Daas et al. Journal of Medical Case Reports 2011, 5:233 http://www.jmedicalcasereports.com/content/5/1/233 and was started on a new regimen that included emtrici- tabine/tenofovir and etravirine. She became more com- pliant with treatment, and her clinical parameters improved. Before March 2009, her CD4 had been 157 cells/mm3 and her viral load had been 120,000 copies/ mL. One month after treatment adjustment, her CD4 went up to 232 cells/mm3 and her viral load was unde- tectable. There was no personal or family history of auto- immune disease. Six months after treatment adjustment she started to experience gradual right upper quadrant pain associated with intermittent night sweats. Her pain increased in intensity and became intractable. A computed tomo- graphic scan of her abdomen was unremarkable. She was seen in the office with fever and tachycardia and was hos- pitalized because of possible sepsis and acute abdomen. Her physical examination revealed that she was febrile (body temperature 102.1°F), tachycardic (130 beats/min) and hypoxic (O2 saturation 84% on room air). Her chest examination revealed fine bibasilar crackles. Her abdom- inal examination demonstrated diffuse abdominal ten- derness with rebound that was most prominent in the right upper quadrant. A hepatobiliary iminodiacetic acid scan showed patent biliary ducts with a normal gallbladder ejection fraction. Computed tomography of the chest showed pericardial effusion that was confirmed by a transthoracic echocardiogram. On day 3 of her hospitalization, she underwent a peri- cardial window, a pericardial biopsy and a laparoscopy with liver biopsy. The laparoscopy revealed a grossly abnormal liver (Figure 1). The liver biopsy demonstrated a dense portal lymphoplasmacytic infiltrate with multifo- cal zones of hepatocellular centrilobular necrosis Page 2 of 4 consistent with AIH (Figure 2). Histological staining for fungi and mycobacterium were negative. Pertinent laboratory findings in this patient included alanine aminotransferase 1526 U/L, aspartate amino- transferase 777 U/L, international normalized ratio, 1.53; albumin level, 2.7 g/dL; anti-nuclear antibody (ANA) titer, 1:1280; negative anti-smooth muscle antibody; negative anti-cardiolipin and anti-ribosomal antibodies; anti-double-stranded DNA (anti-dsDNA) titer, 1:160; and immunoglobulin G level, 4600 mg/dL. Her antibo- dies to hepatitis viruses A, B and C and hepatitis B sur- face antigen were negative. Given her clinical picture, her positive laboratory test for ANA and anti-dsDNA and the histopathology of her liver biopsy, a diagnosis of SLE with AIH was made. Her calculated AIH score was 19 (> 15 is considered a definite diagnosis according to the International Autoimmune Hepatitis Group criteria). The patient was initiated on high-dose steroid therapy (40 mg every 12 hours). By the next day, her abdominal pain had improved, and she was discharged from the hospital on a tapering dose of steroids. One year after her hospitalization the patient remained in remission, with normal liver function and suppressed HIV viral load. Her steroid therapy was tapered off and stopped completely two months after being discharged from the hospital. Figure 1 Laparoscopic image of the liver showing diffuse whitish-gray plaque without nodularity or cirrhosis. Figure 2 Liver biopsy (hematoxylin and eosin stain) showing dense portal lymphoplasmacytic infiltrate and centrilobular hepatocellular necrosis caused by an acute chronic inflammatory infiltrate suggestive of autoimmune hepatitis.