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 21-year old woman using an oral contraceptive, the combination preparation Trigynon containing levonorgestrel (LNG) and ethinyl estradiol (EE), since June 1987 had experienced pain in the groin. In September 1988 she had a single occurrence of bleeding, a sign of lessened effectiveness of the OC. She was treated with 50 mg of minocycline/day as of April 1989, and for inguinal acne conglobata with locally applied clindamycine (10 mg/ml of clindamycine hydrochloride lotion). She switched to another OC, and the next month timely, normal menstruation ensued. A few days later the dose of minocycline was raised to 100 mg/day. Subsequently she had a regular breakthrough bleeding followed by a missed cycle and a positive pregnancy test. There have been several recent reports about the interaction between antibiotics and OCs (breakthrough bleeding and contraceptive failure). Rifampicin and griseofulvin are known to reduce the activity of OCs via induction of liver enzymes. Between 1968-84 there was a total of 62 failures of OCs (15 using OCs with 50 mcg of EE) reported in the UK. The suspected cause was the combined use with antibiotics (70% penicillin and tetracycline). In the Netherlands 6 cases of possible interactions were reported during 1980-86: 2 cases caused by nitrofurantoin and/or trimethoprim, and 1 case by sulfamethoxazol with trimethoprim. The interference of minocycline with the intestinal flora can occur as 34% of it is excreted in feces, and its antibacterial spectrum corresponds to that of tetracycline hydrochloride (reduction of beta-glucuronidase in the feces). The failure of Trigynon cannot be irrefutable ascribed to minocycline as unintended pregnancy also occurs while using OCs without antibiotics. Clindamycine could have also influenced the intestinal flora percutaneously.
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PMID:[Inefficacy of oral contraception during use of minocycline]. 214 63

Chemotactic migration, production of superoxide anion (O2-), and the release of beta-glucuronidase from azurophilic granules were determined in polymorphonuclear leukocytes (PMN) from 135 patients with infectious (e.g., pyoderma, acne conglobata, erysipelas) as well as noninfectious (psoriasis) skin diseases. Purified C5a and the formylated tripeptide FMLP were used as stimuli. In addition, longitudinal profiles of PMN activities were performed at daily intervals in several patients. There was a complete absence of PMN responses (chemotaxis, O2--production, and enzyme release) specifically induced by C5a in 25 patients suffering from various inflammatory diseases of the skin. In these patients PMN responsiveness for the tripeptide FMLP was either normal or increased. The C5a-dependent defect of PMN was transient and correlated with disease activity. When normal PMN were incubated with sera from C5a-defective patients, no inherent stimulatory or inhibitory activities compared to control sera were seen. Pretreatment of normal PMN in vitro with various concentrations of C5a failed to completely deactivate PMN without affecting FMLP dependent functions. These observations demonstrate the presence of a functional defect in circulating PMN during acute cutaneous inflammation. The in vitro experiments suggest transient blocking of C5a-dependent PMN functions by a cell-bound factor which seems not to be C5a or C5adesarg.
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PMID:Transient absence of C5a-specific neutrophil function in inflammatory disorders of the skin. 316 55