Idiosyncratic Drug-Induced Liver Injury Due to Ciprofloxacin: A Report of Two Cases and Review of the Literature.

BACKGROUND Drug-induced liver injury (DILI) can present clinically as a spectrum that includes asymptomatic elevation of transaminases, acute or chronic hepatitis, and acute liver failure. Idiosyncratic DILI is more likely to affect individuals with comorbidities, and to have a wide range of clinical presentations. Although antibiotics are associated with DILI, the fluoroquinolone, ciprofloxacin, is a rarely reported cause. Two cases of idiosyncratic DILI following ciprofloxacin treatment are described, including a review of the literature. CASE REPORT Case 1: A 35-year-old man was treated with ciprofloxacin for periorbital cellulitis. On the second day of ciprofloxacin treatment, he developed abdominal pain, nausea, vomiting and increased serum levels of liver transaminases, aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Further investigations excluded infectious hepatitis, autoimmune disease, or structural liver disease. Exclusion of other causes of DILI and cessation of ciprofloxacin resulted in clinical improvement and normalization of liver function tests (LFTs). Case 2: An 82-year-old man was treated with ciprofloxacin for osteomyelitis. On the tenth day of ciprofloxacin treatment, he developed jaundice and abnormal LFTs, including increased AST, ALT, alkaline phosphatase (ALP), and total bilirubin. Further investigations excluded infectious hepatitis, autoimmune disease, or structural liver disease. Exclusion of other causes of DILI and cessation of ciprofloxacin resulted in clinical improvement and normalization of LFTs. CONCLUSIONS Idiosyncratic DILI due to ciprofloxacin treatment is rare. These two cases have shown that timely diagnosis and discontinuation of ciprofloxacin can prevent the progression of DILI, reduce liver damage, and reduce mortality rates from DILI.

HIV-related pulmonary hypertension.

With the availability of better treatment and prophylactic regimens for the infectious complications of human immunodeficiency virus (HIV), the non-infectious complications are gaining greater attention. HIV-related pulmonary arterial hypertension (HIV-PAH) is one of these. The incidence of HIV-PAH is estimated at 0.5% of HIV-infected individuals. The pathogenesis remains unclear. Patients present with symptoms as diverse as progressive shortness of breath, pedal edema, dry cough, fatigue, syncope, as well as chest pain. Chest X-ray always shows cardiomegaly and prominent pulmonary artery, and evidence of right ventricular hypertrophy can be seen from the electrocardiogram. The pulmonary arterial systolic pressure, diastolic pressure and pulmonary vascular resistance from right heart catheterization are increased. There are a few small studies showing the benefit of prostacyclin analog (epoprostenol and iloprost) and bosentan. The role of antiretrovirals remains controversial, as do those of other agents such as calcium channel blockers and anticoagulants. The prognosis of HIV-PAH is grave. Two thirds of HIV-PAH related mortality is usually secondary to consequences of pulmonary hypertension, with the worst survival noted in New York Heart Association (NYHA) functional class III-IV. The probability of survival in one series was 73%, 60% and 47% at one, two and three years, respectively.