Case Of Drug-induced Hepatitis Research Articles

Temozolomide-induced liver damage

Temozolomide (TMZ) is an alkylating agent used in chemoradiotherapy and adjuvant chemotherapy regimens for treatment of newly diagnosed or recurrent glioblastoma. In Germany alone, 900,000 daily doses of the drug are prescribed each year. Therefore, all severe side effects of TMZ, even those rarely observed, are relevant to radiotherapists. We report a case of severe drug-induced toxic hepatitis that developed during chemoradiotherapy with TMZ in a patient with glioblastoma multiforme. Transaminase elevation was observed after 5 weeks of TMZ treatment, followed by severe jaundice symptoms which only subsided 2 months later. These findings were consistent with diagnosis of the mixed hepatic/cholestatic type of drug-induced toxic hepatitis. Due to the early termination of treatment, no life-threatening complications occurred in our patient. However, rare reports of encephalopathy and fatality as complications of TMZ therapy can be found in the literature. When using TMZ for treatment of glioblastoma, monitoring of liver enzyme levels should be performed twice weekly to prevent fatal toxic hepatitis. In the case of any drug-induced hepatitis, TMZ must be discontinued immediately.

A Case of Drug-Induced Hepatitis from Methyl 1-P, an Anabolic Androgenic Steroid

Purpose: To illustrate the hepatotoxic effect of a commonly available anabolic steroid and the management of the resulting hepatitis. Methods: Case Description: A 28 year-old Caucasian male presented with nausea, vomiting, pruritus and jaundice following flu-like symptoms. Four to five weeks prior to the hospitalization he had consumed methyl 1-P (an anabolic steroid) for a period of 2 months to enhance his muscle mass. He did not take any other medications or drink alcohol. His physical examination showed scleral icterus, yellowish skin and hepatomegaly. The liver profiles showed a total bilirubin of 58 mg/dl with conjugated bilirubin of 45 mg/dl, alkaline phosphatase 238 U/L, AST 48 U/L, ALT 62 U/L and INR 1.0. Viral serologies including hepatitis A, B, C, E, CMV, EBV and HSV were negative. The autoimmune markers, iron studies and markers of Wilson's disease were all normal. His creatinine was 2.5 mg/dl. Ultrasound and MRI/MRCP imaging showed an enlarged liver with a normal biliary tree and patent hepatic vasculature. Liver biopsy revealed centrilobular and canalicular cholestasis without showing bile duct injury or portal/lobular inflammation consistent with drug induced cholestatic hepatitis. A kidney biopsy showed acute interstitial nephritis with tubular injury and bile casts. Results: The patient was managed with ursodeoxycholic acid, hydroxazine and Benadryl with satisfactory symptom relief. One week following discharge his total bilirubin decreased to 34 mg/dl and his creatinine level was improving Conclusion: A variety of side effects including hepatoxicity have been described with the use of anabolic androgenic steroids. However to our knowledge, Methyl 1-P induced cholestasis has not been reported in the literature. Methyl 1-P contains two steroids, progestin and a second steroid that resembles androstenedione. Renal failure due to anabolic steroids is rare but has been reported. Despite FDA regulations against possession, production and marketing of anabolic steroids, these drugs are freely available as dietary supplements. Increased awareness among consumers and the medical community are required regarding the potential lethal complications of anabolic steroid including hepatotoxicity. Obtaining a good drug history, early diagnosis and prompt discontinuation of the offending drug can lead to gradual but complete recovery over a period of several months.

Hepatitis Associated with Low-Dose Venlafaxine for Postmenopausal Vasomotor Symptoms

To report a case of drug-induced hepatitis associated with low-dose venlafaxine. A 60-year-old white woman receiving venlafaxine 75 mg daily for vasomotor symptoms presented after one month of therapy with nonspecific complaints, including abdominal pain. A series of diagnostic and laboratory tests revealed an enlarged liver and elevated alanine aminotransferase (ALT) up to 372 U/L, aspartate aminotransferase (AST) up to 99 U/L, gamma-glutamyltransferase (GGT) up to 962 U/L, and alkaline phosphatase up to 758 U/L. All potential hepatotoxic medications were discontinued. Within one week after stopping venlafaxine, her liver function test results showed marked improvement. Almost 4 weeks after discontinuing therapy, venlafaxine 37.5 mg was reinitiated. Her ALT, AST, GGT, and alkaline phosphatase again increased to 269, 49, 256, and 263 U/L, respectively, 6 days after resuming therapy. Upon discontinuation of venlafaxine, her liver function abnormalities resolved. This case is significant due to the severity of symptoms and consequent liver function test results involved in diagnosing drug-induced hepatitis. It is also remarkable because of the hepatotoxicity that occurred initially and on rechallenge with low-dose venlafaxine. The hepatotoxic effects of venlafaxine have been characterized as rare and idiosyncratic. The Naranjo probability scale revealed that the adverse drug event was probable. Venlafaxine therapy can lead to drug-induced hepatitis, even when used at low doses. Clinicians should be aware of this possible adverse effect of venlafaxine therapy and monitor patients closely after initiation of therapy.

Drug-induced hepatitis with severe cholestasis due to voglibose

A case of drug-induced hepatitis with severe cholestasis caused by voglibose, a new agent for treating noninsulin-dependent diabetes mellitus, is described. The patient presented with icterus and pruritis. Voglibose was administered for 3 months before abnormal liver function was detected. The lymphocyte blast transformation test was positive for voglibose (stimulation index = 536%). One month after the onset of icterus, the patient also developed cholangitis due to methicillin-resistant Staphylococcus aureus, and the serum total bilirubin level increased to above 40 mg/dl. He was treated with plasma exchange, but eventually died. Voglibose is only absorbed slightly after oral administration, and there have been no reports of hepatitis due to this drug. This is the first fatal case of voglibose-induced hepatitis combined with methicillin-resistant Staphylococcus aureus cholangitis.

A case of drug-induced hepatitis caused by Oriental herb-drug, Sai-rei-to

A case of drug-induced hepatitis caused by Oriental herb-drug, Sai-rei-to