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ABSTRACT: The objective was to study the association of antibodies against cyclic citrullinated peptides (anti-CCP) in patients with lupus articular damage. We studied 34 systemic lupus erythematosus patients (30 women) with (n = 14) or without (n = 20) deforming arthropathy. Anti-DNA and arthritis were mandatory inclusion criteria for both groups. As controls, 34 patients with rheumatoid arthritis and nine patients with rheumatoid arthritis and systemic lupus erythematosus (rhupus) were included. Anti-CCP and rheumatoid factor were determined by ELISA and nephelometry respectively. All patients had recent x-ray films of the hands that were evaluated according to Sharp's method. Systemic lupus erythematosus patients had a mean 6.50 +/- 0.86 (SD, range 5-8) American College of Rheumatology (ACR) criteria, rheumatoid arthritis patients met 5.38 +/- 0.60 (range 4-6) ACR criteria for rheumatoid arthritis and rhupus patients had 5.78 +/- 0.44 (range 5-6) criteria for rheumatoid arthritis and 5.11 +/- 0.78 (range 4-6) for systemic lupus erythematosus. Systemic lupus erythematosus patients, with or without deforming arthropathy, had normal serum anti-CCP concentrations. In contrast, rheumatoid arthritis and rhupus patients had 30- and 23-fold higher than normal amounts of anti-CCP (p < 0.001, both comparisons). Rheumatoid arthritis (97%) and rhupus (100%) patients were more frequently positive for anti-CCP than SLE patients with (7%) or without (5%) deforming arthropathy (p < 0.001, both comparisons). Patients with lupus deforming arthropathy were more frequently positive for rheumatoid factor (65%) than patients with non-deforming arthritis (15%) (p = 0.005). Patients with lupus deforming arthropathy had similar frequency of erosions and mean Sharp's score than rhupus patients. Anti-CCP antibodies do not associate with lupus arthropathy, whether deforming, non-deforming or erosive.
Lupus 02/2008; 17(4):300-4. · 2.34 Impact Factor
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ABSTRACT: CD55 and CD59 are glycophosphatidylinositol-anchored proteins with complement inhibitory properties. Lymphopenia in systemic lupus erythematosus (SLE) has been associated with autoantibodies targeting nuclear antigens. The aim of this study was to evaluate the surface density of CD55 and CD59 in T and B lymphocytes from patients with SLE and lymphopenia and its possible correlation with the presence of common SLE autoantibodies. Flow cytometric analyses were performed on CD55 and CD59 stained CD3+ and CD19+ cells from 40 SLE patients, 30 with lymphopenia and 10 without it, and 25 healthy controls. Autoantibodies were detected in the sera by enzyme linked immunosorbent assay. The mean fluorescence intensity of CD55 and CD59 in T and B cells was significantly diminished in SLE patients with lymphopenia when compared with healthy subjects. Interestingly, the opposite was found in T and B cells from non-lymphopenic SLE patients. Although there was no correlation between CD55 and CD59 surface density and the presence of any specificity of the autoantibodies tested, higher titres of anti-dsDNA, anti-SM and anti-ribosomal p antibodies were significantly associated with lymphopenia. The deficiency of CD55 and CD59 expression may play a role in the pathophysiology of lymphopenia, most likely by increasing the susceptibility of cells to complement mediated cytolysis.
Lupus 02/2006; 15(9):600-5. · 2.34 Impact Factor
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ABSTRACT: Headache is common in systemic lupus erythematosus with reported prevalence as high as 70%. The aims of this study were: to estimate the prevalence and types of headache in a sample of patients with systemic lupus erythematosus comparing it with rheumatoid arthritis, to determine clinical and serological associations. Eighty-one systemic lupus erythematosus and 29 rheumatoid arthritis consecutive patients seen in our outpatient clinic were interviewed. Headache was evaluated using the diagnostic criteria proposed by the International Headache Society. Additional evaluations were carried out in the 81 systemic lupus erythematosus patients including depression, disease activity, lupus damage, function disability, quality of life, and severity degree using a validated scales. We analysed the following autoantibodies: anti-double stranded DNA, anti-nucleosomes, anti-histones, anti-ribosomal P, anti-cardiolipin antibodies, anti-beta2-glycoprotein-I (GPI), and antinuclear antibodies. Forty-one per cent of systemic lupus erythematosus and 17% of rheumatoid arthritis patients suffered from headache (P = 0.02). No significant difference for any primary headache type between the two groups was found. Frequency of headache types in systemic lupus erythematosus patients was: migraine 24%, tensional-type headache 11%, and mixed headache 5%. In systemic lupus erythematosus patients the risk factors associated with headaches were Raynaud's phenomenon (OR 3.6; 95% CI 1.3-9.5; P = 0.009) and beta2GPI antibody positivity (OR 4.5; 95% CI 1.2-16.2; p = 0.016). We conclude that headache is more common in systemic lupus erythematosus than in rheumatoid arthritis patients and was independently associated with Raynaud's phenomenon and beta2GP-I antibodies.
Cephalalgia 01/2005; 24(12):1031-44. · 3.43 Impact Factor
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ABSTRACT: Headache is common in systemic lupus erythematosus with reported prevalence as high as 70%. The aims of this study were: to estimate the prevalence and types of headache in a sample of patients with systemic lupus erythematosus comparing it with rheumatoid arthritis, to determine clinical and serological associations. Eighty-one systemic lupus erythematosus and 29 rheumatoid arthritis consecutive patients seen in our outpatient clinic were interviewed. Headache was evaluated using the diagnostic criteria proposed by the International Headache Society. Additional evaluations were carried out in the 81 systemic lupus erythematosus patients including depression, disease activity, lupus damage, function disability, quality of life, and severity degree using a validated scales. We analysed the following autoantibodies: anti-double stranded DNA, anti-nucleosomes, anti-histones, anti-ribosomal P, anti-cardiolipin antibodies, anti-β2-glycoprotein-I (GPI), and antinuclear antibodies. Forty-one per cent of systemic lupus erythematosus and 17% of rheumatoid arthritis patients suffered from headache (P = 0.02). No significant difference for any primary headache type between the two groups was found. Frequency of headache types in systemic lupus erythematosus patients was: migraine 24%, tensional-type headache 11%, and mixed headache 5%. In systemic lupus erythematosus patients the risk factors associated with headaches were Raynaud's phenomenon (OR 3.6; 95% CI 1.3–9.5; P = 0.009) and β2GPI antibody positivity (OR 4.5; 95% CI 1.2–16.2; p = 0.016). We conclude that headache is more common in systemic lupus erythematosus than in rheumatoid arthritis patients and was independently associated with Raynaud's phenomenon and β2GP-I antibodies.
Cephalalgia 11/2004; 24(12):1031 - 1044. · 3.43 Impact Factor
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ABSTRACT: Patients with primary antiphospholipid syndrome (PAPS) may evolve to systemic lupus erythematosus (SLE), even many years later. This makes differentiation between primary and secondary antiphospholipid syndrome a difficult task. Studies in murine models of lupus have shown that the development of antinucleosome (anti-NCS) antibodies may occur from the early stages of life. We therefore hypothesize that anti-NCS antibodies could help predict development of SLE in patients with PAPS. We studied anti-NCS antibodies in 18 PAPS patients (15 female, three male), followed for a mean of 11 years to evaluate the potential development of SLE. When PAPS was diagnosed, nine patients were positive for anti-NCS antibodies. Six of them developed clinical manifestations of SLE. In contrast, none of the patients who were negative to anti-NCS antibodies developed it. These findings suggest that anti-NCS antibodies could help predict which patients with PAPS may eventually develop SLE.
Lupus 02/2004; 13(3):177-81. · 2.34 Impact Factor
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ABSTRACT: We studied antibodies to beta2-glycoprotein 1 (anti-beta2GP1) from 72 patients with systemic lupus erythematosus (SLE) with or without antiphospholipid syndrome (APS) or with or without anticardiolipin antibodies (aCL). Fifteen patients had APS and positive antiphospholipid antibodies [clinical APS(+)/aPL(+)], 12 patients had APS, negative serum IgG and IgM aCL, antiphosphatidylethanolamine, anti-phosphatidylserine and no lupus anticoagulant [clinical APS(+)/ aPL(-)]. A third group included 16 patients without APS but high aCL levels [clinical APS(-)/ aPL(+)]. In a fourth group we studied 29 patients without clinical manifestations of APS or aCL [clinical APS(-)/aPL(-)]. One hundred anticardiolipin and VDRL-negative normal sera were studied as controls. IgG antibodies to cardiolipin proper in a bovine beta2GP-free system, to human beta2GP1 immobilized on cardiolipin or to human beta2GP1 alone were detected in all sera by ELISA using irradiated and nonirradiated plates from two manufacturers. Sera from APS(+)/aPL(+) patients showed IgG binding to CL, CL + beta2GP1 and beta2GP1 in irradiated and nonirradiated plates. APS(+)/ aPL(-) sera had more significant IgG binding to beta2GP1 than normal controls when studied in both irradiated or nonirradiated plates (P = 0.001). This binding was inhibited by solid-phase cardiolipin in a dose-dependent manner. Sera from the APS(-)/aPL(+) subgroup had comparable IgG activity in both the CL and CL + beta2GP1 assays, while no anti-beta2GP1 activity was detected in these sera. Sera from the clinical APS(-)/aPL(-) patients were negative in the three ELISA systems. Antibodies to human beta2GP1 from SLE patients recognize various epitopes. Those from APS(+)/ aPL(+) patients appear to react with an epitope boosted by cardiolipin in addition to another one present in the native protein. In contrast, anti-beta2GP1 from patients with APS(+)/aPL(-) are blocked by cardiolipin, suggesting that their epitope is the phospholipid-binding site.
Lupus 02/2004; 13(3):182-7. · 2.34 Impact Factor
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ABSTRACT: To compare the utility of anti-chromatin antibodies for the diagnosis of systemic lupus erythematosus (SLE) and as markers of disease activity.
We included 73 consecutive patients (62 female) with SLE (four or more ACR criteria) of recent onset (<1 yr since diagnosis). As control groups we included 130 healthy blood donors and 261 patients with 11 systemic autoimmune diseases (SAD). Disease activity was assessed using the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). A venous blood sample was drawn to measure three anti-chromatin antibodies [anti-nucleosome (anti-NCS), anti-double-stranded DNA (anti-dsDNA) and anti-histones (anti-HST)] by enzyme-linked immunosorbent assay.
The prevalence of anti-chromatin antibodies in SLE patients and healthy controls was 100 and 3% respectively for anti-NCS, 63 and 5% for anti-dsDNA, and 15 and 3% for anti-HST. Anti-NCS had a sensitivity of 100% and specificity of 97% for SLE diagnosis. When SLE and SAD patients were compared [excluding mixed connective tissue disease (MCTD)], the sensitivity of anti-NCS, anti-dsDNA and anti-HST antibodies for SLE diagnosis was 93, 71 and 40% respectively and the specificity was 97, 98 and 98%. Anti-chromatin antibodies were not useful in differentiating between SLE and MCTD patients. Anti-NCS antibodies showed the highest correlation with disease activity (r = 0.45, P < 0.0001), especially in patients negative for anti-dsDNA antibodies (r = 0.58, P = 0.001). Anti-NCS antibodies also showed strong association with renal damage (odds ratio 4.1, 95% confidence interval 1.2-13.6, P = 0.01).
Anti-NCS antibodies could be a useful tool in the diagnosis and assessment of disease activity in SLE patients, especially in patients who are negative for anti-dsDNA antibodies.
Rheumatology 02/2004; 43(2):220-4. · 4.06 Impact Factor
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ABSTRACT: To determine the prevalence of antineutrophil cytoplasmic autoantibodies (ANCA) in sera of patients with tuberculosis compared with healthy control subjects and a group of patients with atopic asthma.
The presence of ANCA was examined in patients with tuberculosis, and in asthmatic patients and healthy subjects as control groups, by means of indirect immunofluorescence (IIF) and enzyme-linked immunosorbent assay (ELISA) to detect anti-proteinase 3 (PR3-ANCA) and antimyeloperoxidase (MPO-ANCA) antibodies.
ANCA were present in 20 (44.4%) of 45 tuberculosis patients by IIF (16 c-ANCA, four p-ANCA) and in 18 (40%) patients by ELISA (15 PR3-ANCA, three MPO-ANCA). High odds ratios for ANCA positivity were observed for tuberculosis patients when compared with both control groups. ANCA results were not related to the category of tuberculosis, stage of disease, presence of concomitant diseases or pharmacotherapy.
As many clinical similarities between tuberculosis and Wegener's granulomatosis exist, we propose that a positive ANCA test in patients living in countries with a high prevalence of tuberculosis must be carefully interpreted as indicative of systemic vasculitis, especially when no signs of extrapulmonary involvement occur.
Rheumatology 03/2003; 42(2):223-9. · 4.06 Impact Factor
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ABSTRACT: The coexistence of systemic lupus erythematosus and rheumatoid arthritis (rhupus), is a rare clinical condition. To date, 50 cases of rhupus have been described worldwide; however, the lack of clinical criteria for this rheumatic condition has created confusion in the characterization of this disorder. Nevertheless, in this paper we describe a comprehensive clinical and serological characterization of a cohort of 22 Mexican patients with rhupus, supported by generic HLA-DR phenotyping. We found that rhupus patients have a special clinical behavior. In this setting, the signs and symptoms of rheumatoid arthritis prevail, little organic damage associated with systemic lupus erythematosus (SLE) exists and none of the cases present thrombosis or morbidity during pregnancy in spite of presenting a high frequency of anticardiolipin antibodies. We also found an increased frequency of HLA-DR1 and HLA-DR2 alleles compared to healthy ethnically matched controls, systemic lupus erythematosus and rheumatoid arthritis patients.
Lupus 02/2002; 11(5):287-92. · 2.34 Impact Factor
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Thrombosis Research 08/2000; 99(2):129-33. · 2.44 Impact Factor
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ABSTRACT: Antibodies to beta2-glycoprotein-I are more strongly associated with clinical antiphospholipid syndrome than are anticardiolipin antibodies. We previously found a decrease in anticardiolipin antibodies at the time of thrombosis in 6 patients with systemic lupus erythematosus (SLE). We therefore sought to determine the prevalence and levels of antibodies to beta2-glycoprotein-I and to cardiolipin before, during, and after thrombosis in patients with SLE, and to compare them with patients who did not have thrombosis.
We studied 24 patients with SLE who had at least one episode of thrombosis and 102 patients with SLE without thrombosis. Serum anticardiolipin antibodies were measured by conventional enzyme-linked immunosorbent assay (ELISA) using newborn calf serum as the blocking agent. Serum anti-beta2-glycoprotein-I antibodies were measured by ELISA on nonirradiated plates, using purified human beta2-glycoprotein-I without phospholipid.
All patients with thrombosis had anti-beta2-glycoprotein-I antibodies, compared with only 17% of controls (P <0.0001). We observed a significant decrease in serum anti-beta2-glycoprotein-I levels at the time of thrombosis, as compared with previous and subsequent samples. The prevalence and levels of IgG and IgM anticardiolipin antibodies were similar in patients with and without thrombosis. A decrease in IgG or IgM anticardiolipin titers occurred during thrombosis in 6 patients. Anticoagulant, corticosteroid, and immunosuppressive treatments did not appear to affect anti-beta2-glycoprotein-I levels at the time of thrombosis.
Anti-beta2-glycoprotein-I antibodies are strongly associated with thrombosis in patients with SLE. The decrease of anti-beta2-glycoprotein-I levels at the time of thrombosis may indicate a pathogenic role. This antibody may also be a marker of predisposition for thrombosis in these patients.
The American Journal of Medicine 04/1999; 106(4):417-23. · 5.43 Impact Factor
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ABSTRACT: Heat treatment of normal human serum reveals otherwise masked anti-cardiolipin antibodies (aCL). We studied the mechanism of masking and the nature of the inhibitor of these aCL IgG. Other forms of treatment, besides heating for 30 min at 56 degrees C, can also unmask hidden aCL IgG. These include acid pH, hypermolar buffers and phospholipase digestion. When unmasked, these aCL recognize other anionic and zwitterionic phospholipids, but do not react with DNA, cell antigens or IgG. Using thin layer chromatography we demonstrate that the heat-labile inhibitor(s) of these aCL are phosphatidylserine, phosphatidylethanolamine, phosphatidylglycerol and phosphatidylcholine. These antibodies are not beta2-glycoprotein-I dependent and actually compete with this protein for phospholipid binding. The hidden antibodies are comprised of two populations of IgG autoantibodies: one reactive with cardiolipin, phosphatidylserine, phosphatidylinositol, phosphatidylglycerol, phosphatidylethanolamine and sphingomyelin, and the other reactive almost exclusively with phosphatidylcholine and phosphorylcholine on enzyme-linked immunosorbent assay plates or when exposed by bromelain on the erythrocyte surface. Our data suggest that hidden aCL are natural oligoreactive IgG anti-phospholipid autoantibodies that circulate masked by their antigen.
European Journal of Immunology 08/1998; 28(7):2108-14. · 5.10 Impact Factor
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ABSTRACT: After the initial description of the anticardiolipin syndrome inpatients with systemic lupus erythematosus (SLE), it became clear that phospholipids other than cardiolipin could also be involved, that there could also be a primary syndrome, and that protein cofactors participate in in vitro reactivity of the autoantibodies. We describe 5 patients with SLE with clinical manifestations of antiphospholipid syndrome (APS) but persistently negative antiphospholipid antibodies (aPL). In all their tested sera we found antibodies to phospholipid-free beta 2-glycoprotein I (a beta 2-GPI).
We studied 5 patients with SLE with at least 2 clinical manifestations of APS with no serum aPL detected in routine assays. IgG and IgM a beta 2-GPI were studied by ELISA and by Western blot. We also tested for antibodies to phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine by ELISA. We studied 54 normal sera as controls.
Four patients had livedo reticularis, 2 had thrombocytopenia, 2 had hemolytic anemia, and one each had recurrent venous thromboses, repeated fetal loss, pulmonary arterial hypertension, and transverse myelitis. No patient had serum aPL, but all had high titers of IgG a beta 2-GPI (p < 0.001 vs controls). Reactivity found in ELISA was confirmed by Western blot.
We describe a variant of APS in patients with SLE with negative aPL but serum antibodies to beta 2-GPI.
The Journal of Rheumatology 08/1997; 24(8):1545-51. · 3.69 Impact Factor
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ABSTRACT: Most systemic lupus erythematosus (SLE) patients with two or more clinical manifestations of the antiphospholipid syndrome (APS) and negative antiphospholipid antibodies (aPL) have antibodies to beta 2-glycoprotein-I (a beta 2 GP-I). Herein we describe a similar set of circumstances, but in patients without evidence of SLE.
We studied 6 patients with recurrent venous and/or arterial thromboses without aPL as detected by routine assays nor clinical or serological evidence of other autoimmune disease. Immunoglobin (Ig) G and IgM antibodies to bovine and human phospholipid-free beta 2 GP-I were studied by Western blot test and by enzyme-linked immunosorbent assay (ELISA) utilizing radiated and nonirradiated plates. We also tested antibodies to cardiolipin, phosphatidylserine, and phosphatidylethanolamine by ELISA. As controls, 54 normal sera were studied.
All 6 patients had recurrent arterial and/or venous thromboses. Three also had thrombocytopenia, 1 had livedo reticularis, and 2 had valvular heart disease. None of the patients had aPL, but all had serum IgG reactivity against human and bovine beta 2 GP-I (P < 0.001 versus controls for both). Titers of anti-bovine beta 2 GP-I were higher when studied in irradiated plates but were also higher than normal in nonirradiated plates (P < 0.001). These antibodies did not recognize human or bovine beta 2 GP-I bound to cardiolipin in solid phase. We confirmed by Western blot that these autoantibodies recognize human beta 2 GP-I. We found no IgM a beta 2 GP-I.
We describe a primary condition akin to the antiphospholipid syndrome with negative aPL, but with serum IgG antibodies to human and bovine beta 2 GP-I. These antibodies recognize beta 2 GP-I epitopes that are not accessible when beta 2 GP-I is bound to cardiolipin.
The American Journal of Medicine 11/1996; 101(5):472-81. · 5.43 Impact Factor
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ABSTRACT: To investigate antibodies to phospholipid-free beta 2-glycoprotein-I (a beta 2 GP-I) in the serum of patients with systemic lupus erythematosus (SLE).
We studied alpha beta 2 GP-I by Western blot, dot blot, and ELISA in 94 patients with SLE. Twenty-one had antiphospholipid syndrome (APS) by clinical and serological criteria, 33 had neither of these features, 18 had the clinical criteria for APS but no serum antiphospholipid antibodies (aPL). and 22 had positive aPL but no related clinical manifestations. As controls, we also studied 76 normal sera. Sera were also inhibited with cardiolipin micelles and tested for anticardiolipin antibodies (aCL) or a beta GP-I activities.
Thirty-five of 39 patients with SLE with clinical manifestations of APS has serum a beta 2 GP-I, while only 2 of 55 patients with SLE without such clinical manifestations had them (p = 0.000000001). Sixteen patients with SLE with clinical APS but aPL negative were a beta GP-I positive. All 35 patients with SLE who were a beta 2 GP-I positive had vascular manifestations, but these antibodies were present in only 4 of 55 patients with SLE without vascular manifestations (p = 0.00000001). No patient having either aPL or a beta 2 GP-I had clinical manifestations of APS, whereas all 19 patients positive for both antibodies had clinical APS. The a beta 2 GP-I positive, aPL negative patients with SLE had clinical APS more frequently (16/18) than did a beta GP-I negative, aPL positive patients with SLE (2/24) (p = 0.000000001). The association of clinical manifestations of APS with a beta 2 GP-I was stronger than with aPL. Inhibition studies also indicate that aPL and a beta 2 GP-I are 2 different antigen/antibody systems.
Our findings indicate that the so called APS associates strongly with antibodies recognizing phospholipid-free beta 2 GP-I. There are patients' sera that also recognize cardiolipin and/or its cofactor beta 2 GP-I, the latter perhaps by reacting with a neoepitope on this protein that appears after its interaction with cardiolipin. These would be the previously considered (beta 2 GP-I dependent) aCL.
The Journal of Rheumatology 11/1995; 22(10):1899-906. · 3.69 Impact Factor
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ABSTRACT: To investigate serum anti-beta 2-glycoprotein-I antibodies (a beta 2 GP-I) in patients with primary antiphospholipid syndrome (APS).
We studied a beta 2 GP-I by Western blot, dot blot, and ELISA in the sera of 15 patients with primary APS with high titers of immunoglobulin G (IgG) and/or immunoglobulin M (IgM) anticardiolipin antibodies (aCL) at the time of study and compared findings with the sera of 13 aCL positive patients with syphilis and 76 healthy controls. Sera were also inhibited with cardiolipin micelles and tested for aCL and a beta 2 GP-I activities.
Twelve patients with primary APS but no syphilis patient or control subject had IgG to phospholipid-free beta 2 GP-I (p < 0.0001) for both comparisons). The aCL activity was inhibited with cardiolipin micelles but this treatment had less effect on a beta 2 GP-I activity. We found no IgM a beta 2 GP-I in any serum. Nine of 14 patients had had lupus anticoagulant activity; 8 of these had a beta 2 GP-I.
Patients with primary APS frequently have IgG a beta 2 GP-I that appear to differ from aCL. If aCL present in patients with primary APS actually react with a phospholipid induced neoepitope on beta 2 GP-I, as recently proposed, patients with primary APS have autoantibodies against 2 epitopes on beta 2 GP-I. Lack of a beta 2 GP-I in patients with syphilis might also contribute to protection from developing the APS.
The Journal of Rheumatology 10/1995; 22(10):1894-8. · 3.69 Impact Factor
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ABSTRACT: We investigated the effects of polyoxyethylene sorbitan monolaurate (Tween 20) in the detection of IgG anticardiolipin antibodies (aCL) by the CL-beta 2-glycoprotein-I and the standard aCL solid-phase immunoassays. We found that Tween 20 disengages cardiolipin from a variety of microtiter wells rendering aCL undetectable by both methods. Our results agree with a previous report but are discordant with others. We offer rationale that may explain some of the discrepancies. Based in our findings, we do not recommend the use of Tween 20 for the detection of aCL.
Journal of Immunological Methods 10/1994; 175(1):107-14. · 2.20 Impact Factor
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ABSTRACT: Isolated cases of anti-phospholipid antibody (aPL)-associated idiopathic autoimmune haemolytic anemia (IAHA) have been recently described. To assess the significances of this association, we studied by ELISA the presence of aPL in sera from 18 patients with IAHA and 14 patients with non-autoimmune haemolysis (NON-AH). Four IAHA cases and none of the NON-AH controls showed IgM anticardiolipin antibodies (aCL) that crossreacted extensively with zwitterionic as well as with other anionic phospholipids. IgG aCL were detected in 6 patients with IAHA and in 1 patient with NON-AH; there was little cross-reactivity with other phospholipids. Our results suggest that antiphospholipid antibodies are present in a substantial number of patients with IAHA. This humoral response does not seem to be secondary to the haemolysis proper. The potential pathogenic significance of this finding is discussed.
Autoimmunity 02/1994; 18(1):51-6. · 2.47 Impact Factor
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Thrombosis Research 01/1994; 72(5):471-2. · 2.44 Impact Factor
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ABSTRACT: In an earlier study of a cohort of 667 patients with systemic lupus erythematosus (SLE) followed for 7.5 months with mean antiphospholipid (aPL) testing 2.5 times, we found a 10% prevalence of definite antiphospholipid syndrome (APS) (2 clinical manifestations and high aPL levels). To determine if more followup and aPL testing increased such prevalence we restudied the cohort after a mean followup of 3.1 years and a mean aPL testing of 5.6 times and found a 15% prevalence of definite APS. Another 21% of patients with SLE had probable APS with either high titers of aPL but only one clinical manifestation or low titers with 2 clinical manifestations. The prevalence of high titer positivity of aPL (IgG and/or IgM isotype) reached 41%. One aPL related feature that increased significantly was livedo reticularis possibly from increased awareness. Factors that influenced significantly the mobility upwards in APS category were more pregnancies and further aPL testing. Conversely, immunosuppressive treatment decreased higher aPL levels. The large number of patients with long disease duration in our cohort showed that the maximum prevalence of definite APS is reached after 15-18 years and is 23%. This might be the highest prevalence of definite APS within SLE.
The Journal of Rheumatology 04/1993; 20(3):437-42. · 3.69 Impact Factor
