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  • Title: [Human parvovirus B19 infection mimicking systemic lupus erythematosus: case report].
    Author: Banno S, Matsumoto Y, Sugiura Y, Ueda R.
    Journal: Ryumachi; 1997 Aug; 37(4):581-6. PubMed ID: 9311285.
    Abstract:
    Human parvovirus B19 (HPV-B19) has been known as the etiologic agents of erythema infectiosum in normal childhood, and chronic anemia and thrombocytopenia in immuno-compromised patients. Recently, this virus has been reported as the association with rheumatic manifestation such as rheumatoid arthritis and systemic lupus erythematosus (SLE). We described here a patient whose HPV-B19 infection was mimiking atypical symptoms of SLE at diagnosis, and was persistent because of immuno-suppressive therapy for SLE. A 34-year-old female was admitted to our hospital on 22 June 1995, presenting fever episode and cervical lymph node swelling. Before eighteen months, she was received methyl-predonisolone pulse therapy and plasma exchange by fresh frozen plasma for the treatment of Stevens-Johnson syndrome, and after several weeks these therapy she was suffered from viral infection with lymphadenopathies with a transient appearance of atypical lymphocytes in her peripheral blood smear. On laboratory examination at the present admission, her peripheral blood showed anemia, thrombocytopenia with atypical lymphocytes. Throughout her hospitalization, anti-nuclear antibody (ANA) suspected SLE including anti-DNA and anti-Sm antibody were all negative except of transient week positive ANA screening test. Her physical condition presented poor clinical course with fever elevation, increased ascites and renal dysfunction showing the elevation of CRP and circulating immune-complex (Clq binding method). Her serum was positive for IgM and IgG antibody against VP-1 and VP-2 antigen of HPV-B19 by ELISA in April 1996. And then, HPV-B19 DNA by polymerase chain reaction (PCR) was positive in bone marrow sample in March 1996, and also positive in spleen necropsy at death. We confirmed persistent chronic HPV-B19 infection by measurement of HPV-B19 IgM and IgG antibody by ELISA and HPV-B19 DNA by PCR. The plasmapheresis and administration of intravenous immunoglobulin showed the possible efficacy for her symptom throughout this clinical course. Moreover, bone marrow smear showed the finding of virus-associated hemophagocytic syndrome, and finally, she was died of cervical hemorrhage accompanied with disseminated intravascular coagulation syndrome on July 1996. HPV-B19 infection can present an atypical clinical picture that is highly suggestive of SLE. We suggest that the therapy of steroids and immuno-suppressive agents should be cautious, because these may potentially cause persistent chronic HPV-B19 infection and induced life-threatening clinical course.
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