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PubMed2004

The circulating lymphocyte profiles in patients with discoid lupus erythematosus and systemic lupus erythematosus suggest a pathogenetic relationship.

BACKGROUND: Discoid lupus erythematosus (DLE) and systemic lupus erythematosus (SLE) are chronic inflammatory diseases of unknown aetiology; the relationship of DLE with SLE has been a subject of debate for many years. OBJECTIVES; To find evidence for systemic immune activation in DLE by analysis of the immunophenotypic profiles of circulating lymphocytes, and to compare these changes with those in patients with SLE. METHODS: The immunophenotypic profile of peripheral blood lymphocyte subsets from 23 DLE patients without clinical or laboratory evidence of systemic disease, 25 SLE patients and 38 healthy donors was characterized by two-colour immunofluorescence flow cytometry analysis. None of the patients was receiving corticosteroid or immunosuppressive treatment. RESULTS: Patients with DLE had increased numbers of circulating HLA-DR+ CD3+ T cells and HLA-DR+ CD4+ T cells, indicating systemic T-cell activation, and an expansion of CD5+ CD19+ B cells. Decreased numbers of T-cell subsets expressing the differentiation markers CD11b and CD16/56, and of CD16/56+ natural killer cells were also found. In SLE, the changes were similar but more pronounced. In addition, a profound CD4+ T-cell lymphopenia and an increase of HLA-DR+ CD8+ T cells were found only in SLE. CONCLUSIONS: Our data provide evidence for systemic activation of the cellular immune system in patients with purely cutaneous DLE. Similarities in the lymphocyte immunophenotypic profiles in patients with DLE compared with SLE suggest that there are common immunopathological processes in these two conditions.

Adolescent↗
PubMed2004

Lupus erythematosus tumidus in systemic lupus erythematosus: novel association and possible role of early treatment in prevention of discoid lupus erythematosus.

Skin involvement in systemic lupus erythematosus (SLE) occurs in varied forms. Lupus erythematosus tumidus (LET) is not known to occur with SLE. In our patient presented below, LET occurred in a patient with SLE. Some of the lesions progressed to scarring discoid lesions, while others responded very well to hydoxychloroquine treatment. We, as rheumatologists, are not very aware of this entity, which is so amenable to prevention and treatment if recognized correctly.

Adult↗
PubMed1992

Cutaneous lupus erythematosus without systemic lupus erythematosus: clinical and laboratory features.

Sixty-seven patients with cutaneous lupus erythematosus (CLE) were followed up as part of a series of 570 lupus erythematosus patients seen in a private practice between 1980 and 1989. Clinical and laboratory features, treatment, and natural course were observed. Findings of interest included (1) a ratio of at least one CLE case for every seven cases of systemic lupus erythematosus (SLE); (2) occurrence of CLE in fewer women and apparently associated with an older age at diagnosis than SLE; (3) similar frequency of cutaneous lupus subsets in CLE and SLE; (4) strong family history for SLE but not CLE in CLE patients; (5) other cutaneous and musculoskeletal features in a majority of CLE patients and constitutional symptoms in 10%; (6) positive ANA titers, high sedimentation rates, and leukopenia common in CLE; (7) anticardiolipin antibody in 31% of CLE patients but not associated with systemic complications; (8) antimalarials required by 75% of patients and systemic steroids by 33%; and (9) an excellent prognosis associated with CLE, organ-threatening disease being rare.

Adult↗
PubMedDate not supplied

Hair and nail involvement in lupus erythematosus.

Lupus erythematosus (LE) is a systemic autoimmune disorder associated with polyclonal B-cell activation, resulting in diverse patterns of autoantibody production and a heterogeneous clinical expression constituting a spectrum extending from limited cutaneous disease (cutaneous lupus LE) to a life-threatening systemic disease process (systemic LE). While the clinical characteristics of cutaneous LE are well defined in terms of morphology, and for the classification of systemic LE (SLE), clinical and laboratory criteria are available, recent advances in basic and clinical research have contributed to a better understanding of the cellular and molecular events that lead to LE. The importance of genetic susceptibility, environmental factors, and hormonal elements are well appreciated, although we as clinicians are faced with relatively late-term manifestations of the immunologic events that lead to the clinical manifestations of disease. Nevertheless, combining our knowledge of the clinical patterns of LE with the advances in our understanding of the underlying immunology, has led to the concept of "subsets" of disease, where a correlation between immune genetic markers, autoantibody profiles, distinctive cutaneous morphology, and clinical outcome has become possible.

Hair Diseases↗
PubMed2006

Lupus erythematosus and lupus valgaris: a case report and historical remarks.

Lupus erythematosus and lupus valgaris, i.e., cutaneous tuberculosis, are confusing skin lesions in the history. Here, we reported on a Chinese lupus patient manifested with multiple nodular erythematous rashes on both upper extremities, which turned out to be cutaneous mycobacterial infection.

Antitubercular Agents↗
PubMed2004

Myocarditis as a prognostic indicator in systemic lupus erythematosus.

Lupus myocarditis is a life threatening complication of systemic lupus erythematosus (SLE). A case of left ventricular failure secondary to myocarditis occurring in a patient with SLE is reported. Despite resolution of the cardiac failure with pulsed cyclophosphamide and steroids, she eventually died of non-cardiac complications 18 months later. The literature is also reviewed.

Adult↗
PubMed1996

Autoantibodies in systemic lupus erythematosus.

Lupus anti-DNA may have higher homology with germline than those from normal subjects. However, in NZB/NZW mice, bacterial DNA is more antigenic than mammal DNA, which could indicate an antigen-driven origin. High-affinity antibodies to double-stranded DNA cross-react with small nuclear ribonucleoprotein and ribosomal P proteins. These cross-reactive anti-DNA may penetrate live cells. Antibodies to ribosomal P proteins are associated with neuropsychiatric, renal, and hepatic lupus involvement. IgG antibodies to (H2A-H2B)-DNA complexes antedate procainamide-induced lupus. Autoantibodies to some La/Ro peptides in a mother indicates that her children may develop neonatal lupus and determine who will have congenital heart block. Perinuclear antineutrophil cytoplasmic antibodies are present in 25% of systemic lupus erythematosus patients without correlation with anti-DNA or disease activity. Different antiphospholipid antibodies require different protein cofactors for reactivity. Those to anionic phospholipids require beta 2-glycoprotein I, whereas anti-phosphatidylethanolamine antibodies require kininogen or its binding protein. Antibodies to phospholipid-free beta 2-glycoprotein I are associated more strongly with clinical antiphospholipid syndrome than are antiphospholipid antibodies.

Animals↗
PubMed1998

[Extracorporeal photopheresis in therapy-refractory disseminated discoid lupus erythematosus].

Lupus erythematosus (LE) is a disease with a wide spectrum of cutaneous and systemic manifestations. Discoid LE (DLE) is the most common form of cutaneous LE; the disseminated form of DLE is rare. We report an encouraging response to treatment with extracorporeal photopheresis (ECP) in a single patient with disseminated DLE who did not respond to conventional therapy. To the best of our knowledge this is the first successful use of ECP in the management of such a patient. Extracorporeal photopheresis is a therapeutic modality that has been under investigation for more than 12 years. Although originally developed for the treatment of cutaneous T-cell lymphoma, ECP has recently been used for the management of autoimmune diseases including systemic scleroderma, pemphigus vulgaris and SLE, as well as prevent organ rejection in patients with cardiac or kidney transplants and graft versus host disease after bone marrow transplantation.

Dose-Response Relationship, Drug↗
PubMed2005

Photosensitivity in lupus erythematosus.

Lupus erythematosus (LE) is an autoimmune disease which can be triggered by environmental factors such as solar irradiation. It has long been observed that especially ultraviolet (UV) exposure can induce and exacerbate skin lesions in patients with this disease. However, despite the frequency of photosensitivity in LE, the mechanisms by which UV irradiation activates autoimmune responses is only now becoming increasingly unfolded by advanced molecular and cellular biological investigations. Phototesting, according to a standardized protocol with UVA and UVB irradiation has proven to be a valid model to study photosensitivity in various subtypes of LE and to evaluate the underlying pathomechanisms of this disease. Detailed analysis of the molecular events that govern lesion formation in experimentally photoprovoced LE showed increased accumulation of apoptotic keratinocytes and impaired expression of the inducible nitric oxide synthase (iNOS). In the near future, gene expression profiling and proteomics will further increase our knowledge on the complexity of the "UV response" in LE. This review summarizes the current understanding of the clinical and molecular mechanisms that initiate photosensitivity in this disease.

Humans↗
PubMed1997

Guidelines for looking at the antiphospholipid antibodies in systemic lupus erythematosus.

Lupus anticoagulant (LA), anticardiolipin (aCL), and/or antiphospholipid (aPL) antibodies are the hallmarks of the antiphospholipid syndrome, characterized by widespread thrombosis. The syndrome has been described as primary or secondary when aCL/aPL are the only classes of detectable autoantibodies or occur in the context of systemic lupus erythematosus (SLE) or SLE-like disease. However, since LA/aCL/aPL have been extensively looked for, it has become evident that they may also be detected in the absence of any clinical correlation with thrombosis. In particular, among SLE patients, these antibodies mean a high risk of thrombosis only in a small subset, sharing clinical features with primary antiphospholipid syndrome. As laboratory examination is still unable to distinguish between high-risk and non-high-risk antiphospholipid antibodies, it is crucial to have some reasonable criteria able to guide the day-to-day clinical practice. We attempt to trace the following guidelines: (1) distinguish between transient and persistent LA/aCL/aPL results; (2) do not forget the LA phenomenon in the era of aCL/aPL; (3) maintain a strict communication with the laboratory; (4) exclude other causes of primary coagulation abnormalities; (5) look at the time of appearance of LA/aCL/aPL with respect to thrombosis; (6) analyze any possible laboratory clue putatively useful to distinguish between 'rouge' and 'non-rouge' LA/aCL/aPL; (7) look for signs of widespread noninflammatory vasculopathy; (8) do not engage a war to the knife against LA/aCL/aPL by immunosuppressive therapies.

Antibodies, Antiphospholipid↗
PubMed1996

Antiphospholipid antibodies (aPL) increase the potential monocyte procoagulant activity in patients with systemic lupus erythematosus.

Lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) are frequently detected in sera from patients affected by systemic lupus erythematosus (SLE). However, the role of antiphospholipid antibodies (aPL) in thrombus formation has not been defined as yet. Twenty-two patients affected by SLE, all fulfilling the 1982 ARA revised criteria, and twenty healthy subjects were investigated for the presence of LA, aCL and other aPLs. Monocyte procoagulant activity-PCA (Tissue Factor production) was evaluated by one stage plasma recalcification time. In all patients the plasma levels of F1 + 2 and of plasminogen activator inhibitor (PAI) were also determined. Monocyte PCA was significantly higher in SLE patients with LA and/or aCL in comparison to SLE patients without LA and/or aCL (p < 0.01) and to controls (p < 0.05). However, no connection was observed between PCA expression by mononuclear cells and LA or aCL levels. No differences in F1 + 2 and PAI plasma levels were found between SLE patients with or without aPL and controls. In our SLE patients LA and/or aCL positivity appears strictly related to an increased monocyte activation that could play an important role in the occurrence of thrombotic events.

Adult↗
PubMed1995

Pulmonary thromboembolic hypertension in systemic lupus erythematosus with lupus anticoagulant: histopathological analysis of localization and distribution of thromboemboli in pulmonary vasculature.

We report a systemic lupus erythematosus patient with lupus anticoagulant accompanied by pulmonary thromboembolic hypertension possibly due to large vegetation of the tricuspid valve of the heart. Histopathological analysis of localization and distribution of thromboemboli in pulmonary vasculature revealed that the organized thromboembolic occlusion of multiple blood vessels (99 out of 222 arteries), might be responsible for the pulmonary hypertension both in quality and quantity. The contribution of lupus anticoagulant to the pathogenesis of Libman-Sacks endocarditis in systemic lupus erythematosus, and its possible relationship to pulmonary thromboembolic hypertension are discussed.

Adult↗
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↗
PubMed2001

De novo fibrillary glomerulopathy in the renal allograft of a patient with systemic lupus erythematosus.

Lupus glomerulonephritis is a complication of systemic lupus erythematosus, with 10% of the patients developing end-stage renal disease. It is accepted that lupus patients are good candidates for kidney transplantation and that the disease activity is subdued after transplantation due to rigorous immunosuppression, with a low rate of graft loss due to recurrent glomerulonephritis. While recurrent fibrillary glomerulopathy has been reported in renal allografts, de novo disease has not. We report a patient with systemic lupus who underwent a renal transplantation and subsequently lost her allograft due to de novo fibrillary glomerulopathy. Four years after her first kidney transplant, the patient presented with acute deterioration of her renal function. A renal biopsy was performed, and it revealed a focal mesangioproliferative pattern with positive amorphous mesangial immunofluorescence staining for IgG and C3. Congo red staining was negative. Electron microscopy demonstrated the presence of randomly oriented nonamyloid fibrils in the mesangiun. The diagnosis of de novo fibrillary glomerulopathy was made. The patient lost her allograft and received a second cadaveric renal transplant 1 year later. She has had a stable renal function since then.

Adult↗
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↗
PubMed1982

Carpal tunnel syndrome in cutaneous connective tissue disease: generalized morphea, lichen sclerosus, fasciitis, discoid lupus erythematosus, and lupus panniculitis.

Carpal tunnel syndrome developed concurrently with cutaneous connective tissue disease in five patients. The skin lesions varied from morphea, lichen sclerosus, fasciitis, and discoid lupus erythematosus to lupus panniculitis. Variable and transitory serologic and direct immunofluorescent findings were noted. In two cases, surgical specimens from carpal tunnel operations had lymphoid nodules. Treatment of the cutaneous connective tissue syndrome (antimalarials, four cases; corticosteroids, two cases) brought healing of the carpal tunnel syndrome as well as improvement of the skin lesions.

Adult↗
PubMed1994

Conversion of antinuclear antibody specificity as a marker of deterioration of cutaneous lupus erythematosus into lupus nephritis.

A 34-year-old male systemic lupus erythematosus patient (SLE) with cutaneous vasculitis developed renal failure after switching anti-nuclear antibody (ANA) specificity. He developed cutaneous lupus erythematosus with homogeneous and speckled type ANA and a high titer of anti-DNA antibody without renal involvement at 21 years of age. After developing lupus nephritis at the age of 27, the original ANA disappeared gradually. Two years later, a discrete speckled type ANA titer elevated abruptly to as high as 1:640 with low complementemia and without DNA antibody. Within five years, he suffered renal failure. This case of SLE suggests a direct correlation with ANA pattern and organ involvement.

Adult↗