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Items 1 - 7 of 7
One page.

1: Ann Pharmacother. 2004 Jun;38(6):1074-9. Epub 2004 Apr 30. Related Articles, Links
Click here to read 
Incidence of hepatotoxicity due to antitubercular medicines and assessment of risk factors.

Shakya R, Rao BS, Shrestha B.

Department of Pharmacy, Kathmandu University, Dhulikhel, Nepal. rajani@ku.edu

BACKGROUND: Antitubercular drugs cause derangement of hepatic function revealed by clinical examination and abnormal liver function test results. Potential hepatotoxicity of some of the first-line antitubercular agents remains a problem, especially during the initial period of treatment. OBJECTIVE: To determine the incidence of antitubercular drug-induced hepatotoxicity in a Nepalese urban population and assess the risk factors. METHOD: Fifty patients diagnosed with active tuberculosis infection with normal pretreatment liver function were monitored clinically as well as biochemically in a prospective cohort analysis. RESULTS: Antitubercular drugs were found to be associated with derangement of hepatic function, resulting in elevation of liver enzymes to a variable extent (t = -4.550, p < 0.01 for aspartate aminotransferase [AST]; t = -5.467, p < 0.01 for alanine aminotransferase [ALT] at 95% CI). Thirty-eight percent of patients had 2 times and 30% had >3 times elevation of ALT. Similarly, 40% and 29% of patients showed 2 and >3 times elevation of the AST level, respectively. Four patients (8%) developed drug-induced hepatotoxicity. Jaundice was the presenting symptom in all patients. The time interval for onset of hepatotoxicity after initiation of therapy was 12-60 days (median 28). Antitubercular drug-induced hepatotoxicity was found more often in younger patients (6% vs 2%; p = 0.368, OR 2.75). Female gender was also a higher risk (p = 0.219, OR 4.2). Most patients who had developed hepatitis were diagnosed per sputum-smear positive reactions. Nutritional status, assessed by body mass index and serum albumin level, was the next predisposing factor. CONCLUSIONS: A finding of an 8% incidence of hepatotoxicity is considerably high. Risk factors of hepatotoxicity included female gender, disease extent, and poor nutritional status. Timely detection and temporary withdrawal of the offending agent can completely cure antitubercular drug-induced hepatotoxicity.

Publication Types:
  • Clinical Trial

PMID: 15122004 [PubMed - indexed for MEDLINE]


2: Ann Pharmacother. 2004 Jun;38(6):1088-9. Epub 2004 Apr 30. Related Articles, Links
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Ursodeoxycholic acid for terbinafine-induced toxic hepatitis.

Agca E, Akcay A, Simsek H.

Publication Types:
  • Case Reports
  • Letter

PMID: 15122001 [PubMed - indexed for MEDLINE]


3: Ann Pharmacother. 2004 Jun;38(6):996-8. Epub 2004 Apr 27. Related Articles, Links
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Rash associated with piperacillin/tazobactam administration in infectious mononucleosis.

LeClaire AC, Martin CA, Hoven AD.

Pharmacy Services, Chandler Medical Center, University of Kentucky, 800 Rose Street, Lexington, KY 40536-0293, USA.

OBJECTIVE: To report a case of piperacillin/tazobactam-induced rash in a patient with infectious mononucleosis. CASE SUMMARY: A 25-year-old white man developed a rash while receiving piperacillin/tazobactam 3.375 g intravenously every 6 hours and gentamicin for osteomyelitis complicating a left femur fracture secondary to a motorcycle accident. Due to progression of the rash following additional doses of piperacillin/tazobactam during hospitalization, the patient's antimicrobial regimen was changed to vancomycin and meropenem. Subsequently, a mononucleosis spot test was positive, and both Epstein-Barr virus (EBV) immunoglobulin (Ig) G and IgM antibodies were positive. The rash rapidly resolved with the discontinuation of piperacillin/tazobactam. DISCUSSION: Although the development of rash following the administration of several different antimicrobials, especially ampicillin, has been previously reported, this is the first report of piperacillin/tazobactam-induced rash in infectious mononucleosis. The rash is generally self-limiting and usually resolves within days of discontinuing the causative antimicrobial agent. An altered drug metabolism or an immune-mediated process has been suggested as the potential mechanism for rash development. CONCLUSIONS: Prior reports of antimicrobial-induced rash in infectious mononucleosis and a positive laboratory diagnosis of EBV in our patient with no history of penicillin allergy support the identification of piperacillin/tazobactam as the inducer of the rash. According to the Naranjo probability scale, the association of piperacillin/tazobactam with the rash was classified as probable.

Publication Types:
  • Case Reports

PMID: 15113982 [PubMed - indexed for MEDLINE]


4: Ann Pharmacother. 2004 May;38(5):895-7. Epub 2004 Mar 25. Related Articles, Links

Comment on: Click here to read 
More evidence supporting the ban of ephedra dietary supplements.

Chavez ML.

Publication Types:
  • Comment
  • Editorial

PMID: 15044656 [PubMed - indexed for MEDLINE]


5: Ann Pharmacother. 2004 May;38(5):776-80. Epub 2004 Mar 18. Related Articles, Links
Click here to read 
Toxic effects from metformin exposure.

Spiller HA, Quadrani DA.

Kentucky Regional Poison Center, Louisville, KY 40232-5070, USA. henry.spiller@nortonhealthcare.org

BACKGROUND: The major risk associated with metformin is lactic acidosis. The incidence of lactic acidosis is not clear. Hypoglycemia is not expected to be a major concern after metformin exposure. OBJECTIVE: This study assessed the demographics, toxic effects, and clinical syndromes of metformin exposures reported to poison centers nationally. METHODS: The Toxic Exposure Surveillance System (TESS) of the American Association of Poison Control Centers was searched for all metformin-only exposures occurring from January 1, 1996, through December 31, 2000. RESULTS: There were 10,958,526 total poisoning exposures reported to TESS during the study period. Of those, 4072 cases met the study criteria. Exposures occurred in 2421 (59%) women and were categorized in all patients as acute (3074; 75%), acute-on-chronic (767; 19%), chronic (200; 5%), and chronicity unknown (31; 1%). Children < or =12 years old experienced few adverse outcomes and no deaths. There were 20 moderate-effect outcomes (1.8%) and 2 major-effect outcomes (0.2%) in children <6 years old and 4 moderate-effect outcomes (2.3%) and no major-effect outcomes in children 6-12 years old. In the adult population, the adverse outcomes were distributed evenly across the age span, with a trend toward more serious outcomes in the elderly. There were 9 deaths (0.2%), 32 major-effect cases (0.8%), and 187 moderate-effect cases (4.6%). In all age groups, acidosis was rare (n = 68; 1.6%). Hypoglycemia is more common than previously reported (n = 112; 2.8%). Clinical effects associated with a major outcome or death were hyperglycemia, acidosis, elevated anion gap, elevated creatinine, hypotension, and coma. CONCLUSIONS: Severe adverse events after exposure to metformin are not common, occurring in approximately 1% of cases; this is in agreement with previous reports. The presence of hypotension, acidosis, elevated anion gap, hyperglycemia, and coma may be prognostic of severe or fatal outcome.

PMID: 15031415 [PubMed - indexed for MEDLINE]


6: Ann Pharmacother. 2004 May;38(5):795-8. Epub 2004 Mar 16. Related Articles, Links
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Lichenoid drug eruption probably associated with rofecoxib.

Abu-Shraie NA, Alfadley AA.

Department of Pharmacy Services, King Faisal Specialist Hospital and Research Center, Riyadh, Kingdom of Saudi Arabia. Nada@kfshrc.edu.sa

OBJECTIVE: To report a case of lichenoid drug eruption (LDE) probably induced by rofecoxib. CASE SUMMARY: A 73-year-old woman was prescribed rofecoxib 25 mg/day for rheumatoid arthritis in addition to other medications on which the patient had been stabilized. Six months after initiation of rofecoxib, linear plaques over the infra-orbital and bitemporal areas of both eyes were observed. Several itchy violaceous papules also developed on her right wrist and dorsum of the left foot. She also had a hyperpigmented macule on her right buccal mucosa. As the skin rash was localized and the patient was initially unwilling to undergo skin biopsy, rofecoxib was continued and a topical steroid was started. One month later, the patient was seen in the dermatology clinic, and the improvement of her skin reaction was significant. A skin biopsy performed during this visit was consistent with LDE. On the next day, her rheumatologist decided to discontinue the offending drug, rofecoxib. Two months later, all skin lesions had completely resolved. No rechallenge with rofecoxib was attempted. DISCUSSION: LDE is a rare skin reaction that can be associated with several drugs. Rofecoxib, a cyclooxygenase-2 inhibitor, has never before been reported to cause LDE. An objective causality assessment indicates that rofecoxib was the probable cause of the skin reaction. CONCLUSIONS: As of this writing, to our knowledge, this is the first case report in the English literature in which rofecoxib had led to the development of LDE.

Publication Types:
  • Case Reports

PMID: 15026562 [PubMed - indexed for MEDLINE]


7: BMJ. 2004 Aug 21;329(7463):459-60; author reply 460. Related Articles, Links

Comment on: Click here to read 
Adverse drug reactions as cause of admission to hospital: definition of adverse drug reactions needs to include overdose.

Laws MB.

Publication Types:
  • Comment
  • Letter

PMID: 15321917 [PubMed - indexed for MEDLINE]


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