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Parvovirus B19 causes polyarthritis in adults.1 Several observers have noted a lupus-like syndrome2,3 and production of autoantibodies associated with this infection.4 We describe here two white patients with acute parvovirus B19 infection and a transient lupus-like syndrome.
A 41 year old woman had a transient polyarthritis of the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints after her first delivery at the age of 30, and she developed photosensitivity, and reported dryness of the eyes for some years.
In 1998 she had an influenza-like illness with polyarthralgia, myalgia, and fever. She also had a massive UV light exposure with tanning. Two days later she developed polyarthritis of the wrists, MCP, and PIP joints. Her 4 year old child had a fever and facial skin rash just before her disease.
One week after the start of her polyarthritis she had a normal blood count, erythrocyte sedimentation rate (ESR), rheumatoid factor, complement, immunoglobulin levels, urine analysis, liver enzymes, creatinine kinase, and slightly raised (15 mg/l) C reactive protein (CRP). Anti-dsDNA, anticardiolipin, IgG and IgM were increased, and anti-SS-A, anti-SS-B antibodies were also detected by enzyme linked immunosorbent assay (ELISA). An antinuclear antibody (ANA) test was negative, with an anti-cytoskeletal staining on HEp-2 cells. Both IgM and IgG antibodies to human parvovirus B19 were positive, and parvovirus DNA was detected by nested polymerase chain reaction (PCR) in serum.
After eight weeks the autoantibody tests became negative, and her symptoms completely resolved. At two years follow up she remained asymptomatic, and the parvovirus PCR was negative.
A 34 year old woman was examined in June 1998 with an acute painful occipital lymph node and polyarthritis in the MCP and PIP joints. She had had photosensitivity from the age of 10. Two weeks before symptoms, her child had a rash and flu-like illness, and in the meantime she was exposed to UV light with tanning.
Urine analysis, blood count, liver enzymes were normal, but the ESR and CRP were slightly raised (22 mm/1st h, and 11 mg/l, respectively). No rheumatoid factor was detected. Anti-dsDNA and anti-Sm autoantibody were positive by ELISA. An ANA test was negative on HEp-2 cells, with an atypical cytoplasmic staining. IgM and IgG antibodies to human parvovirus B19 were present, and parvovirus DNA was detected by PCR in serum. The patient was three weeks' pregnant but she decided to terminate the pregnancy. After 10 weeks the autoantibody ELISA became negative, but the ANA test became positive with homogeneous staining pattern. Apart from periodic myalgia and arthralgia the patient remained without symptoms for two years. The diagnosis may be systemic lupus erythematosus (SLE) in view of the photosensitivity, polyarthritis, ANA, and anti-dsDNA positivity. At 500 days after the onset PCR was positive in serum.
After the infection four criteria of SLE were fulfilled in case 2, and case 1 was compatible with the diagnosis of undifferentiated connective tissue disease.5 The autoimmune process was self limited in both patients.
The patients' children had symptoms of erythema infectiosum, and the mothers were examined for parvovirus B19. They were IgM and IgG positive (table 1). The VP1-IgG avidity6 and VP2-IgG epitope type specificity7 results (table 1) confirmed acute B19 infection in our patients. Nested PCR was performed on the patients' sera.8 Both patients were PCR positive in the acute phase (table 1). In immunocompetent patients PCR may remain positive for four months, but more prolonged persistence in healthy subjects is unusual. Parvovirus DNA was not detectable in the first patient after 400 days, but in patient 2 the blood sample taken at 500 days was positive.
At the time of the infection other provoking factors for SLE could also be identified. The second patient had an early phase pregnancy. Although the patients had earlier had photosensitivity, they were tanning during the initial period of infection. The typical rash of parvovirus infection, like the skin manifestations of SLE, can be provoked by UV light. Possibly, the virus and the UV light had additional effects on the autoimmune process.
Typing for HLA-A, B, C, and DR, DQ showed common alleles. They had DR2 (DRB1*1501) and DQ6 (DQB1*0602) with the same subtypes (table 2). Four HLA alleles of the patients have been previously described as associated with SLE.9
In conclusion, we have found several common provoking factors of the autoimmune process in our cases. The patients had a genetic predisposition to lupus and also signs of autoimmune diseases in the past. They had also been exposed to UV light and pregnancy, which are known provoking factors for SLE. Furthermore, parvovirus infection seemed to be also a provoking factor for the development of SLE and lupus-like disease, although the symptoms of connective tissue diseases were transient.
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