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Raúl J Andrade

Publications and source records attributed to Raúl J Andrade.

28 records · Page 2Linked to original sources
PubMed2003

Antidepressant-induced hepatotoxicity.

Depression is a chronic, severe and increasingly prevalent illness associated with substantial morbidity, mortality and healthcare costs. Antidepressant drugs, the cornerstone of depression treatment, are not devoid of adverse effects, including hepatotoxicity. To review the risk of liver toxicity related to major antidepressants, the authors have followed structural criteria focusing on the underlying mechanism presumably involved and the role of particular chemical structures. The clinicopathological expression goes from transient increases in liver enzymes to fulminant liver failure. Classical antidepressants such as monoamine oxidase inhibitors (MAOIs) or tricyclic antidepressants (TCAs) seem to have the highest potential to induce liver damage compared with the newer drugs such as selective serotonin re-uptake inhibitors (SSRIs). The potential for severe hepatotoxicity associated with nefazodone is stressed. Guidelines for therapy and prevention of antidepressant-induced hepatotoxicity are also discussed.

Antidepressive Agents↗
PubMed2002

Multicenter hospital study on prescribing patterns for prophylaxis and treatment of complications of cirrhosis.

OBJECTIVE: To describe the prescribing patterns for liver disease management. METHODS: A multicenter cross-sectional prospective observational study was carried out in 25 Spanish hospitals. Inpatients, admitted to gastrointestinal and liver units with a diagnosis of liver cirrhosis, were included in five centrally assigned index days between February and June 1999. Information was collected about demographic variables and pharmacological treatments used on admission and recommended at discharge. RESULTS: Five hundred and sixty-eight patients (70% men, mean age 61 years) were studied. Alcoholic cirrhosis of the liver accounted for 44% of the sample, ascites being the most prevalent complication. The most frequent diuretic schedule on admission was the combination of spironolactone and furosemide at a ratio of 1 (100 mg/40 mg). Hospitalization resulted in an increase in the percentage of patients that received the combination at a ratio higher than 1. Diuretics were a major cause of adverse drug events on admission (7.5%). Ulcer-healing drugs showed a notable increase at discharge (35%; range 10-59%) compared with 24% (6-37%) on admission. Utilization rates at discharge were 65% (59-74%) for diuretics, 51% (38-76%) for laxatives, 31% (0-75%) for vitamin K, 24% (4-53%) for beta-adrenergic blocking agents, and 13% (0-47%) for nitrates, which were significantly higher than on admission. CONCLUSION: These results provide the first quantitative data of drug utilization in liver disease and highlight the wide variability in prescribing practices across centers and the higher than expected use of non-evidence-based treatments, especially vitamin K and antiulcer drugs.

Adult↗
PubMed2002

Cholestatic hepatitis related to use of irbesartan: a case report and a literature review of angiotensin II antagonist-associated hepatotoxicity.

We report a patient who developed cholestatic hepatitis shortly after starting therapy with irbesartan, one of the new, recently marketed angiotensin II antagonists. Serological studies and ultrasonography ruled out viral hepatitis and extrahepatic obstructive jaundice, respectively. A percutaneous liver biopsy showed a portal inflammatory infiltrate with eosinophils and marked cholestatic features in the perivenular area. Irbesartan was discontinued and the patient's jaundice resolved slowly over a period of several weeks, although mild biochemical cholestasis lasted for more than 1 year. There have been seven prior cases of angiotensin II antagonist-induced hepatotoxicity reported in the literature. A class warning for hepatotoxicity for these compounds should probably be considered.

Acute Disease↗