[Tuberculosis. Persistence of the febrile syndrome despite correct tuberculostatic treatment].
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Biomedical subjects
Publications and source records attributed to M Ingelmo.
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OBJECTIVE: To determine the prevalence and correlation with clinical manifestations of the IgG and IgM isotypes of antibodies to cardiolipin (aCL), phosphatidic acid (aPA), phosphatidylinositol (aPI) and phosphatidylserine (aPS) in patients with systemic lupus erythematosus (SLE). METHODS: Clinical and laboratory features of 92 consecutive unselected patients with SLE were prospectively studied over two years. aCL, aPA, aPI and aPS were determined by ELISA. RESULTS: aCL were detected in 34 (37%) patients, aPA in 26 (28%), aPI in 22 (24%), and aPS in 29 (32%). A significant association was found between the appearance of thrombosis and the presence of IgG aCL (p < 0.001) and IgG aPS (p < 0.05). A significant association was also found between thrombocytopenia and the presence of IgG aCL (p < 0.001), IgG aPA (p < 0.01), IgG aPI (p < 0.05), and IgG aPS (p < 0.001). The development of hemolytic anemia was associated with the detection of IgM aCL (p < 0.001), IgM aPA (p < 0.05), IgM aPI (p < 0.001), and IgM aPS (p < 0.01). CONCLUSION: We found a relatively high prevalence of aCL, aPA, aPI and aPS in our SLE population and confirmed the presence of a correlation between the IgG isotype of these antibodies and thrombosis and thrombocytopenia, and also between the IgM isotype and hemolytic anemia. These results demonstrate the variety of antiphospholipid antibodies that can be detected in SLE patients, as well as their association with the clinical manifestations of the antiphospholipid syndrome.
OBJECTIVE: To determine the prevalence and clinical significance of antiphospholipid antibodies (aPL) in a cohort of patients with primary Sjögren's syndrome (SS). METHODS: Eighty patients with primary SS were studied prospectively. The prevalence of aPL and characteristics of the clinical and laboratory features of these patients were compared with those of the following groups of patients: (i) 50 patients with SS associated with systemic lupus erythematosus (SLE); (ii) 100 patients with SLE without SS; and (iii) 100 healthy blood donors from the blood bank of our hospital. RESULTS: Only 11 (14%) patients with primary SS were found to have aPL (anticardiolipin antibodies or lupus anticoagulant, or both) in their sera, but anti beta 2-glycoprotein I antibodies were not detected in any patient. In contrast, aPL were detected in 12 (24%) patients with SS secondary to SLE and in 21 (21%) patients with SLE without SS. None of the healthy controls presented aPL in their sera. Patients with primary SS presented a lower prevalence of thrombocytopenia (p < 0.05) and livedo reticularis (p < 0.01) compared with the other two groups of patients. No patient with primary SS was diagnosed as having an antiphospholipid syndrome (APS), while 4 (8%) patients with secondary SS and 9 (9%) with SLE without SS were found to have APS (p < 0.05). CONCLUSION: In patients with primary SS, aPL are present in a lower percentage than in patients with SS secondary to SLE or in patients with SLE without SS. The presence of aPL in these primary SS patients is not associated with the clinical events of APS.
The antiphospholipid syndrome (APS) is characterized by the presence of venous and arterial thrombosis, recurrent fetal losses and thrombocytopenia, associated with the presence of antiphospholipid antibodies (aPL). This syndrome may be "primary" or may be associated with other diseases, mainly systemic lupus erythematosus (SLE). However, some patients present the clinical picture of this syndrome but without evidence of aPL in their serum. The term "seronegative" APS has been proposed to categorize these patients. Here with we present two patients with seronegativity for aPL at the time of a thrombotic event, but in whom these antibodies were detected 2 and 7 months later.
BACKGROUND: Recently, tumor markers (CA 125 and SCC) have been suggested as possible activity markers of systemic lupus erythematosus (SLE), but study results have been contradictory. OBJECTIVE: The aim of this study was to evaluate the possible relationship between CA 125 and SCC serum levels and SLE activity. PATIENTS AND METHODS: Serum levels of CA 125 from 59 patients and levels of SCC from 53 patients with SLE were analyzed. Both tumor markers were determined by ELISA, considering 35 U/ml (CA 125) and 2.5 ng/ml (SCC) respectively as the upper limit of normality. The serum levels of these tumor markers were correlated with the SLE disease activity index (SLEDAI). RESULTS: The CA 125 concentrations in active SLE (mean 13.8 + 15.3) were similar to those in inactive patients (mean 13.1 + 11.7 U/ml). Significantly high CA 125 serum levels were found only in SLE patients with nephrotic syndrome (p = 0.001). No significant differences were found in SCC serum levels in SLE patients with (mean 0.9 +/- 0.8 ng/ml) or without activity (mean 1.1 +/- 1.3 ng/ml). Likewise, no relationship between SCC serum levels and parameters related to SLE activity were found, excluding slight increases associated with renal failure. CONCLUSIONS: The correlation that some authors have found between elevated serum levels of CA 125 and SLE activity is only associated with the presence of nephrotic syndrome. Likewise, SCC is not related with SLE activity and the increases found may be due to renal failure.