In the latest Case Record of the Massachusetts General Hospital, a 41-year-old woman with a history of HIV infection was admitted to the hospital because of malaise and chest and abdominal pain. Initial laboratory evaluation was notable for elevated hepatic aminotransferase levels. Diagnostic procedures were performed.
Hepatic injury with significant elevations in transaminases has been reported in primary Epstein-Barr virus (EBV) and cytomegalovirus (CMV) infections. Reactivation of each of the following viruses has been described as a cause of hepatitis, particularly in immunosuppressed hosts: EBV, CMV, varicella-zoster virus, HSV type 1 (HSV-1), and HSV-2.
• What etiologies of ischemic hepatitis should be considered in a patient infected with HIV type 1 (HIV-1)?
Acute liver injury with high transaminases may occur as a result of ischemia caused by hepatic congestion or diminished perfusion. Thrombotic complications are prevalent in persons with HIV-1 infection, and therefore, the Budd-Chiari syndrome and portal-vein thrombosis should be considered. The Budd-Chiari syndrome is more common in women, especially during pregnancy. Hepatomegaly, ascites, or both frequently accompany hepatic-outflow obstruction. Ischemic hepatitis may also occur in association with acute vasoconstriction (e.g., that caused by cocaine use) or prolonged hypotension, especially in persons who have known preexisting liver disease or congestive hepatopathy. A large pulmonary embolism could cause both hypoperfusion and hepatic congestion due to pulmonary hypertension.
• What are the typical features of hepatitis A virus (HAV) infection?
HAV is acquired through a fecal-oral route of transmission. HAV infection is very likely to be symptomatic in adults, and evanescent rashes have been described during the illness. It is important to elicit any travel history to areas where HAV is endemic. The incidence of HAV continues to decline throughout the United States. The average incubation period is 30 days. Illness presents with prodromal symptoms, which may include malaise, nausea and vomiting, fever, and right upper quadrant pain. Subsequently, dark urine, acholic stool and jaundice appear. At the onset of jaundice, prodromal symptoms typically disappear. Jaundice usually peaks within 2 weeks. Vaccine administration even after an exposure is associated with a decrease in symptomatic illness. A diagnosis of HAV infection can be made if HAV-specific IgM is detected in the blood or if the virus is isolated from stool.
Morning Report Question
Q: What are the typical features of HCV infection and how might coinfection with HIV alter these manifestations?
A: HCV is most efficiently transmitted through the blood, and the usual mode of transmission is the sharing of paraphernalia related to injection-drug use, a behavior that is sometimes underreported by patients to their providers. Although sexual transmission of HCV across mucosal surfaces is inefficient, it is possible. HIV-1 infection in either partner increases the likelihood of HCV transmission. Acute HCV infection is most often associated with few or no symptoms. Therefore, infected patients rarely seek medical attention, and the diagnosis may be easily missed, unless there is a high index of suspicion. No single laboratory test defines this stage of infection, since tests for HCV antibodies may be negative at the same time as tests for HCV RNA are positive (the infectious window period of seronegativity), hepatic aminotransferase levels may vary considerably, and serum HCV RNA levels may be low or even undetectable. The seronegative window period (the interval from HCV infection to anti-HCV seroconversion) in persons infected with HIV-1 may be longer than that in persons without HIV-1.
Q: In a patient coinfected with HCV and HIV, what factors predict the ability to spontaneously clear HCV?
A: Although preexisting HIV may decrease a patient’s chance of spontaneous recovery, several other factors are positive predictors of viral clearance — female sex, maintenance of a high CD4+ T-cell count, and very symptomatic illness. If the virus does not clear, HIV positive patients are at substantial future risk for HCV-related liver disease due to accelerated fibrosis associated with HIV-1 coinfection. The time until the development of cirrhosis may be substantially shorter than for an HIV-negative patient. Another prognostic factor that may be worth pursuing is the detection of a single-nucleotide polymorphism related to the beta subunit of the interleukin-28 gene (IL28B), which has been implicated in spontaneous clearance of the virus.