Female patient, 16 years old with a history of hepatitis A in 1998.
Established for the first time in June 2001 reporting symmetrical polyarthralgia of large and small intestines accompanied by morning stiffness of 30 min duration.
The previous picture was accompanied by photosensitivity and alopecia, with no other clinical elements suggesting mesenchymopathy.
Clinical examination revealed polyarthritis in affected patients.
Their study highlighted antinuclear antibodies (ANA) in HEP-2 positive cells for a dilution of 1/1280; negative rheumatoid factor, decreased complement C3 and C4 positive and anti-DNA antibodies.
The diagnosis of systemic lupus erythematosus (SLE) was made and treatment with hydroxychloroquine 400 mg daily, azathioprine 100 mg daily and methylprednisolone 32 mg daily was initiated.
The patient had partial response to treatment and weekly intolerance to azathioprine (severe anemia and persistent vomiting), so the drug was discontinued and methotrexate (MTX) was started in June 2002.
He remained under periodic control, with persistent arthritis that was exacerbated by reducing methylprednisolone to 32 mg/day, so that MTX progressively increased to a dose of 20 mg/week.
She remained oligosymptomatic with mild synovitis receiving 16 mg/day of methylprednisolone, hydroxychloroquine 200 mg/day and MTX (20 mg/week) until June 2004, when she consulted for exacerbated fever.
Leukopenia of 3,790 with 758 lymphocytes and erythrocyte sedimentation rate (HSV) of 89 mm/hr, hypocomplementemia with C3dl = 1104 dl (baseline) was investigated within the laboratory tests.
The etiologic study included negative blood cultures, negative urine culture, chest X-ray with no evidence of condensation, serology for cytomegalovirus (CMV), Toxoplasma gondii and influenza A and B negative viruses.
Computed axial tomography (CAT) of the abdomen and thorax, cervical and axillary ultrasound show only small lymphadenopathies.
Anti-capsid virus IgM was positive, so infectious mononucleosis was diagnosed and an expectant management was decided.
The patient had fever and fever for three months, persistently elevated ESR and decreased complementemia.
A new study was conducted to search for an infectious etiology, which was completely negative, including PCR for Epstein&#146;s anomaly.
Procalcitonin was performed which was normal.
A new chest CT showed persistent lymph nodes and mild bilateral pleural effusion.
It was decided to increase the dose of methotrexate to 25 mg weekly for 4 weeks without clinical response so it was decided to change mycophenolate mofetil 2 g daily.
This scheme assisted to the appearance of secondary leukopenia severe that required the use of granulocyte colony stimulating factor.
Given the persistence of fever, arthritis, lymphadenopathies and the appearance of proteinuria and hematuria in an isolated sample, it was concluded that it was an active SLE refractory to treatment.
Rituximab was started at a dose of 375 mg/m2 every seven days for four doses with disappearance of fever, lymphadenopathy and arthritis, decrease of ESR up to 35 mm/hr and normalization of C3 fraction.
To date (3 months after treatment), the patient is asymptomatic on treatment with methylprednisolone 16 mg/day, hydroxychloroquine 200 mg/day and methotrexate (10 mg/week).
