Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A sensitive technique was used to estimate two acid hydrolases--N-acetyl-beta-glucosaminidase (N.A.G.) and beta-glucuronidase (B.G.)--produced by peripheral-blood monocytes. Enzyme levels were measured after in-vitro incubation of monocytes with or without stimulation by zymosan and endotoxin. Compared with controls, enzyme production and release in inflammatory bowel disease, chronic liver disease, and rheumatoid arthritis were markedly raised. It is suggested that various stimuli, including immunological ones, may be responsible for the release of such enzymes from monocytes and that such release may be a factor in the production of the chronic inflammation seen in these disorders.
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PMID:Acid hydrolases in monocytes from patients with inflammatory bowel disease, chronic liver disease, and rheumatoid arthritis. 7 70

Although oral glucocorticoids are the treatment of choice for moderate to severe ulcerative pancolitis, their systemic side effects and adrenal suppression account for considerable morbidity. An oral glucocorticoid-conjugate (prodrug), budesonide-beta-D-glucuronide, which is not absorbed in the small intestine but is hydrolysed by colonic bacterial and mucosal beta-glucuronidase to release free budesonide into the colon was synthesised. The objective of this study was to compare treatment with budesonide-beta-D-glucuronide with treatment with free budesonide by examining: (1) the healing of experimental colitis and (2) the extent of adrenal suppression. Pancolitis was induced with 4% acetic acid. Animals were then randomised to receive oral therapy for 72 hours with (1) budesonide-beta-D-glucuronide, (2) free budesonide, or (3) vehicle. Drug efficacy and colitic healing was determined by measuring gross colonic ulceration, myeloperoxidase activity, and in vivo colonic fluid absorption. Adrenal suppression was determined by measuring plasma adrenocorticotrophic hormone and serum corticosterone. Vehicle-treated colitis animals had gross ulceration, increased myeloperoxidase activity, and net colonic fluid secretion. Treatment with oral budesonide-beta-D-glucuronide accelerated all measures of colitis healing at a fourfold lower dose than did free budesonide. Furthermore, treatment with budesonide-beta-D-glucuronide did not result in adrenal suppression whereas free budesonide treatment did. A newly synthesised orally administered glucocorticoid-conjugate accelerates colitis healing with limited adrenal suppression. Development of an orally administered colon-specific steroid delivery system represents a novel approach to inflammatory bowel disease treatment.
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PMID:A budesonide prodrug accelerates treatment of colitis in rats. 795 2

To investigate the possibilities of differentiating between inflammatory bowel disease (IBD) and infectious colitis on clinical, microbiological, laboratory and histological grounds, a prospective study of 105 patients with a first attack of colitis was undertaken. Rectal biopsy was performed on four occasions during 1 year. In 56% of the patients who proved to have IBD, the mode of onset of diarrhoeal symptoms was insidious and in 44% it was more acute, while in 81% of those who proved to have infectious colitis the onset was acute. Most patients with infectious colitis presented within 1 week, had early fever, and did not show any histological features characteristic of IBD. In most IBD patients with a non-insidious onset there were clinical warning signs of IBD, such as slight previous bowel symptoms, a late presentation time (> 1 week) and absence of early fever, or histological features characteristic of IBD. Moreover, 62% of the IBD patients with a non-insidious onset fell ill in connection with travelling abroad, gastrointestinal infection or treatment with antibiotics. Travel abroad seemed to be associated with an increased risk of developing IBD. The strongest histological predictor of IBD was basal plasmocytosis, followed by more than two vertical crypt branches/MPF, crypt distortion, villous mucosa, mucosal atrophy, epithelioid granulomas and Paneth cell metaplasia. These signs were rarely or never found among patients with infectious colitis. Their frequency increased with the interval between the initial symptoms and the first biopsy. The presence of focal basal plasmocytosis seems to be the earliest sign of IBD. The frequency of histological signs indicating IBD was maximal (88%) at the 1-week biopsy. During treatment the basal plasmocytosis and villous mucosa decreased, while crypt distortion and mucosal atrophy remained unchanged. Early treatment did not prevent the appearance of any feature. Nor did it prevent relapse. In 21% of the IBD patients microbial findings were positive. The findings consisted in known colitis-causing agents in 14% and other agents, such as viruses, in another 7%. In 78% of the patients with non-relapsing colitis (NRC), colitis-causing agents were found. Haemolytic strains of E. coli were detected more often in IBD. Among the IBD patients, 65% showed positive immunofluorescence reactivity to neutrophil granulocytes, indicating the presence of antineutrophil antibodies (ANCA). The corresponding figure for NRC patients was 5%. Antibodies against beta-glucuronidase were found in 42% of the patients with granulocyte reactivity.
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PMID:First attack of inflammatory bowel disease and infectious colitis. A clinical, histological and microbiological study with special reference to early diagnosis. 811 39

Inflammatory bowel disease refers to ulcerative colitis and Crohn's disease, two gut diseases with unknown causes. The dramatic increase in the last half century and the big difference in incidence for people with the same ethnic background but living in different areas strongly suggested that environmental factors played the dominant role for these diseases. The similarity in many aspects for these two diseases suggested a common causative factor. Here I suggest the impaired inactivation of digestive proteases by deconjugated bilirubin, as the result of the inhibition of bilirubin deconjugation enzyme, beta-glucuronidase, originated from the luminal bacteria and mucosa of the gut, to be a possible mechanism for both ulcerative colitis and Crohn's diseases. I also provide evidence to suggest that saccharin could be the causative or one of the most important risk factors for inflammatory bowel disease as for its inhibition on beta-glucuronidase in the intestine.
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PMID:Impaired inactivation of digestive proteases by deconjugated bilirubin: the possible mechanism for inflammatory bowel disease. 1220 2

The aim of the study was to analyze the differences in the activity of beta-glucuronidase and beta-glucosidase in stool specimens of children with Inflammatory Bowel Diseases (IBD) and healthy subjects. The disease activity was determined according to the PCDAI scale (Crohn disease) and Truelove-Witts scale (Ulcerative colitis). Enzyme activity was determined by spectrophotometry. There was a correlation between the level of beta - glucosidase activity in stool and patient's age in the group of healthy controls, but not in the IBD group. beta-glucosidase activity in IBD and healthy subjects stool specimens did not differ significantly. The activity of beta-glucuronidase in children with IBD was two times lower than in the healthy group and was correlated with age in children with IBD, but not in the group of healthy ones.
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PMID:Beta-glucuronidase and Beta-glucosidase activity in stool specimens of children with inflammatory bowel disease. 2445 40