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Items 1 - 6 of 6
One page.
1: Ann Intern Med. 2004 Oct 19;141(8):650-1. Related Articles, Links
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Senna-induced hepatitis in a poor metabolizer.

Seybold U, Landauer N, Hillebrand S, Goebel FD.

Publication Types:
  • Case Reports
  • Letter

PMID: 15492352 [PubMed - indexed for MEDLINE]


2: Ann Pharmacother. 2004 Sep;38(9):1439-42. Epub 2004 Aug 03. Related Articles, Links
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Intentional topiramate ingestion in an adolescent female.

Chung AM, Reed MD.

Assistant Clinical Professor of Pharmacy Practice and Adjunct Assistant Harrison School of Pharmacy, Auburn University, Auburn, AL, USA.

OBJECTIVE: To describe an intentional topiramate ingestion by an adolescent and warn of the potential for topiramate abuse. CASE SUMMARY: A 17-year-old female intentionally ingested approximately eight 100-mg topiramate tablets for the purpose of "getting high." Soon after ingestion, she was found at school obtunded and nonresponsive. Upon transfer to the emergency department, she became combative and aggressive with evolving neurologic abnormalities including incoherence, confusion, disorientation, and significant speech impairments including echolalia. Approximately 24 hours after ingestion, the patient had completely recovered without requiring specific treatment or experiencing sequelae. DISCUSSION: The clinical effects following acute topiramate intoxication appear consistent with the drug's known pharmacologic properties. There are few other reports of topiramate ingestions and most cases have had mild outcomes. CONCLUSIONS: Due to the multifactorial effects topiramate may have upon the central nervous system and its anorectic effect, abuse of this drug by adolescents should be considered upon presentation of an adolescent with mental status changes.

Publication Types:
  • Case Reports

PMID: 15292499 [PubMed - indexed for MEDLINE]


3: Ann Pharmacother. 2004 Sep;38(9):1443-5. Epub 2004 Jul 27. Related Articles, Links
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Alfuzosin-induced acute hepatitis in a patient with chronic liver disease.

Yolcu OF, Koklu S, Koksal AS, Yuksel O, Beyazit Y, Basar O.

Department of Gastroenterology, Turkiye Yuksek Ihtisas Hospital, Ankara, Turkey. omerfarukyolcu@hotmail.com, gskoklu@yahoo.com

OBJECTIVE: To report a new case of probable alfuzosin-induced hepatitis. CASE SUMMARY: An 80-year-old man was evaluated because of jaundice and pruritus. He was diagnosed as having Child-Pugh A chronic liver disease due to hepatitis B virus. Other etiologies of hepatitis were appropriately ruled out, and the hepatitis B was non-replicative. Therefore, elevated liver enzyme levels were ascribed to alfuzosin treatment. DISCUSSION: Although alfuzosin-related mixed-type hepatotoxicity has been previously reported, this is the first published case describing probable hepatocellular-type hepatotoxicity resulting from use of alfuzosin in a patient with underlying chronic liver disease. According to the Naranjo probability scale, alfuzosin was a probable cause of the hepatotoxicity. The mechanism of alfuzosin-induced liver damage is unknown. Several features, such as absence of predictable dose-dependent toxicity of alfuzosin in previous studies and absence of hypersensitivity manifestations in our case, are suggestive of a metabolic type of idiosyncratic toxicity. CONCLUSIONS: Alfuzosin rarely causes hepatotoxicity; however, clinicians must be alert for this adverse effect while using alfuzosin.

Publication Types:
  • Case Reports

PMID: 15280514 [PubMed - indexed for MEDLINE]


4: Ann Pharmacother. 2004 Sep;38(9):1540-1. Epub 2004 Jul 20. Related Articles, Links
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Is the Naranjo probability scale accurate enough to ascertain causality in drug-induced hepatotoxicity?

Garcia-Cortes M, Lucena MI, Andrade RJ, Camargo R, Alcantara R.

Publication Types:
  • Letter

PMID: 15266043 [PubMed - indexed for MEDLINE]


5: Ann Pharmacother. 2004 Sep;38(9):1419-23. Epub 2004 Jul 20. Related Articles, Links
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Second-generation thiazolidinediones and hepatotoxicity.

Marcy TR, Britton ML, Blevins SM.

Department of Pharmacy, Clinical and Administrative Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73117-1223, USA. todd-marcy@ouhsc.edu

OBJECTIVE: To report a case of hepatotoxicity probably caused by pioglitazone, summarize case reports of hepatotoxicity induced by rosiglitazone or pioglitazone, and make recommendations regarding routine liver enzyme measurement in patients taking these agents. CASE SUMMARY: A 39-year-old black woman with type 2 diabetes mellitus, hypertension, and congestive heart failure presented to a pharmacist-staffed diabetes comanagement service. She reported fatigue, dark brown urine, nausea, itching, and loss of appetite. Pioglitazone was promptly discontinued because her symptoms were consistent with those of hepatic dysfunction and pioglitazone was identified as a potential cause. The patient was referred to her physician. Liver enzyme levels were checked 13 days after initial presentation and found to be abnormal: alanine aminotransferase 490 U/L, aspartate aminotransferase 360 U/L, alkaline phosphatase 851 U/L, total bilirubin 3.1 mg/dL, direct bilirubin 2.0 mg/dL, and indirect bilirubin 1.1 mg/dL. Within 2(1/2) months of discontinuing pioglitazone, the patient's symptoms resolved and liver enzyme levels returned to normal. DISCUSSION: Troglitazone, a thiazolidinedione (TZD), was removed from the market because of hepatotoxicity. Reported cases involving the newer TZDs, rosiglitazone and pioglitazone, have been few in number and less severe in consequence. Six cases of rosiglitazone-induced hepatotoxicity and 5 of pioglitazone-induced hepatotoxicity have been reported. Most patients improved symptomatically 2-4 weeks following discontinuation of the offending TZD, with normalization of liver enzyme levels in 2 weeks to 6 months following TZD discontinuation. CONCLUSIONS: Although the timeline and extent of liver enzyme elevation in this case are unclear, the Naranjo probability scale suggests that a causal relationship between pioglitazone and liver disease is probable. Patients with previous TZD-induced hepatotoxicity should not be rechallenged. Cases of hepatotoxicity with second generation TZDs, although clearly linked, have been few in number and less severe in consequence when compared to troglitazone. We agree with current package labeling that requires baseline and then periodic measurement of liver enzymes in patients taking pioglitazone or rosiglitazone.

Publication Types:
  • Case Reports

PMID: 15266041 [PubMed - indexed for MEDLINE]


6: Gastroenterol Clin Biol. 2004 Jan;28(1):94-5. Related Articles, Links
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[Nome gesrol (lutenyl) induced severe acute hepatitis]

[Article in French]

Daghfous R, El Aidli S, Rjeibi I, Hedi Loueslati M, Lakhal M, Belkahia C.

Publication Types:
  • Case Reports
  • Letter

PMID: 15041823 [PubMed - indexed for MEDLINE]


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