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Various toxicities following drug interaction or off-label use A 30-year-old woman developed drug-induced liver injury (DILI) during antitubercular treatment with ethambutol, pyrazinamide, isoniazid and rifampicin for active tuberculosis (TB). It was also determined that there was an increased risk of hepatotoxicity as a drug-drug interaction might have occurred between isoniazid and rifampicin. Additionally, she developed nausea and vomiting following off-label treatment with acetylcysteine for acute liver failure (ALF) [not all dosages and routes stated]. The woman presented with complaints of fever, shortness of breath and productive cough. She had a history of recent hospitalisation due to shortness of breath. She was empirically treated with unspecified IV antibiotics. She was eventually diagnosed with fungal infection and was found to be positive for Mycobacterium tuberculosis. She was thus diagnosed with disseminated tuberculosis. Therefore, anti-tubercular therapy with rifampicin [rifampin], isoniazid, pyrazinamide and ethambutol (RIPE therapy) was initiated, which was scheduled to be administered for 4 months, followed by dual therapy for another 2 months. She was then admitted to the medical/surgical ward. However, after 4 days of RIPE therapy, she was noted to have elevated prothrombin time (PT) and an increased International Normalized Ratio (INR), from baseline values, along with right upper quadrant tenderness on palpation, she also experienced nausea and vomiting. Her liver enzyme levels were found to be elevated (AST, ALT and total bilirubin). Based on the presentation and laboratory reports, anti-tubercular drugs-induced liver injury (DILI) was suspected. In addition to that, it was also determined that there was an increased risk of hepatotoxicity, as a drug-drug interaction might have occurred between isoniazid and rifampicin. Further, she also exhibited hypotension, tachycardia and tachypnoea. The woman was treated with unspecified fluids and shifted to the MICU for treatment of DILI and a possible sepsis. Upon transfer, a CT scan of the pelvis and abdomen showed likely TB involvement in the spleen, in addition to findings of fatty liver and ascites. Her RIPE therapy was therefore discontinued, and phytomenadione was initiated. She also exhibited persistent hypoglycaemia, which was determined to be due to ALF (a complication of DILI). Hence, 10% dextrose was also initiated. Liver transplant was considered due to a continued rise in the liver function tests. However, hepatic transplant was denied due to active TB. Acute hepatitis panels revealed previous hepatitis-A virus exposure and factor-V concentration was found to be less than 3%, which indicated a poor prognosis. Hepatic encephalopathy was also diagnosed, which required treatment with lactulose and rifaximin. She also received plasma exchange to correct the INR and for management of coagulopathies. Brain MRI showed parenchymal and leptomeningeal enhancements, indicating possible tuberculoma of the brain (a part of disseminated TB). S