Blueprint for change: will new hospitals be safer hospitals?

2006 
To the Editor, We read Grand Rounds in Gastroenterology, which was published in your February issue, with interest[1] and want to report a case of acute hepatitis C in a US resident who returned from Pakistan after a 3-month stay. A 60-year-old man from Pakistan who lived in the United States for a decade presented to the clinic with complaints of nausea, decreased appetite, and malaise of 4 weeks. He had a history of DM [diabetes mellitus] and hyperlipidemia, for which he was taking oral glipizide 10 mg and atorvastatin 10 mg daily for several years. His HCVAb [hepatitis C virus antibody] was negative 2 years earlier when his wife was being treated for HCV. He had no history of alcohol use, multiple sexual partners, blood transfusion, or drug use. Several sets of liver function tests in the preceding 3 years while he was receiving atorvastatin were normal. While in Pakistan, he was emergently seen in a clinic outside his village after he sustained a syncopal episode due to hypoglycemia and received an IV [intravenous] glucose infusion. Two weeks later, he underwent extraction of 4 teeth. On examination, he had mild tenderness in the right upper quadrant. His AST [aspartate aminotransferase] level was 385 IU/mL, ALT [alanine aminotransferase] level was 509 IU/mL, alkaline phosphatase was 86 IU/mL, albumin level was 3.9 g/L, and bilirubin level was 1 mg/dL. An HCV antibody was initially indeterminate but became positive 2 weeks later. He was found to be HCV genotype 3a with a viral load of 97,719 IU/cc. A liver biopsy showed moderate spotty apoptosis with surrounding lymphocytes in the lobule, mild portal inflammation, and no fibrosis (Figure). He was started on peginterferon alfa-2a at 180 mcg subcutaneously every week along with ribavirin at 1000 mg daily for treatment of HCV, and showed near normal liver function tests 2 weeks after starting the treatment. Figure 1 Liver biopsy – lobular inflammatory Infiltrates × 100. The rise of LFTs [liver function tests], seroconversion of HCVAb, and liver biopsy findings favor a diagnosis of acute HCV infection. He developed acute HCV upon return from Pakistan where unique risk factors associated with acquiring HCV, including contaminated injection use by healthcare providers and dental extraction, have been reported.[2] He was married for 30 years, and his wife was HCV-RNA-negative after completion of 1 year of therapy for HCV, making sexual transmission unlikely. One case of acute hepatitis C that occurred in an individual who traveled to India from France has been reported.[3] This case highlights that besides hepatitis A, B, and E, HCV is a risk to an unsuspecting traveler. The public in the United States should be educated about avoiding elective medical procedures upon traveling to highly endemic areas for HCV and use healthcare facilities with a good reputation. Sincerely, Readers are encouraged to respond to George Lundberg, MD, Editor of MedGenMed, for the editor's eye only or for possible publication via email: ten.epacsdem@grebdnulg
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