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Pericardial involvement is the most common cardiovascular complication in systemic lupus erythematosus (SLE).1 The clinical picture varies from subclinical pericardial effusion and classic acute pericarditis to cardiac tamponade.1 2Immunological studies of pericardial fluid (PF) have been limited to determination of autoantibodies, complements and immune complexes.3 4 To further study the pathogenic mechanisms involved in lupus pericarditis we examined the lymphocytic populations and cytokine concentration pattern in PF and peripheral blood (PB) from a SLE patient with cardiac tamponade.
We report a case of a 38 year old man with SLE diagnosed in December 1995 when he presented with polyarthritis, photosensitivity, oral ulcers, nephritis, non-hemolytic anaemia, positive ANA, increase of anti-dsDNA and hypocomplementaemia. The patient improved with corticosteroid and intravenous cyclophosphamide treatment. However, on 18 June 1997 he presented with syncope, hypotension (80/40 mm Hg), a tachycardia, jugular vein distension and cardiomegaly. The two dimensional echocardiogram showed a large pericardial effusion with right atria and ventricle collapse in diastole. Pericardiocenthesis was performed and 180 ml of an orange fluid was aspirated. Examination of PF showed white blood cell count of 5280/mm3(polymorphonuclear cells = 96%). The absolute number of lymphocytes was lower in PF than in PB (211 v700/mm3). PF level of protein was 4.1 g/dl (serum = 5.3 g/dl), glucose was 53 mg/dl (serum = 110 mg/dl) and LDH was 471 IU/l (serum = 110 IU/l). PF cultures were negative. No malignant cells were seen. He was treated with high dose corticosteroids and azathioprine. Prednisone was gradually decreased to 10 mg daily over a three month period. After a 22 month follow up, he remained clinically stable without recurrent pericardial involvement or SLE exacerbations.
Before starting immunosuppressive treatment, PF and PB were obtained simultaneously for immunological analysis. Mononuclear cells from both sources were isolated by gradient centrifugation and the frequency of lymphocyte populations was determined by flow cytometry. The cytokine concentrations from plasma and PF were determined by ELISA. Table 1shows the results. Among lymphocytes, the percentage of CD4+ T cells and NK cells was higher in PF, while the frequency of CD8+ T cells was higher in PB. IL6 concentration was much higher in PF than plasma. Also, IL1β and IL10 concentrations were higher in PF. IL2 was detected in plasma but not in PF.
The considerable increase in pericardial IL6, with respect to plasma, is particularly interesting. PF concentrations of IL6 in our patient were substantially higher than those observed in PF from patients with inflammatory and non-inflammatory heart conditions.5 6IL6, not only can increase antibody production, but in SLE, B cells have increased reactivity to this cytokine.7 As in our case, IL6 is usually expressed or increased in the affected organ or system rather than PB. IL6 has been found to be higher in cerebrospinal fluid and urine than in serum of SLE patients with CNS disease and active nephritis respectively.8 9
The decreased pericardial lymphocyte count and fluid characteristics observed here are in agreement with other studies.10 The higher frequency of CD4+ T cells and NK cells in PF could be associated with the observed cytokine concentration pattern. For example, CD4+ memory T cells from SLE patients highly secrete IL10 compared with normal controls.11
In summary, different patterns of lymphocyte populations and cytokines were found in both sources, with type 2 cytokines predominating in PF and type 1 in PB. Further studies would be required to confirm the results presented here. In addition, immunocytochemical studies of pericardial tissue are necessary as the composition of lymphocyte and cytokine profiles may differ between pericardial fluid and tissue.
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