Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sulfapyridine (SP), one of the metabolites of sulfasalazine (SASP), is further metabolized into N-acetylsulfapyridine (AcSP) by polymorphic N-acetyltransferase 2 (NAT2). NAT2 activity has been diagnosed by phenotyping, that is, evaluating plasma concentrations or urinary excretions of tentatively administered test drugs for dose individualization and avoidance of serious adverse events. Herein, we investigated the relationship between NAT2 genotypes and the pharmacokinetics of SP in healthy Japanese subjects, as well as the adverse events of SASP in patients with inflammatory bowel disease (IBD). Eight healthy subjects and 13 IBD patients were classified into three groups by NAT2 genotyping; the homozygote for the wild-type allele (Rapid Types), the compound heterozygote for the wild-type and mutant alleles (Intermediate Types), and the homozygote for mutant alleles (Slow Types). A single oral dose of 40 mg/kg SASP was administered to each healthy subject, and plasma and urine samples were taken until 51 and 72 h after administration, respectively. Both the SP and AcSP concentrations in each sample were determined by the HPLC method. The NAT2 genotypes were well-correlated with the plasma concentrations or urinary excretions of SP and AcSP in 8 healthy subjects, except for one Slow Type. In patients with IBD, skin rash was seen in 3 of 6 Rapid Types and 1 of 6 Intermediate Types, consistent with the concept that hypersensitive reactions are independent of serum SP concentrations. In contrast, SASP dosing-related acute pancreatitis was found in the Slow Type patient. In this case, the NAT2 activity was diagnosed by genotyping in advance, and the medical staff could pay scrupulous attention, resulting in no serious subjective symptoms such as abdominal pain, anorexia or fever. Further investigations on the relationship between the NAT2 genotype and adverse events are required, although genotyping appeared to be a promising method to avoid such serious adverse events.
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PMID:N-acetyltransferase 2 genotype-related sulfapyridine acetylation and its adverse events. 1218 10

Growth failure (GF) is one of the major complications affecting children with inflammatory bowel disease. The faltering is temporary in 40-50% of cases and prolonged in 10-20% in Crohn's disease (CD). Such failure is rare in children with ulcerative colitis (5%). This complication is often associated with retarded bone development and delayed onset of sexual maturation. The delayed linear growth has a variety of causes including insufficient intake due to anorexia and the inflammatory process with increased energy and protein expenditure. Other factors are increased intestinal loss, secondary hypopituitarism and treatment with steroids. Therapeutic strategies of CD in children have changed this last decade by introducing new therapeutic agents such as topic steroids, immunosuppressors, anti-TNF (antibody and notably in children enteral nutrition which has shown its efficacy in inducing remissions of active CD, restoring nutritional status and stimulation of linear growth. The results of a recent prospective multicentric study over 2 years in 82 CD show that severe GF (-2 SD) is initially present in 15% (n = 12), among them 11 remain < -2SD after 2 years of follow-up. Six patients who were on the normal range initially increased their GF during the follow-up (< -2SD) (total 21% < -2SD (n = 17) at 2 years). At inclusion in this group there was no difference in growth velocity, used of steroids, enteral nutrition or severity of CD as compared to the group with no GF. It suggests that new treatment strategy should be developed in the future for this specific complication of paediatric CD.
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PMID:Growth in paediatric Crohn's disease. 1237 7

In the last years the research on the etiopathogenesis of the inflammatory bowel disease (IBD) is focused around immunological aspects. Many authors consider that the intestinal inflammation is due to an inappropriate immunological response to normally present antigens in the gut. Two aspects must to be considered between IBD: Crohn's disease and ulcerative colitis. IBD's diagnosis is based on the symptomatology, (cramps, liquid feces with mucus and blood, anorexia and weight loss), hemato-clinical tests (ESR, PCR, blood platelet, mucoprotein, sideremia) and radiological tests (tenuis Rx, abdominal echography, fibro endoscophy and scintigraphy). Principal aim of the therapy is the clinical remission. Following the remission starts a maintenance protocol. Parenteral nutrition is used in paediatric and adolescent age. Diets have been used to provide a convenient nutritious contribution with growth improvement and partial remission of activity index of the disease. Pharmacology therapy represents a valid instrument to obtain the remission. Colectomy is performed on unsuccessful medical therapy. Early studies on IBD's pathogenesis bring to the use of biological therapies that show beneficial effects on the disease.
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PMID:[Chronic intestinal inflammatory diseases]. 1240 Feb 15

Weight loss, day-time sleep and loss of appetite were leading symptoms in a thirteen years old girl, in whom consecutively the diagnosis of Crohn's disease of the stomach and the duodenum was made after endoscopy and biopsy were performed. There were no complaints of diarrhea, abdominal pain or other symptoms suspicious for this chronic inflammatory bowel disease.
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PMID:[An interesting case in the pediatric polyclinic. Crohn disease with involvement of the distal esophagus, stomach and duodenum]. 1244 46

Inflammatory bowel disease (IBD) is a group of chronic intestinal inflammatory diseases that consists of ulcerative colitis (UC), an inflammation of the large intestine, and Crohn's disease (CD), which can affect any part of the gastrointestinal tract. IBD affects approximately 1 in every 1000 individuals in western countries. There is a marked tendency in the age of onset toward gradually younger people. IBD represents a genuine problem in public health because of the absence of etiologic treatment. The clinical image is characterized by recurrent segmental or total inflammatory involvement of the large and/or small intestine, often resulting in a chronic, unpredictable course. The symptoms of both are extremely unpleasant and impact all aspects of quality of life. They include diarrhea, abdominal pain, rectal bleeding, fever, nausea, weight loss, lethargy, and loss of appetite. If left untreated, malnutrition, dehydration, and anemia follow, which, in extreme cases, can even lead to death. Although many patients are managed successfully with conventional medical therapy, such as anti-inflammatory corticosteroid treatment, some stay refractory to treatment, most will have recurrent activity of disease, and two thirds will require surgery. Administered orally or by injection, only a fraction of the active components of most conventional drugs reaches the intended target site, the inflamed intestinal lining. This is not only an inefficient way to deliver drugs, but, more important, means that patients are often subject to a spectrum of unpleasant side effects that result from the high levels of the drugs in other, otherwise healthy tissues and organs of the body.
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PMID:Lactococcus lactis, a tool for the delivery of therapeutic proteins treatment of IBD. 1280 77

Milk kappa-casein-derived glycomacropeptide has immunomodulatory and bacterial toxin binding effects. The intestinal anti-inflammatory activity of glycomacropeptide was assessed in trinitrobenzenesulfonic acid-induced colitis in rats. Rats were administered glycomacropeptide daily starting either 2 d before (pretreatment) or 3 h after (post-treatment) colitis induction. Pretreatment with glycomacropeptide had a dose-dependent anti-inflammatory effect, characterized by lower body weight loss, decreased anorexia (57%), colonic damage (65%), and weight to length ratio (32%), as well as a reduction in colonic alkaline phosphatase activity (42%) and interleukin 1, trefoil factor 3, and inducible nitric oxide synthase mRNA levels (P < 0.05). The mechanism of action of glycomacropeptide is unknown but is consistent with an inhibition of the activation of immune cells. The magnitude of the anti-inflammatory effect was generally comparable to that of sulfasalazine, an established drug used in the treatment of inflammatory bowel disease. Bovine glycomacropeptide may play a role in the management of patients with inflammatory bowel disease.
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PMID:Bovine glycomacropeptide is anti-inflammatory in rats with hapten-induced colitis. 1586 98

Anorexia, malnutrition, altered body composition and development of mesenteric obesity are well known features of inflammatory bowel disease (IBD). Recent data suggest that dysregulation of protein secretion by white adipose tissue is involved in these manifestations of patients with IBD. Adipocytes are recently recognized as endocrine cells that secrete a variety of bioactive substances known as adipocytokines. There is evidence that adipocytokines are involved in inflammatory and metabolic pathways in human beings. Overexpression of adipocytokines such as leptin, adiponectin and resistin in mesenteric adipose tissue of operated patients with Crohn's disease has recently been reported, suggesting that mesenteric adipocytes in IBD may act as immunoregulating cells. Therefore, it could be suggested that adipocytokines play an important role in the disease pathogenesis. Moreover, modulators of mesenteric adipose function have been suggested as potential therapeutic drugs in IBD. In this review, the importance of white adipose tissue function and adipocytokines, is discussed with respect to IBD.
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PMID:The emerging role of adipocytokines as inflammatory mediators in inflammatory bowel disease. 1611 20

Oligosaccharides are included among the anti-inflammatory components of milk because of their prebiotic properties and their capacity to act as receptors of microorganisms. Here the intestinal anti-inflammatory effect of goat milk oligosaccharides (O) was assessed in trinitrobenzenesulfonic (T) acid-induced colitis in rats. Rats were randomly assigned to three different groups. Two groups (T and OS) of colitic rats and a control group (C) were studied. Group OS received 500 mg/(kg.d) of goat milk oligosaccharides orally, starting 2 d before the colitis induction until d 6, and groups T and C received the vehicle. When compared with the T group, the OS group showed decreased anorexia and body weight loss; reduced bowel wall thickening and longitudinal extension of necrotic lesions; downregulated colonic expression of interleukin 1beta, inducible nitric oxide synthase, cyclooxygenase 2, and mucin 3; and increased trefoil factor 3. Thus, goat milk oligosaccharides have anti-inflammatory effects in rats with experimental colitis and may be useful in the management of inflammatory bowel disease.
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PMID:Goat milk oligosaccharides are anti-inflammatory in rats with hapten-induced colitis. 1648 41

A case of eosinophilic granulomatous gastroenterocolitis and hepatitis in a 1-year-old male Siberian Husky is described. The dog presented with a history of diarrhea, weakness, lethargy, and anorexia of several months' duration. Hematologic and biochemical examinations, abdominal ultrasonography, computer tomography, and exploratory laparotomy were performed. Histopathologic examination of full-thickness biopsies from the gastrointestinal tract and liver revealed the presence of eosinophilic granulomatous lesions in the submucosa and tunica muscularis of stomach, jejunum, ileum, colon, and liver. Infectious agents were not detected by light microscopic and electron microscopic examination or by immunohistochemistry. On the basis of the findings, it is concluded that the disease in this dog represents an unusual manifestation of chronic idiopathic inflammatory bowel disease.
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PMID:Eosinophilic granulomatous gastroenterocolitis and hepatitis in a 1-year-old male Siberian Husky. 1709 65

Blastocystis hominis (B. hominis) is a parasite of uncertain role in human disease. It may be identified during a workup for gastrointestinal symptoms, usually in stools. The clinical consequences of B. hominis infection are mainly diarrhea and abdominal pain as well as nonspecific gastrointestinal symptoms such as nausea, anorexia, vomiting, weight loss, lassitude, dizziness, and flatulence. Case reports and series have suggested a pathogenic role of B. hominis in causing intestinal inflammation. Also some studies have suggested that inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) are associated with B. hominis infection. The investigators indicate that the stools of all patients presenting with IBD or IBS should be examined, and culture methods for B. hominis carried out. Invasion and mucosal inflammation of the intestine with B. hominis have been observed in studies of gnotobiotic guinea pigs. The transmission, pathogenicity, culture characteristics, taxonomy, life cycle, biochemistry and molecular biology of B. hominis remain unclear. More studies are necessary for this parasite.
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PMID:[Blastocystis hominis and bowel diseases]. 1710 62


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