Dosing of proton pump inhibitors is suboptimal among otolaryngologists treating reflux-induced upper-respiratory disease.

OBJECTIVE: To evaluate the practice of otolaryngologists treating reflux-induced upper-respiratory disease in a nationwide survey. STUDY DESIGN: Survey study using an anonymous questionnaire containing clinical vignettes. SUBJECTS AND METHODS: The survey was mailed to all 6,899 board-certified fellow members in practice in the American Academy of Otolaryngology-Head and Neck Surgery residing in the United States. RESULTS: One thousand seven hundred twenty questionnaires were returned. Respondents empirically treated reflux-induced upper-respiratory disease with proton pump inhibitors once daily and twice daily 63% and 31%, respectively. Fifteen percent did not instruct their patients on how to take the proton pump inhibitors. Of those who instructed their patients, 22% advised dosing before breakfast, 32% before breakfast and again before dinner, and 46% recommended other timings. When prescribing twice-per-day dosing, 64% responded to give before breakfast and dinner and 28% responded before breakfast and at bedtime. CONCLUSION: Suboptimal dosing of proton pump inhibitors is prevalent among otolaryngologists treating reflux-induced upper-respiratory disease.

A fatal case of bupropion (Zyban) hepatotoxicity with autoimmune features: Case report.

BACKGROUND: Bupropion is approved for the treatment of mood disorders and as an adjuvant medication for smoking cessation. Bupropion is generally well tolerated and considered safe. Two randomized controlled trials of bupropion therapy for smoking cessation did not report any hepatic adverse events. However, there are three reports of severe but non-fatal bupropion hepatotoxicity published in the literature. CASE PRESENTATION: We present the case of a 55-year old man who presented with jaundice and severe hepatic injury approximately 6 months after starting bupropion for smoking cessation. Laboratory evaluation demonstrated a mixed picture of hepatocellular injury and cholestasis. Liver biopsy demonstrated findings consistent with severe hepatotoxic injury due to drug induced liver injury. Laboratory testing was also notable for positive autoimmune markers. The patient initially had clinical improvement with steroid therapy but eventually died of infectious complications. CONCLUSION: This report represents the first fatal report of bupropion related hepatotoxicity and the second case of bupropion related liver injury demonstrating autoimmune features. The common use of this medication for multiple indications makes it important for physicians to consider this medication as an etiologic agent in patients with otherwise unexplained hepatocellular jaundice.