D K Farver1, M N Lavin. 1. College of Pharmacy, South Dakota State University, Sacred Heart Hospital, Yankton 57078, USA. dfarver@sunflowr.usd.edu
Abstract
OBJECTIVE: To report a case of quinine-induced hepatotoxicity presenting within 24 hours following the ingestion of the first dose. DATA SOURCES: Case report information was obtained from the medical record, the patient, and the physicians involved in this patient's case. MEDLINE and Index Medicus were searched to obtain relevant published literature from January 1942 to May 1997 using the terms quinine, muscle cramps, liver disease, and hepatotoxicity. CASE SUMMARY: A 57-year-old Native American woman presented with symptoms of nausea, vomiting, generalized myalgia, headache, fever, chills, and rigor. The alkaline phosphatase, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyltranspeptidase concentrations were dramatically elevated. Quinine was suspected as the cause after several days of hospitalization and continued therapy. With discontinuation of the quinine, the patient's symptoms resolved within 48 hours and the liver enzyme concentrations declined within 72 hours. CONCLUSIONS: Documented hepatotoxicity has occurred with quinidine, the optical isomer of quinine. Limited awareness of quinine-induced hepatotoxicity may result in an unrecognized adverse effect.
OBJECTIVE: To report a case of quinine-induced hepatotoxicity presenting within 24 hours following the ingestion of the first dose. DATA SOURCES: Case report information was obtained from the medical record, the patient, and the physicians involved in this patient's case. MEDLINE and Index Medicus were searched to obtain relevant published literature from January 1942 to May 1997 using the terms quinine, muscle cramps, liver disease, and hepatotoxicity. CASE SUMMARY: A 57-year-old Native American woman presented with symptoms of nausea, vomiting, generalized myalgia, headache, fever, chills, and rigor. The alkaline phosphatase, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyltranspeptidase concentrations were dramatically elevated. Quinine was suspected as the cause after several days of hospitalization and continued therapy. With discontinuation of the quinine, the patient's symptoms resolved within 48 hours and the liver enzyme concentrations declined within 72 hours. CONCLUSIONS: Documented hepatotoxicity has occurred with quinidine, the optical isomer of quinine. Limited awareness of quinine-induced hepatotoxicity may result in an unrecognized adverse effect.
Authors: Mark A Howard; Andrea B Hibbard; Deirdra R Terrell; Patrick J Medina; Sara K Vesely; James N George Journal: Proc (Bayl Univ Med Cent) Date: 2003-01