Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LUPUS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed1998

Sudden sensorineural hearing loss in patients with systemic lupus erythematosus or lupus-like syndromes and antiphospholipid antibodies.

Although the pathogenesis of sudden sensorineural hearing loss (SNHL) in patients with systemic lupus erythematosus (SLE) is not clear, several reports suggest an association with the antiphospholipid antibody (aPL). We describe 6 patients with SLE or a lupus-like syndrome, who had sudden SNHL and had elevated levels of anticardiolipin antibodies (aCL) or the lupus anticoagulant. In a literature search, of 5 additional reported cases, 2 were not tested for aPL; the remaining 3 had elevated aCL levels. Thus, acute SNHL in patients with SLE who have aPL may be a manifestation of the antiphospholipid syndrome. We recommend anticoagulation treatment of these patients.

Adult↗
PubMedDate not supplied

[Oral lesions in systemic lupus erythematosus. I. The etiopathogenic aspects of lupus erythematosus].

The authors investigate lupus erythematosus systemicus, characterized by the multiform etiology and autoimmune pathogenesis. Cutaneous lesions, large confluent areas of erythema, poikilodermatous lesions, atrophy and necrotizing vasculitis (leukocytoclastic vasculitis) occur in patients with lupus erythematosus (SLE). Ulcerative lesions are an ACR (American College of Rheumatology), (formerly ARA), criterion for the diagnosis of SLE. These lesions are suspected of being caused by a mechanism involving circulating immune complexes and neutrophils. This observation further supports previous evidence that all oral lesions in SLE result from vacuolar degeneration of basal keratinocytes. Immunopathologic study of lupus erythematosus shows the correlation between HLA-dr positive keratinocytes or Langerhans cells and epidermotropic T cells and the immunobiological significance of the antigen-antibody system in LES.

Antibody Formation↗
PubMed1992

Lupus anticoagulant in systemic lupus erythematosus: a clinical and renal pathological study.

Circulating lupus anticoagulant (LA) is associated with thrombosis in large and small vessels. To determine how often the presence of LA is associated with thrombosis within the renal microcirculation, 33 patients with systemic lupus erythematosus (SLE), renal dysfunction, and LA were identified over a 25-year period (LA group) and 32 patients with renal SLE but with normal gross coagulation screen were matched for age, sex, and biopsy timing (C group). Prevalences of serositis, neuropsychiatric illness, leukopenia, thrombocytopenia, hemolysis, anti-DS-DNA elevation, and complement reduction were similar. Arthritis was less and biologic false-positive (BFP) syphilis serology more common in LA. More LA patients had thrombotic events (LA 39% v C 13%; P = 0.014); bleeding episodes, including postbiopsy, were similar. At biopsy, hypertension (LA 55%, C 41%), serum creatinine (mean +/- SD: LA 186 +/- 168 mumol/L [2.1 +/- 1.9 mg/dL] v C 150 +/- 168 mumol/L [1.7 +/- 1.9 mg/dL]) and proteinuria (LA 2.6 +/- 3.1 g/24 h v C 3.1 +/- 2.7) were similar. Lesions by World Health Organization (WHO) class, activity, and chronicity indices, as well as immunofluorescence (IF) and electron microscopy (EM) findings, were not significantly different. Occlusive glomerular, arteriolar, and arterial fibrin thrombi, along with varying degrees of renal thrombotic microangiopathy, were seen in five of 33 patients with LA, but zero of 32 C patients (P = 0.053); three of these five patients died soon after biopsy. Overall, mortality was not different between LA and C. We conclude that the majority of patients with SLE, renal dysfunction, and LA exhibit renal morphologic findings indistinguishable from patients without LA. However, a significant minority of LA patients have thrombotic microangiopathy in their biopsy, which is accompanied by a worse prognosis.

Adolescent↗
PubMed1997

ARA and EADV criteria for classification of systemic lupus erythematosus in patients with cutaneous lupus erythematosus.

OBJECTIVE: To verify (1) how many patients with cutaneous lupus erythematosus (CLE) fulfill 4 or more American Rheumatism Association (ARA) and European Academy of Dermatology and Venereology (EADV) criteria for classification of systemic lupus erythematosus (SLE); (2) which criteria are mostly fulfilled; (3) the severity of the disease in patients fulfilling criteria; (4) how many patients with systemic involvement fail to fulfill 4 ARA and EADV criteria. METHODS: We studied 207 patients with chronic and subacute CLE, classified according to ARA and EADV criteria. RESULTS: Twenty-four patients with localized discoid (L-DLE; 21.8%), 22 with disseminated discoid (D-DLE; 30.5%) and 7 with subacute CLE (SCLE; 28%) had 4 or more ARA criteria. With EADV criteria, these figures fell to 7 (6.4%), 7 (9.7%) and 6 (24%), respectively. Only 3 L-DLE (2.7%), 5 D-DLE (6.9%) and 3 SCLE cases (12%) defined as SLE by ARA criteria and 1, 3 and 3, respectively, by EADV criteria had a renal or neurological disorder, hemolytic anemia and/or thrombocytopenia, vasculitis or serositis. ARA criteria did not classify 7 patients with a similar visceral involvement, while EADV criteria failed in 11 patients. CONCLUSION: In our patients, ARA criteria showed a sensitivity of 88%, a specificity of 79%, a positive predictive value of 56% and a negative predictive value of 96%. EADV criteria showed a sensitivity of only 64%, but a specificity of 93%, a positive predictive value of 61% and a negative predictive value of 94%. ARA criteria should not be used in CLE patients as they are too sensitive, poorly specific and altogether misleading. EADV criteria are more specific, but less sensitive.

Anemia, Hemolytic↗
PubMed2002

Systemic lupus erythematosus in three ethnic groups. XII. Risk factors for lupus nephritis after diagnosis.

The purpose of this study was to determine the cumulative incidence of lupus nephritis (LN) and the factors predictive of its occurrence in a multiethnic systemic lupus erythematosus (SLE) cohort. We studied 353 SLE patients as defined by the American College of Rheumatology (ACR) criteria (65 Hispanics, 93 African-Americans and 91 Caucasians). First, we determined the cumulative incidence of LN in all patients. Next, we determined the predictors for LN in those with nephritis occurring after diagnosis. The dependent variable, LN, was defined by: (1) A renal biopsy demonstrating World Health Organization (WHO), class II-V histopathology; and/or (2) proteinuria > or = 0.5 g/24 h or 3+ proteinuria attributable to SLE; and/or (3) one of the following features also attributable to SLE and present on two or more visits, which were performed at least 6 months apart--proteinuria > or = 2+, serum creatinine > or = 1.4 mg/dl, creatinine clearance < or = 79 ml/min, > or = 10 RBCs or WBCs per high power field (hpf), or > or = 3 granular or cellular casts per hpf. Independent variables assessed at diagnosis, and if absent, at baseline, were from four domains: sociodemographic, clinical, immunologic and immunogenetic (including the complete antibody profile and MHC class II alleles), and health habits. Variables with P < 0.05 by chi square analyses were entered into domain-specific stepwise logistic regression analyses controlling for disease duration, with LN as the dependent variable. Significant domain-specific regression variables (P < or = 0.1) were then entered into an overall model. The cumulative incidence of LN was 54.3% in all patients, and 35.3% for those developing LN after diagnosis. LN after diagnosis occurred in 43.1% of 65 Hispanics, 50.5% of 93 African-Americans, and 14.3% of 91 Caucasians, P < 0.0001. The duration of follow-up for those with LN after diagnosis was 5.5+/-2.4 vs 4.0+/-2.9 years for those without LN. Hispanic (odds ratio (OR) = 2.71, 95% confidence limits (CL) = 1.07-6.87, P < 0.04) and African-American ethnicities (OR = 3.13, 95% CL = 1.21-8.09, P < 0.02), not married or living together (OR = 3.45, 95% CL = 1.69-7.69, P < 0.0003), higher SLAM score (OR = 1.11, 95% CL = 1.02-1.19, P < 0.007), anti-dsDNA (OR = 3.14, 95% CL = 1.50-6.57, P < 0.0001) and anti-RNP (OR = 4.24, CL = 1.98-9.07, P < 0.0001) antibodies were shown to be significant predictors of the occurrence of LN. Repeated analyses excluding the patients with missing HLA data showed that absence of HLA-DQB1*0201 was also a significant predictor for the occurrence of LN (OR = 2.34, CL = 1.13-5.26, P < 0.04). In conclusion, LN occurred significantly more often in Hispanics and African-Americans with SLE. Sociodemographic, clinical and immunologic/immunogenetic factors seem to be predictive of LN occurring after the diagnosis of SLE has been made.

Black or African American↗
PubMed1999

Strong association of autoantibodies to human nuclear lamin B1 with lupus anticoagulant antibodies in systemic lupus erythematosus.

OBJECTIVE: To determine the frequency and clinical significance of high titers of IgG autoantibodies to nuclear lamin B1 in a large number of unselected and well-characterized systemic lupus erythematosus (SLE) patients, disease controls, and normal healthy controls. METHODS: A cross-sectional study of anti-lamin B1 autoantibodies, as measured by enzyme-linked immunosorbent assay using human recombinant lamin B1 autoantigen, was performed on serum samples obtained at first evaluation of 238 consecutive French Canadian adults: 61 healthy control subjects, 20 patients with osteoarthritis, 22 with ankylosing spondylitis, 11 with autoimmune hepatitis, 30 with rheumatoid arthritis, and 94 with SLE. SLE patients were studied for 57 disease manifestations. A case-control study was performed to analyze the relationship between anti-lamin B1 status and thrombotic manifestations between SLE onset and last followup. RESULTS: High titers of anti-lamin B1 were strikingly restricted to a subset of 8 SLE patients (8.5%). The mean anti-lamin B1 titer was higher in this subset than in the other SLE patients or any control group (P<0.001). By univariate analysis and stepwise multiple logistic regression, the most striking association of anti-lamin B1 was with lupus anticoagulant (LAC) antibodies (P = 0.00001). Although LAC were significantly associated with thrombosis in our SLE patients, anti-lamin B1 was not. The frequency of thrombosis in SLE patients expressing both LAC and anti-lamin B1 was similar to that in patients without LAC (P = 1.0). However, patients expressing LAC without anti-lamin B1 had a greater frequency of thrombosis (P = 0.018). CONCLUSION: High titers of IgG anti-lamin B1 autoantibodies are highly specific for a subset of SLE patients whose clinical characteristics include the presence of LAC and other laboratory manifestations of the antiphospholipid syndrome. The presence of LAC without anti-lamin B1 may define a subset of SLE patients at greater risk for thrombosis.

Adult↗
PubMed2002

Diagnosis of lupus anticoagulant in the lupus anticoagulant-hypoprothrombinemia syndrome: report of two cases and review of the literature.

We report a severe hemorrhagic disorder in two pediatric patients with lupus anticoagulant (LA) associated to acquired factor II (prothrombin) deficiency. In both patients, hemorrhagic symptoms resolved after corticosteroid therapy. Serial coagulation studies showed that Staclot LA assay was more sensitive than DVVconfirm and Staclot PNP tests to confirm the presence of LA when associated with severe factor II deficiency. Both patients had non-neutralizing anti-prothrombin antibodies and their titers inversely correlated with factor II activity (r = -1.0, P < 0.0001). Associated findings in these patients included positive immunologic tests for systemic lupus erythematosus, a positive anti-cardiolipin antibody, and anti-beta(2) GPI antibodies in one case. Our findings point out the difficulty in diagnosing LA associated with acquired factor II deficiency and suggest that, in confirmation of its phospholipid dependency, the inclusion of a source of normal human plasma in the test sequence to correct for any factor deficiency and a confirmatory step utilizing hexagonal (II) phase phospholipids may be crucial to the diagnosis of LA in some patients with LA-hypoprothrombinemia syndrome.

Adolescent↗
PubMed1994

Anti-annexin V antibody in systemic lupus erythematosus patients with lupus anticoagulant and/or anticardiolipin antibody.

We investigated anti-annexin V antibody (aANX) in patients with systemic lupus erythematosus (SLE), and correlated to positivity with lupus anticoagulant (LA)/anticardiolipin antibody (aCL). aANX was positive in 12/47 SLE patients (26%), including 7 with beta 2-glycoprotein 1 (GPI)-dependent aANX. The positivity of aANX was higher in patients with aCL (19%) and LA/aCL (50%) than in those without LA/aCL (10%). From these results, it is concluded that aANX is an autoantibody closely related to LA/aCL, and can be a possible new risk marker for thrombosis.

Annexin A5↗
PubMed1990

The expression of C3b receptors in the differentiation of discoid lupus erythematosus and systemic lupus erythematosus.

We studied the expression of the C3b receptor, CR1, on erythrocytes (E-CR1) of patients who, in spite of having mild systemic symptoms, were diagnosed as having discoid lupus erythematosus and followed accordingly. We found that E-CR1 was markedly reduced in these patients, similar to that seen in patients with systemic disease. In contrast, those patients with completely asymptomatic discoid lupus erythematosus had the same expression of E-CR1 as the normal population.

Complement C3b↗
PubMed2005

Familial aggregation of systemic lupus erythematosus, rheumatoid arthritis, and other autoimmune diseases in 1,177 lupus patients from the GLADEL cohort.

OBJECTIVE: To determine whether there is familial aggregation of systemic lupus erythematosus (SLE) and/or other autoimmune diseases in SLE patients and to identify clinical differences between patients with and those without familial autoimmunity. METHODS: We interviewed members of the Grupo Latinoamericano de Estudio del Lupus Eritematoso (GLADEL) inception cohort of 1,214 SLE patients to ascertain whether they had relatives with SLE and/or other autoimmune diseases. Identified relatives were studied. Familial aggregation was tested using reported highest and intermediate population prevalence data for SLE, rheumatoid arthritis (RA), or all autoimmune diseases, and studies were performed to identify the genetic model applicable for SLE. RESULTS: We identified 116 first-, second-, or third-degree relatives with SLE, 79 with RA, 23 with autoimmune thyroiditis, 3 with scleroderma, 1 with polymyositis, and 16 with other autoimmune diseases, related to 166 of the 1,177 SLE patients in the GLADEL cohort who agreed to participate. Forty-two SLE patients had 2 or more relatives with an autoimmune disease. We found a lambda(sibling) of 5.8 and 29.0 for SLE and of 3.2-5.3 for RA, when comparing with their reported high or intermediate population prevalence, respectively. We also found familial aggregation for autoimmune disease in general (lambda(sibling) = 1.5) and determined that for SLE, a polygenic additive genetic model, rather than a multiplicative one, is applicable. CONCLUSION: In SLE there is familial aggregation of SLE, RA, and autoimmune disease in general. A polygenic additive model applies for SLE. American Indian-white Mestizo SLE patients and those with higher socioeconomic level were more likely to have familial autoimmunity.

Arthritis, Rheumatoid↗
PubMed2006

Revised British Isles Lupus Assessment Group 2004 index: a reliable tool for assessment of systemic lupus erythematosus activity.

OBJECTIVE: To test the interrater reliability of the revised British Isles Lupus Assessment Group 2004 (BILAG-2004) index for the assessment of systemic lupus erythematosus (SLE) activity. METHODS: Patients with SLE were recruited from 11 centers. Two physician raters separately assessed the patients' disease activity using the BILAG-2004 index in routine clinical practice. Scores ranged from A (for very active disease) to E (for inactivity). Two reliability exercises were performed. Changes were made to the index after the first exercise (E1), and additional training was provided to the raters before the second exercise (E2). E1 and E2 involved 12 and 14 raters, respectively. Interrater reliability was assessed using kappa statistics and intraclass correlation coefficients. Levels of agreement and the extent of major disagreement were also examined. Major disagreement was defined as a score difference between raters of A versus C, D, or E or B versus D or E. RESULTS: For each exercise, 97 patients were recruited. In E1, the mean age of the patients was 42.3 years (range 18.5-82.2 years), 89.7% were women, and 74.2% were white, 8.2% were Afro-Caribbean, and 13.4% were South Asian, and in E2, the mean age was 43.7 years (range 17.7-75 years), 90.7% were women, and 68% were white, 15.5% were Afro-Caribbean, and 11.3% were South Asian. The mean disease duration was 9.4 years (range 0-32.1 years) for patients in E1 and 10 years (range 0-34.8 years) in E2. There was improvement in the interrater reliability and the level of agreement from E1 to E2. Further improvement was achieved after removal of poorly performing items. CONCLUSION: The BILAG-2004 index is a reliable tool to assess SLE activity. The use of a well-defined glossary and training of raters are essential to ensure the optimal performance of the index.

Activities of Daily Living↗
PubMed1994

Heterogeneity and diversity of IgM and IgG lupus anticoagulants in an individual with systemic lupus erythematosus.

From one patient with systemic lupus erythematosus retaining lupus anticoagulant (LAC), we established 6 Epstein-Barr virus-transformed human B cell clones secreting antibodies that affect the coagulation assay. Two and 4 of the clones secreted IgM and IgG antibodies, respectively. Although all 6 antibodies displayed anticardiolipin activity in ELISA, the increased binding activity in the presence of beta 2-glycoprotein I was limited only to the IgG antibodies. Five antibodies (two IgM and three IgG) had LAC activity which prolonged the activated partial thromboplastin time (APTT), whereas one IgG antibody shortened the APTT. Two of the IgG producing clones had an identical Ig heavy chain gene rearrangement despite their opposite effects on the coagulation assay. These results demonstrated the heterogeneity of LACs and diversity among their physiological functions.

Adult↗
PubMed1994

Plasma concentrations of total/free and functional protein S are not decreased in systemic lupus erythematosus patients with lupus anticoagulant and/or antiphospholipid antibodies.

We conducted an investigation to clarify whether or not the levels of total, free, and functional protein S and C4-binding protein (C4bp) in plasma are decreased in systemic lupus erythematosus (SLE) patients, especially those with antiphospholipid antibody (aPL), which is known to be a causative factor of such complications as habitual abortion and arteriovenous thrombosis. Fifty patients with SLE were recruited as subjects of the study. Serum aPL (anticardiolipin, antiphosphatidyl serine, antiphosphatidyl inositol, and antiphosphatidic acid antibodies) were measured by ELISA. Lupus anticoagulant was determined by a PTT, KCT, and diluted RVVT. Furthermore, plasma concentrations of total, free, and functional protein S and C4bp were measured. There were no significant differences in the mean levels of total, free, or functional protein S and C4bp between aPL-positive, aPL-negative SLE patients, and the healthy controls. From these results, we concluded that the protein S level is not the sole factor causing complications, and that other factor(s) may be involved in the induction of such complications in this clinical setting.

Antibodies, Antiphospholipid↗
PubMed1992

Anticardiolipin antibodies and lupus anticoagulant in patients treated with different methods of renal replacement therapy in comparison to patients with systemic lupus erythematosus.

Antiphospholipid antibodies were found to be associated with certain clinical manifestations such as recurrent venous thrombosis or arterial occlusions in a wide spectrum of immune disorders [6]. We analyzed the plasma concentration of two isotypes (IgG, IgM) of anticardiolipin antibodies (ACA) and lupus anticoagulant (LAC) activity in 84 patients with end-stage renal disease. They were receiving different types of renal replacement therapy and had a high frequency of thrombotic vascular complications. The prevalence of positive tests and the mean ACA concentration obtained in the plasma of renal patients were compared with those in patients with systemic lupus erythematosus (SLE) and in healthy controls. When analyzed as a whole group, renal patients maintained on dialysis (n = 45: hemodialysis, n = 20; peritoneal dialysis) or with a functioning kidney transplant (n = 19) did not differ in mean ACA concentration and LAC activity (n = 84, ACA: IgG 10 +/- 7 U/ml, IgM 2 +/- 1 U/ml, LAC ratio: 1.0 +/- 0.2) from healthy subjects (n = 50, ACA: IgG 10 +/- 3, IgM 2 +/- 1 U/ml, LAC ratio: 1.0 +/- 0.1) but they had a higher incidence of raised IgG-ACA titers (renal replacement 14% vs. normal controls 4%, p less than 0.05). No significant correlation was found between thrombotic events and raised ACA or LAC activity in dialysis patients. In contrast, the proportion of SLE patients (n = 51) with a raised concentration of ACA was significantly higher (IgG: 69%, IgM: 29%) than that among patients with renal replacement therapy (IgG: 14%, IgM: 4%) or normal controls (IgG: 4%, IgM: 2%, p less than 0.002). Moreover, recurrent manifestations of thrombosis in SLE were associated with very high IgG-ACA (n = 11, IgG 117 +/- 91 U/ml) and LAC activity (LAC ratio: 2.4 +/- 0.7) in comparison to SLE patients without thrombotic events (n = 40, ACA: IgG 23 +/- 13). The results of our investigations demonstrate that the pathogenetic role of these phospholipid antibodies in end-stage renal disease is far from established.

Adult↗
PubMed2004

Lupus anticoagulant, factor V Leiden, and methylenetetrahydrofolate reductase gene mutation in a lupus patient with cerebral venous thrombosis.

We describe the case of a young Lebanese woman with systemic lupus erythematosus (SLE) and a positive lupus anticoagulant (LAC) who developed right internal jugular vein and sigmoid sinus thrombosis. Coagulation studies showed that in addition to the LAC the patient was heterozygous for the factor V (FV) Leiden mutation, and C677T mutation of the methylenetetrahydrofolate reductase gene. The high prevalence of FV Leiden in the eastern Mediterranean region suggests that we should probably screen our SLE patients in this area, especially those with anticardiolipin antibodies and/or LAC who have no history of thrombosis, for this and other thrombophilia markers. The detection of such abnormalities may have major practical consequences for the long-term management of these patients to prevent further thrombotic episodes.

Adolescent↗
PubMed1994

Recovery of both acute massive pulmonary hemorrhage and acute renal failure in a systemic lupus erythematosus patient with lupus anticoagulant by the combined therapy of plasmapheresis plus cyclophosphamide.

Acute massive pulmonary hemorrhage (AMPH) is a rare and highly fatal complication in systemic lupus erythematosus (SLE). We report here survival in a case of AMPH in a SLE patient with both rapidly progressive glomerulonephritis and lupus anticoagulant. The AMPH occurred while the nephritis was refractory to 2 courses of pulse methylprednisolone therapy. After combined therapy with plasmapheresis plus cyclophosphamide, circulating immune complex levels declined, AMPH recovered, and serum creatinine levels returned to normal. In conclusion, the combined therapy of plasmapheresis plus cyclophosphamide should be considered for treating AMPH especially in those SLE patients with rapidly progressive glomerulonephritis.

Acute Disease↗
PubMed1998

Subacute cutaneous lupus erythematosus versus systemic lupus erythematosus: diagnostic criteria and therapeutic implications.

BACKGROUND: The nosologic position of subacute cutaneous lupus erythematosus (SCLE) is controversial. More than four American Rheumatism Association (ARA) criteria for systemic lupus erythematosus (SLE) are found in a proportion of patients diagnosed as having SCLE; thus such cases could be classified as SLE. OBJECTIVE: Our purpose was to determine whether ARA criteria for SLE are helpful in differentiating SCLE from SLE and whether cutaneous and visceral changes, immunologic findings, and photosensitivity provide a basis for diagnosis of SCLE. METHODS: A cohort of 143 patients (79 with SCLE, 58 with SLE, and six with overlapping features of SCLE and SLE) was studied clinically, histologically, and immunologically as well as by phototesting. The patients were observed for up to 10 years, and the course of the disease and response to therapy were evaluated in each group. RESULTS: SCLE differed from SLE by cutaneous changes, significantly less frequent kidney involvement, serositis and arthritis, and the rare presence of double-stranded DNA, U1RNP, and Sm antibodies characteristic of SLE. Ro(SS-A) and La(SS-B) antibodies were detected with similar frequency, and photosensitivity was not related to the presence of Ro antibody. In contrast, photoreproduction (appearance of LE lesion in irradiated area) was significantly more frequent in patients with SCLE. The course of SCLE in older patients was less severe than in younger patients, and aggressive therapy was usually not required. CONCLUSION: Patients with SCLE (although the majority fulfill more than four ARA criteria for SLE) show significant differences from those with SLE in terms of cutaneous and visceral involvement, immunologic findings, photosensitivity, course of the disease, and the requirement for therapy. Therefore SCLE should be recognized as a separate subset. However, cases of overlapping SLE and SCLE suggest a close relation.

Adult↗
PubMed1997

Increased factor VIIa levels in systemic lupus erythematosus patients with lupus anticoagulant.

Recurrent fetal loss, and/or arterio-venous thrombosis are frequent complications in patients with the antiphospholipid antibodies (aPL), anticardiolipin antibody (aCL) and/or lupus anticoagulant (LA). Furthermore, patients with LA have been found to be more susceptible to thrombosis than those with aCL, thus suggesting differences in the pathogenesis of aCL and LA. We examined the systemic lupus erythematosus (SLE) patients with aCL and/or LA for differences in the markers for hypercoagulable state, including thrombin-antithrombin complex (TAT), prothrombin fragment 1 + 2 (F1 + 2), thrombomodulin (TM) and activated factor VII (FVIIa), and lipoprotein (a) (Lp(a)), which is a well-known risk factor for thrombosis. The FVIIa concentration was significantly higher in the LA-positive patients than in the aCL-positive and aPL-negative patients. No significant differences in TAT, F1 + 2, TM, and Lp(a) values were found among the aCL-positive, LA-positive and LA-negative patients groups. These findings indicate that patients with LA were in a more prethrombotic state than those with aCL. The measurement of FVIIa may serve as a useful predictive marker for thrombosis, but further studies are needed to clarify the mechanisms of thrombosis in this clinical setting.

Adult↗