In most of these patients clinical remission of IBD was achieved by treating the intercurrent infection. These data indicate that in the presence of an acute attack of colitis an infective etiologic agent must always be sought, and that an attack of chronic idiopathic inflammatory bowel disease may be caused by an intercurrent infection.
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PMID:Acute infective colitis caused by endemic pathogens in western Europe: endoscopic features. 714 Jun 55


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