{'fraction_non_alphanumeric': 0.035977859778597784, 'fraction_numerical': 0.02060270602706027, 'mean_word_length': 4.840215439856373, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Systemic lupus erythematosus associated with cytomegalovirus infection

Viruses are considered to be possible aetiologic agents in autoimmune disease. Cytomegalovirus (CMV) has recently been considered as an environmental factor that may trigger the development of systemic lupus erythematosus (SLE). We report a case of SLE with concurrent laboratory evidence of CMV infection. A 16-year-old girl was admitted to our hospital because of fatigue, bilateral wrist pain and finger eruption for 2 weeks. On admission, significant physical findings were low-grade fever and purplish eruptions on her fingers and toes. Her white blood cell count was 5900/mL, 4% of which included atypical lymphocytes. The C-reactive protein (CRP) level was negative. Levels of glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) were elevated to 173 IU/L and 133 IU/L, respectively. Urine analysis showed no haematuria or proteinuria. Complement components C3 and C4 were 20.0 mg/dL and 1.0 mg/dL, and the plasma level of complement (CH50) was 11 U/mL. Immunological tests showed high titers of antinuclear antibody (Ab) (|1280) and anti dsDNA Ab (950 IU/mL). Tests for viral infection revealed an increase of anti-CMV IgM Ab (2.20; normal v1.0 while anti-CMV IgG Ab was negative. Skin biopsy demonstrated IgG deposition in the junction between the epiderm and corium by immunofluorescence staining, which is a finding compatible with SLE. From hospital Day 15, urine examination began to present haematuria 3z, proteinuria of 3.5 g/day, and granular cylindruria. At the onset of SLE, nephritis was suspected, we performed a renal biopsy on Day 21. Light microscopy presented focal mesangial cell proliferation in 80% of the glomeruli and wire-loop lesions in two glomeruli. Electron microscopy demonstrated diffuse deposits in the subendothelium. After renal biopsy, we started oral administration of prednisolone at 60 mg/day. However, the patient’s proteinuria was only partially improved to 3.0 g/day. Methylprednisolone (mPSL) pulse therapy was therefore performed from Day 38 – 40. The fever was alleviated and eruptions on the fingers and toes began to improve. Proteinuria drastically decreased to v1.0 g/day within a week after the completion of the mPSL therapy. Prednisolone was tapered to 30 mg/day, and the patient was discharged on Day 76. She is now taking prednisolone 15 mg/day without further exacerbation of SLE. Anti-CMV IgM Ab has been negative for 1 year of follow-up, while other autoantibodies, such as anti-DNA Ab, remain positive. The clinical course is shown in Figure 1. Many reports have been concerned with opportunistic infections of CMV in SLE patients under the administration of steroids or immunosuppressants (1). Recent researchers have come to suggest direct effects of CMV infection on the onset of SLE, but the precise mechanism is still unclear. According to some reports, CMV is responsible for cutaneous exacerbation of SLE (2). On the other hand, it has been demonstrated that there is a cross reactivity between antibodies to Sm/RNP antigens and antibodies to CMV in patients with SLE (3). In treating such patients, we often face difficulty in judging whether clinical conditions are brought about by