Clinical Pearls & Morning Reports
Published February 21, 2018
Although acute parvovirus B19 infection often causes temporary suppression of erythropoiesis, it rarely leads to a severe decline in hemoglobin level. Read the latest Case Records of the Massachusetts General Hospital here.
Q: What are some of the diagnoses to consider in a patient with a hypoproliferative anemia?
A: Deficiencies of folate, vitamin B12, and iron can lead to hypoproliferative anemia. Anemia of chronic disease, hypothyroidism, and chronic kidney disease can affect the activity of erythrocyte precursor cells through aberrant or absent hormonal signaling. Infiltrative processes involving the bone marrow that can lead to hypoproliferative anemia include mycobacterial infection, granulomatous diseases (e.g., sarcoidosis), and other disorders, such as myelofibrosis, lysosomal storage diseases, and cancer.
Q: What are typical symptoms of parvovirus B19 infection?
A: Initial symptoms of fever, malaise, and headache are typical of parvovirus B19 infection in adults. In children, the classic manifestation of parvovirus B19 infection is erythema infectiosum (fifth disease), which is characterized by a “slapped cheek” rash. The rash is considered to be diagnostic of parvovirus B19 infection in children, and serologic testing is typically not pursued.
A: Antibody-mediated pure red-cell aplasia can be induced by pregnancy, viral hepatitis, HIV infection, leukemia, lymphoma, thymoma, and autoimmune conditions. It is far more common with rheumatoid arthritis and systemic lupus erythematosus than with inflammatory bowel disease. Parvovirus B19 infection may also be associated with pure red-cell aplasia; this virus directly infects erythrocytes and erythrocyte precursor cells and causes hypoproliferative anemia. Among patients with parvovirus B19 infection, a transient aplastic crisis typically occurs in those who are immunocompetent, whereas chronic pure red-cell aplasia typically occurs in those who are immunocompromised.
A: Maternal parvovirus infection during pregnancy may have several devastating consequences for the developing fetus. Intrauterine fetal death occurs at a very high rate (≥10%) in mothers who are infected before 20 weeks of gestation and occurs at a much lower rate (<1%) in mothers who are infected at 20 weeks of gestation or later. Anemia, high-output heart failure, and hydrops fetalis can occur in the fetus as a result of destruction of fetal red-cell precursor cells and myocardial cells. If these conditions develop, the risk of intrauterine fetal death is high unless intrauterine transfusion of red cells is possible.