Parvovirus B19 in anemic liver transplant recipients.

Five hundred thirty-three liver transplant recipients were seen for follow-up care over a 6-month period. Of these,23(4.3%)hadahemoglobinlevelof <9g/dl,with19beingeligibleforinclusioninthisstudy.Themedian hemoglobinlevelwas8.7g/dlwithalowof7.1g/dl.Twopatientshadiron-deficiencyanemia.Allofthepatients were on therapeutic drugs which can suppress erythropoiesis or shorten the lifespan of mature erythrocytes. Sixpatients(31.6%)wereviremicforhumanparvovirusB19butnonewasB19immunoglobulinMseropositive. TwopatientswereimmunoglobulinMseropositiveforcytomegalovirus.ThepatientswithcirculatingB19DNA were not easily distinguished from those without the virus by their laboratory results. The absence of reticulocyte counts for these patients contributed to this inability to differentiate B19 infection from other causes of anemia, particularly drug myelotoxicity. The high likelihood of making a specific diagnosis with the increasing availability of PCR should spur the search for this virus in the liver transplant population. Theanemicstateinpatientswithchronicliverdiseasecanbe associated with a number of factors including decreased erythropoietin production due to concomitant renal insufficiency, drug- or virus-induced marrow suppression, iron loss from bleeding, other nutritional deficiencies, hypersplenism, and acquired hemolytic anemia associated with congestive splenomegaly (18). In advanced liver disease associated with marked liverfibrosis and portal hypertension, the differential diagnosis of anemia must also include upper gastrointestinal bleeding. As in the case of patients with chronic liver disease, liver transplant recipients are subject to several different medical conditions, each of which can produce an anemia. For example, they are invariably on immunosuppressive regimens such as tacrolimus (FK506), a recognized cause of myelosuppression (20). An additional myelosuppressive agent, trimethoprim-sulfamethoxazole, which interferes with folic acid metabolism, is administered routinely to these patients for prophylaxis against common microbial pathogens and various opportunistic infections. In 1975, the list of putative causes of anemia in individuals with liver disease grew with the discovery of human parvovirus B19 (B19) (2, 8, 14). This viral agent causes anemia by infecting and lysing globoside-containing erythrocyte precursors (5). Initial reports link B19 infection with the aplastic crisis that occurs in patients with underlying hereditary anemias (17, 21). Other studies demonstrate a relationship between the agent and arthritis (19), hydrops fetalis (6, 9), and anemia in pediatric liver transplant recipients (16) and in individuals transplanted for fulminant liver failure (7). To date, however, there have been no large-scale studies of B19 infections in adults who have undergone liver transplantation for chronic liver diseases. Furthermore, the available literatureinsufficientlycharacterizestheanemiaand/orclinical status of patients reported with B19 infection, making it difficult to generate medically useful paradigms. The goal of this investigation was to determine the prevalence of B19 infection in a cohort of anemic liver transplant recipients. Concurrent causal factors for anemia were surveyed to permit a fuller characterization of anemia in this unique group of patients.