Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatosplenic candidiasis has increased in frequency among immunocompromised hosts. Risk factors include hematologic malignancy, intensive chemotherapy, prolonged neutropenia, and treatment with broad-spectrum antibiotics. Patients most commonly present with abdominal pain, persistent fevers despite antibiotic therapy, and an elevated alkaline phosphatase level that is out of proportion to other hepatic enzyme levels. Gastrointestinal mucosal damage secondary to intensive chemotherapy may allow colonization with Candida species and subsequent seeding of the portal vein. Treatment has consisted of prolonged courses of amphotericin B, with mortality rates approaching 50%. We report a case of hepatosplenic candidiasis in a patient with acute myelogenous leukemia who had clinical and radiographic improvement during fluconazole therapy. Fluconazole may be an efficacious and less toxic alternative to amphotericin B.
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PMID:Fluconazole in the treatment of hepatosplenic candidiasis. 173 74

We have reviewed the efficacy of the use of fluconazole in patients with definitely proven Candida esophagitis (CE) associated with human immunodeficiency virus (HIV) infection, using a single 400 mg oral dose of fluconazole and evaluating the patient three days afterwards. This drug showed to be effective for the clinical and endoscopic cure in all patients (100%), and with microbiological cure in ten cases. There was no clinical feature of toxicity. The only side effect was an increased alkaline phosphatase and transaminase activity without hyperbilirubinemia, but this finding was not statistically significant (p greater than 0.05). Fluconazole, given in a single 400 mg dose, was absolutely effective to cure esophagitis in AIDS, thus permitting to avoid parenteral amphotericin.
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PMID:[Candida esophagitis treated with a single dose of fluconazole in patients with HIV: presentation of 11 cases]. 209 54

Eleven kidney transplant recipients with the oral or/and throat candidiasis which occurred during the first 3 months after transplantation were studied. Fluconazole was administered orally in the dose of 50 mg each 24, 48, 72 h, according to creatinine clearance. No clinical symptoms of candidiasis on the third day of the treatment were observed. In all patients, negative mucosal cultures were noted at the 8th day after first fluconazole dose. During fluconazole was with in normal range. Furthermore, no changes in serum bilirubin alanine transaminase, lactate dehydrogenase and alkaline phosphatase activities were observed. Serum creatinine decreased during this follow-up. In the 30th day after fluconazole administration cessation the mycological evidence of Candida p. reinfection were noted in 25% of patients. Fluconazole is highly efficient and safe agent to manage the oral and throat candidiasis in renal transplant recipients.
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PMID:[Testing the efficacy of fluconazole in treatment of oral and throat candidiasis in patients after kidney transplantation]. 797 12

Itraconazole and fluconazole are potent wide spectrum antifungal drugs. Both of these drugs induce hepatotoxicity clinically. The mechanism underlying the hepatotoxicity is unknown. The purpose of this study was to investigate the role of phenobarbital (PB), an inducer of cytochrome P450 (CYP), and SKF 525A, an inhibitor of CYP, in the mechanism of hepatotoxicity induced by these two drugs in vivo. Rats were pretreated with PB (75 mg/kg for 4 days) prior to itraconazole or fluconazole dosing (20 and 200 mg/kg for 4 days). In the inhibition study, for 4 consecutive days, rats were pretreated with SKF 525A (50 mg/kg) or saline followed by itraconazole or fluconazole (20 and 200 mg/kg) Dose-dependent increases in plasma alanine aminotransferase (ALT), gamma-glutamyl transferase (gamma-GT), and alkaline phosphatase (ALP) activities and in liver weight were detected in rats receiving itraconazole treatment. Interestingly, pretreatment with PB prior to itraconazole reduced the ALT and gamma-GT activities and the liver weight of rats. No changes were observed in rats treated with fluconazole. Pretreatment with SKF 525A induced more severe hepatotoxicity for both itraconazole and fluconazole. CYP 3A activity was inhibited dose-dependently by itraconazole treatment. Itraconazole had no effects on the activity of CYP 1A and 2E. Fluconazole potently inhibited all three isoenzymes of CYP. PB plays a role in hepatoprotection to itraconazole-induced but not fluconazole-induced hepatotoxicity. SKF 525A enhanced the hepatotoxicity of both antifungal drugs in vivo. Therefore, it can be concluded that inhibition of CYP may play a key role in the mechanism of hepatotoxicity induced by itraconazole and fluconazole.
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PMID:Involvement of phenobarbital and SKF 525A in the hepatotoxicity of antifungal drugs itraconazole and fluconazole in rats. 1677 3