Reactivation of sarcoidosis during interferon therapy.

The exacerbation of a co-existing autoimmune disease is often a concern for physicians who use immunomodulating agents for the treatment of a concomitant process. As physicians begin to treat chronic hepatitis C more often and more aggressively, this potential problem with occur more frequently. Herein we reported a case of reactivation of sarcoidosis occurring during the treatment of chronic hepatitis C, and we present a literature review of other centers' experiences with this problem. Depending upon the severity of the exacerbation and the type of organ involvement, reactivation of sarcoidosis may require discontinuation of the interferon therapy, with or without the use of additional steroids. The majority of patients, however, do not require the use of steroids. Interestingly, continuation of the interferon therapy in the presence of a mild-to-moderate exacerbation of sarcoidosis may be safe in a minority of patients with noncritical organ involvement.

Prochlorperazine-induced cholestasis in a patient with alpha-1 antitrypsin deficiency.

A case of a 58-year-old woman with history of bilateral lung transplant secondary to alpha-1 antitrypsin deficiency (PIZZ), who presented with a severe drug-induced cholestasis secondary to prochlorperazine is reported. After 27 months of prochlorperazine use, she developed liver failure consisting of jaundice with ascites. Computed tomography of the abdomen, abdominal ultrasonography as well as an endoscopic retrograde cholangiopancreatography showed no evidence for biliary obstruction. Liver biopsy demonstrated diffuse ongoing advanced chronic cholestasis, moderate portal and periportal inflammation as well as bridging fibrosis. During her hospitalization, her total bilirubin increased to 38.6 mg/dL; alkaline phosphatase to 362 IU/L, alanine aminotransferase to 71 IU/L and aspartate aminotransferase to 88 IU/L. After several weeks of ursodiol therapy without clinical improvement the prochlorperazine was discontinued and was followed by a rapid improvement in her measures of liver injury. An immediate decline of her serum total bilirubin and alkaline phosphatase to 21.4 mg/dL and 258 IU/L, respectively, occurred strongly suggesting the idea of a prochlorperazine-induced injury.