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PubMed1978

Drug-induced lupus erythematosus with in vivo lupus erythematosus cells in pleural fluid.

Pleural involvement in drug-induced lupus erythematosus is not uncommon. Lupus erythematosus cells were found in vivo in the pleural of an elderly patient who had received procainamide (Pronestyl) hydrochloride (2 gm daily) for nine months. Patients who initially have pleural effusions while receiving drugs capable of inducing lupus erythematosus should have the fluid analyzed for lupus erythematosus cells to help clarify the cause of the effusion.

Aged↗
PubMed1999

Toxoplasma infection in systemic lupus erythematosus mimicking lupus cerebritis.

An opportunistic infection is a known, although under-diagnosed, complication of systemic lupus erythematosus (SLE). A 48-year-old woman with a recent diagnosis of SLE was admitted to the hospital because of a fever, confused state, and convulsive episode. Her symptoms were interpreted as being compatible with lupus cerebritis. Treatment with methylprednisolone resulted in a temporary improvement in the patient's condition. Nevertheless, during the next few weeks, her physical and mental condition deteriorated, and she died of massive pulmonary emboli. An autopsy revealed no signs of lupus cerebritis; however, disseminated cerebral toxoplasmosis was found. Cerebral toxoplasmosis is a rare complication of SLE that may be misdiagnosed as lupus cerebritis.

Autopsy↗
PubMed1983

Gangrene developing after minor surgery in a patient with undiagnosed systemic lupus erythematosus and lupus anticoagulant.

We report a case of progressive peripheral ischaemia and gangrene as a presenting feature of systemic lupus erythematosus. It developed in a previously asymptomatic 40-year-old woman following minor surgery to her toe. Eventually she required a below-knee amputation and despite systemic corticosteroids continued to deteriorate, presenting later with signs of systemic intravascular thromboses. Histopathology and immunofluorescence on vessels repeatedly failed to demonstrate any evidence for vasculitis. A full coagulation screen confirmed the presence of 'lupus' anticoagulant. A plasma exchange was performed to remove circulating immunoglobins and she made a rapid and sustained recovery. Peripheral gangrene has not previously been described in association with lupus anticoagulant. We would suggest that in all cases of systemic thrombosis or unexplained peripheral vascular ischaemia lupus anticoagulant should be considered.

Adult↗
PubMed2002

Endogenous retroviruses in systemic lupus erythematosus: candidate lupus viruses.

Although the etiology of systemic lupus erythematosus (SLE) remains unclear, there is substantial circumstantial evidence that the development of SLE is dependent on environmental, genetic, and retroviral factors. SLE patients produce high titer antibodies to various retroviral proteins, including Gag, Env, and Nef of HIV and HTLV, in the absence of overt retroviral infection. We review the factors linking HERVs to SLE and consider the various processes utilized by endogenous retroviruses in the etiopathogenesis of SLE. In particular, we consider the role of HTLV-1-related endogenous sequence (HRES-1) in SLE. We propose that molecular mimicry between HRES-1 and the small ribonucleoprotein complex initiates the production of autoantibodies, leading to immune complex formation, complement fixation, and pathological tissue deposition.

Antibodies, Viral↗
PubMed1985

Ancrod: normalization of fibrinolytic enzyme abnormalities in patients with systemic lupus erythematosus and lupus nephritis.

Ancrod is a thrombinlike enzyme from Malayan pit viper (Agkistrodon rhodostoma) venom that has a selective enzyme substrate specificity for fibrinogen. Unlike thrombin, it splits only fibrinopeptide A from the fibrinogen molecule and does not activate factor XIII. Simultaneously with the occurrence of hypofibrinogenemia there is a reduction of plasma plasminogen and a rise in fibrin degradation products, suggesting secondary recruitment of the fibrinolytic enzyme system. Ancrod was given to 18 patients with systemic lupus erythematosus and glomerular and vascular microthrombi. Before treatment vascular plasminogen activator (VPA) was low or unmeasurable in 14, an inhibitor of urokinase-induced plasminogen activation (IPA) was elevated in 18, and an inhibitor of plasmin (PI) was elevated in five. Ancrod treatment resulted in prompt normalization of IPA levels in 13 patients; they were classified as fibrinolysis responders. In five patients IPA levels remained elevated throughout treatment with ancrod; they were classified as fibrinolysis nonresponders. In these five the PI level was elevated before treatment and decreased slowly toward the normal range during ancrod administration. The PI did not appear related to the nonspecific serine protease inhibitors, and was shown to be identical with alpha 2-antiplasmin. In the fibrinolysis responders serial histologic studies showed a striking decrease of disappearance of microvascular thrombosis; in the fibrinolysis nonresponders microvascular thrombosis persisted. The action of ancrod is discussed.

Adult↗
PubMed1981

[Comparison of severity and native anti-DNA antibody levels in systemic lupus erythematosus. Serodiscordant lupus].

The authors studied the clinicobiological correlations between the severity of systemic lupus erythematosus (SLE) and native anti-DNA antibody levels in 176 patients suffering from this disease. Certain patients were studied at different stages of their disease. This correlation was very close in one out of two cases and relative in one case out of four. In one-fourth of these patients, a significant and persistent discordance existed, and these patients were therefore studied apart. Certain SLE which have been suppressed over long periods of time continue to have elevated anti-DNA levels which are occasionally associated with lowered levels of complement. This has been previously reported in the literature. All decisions to modify corticosteroid treatment based only on biological data is therefore questionable. In contrast, in certain cases of SLE where the evolution of the disease is relatively severe, no anti-DNA or antinuclear antibodies are present. These "seronegative" SLE cases are proof that the "specific" biology of this disease may be erroneous for diagnosis as well as for prognosis. The authors review the possible or known causes for the absence of these antibodies in SLE. They believe that native anti-DNA levels are only of relative value in SLE and feel that these values must be examined with respect to clinical and other biological data in order to treat and survey patients affected with this disease.

Antibodies, Antinuclear↗
PubMed2005

Lupus erythematosus panniculitis (lupus profundus): clinical, histopathological, and molecular analysis of nine cases.

BACKGROUND: The diagnosis of lupus erythematosus panniculitis (LEP) may be very difficult in cases in which involvement of the subcutaneous fat is the only manifestation of the disease. The main differential diagnosis is subcutaneous panniculitis-like T-cell lymphoma (SPTCL). METHODS: We performed a retrospective study reviewing the histopathologic features of 11 biopsy specimens from nine patients with LEP (M : F = 2 : 7; median age: 48 years; range: 20-71 years). RESULTS: Histopathologically, all biopsies revealed a lobular panniculitis, with concomitant septal involvement in 82% of them. Dermal changes included the presence of superficial and deep infiltrates (82%) and mucin deposition (73%). The majority of cases (73%) presented also some form of epidermal involvement. The subcutaneous infiltrate was composed of lymphocytes in all cases, admixed with plasma cells in 91% of cases. Lymphoid follicles with reactive germinal centers were detected in 45% of cases. Immunohistochemistry showed a predominance of alpha/beta-T-helper and cytotoxic lymphocytes in 80% of cases admixed with B lymphocytes. The polymerase chain reaction analysis of the T-cell receptor (TCR)-gamma gene showed a polyclonal smear in all cases. CONCLUSIONS: Our study shows that the most useful histopathologic criteria for distinguishing LEP from SPTCL are the presence of involvement of the epidermis, lymphoid follicles with reactive germinal centers, mixed cell infiltrate with prominent plasma cells, clusters of B lymphocytes, and polyclonal TCR-gamma gene rearrangement.

Adult↗
PubMed2005

Association of anti-nucleoprotein autoantibodies with upregulation of Type I interferon-inducible gene transcripts and dendritic cell maturation in systemic lupus erythematosus.

Lupus patients selectively produce autoantibodies against nucleoproteins. Since the RNA/DNA components of these autoantigens are endogenous TLR ligands capable of stimulating Type I interferon (IFN-I) production, we asked whether autoantibodies against the ribonucleoproteins Sm/RNP and Ro60 and double-stranded DNA are associated with high levels of IFN-I. IFN-I levels were increased in SLE (n = 88) vs. other autoimmune diseases (n = 82) and controls (n = 57) (P < 0.0001) and were associated positively with autoantibodies against Sm/RNP, Ro60/La, and dsDNA but negatively with anti-phospholipid. Low numbers of circulating plasmacytoid and myeloid dendritic cells also were associated with these autoantibodies. The IFN-I and dendritic cell abnormalities correlated with disease severity and were not therapy-related. These findings suggest that immunostimulatory nucleic acid components of autoantigens may act as endogenous adjuvants by promoting IFN-I production and dendritic cell maturation, helping to explain the high prevalence of autoantibodies against nucleoprotein antigens in SLE.

Antibodies, Antinuclear↗
PubMed2000

Sex hormones and systemic lupus erythematosus.

Lupus is one disease in which sex hormones and gender are quite important. Studies of autoimmune diseases like lupus have made the hormone connection more important and increased our overall understanding of the sexual dimorphism of the immune system. It is clear that some fundamental biologic mechanism is at work here and that only knowledge of the molecular mechanisms behind the action of the hormones can help us to understand the gender preference in this illness. Hormones may be potent regulators of cytokine levels and, consequently, disease activity.

Animals↗
PubMed1979

Different histological manifestation of glomerular lesions in familial systemic lupus erythematosus.

Lupus nephritis in a sister and brother pair was histologically analyzed. The 12-year-old sister showed clinically progressive renal failure and her renal pathology disclosed segmental necrotizing and disorganizing glomerulonephritis. On the contrary, the 14-year-old brother exhibited nephrotic syndrome and his renal biopsy showed diffuse exudative and proliferative glomerulonephritis with segmental membraneous changes. Although the familial incidence of SLE suggests both genetic and environmental factors existing in the background of SLE of identical twins and siblings, the differences of clinical manifestation and histopathological findings imply that there might be little direct genetic and environmental control on determining the expression of the disease.

Adolescent↗
PubMed2004

Update on the immunology, diagnosis and management of systemic lupus erythematosus.

Lupus occurs with a prevalence of 2-9 in 10,000 people, targeting female and indigenous populations in particular. Lupus and related systemic autoimmune syndromes (scleroderma, Sjögren's syndrome, rheumatoid arthritis and polymyositis) result from a similar set of genetically and environmentally modulated immune disturbances, and the diagnostic and management approach to these conditions is broadly comparable. Evanescent, vague symptoms, restrictive diagnostic criteria and low diagnostic suspicion might have resulted in the under-diagnosis of these problems in the past, imposing considerable burdens on sufferers and the community. Serological screening should be employed cautiously and wisely, given the rapidly occurring changes in methodology, which have lowered their specificity. Close liaison with the immunology laboratories performing these tests is therefore advisable. Clinicians should emphasize the improving prognosis of lupus and related conditions as a result of earlier disease detection, improved educational support systems and refined medical therapies.

Autoimmunity↗
PubMed1990

Pregnancy associated with systemic lupus erythematosus.

Lupus pregnancies may be complicated by difficulties in the diagnosis of flare, by complications related to aPL antibody, complications related to neonatal lupus, and by a high frequency of preeclampsia. Lupus pregnancies are often difficult to manage, but most complications can be anticipated and, with care, successfully managed.

Female↗
PubMed1996

[Lupus anticoagulants in patients with systemic lupus erythematosus].

Lupus anticoagulants (LA) and anticardiolipin antibodies (aCL) are known as thrombosis-related antiphospholipid antibodies. LA is not as well characterized as aCL, and the relation between LA and aCL is not clarified. Since standardized method for the detection of LA has not been established, we measured LA activities in outpatients with SLE by using two different methods (KCT and dRVVT), and analyzed the characteristics of LA in SLE. LA was detected in 29.8% of all samples (14.3% in both methods, 15.5% in one method). IgG-aCL and IgM-aCL was detected in 38% and 20%, respectively, of all LA positive samples. Though a good correlation was observed between LA activities and IgG-aCL levels, a considerable number of LA positive samples were negative for aCL. This indicated the presence of factors with LA activity other than aCL. On the contrary there was also a high percentage of LA negative samples with positive aCL (42.4% in IgG-aCL, 47.4% in IgM-aCL), suggesting the presence of aCL with poor or low LA activity. These findings showed the heterogeneity of antiphospholipid antibodies both in LA and in aCL. The platelet function tests showed increased platelet adhesiveness and normal platelet aggregation in LA positive patients with SLE even in the inactive phase. The serum levels of factors such as protein C, protein S, antithrombin III and thrombomodulin were within normal range. Clinical features such as hemolytic anemia, thrombosis and abortion were more frequently observed in LA positive population than in LA negative population. The clinical features tend to be different between patients with dRVVT-LA and those with KCT-LA, though not significant. Because of the heterogeneity in LA, a combination of more than two different methods including dRVVT was recommended for the detection and the evaluation of LA.

Adult↗
PubMed2002

Role of the Fcgamma receptor IIa polymorphism in susceptibility to systemic lupus erythematosus and lupus nephritis: a meta-analysis.

OBJECTIVE: To assess the impact of the Fcgamma receptor type IIa (FcgammaRIIa)-R/H131 polymorphism on the risk for systemic lupus erythematosus (SLE) and development of lupus nephritis. METHODS: A meta-analysis was performed based on the Medline and Embase databases (last retrieval August 2001), assessment of bibliographies of pertinent articles, and additional data gathered after contact with primary investigators. RESULTS: A total of 25 comparisons from 17 studies involving R/H131 genotyping of 1,405 patients with lupus nephritis, 1,709 SLE patients without nephritis, and 2,580 non-SLE controls were included. No association between RR genotype and risk of lupus nephritis relative to both other genotypes (odds ratio [OR] 1.05, 95% confidence interval [95% CI] 0.88-1.27) was demonstrated in the total meta-analysis or in any racial subgroup. The RR genotype was more frequent in SLE patients as a whole (OR 1.30, 95% CI 1.10-1.52) and in SLE patients without nephritis (OR 1.27, 95% CI 1.04-1.55) compared with disease-free controls. A potential dose-response relation between the R131 allele and the risk of SLE was also identified, with an OR of 1.23 for RR versus RH (95% CI 1.03-1.46). The OR was 1.55 for RR versus HH (95% CI 1.21-1.98). There was no significant heterogeneity between racial subgroups. The population-attributable fractions of SLE cases due to the FcgammaRIIa-R131 allele were 13%, 40%, and 24% in subjects of European, African, and Asian descent, respectively. CONCLUSION: The FcgammaRIIa-R/H131 polymorphism represents a significant risk factor for SLE but has no clear effect on susceptibility for lupus nephritis.

Antigens, CD↗