Onset of Celiac Disease after Treatment of Chronic Hepatitis C with Interferon Based Triple Therapy.

Background. Patients treated with interferon (IFN) based therapies may develop exacerbation of autoimmune disease. We herein present the case of a 53-year-old female patient who developed celiac disease (CD) as a result of triple therapy (interferon, ribavirin, and boceprevir) for chronic HCV. Case. 53-year-old Caucasian female with past medical history of IV drug abuse was referred for abnormal LFTs. Laboratory data showed HCV RNA of 4,515,392 IU/mL, HCV genotype 1a, with normal LFTs. She was treated with 4 weeks of pegylated interferon alfa-2a plus ribavirin, followed by triple therapy using boceprevir for a total of 28 weeks. Approximately 4 weeks after initiation of triple therapy patient developed loose nonbloody bowel movements and was also found to have anemia. Biopsies from first and second portions of the duodenum were consistent with CD. The patient was treated with a gluten-free diet. Her intestinal symptoms improved and the hemoglobin returned to normal. Conclusion. Chronic HCV patients being treated with interferon alfa can develop celiac disease during or after therapy. For patients with positive autoantibodies, all-oral-IFN-free regimens should be considered. Celiac disease should be considered in patients who develop CD-like symptoms while on and shortly after cessation of interferon alfa therapy.

Penetrating aortic atherosclerotic ulcer complicated by periesophageal hematoma.

Penetrating aortic atherosclerotic ulcers have been recently recognized as an entity among the acute aortic syndromes with a potentially fatal outcome. We describe the case of a patient presenting with severe chest pain who died as a result of a thoracic-aorta penetrating atherosclerotic ulcer complicated by a intramural hematoma of the esophagus and stomach, leading to exsanguination. To our knowledge this is the first case reported in the literature of such a complication from penetrating aortic atherosclerotic ulcers.

Terbinafine-associated hepatotoxicity.

Terbinafine, an orally and topically active agent licensed for treatment of dermatophytic infection, has gained rapid worldwide acceptance in medical practice. Despite its fairly benign profile of adverse reactions, liver toxicity has occasionally been linked to terbinafine. This report describes a patient with severe cholestatic hepatitis associated with use of terbinafine. The patient was treated successfully with corticosteroids after partial response to ursodeoxycholic acid and cholestyramine. We attempt to identify risk factors for terbinafine-induced hepatotoxicity by an analytical review of all relevant literature. The mechanism underlying terbinafine hepatotoxicity could be more than just an idiosyncratic reaction. 7,7-dimethylhept-2-ene-4-ynal (TBF-A), the allylic aldehyde metabolite of terbinafine, may play a role in the pathogenesis of its hepatotoxicity. Our analysis supports monitoring patients clinically and measuring liver biochemistry through periodic blood tests, after confirming normal liver function at the onset of therapy with terbinafine. Early detection of abnormal hepatic function should prompt immediate discontinuation of this drug along with further evaluation.

Development and validation of a model to diagnose cirrhosis in patients with hepatitis C.

OBJECTIVE: Although noninvasive markers predictive of cirrhosis in patients with chronic hepatitis C have been examined, none has proved sufficiently accurate for clinical use. The aim of this study was to develop an accurate model that can be easily used by clinicians to predict the probability of cirrhosis in hepatitis C patients from readily available clinical and laboratory information. METHODS: We identified 264 consecutive patients with established chronic hepatitis C infection and extracted multiple physical examination and biochemical variables (recorded before liver biopsy). Similar data were extracted from charts at another hospital. RESULTS: Logistic regression identified the following independent predictors of cirrhosis: platelet count < or = 140,000/ mm3, spider nevi, AST > 40 IU/L, and male gender. Male and female patients with normal values for platelet count and AST and no spider nevi had low probabilities of cirrhosis: 1.8% (95% CI = 0.4-7) and 0.03% (95% CI = 0.003-0.04), respectively. Male patients with abnormal values on all three other predictors had a probability of cirrhosis of 99.8% (95% CI = 98.7-100). Over 48% of study patients had a low (< or = 1.8%) or a very high (> or = 99.8%) predicted probability of cirrhosis. The model had area under the receiver operating characteristic curve of 0.938 (95% CI = 0.91-0.97) and 93.4% in an internal validation. The model accurately distinguished patients with and without cirrhosis (area under the receiver operating characteristic curve = 93.3%) in 102 hepatitis C patients from another hospital. CONCLUSIONS: In patients with hepatitis C, four readily available variables together predict cirrhosis accurately. Successful validation in hepatitis C patients at another hospital with lower prevalence of cirrhosis suggests this model's potential for broad applicability.