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Results for “LUPUS ERYTHEMATOSUS, SYSTEMIC”

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PubMed1995

Tc-99m DTPA aerosol lung clearance test in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) can affect every organ. Involvement of the lung in systemic lupus erythematosus may be a significant cause of morbidity and mortality. To evaluate alveolar epithelial damage in SLE, we studied lung epithelial permeability by measuring the clearance of inhaled Tc-99m DTPA aerosol. Twenty-three SLE patients without clinical pulmonary manifestations were studied. Of the 23 patients, 16 had normal clearance rates of Tc-99m DTPA (T1/2 > 60mins) and normal chest X-ray findings. A mild increase in the clearance rate was found in 5 cases (T1/2 between 40-60 min) and a significant increase in clearance rate in the remaining 2 (T1/2 < 40mins). Totally, 30% (7/23) of SLE patients have abnormal lung permeability. Of the 7 patients with abnormal clearance of Tc-99m DTPA, 3 had abnormal findings in chest X-rays and four had normal chest X-rays. Our study suggests that the clearance of Tc-99m DTPA aerosol may be a useful complementary study to assess pulmonary involvement in SLE.

Adolescent↗

PubMed2000

Favourable interactions of cytostatic and steroid drugs in treatment of systemic lupus erythematosus.

Systemic lupus erythematosus (referred to below as SLE) is a disorder associated with formation of immune complexes in the circulatory system and their deposition in the internal organs, as well as in the skin. The disease can appear at any age, but the vast majority of cases are women between 15 and 40 years of age. The paper presents the case of a thirty-year-old woman with systemic lupus erythematosus. She was admitted to hospital because of erythematous and haemorrhagic lesions in the skin of her face, hands and feet and febrile states. SLE was diagnosed in the patient on the basis of criteria established by the American Rheumatological Association. The following abnormalities were observed in the patient: skin lesions of erythematous type on the face, hypersensitivity to UV light, erosions of the mucous membranes of the oral cavity, changes in the kidneys confirmed by biopsy, haematological symptoms, immune disorders. Additional criteria to establish the diagnosis included: febrile states. Raynaud's sign, hair loss, presence of immunoglobulin complexes in the skin, decreased complement level. The paper discusses modern therapy of visceral lupus erythematosus, based on corticosteroids and immunosuppressants. The interactions of these drugs were observed in the patient. The woman was treated with combined corticosteroid and cytostatic therapy, which led to the remission of the pathologic process confirmed by the clinical condition of the patient and laboratory tests.

Adrenal Cortex Hormones↗

PubMed2005

The role of host CD4 T cells in the pathogenesis of the chronic graft-versus-host model of systemic lupus erythematosus.

Systemic lupus erythematosus is characterized by production of autoantibodies and glomerulonephritis. The murine chronic graft-vs-host (cGVH) model of systemic lupus erythematosus is induced by allorecognition of foreign MHC class II determinants. Previous studies have shown that cGVH could not be induced in CD4 knockout (CD4KO) mice. We have further explored the role of host CD4 T cells in this model. Our studies now show that B cells in CD4KO mice have intrinsic defects that prevent them from responding to allohelp. In addition, B cells in CD4KO mice showed phenotypic differences compared with congeneic C57BL/6 B cells, indicating some degree of in vivo activation and increased numbers of cells bearing a marginal zone B cell phenotype. The transfer of syngeneic CD4 T cells at the time of initiation of cGVH did not correct these B cell abnormalities; however, if CD4 T cells were transferred during the development and maturation of B cells, then the B cells from CD4KO mice acquire the ability to respond in cGVH. These studies clearly indicate that B cells need to coexist with CD4 T cells early in their development to develop full susceptibility to alloactivation signals.

Adoptive Transfer↗

PubMed2001

Genetic epidemiology: systemic lupus erythematosus.

Systemic lupus erythematosus is the prototype multisystem autoimmune disease. A strong genetic component of susceptibility to the disease is well established. Studies of murine models of systemic lupus erythematosus have shown complex genetic interactions that influence both susceptibility and phenotypic expression. These models strongly suggest that several defects in similar pathways, e.g. clearance of immune complexes and/or apoptotic cell debris, can all result in disease expression. Studies in humans have found linkage to several overlapping regions on chromosome 1q, although the precise susceptibility gene or genes in these regions have yet to be identified. Recent studies of candidate genes, including Fcgamma receptors, IL-6, and tumour necrosis factor-alpha, suggest that in human disease, genetic factors do play a role in disease susceptibility and clinical phenotype. The precise gene or genes involved and the strength of their influence do, however, appear to differ considerably in different populations.

Animals↗

PubMed2004

Global cerebral edema and subarachnoid hemorrhage in a patient with systemic lupus erythematosus.

Systemic lupus erythematosus is a multifactorial autoimmune disease of complex etiology, which may be associated with cognitive dysfunction, seizures, and headache. The authors present an unusual presentation of systemic lupus erythematosus complicated by global cerebral edema and subarachnoid hemorrhage secondary to rupture of a cerebral aneurysm. The complicated patient management issues are discussed.

Adolescent↗

PubMed1990

[Central nervous symptoms and findings in patients with systemic lupus erythematosus].

Systemic lupus erythematosus is a disease characterized by multiple autoimmune phenomena, and a broad clinical spectrum. Involvement of the central nervous system is common, and in the majority of patients occurs mainly as an organic brain syndrome or as migraineous headache. Cerebral atrophy as judged by CT scan is common. Cerebral infarction occurs in a minority of patients, mainly those with high disease activity and a high titer of anti-phospholipid antibodies. Systemic lupus erythematosus should be considered as a possible diagnosis in patients with certain central nervous system aberrations, especially young females.

Adult↗

PubMed1998

[Treatment of systemic lupus erythematosus systemic].

Patients with systemic lupus erythematosus require adequate information (sun avoidance, fair compliance, smoking discontinuation, adequate contraception and diet, pregnancy planning). Nonsteroidal antiinflammatory drugs and antimalarials are effective in patients presenting with skin and articular involvement. Visceral lesions and hemocytopenias require the use of steroids, alone or in association with immunosuppressive agents. Long-term anticoagulation with an INR of 3-3.5 achieves the prevention of recurrent thrombotic events. Experimental data suggest that more specific treatments and even regimens aimed at eradication of human lupus might soon arise.

Adrenal Cortex Hormones↗

PubMedDate not supplied

Treating systemic lupus erythematosus.

Systemic lupus erythematosus is one of the more common rheumatic complaints, affecting mainly women of child-bearing age. It is a life-threatening condition that affects the immune system and causes damage to the main organs of the body. To coincide with Lupus Awareness Week (10-17 April), this article reviews the symptoms, causes, diagnosis and treatment of systemic lupus erythematosus and examines ways in which research is improving management of the condition.

Female↗

PubMed1969

Systemic lupus erythematosus.

Systemic lupus erythematosus is a polysystemic disease with a high incidence of associated glomerulonephritis. Patients with sle rarely have the destructive arthritis so characteristic of rheumatoid arthritis. An unusual case is presented in which both glomerulonephritis and destructive arthritis occurred simultaneously, justifying the diagnosis of both systemic lupus erythematosus and rheumatoid arthritis.Immunohistochemical studies in lupus glomerulonephritis suggest that the pathogenetic mechanisms involve the deposition of immune complexes containing "nuclear" antigens and antinuclear antibodies in the lesions. The detection of mixed cryoglobulins in the sera of patients with sle suggests that a portion of the circulating immune complexes may precipitate at reduced temperatures and be detected as mixed cryoglobulins. The therapy of lupus glomerulonephritis with combinations of corticosteroids and azathioprine, though still in an investigative state, holds great promise. Similar abnormalities in diseases of minks and mice and in sle suggest similar pathogenetic mechanisms in the three species involved. Since the diseases in the lower animals have been associated with persistent viral infection, the investigation of the role of persistent infection in sle seems warranted.

Adolescent↗

PubMed1994

Epidemiology, genetics, etiology, and environment relationships of systemic lupus erythematosus.

Systemic lupus erythematosus continues to provide a major etiologic challenge. Current investigation is focusing on the possibilities of environmental factors, including infection. How these factors are related to genetic factors, including the major histocompatibility complex and more recently observed defects in apoptosis genes, remains unclear. Ethnic and geographic studies of systemic lupus erythematosus are providing important clues, as are continued clinical observations on the various subsets of disease and the patterns of therapeutic response. Different pathogenic mechanisms are constantly being uncovered and in turn need to be related to the various etiologies.

Contraceptives, Oral↗

PubMed1990

Identification of human immunodeficiency virus hybridizing sequences in the peripheral blood of a patient with systemic lupus erythematosus.

Systemic lupus erythematosus, a multisystemic disorder, is considered a prototype of the autoimmune diseases. Although its cause remains unknown, a viral etiology has been proposed. We report that a rapid and sensitive messenger RNA in situ hybridization technique detected hybridizing sequences to the human immunodeficiency virus type in the peripheral blood cells of a woman with systemic lupus erythematosus in whom the presence of acquired immuno-deficiency syndrome was reasonably excluded.

Adult↗

PubMed2003

Apoptosis in systemic lupus erythematosus.

Systemic lupus erythematosus is a complex, multisystem autoimmune disease characterized by production of high-titer autoantibodies directed against ubiquitously expressed self-antigens. Autoantigens in systemic lupus erythematosus are highly diverse in terms of structure and location in control cells, but become clustered in and on the surface blebs of apoptotic cells. The past several years have provided significant evidence that the apoptotic cell plays a central role in tolerizing B cells and T cells to both tissue-specific and ubiquitously expressed self-antigens, and may drive the autoimmune response in systemic autoimmune disease. The authors review the significant recent advances in this area. Recent studies suggest that predisposing factors to subsequent development of systemic autoimmunity may be the incomplete induction of tolerance to apoptotic antigens, potentially through abnormal apoptotic signaling and effector pathways, decreased apoptotic cell clearance, or abnormal signaling thresholds on responding lymphocytes. In such genetically susceptible hosts, proinflammatory events at the host-environment-immune system interface that lead to the binary change in the response to apoptotic material from tolerance to immunity may be responsible for initiation of autoimmunity and subsequent disease amplification. Such pathways may be amenable to therapeutic and preventive interventions.

Apoptosis↗

PubMed2002

A role for the Cr2 gene in modifying autoantibody production in systemic lupus erythematosus.

Systemic lupus erythematosus is an autoimmune disease characterized by autoantibody production against nuclear Ags. Recent studies suggest that the Cr2 gene, which encodes for complement receptor (CR)1 and CR2, is important in disease susceptibility. Because the precise disease phenotype related to this gene, in isolation or in relation to other genetic loci, is not known, we analyzed C57BL/6 mice with a targeted mutation in Cr2 (C57BL/6.Cr2(-/-)) with or without a concomitant mutation in Fas (C57BL/6.lpr Cr2(-/-)). The Cr2(null) mutation in a C57BL/6.lpr background markedly increases the serum concentrations of IgG1 and IgG2b and the levels of antinuclear and anti-dsDNA Abs as compared with C57BL/6.lpr controls. There is also a trend for higher concentrations of IgG2a and IgG3. In contrast, isolated deficiencies in either these CRs or Fas have a limited effect in the production of anti-dsDNA Abs. Moreover, the Cr2(null) mutation does not affect other disease manifestations. These findings demonstrate that abnormalities in CR1 and CR2 may be linked to the production of autoantibodies by modifying the effect of other systemic lupus erythematosus susceptibility genes. Phenotypic expression of other disease manifestations need additional Cr2-independent genetic factors.

Animals↗

PubMed2002

[Prevalence and clinical features of fibromyalgia in systemic lupus erythematosus, systemic sclerosis and Sjögren's syndrome].

BACKGROUND: We studied the prevalence of fibromyalgia in 3 different groups of patients affected respectively with systemic lupus erythematosus, systemic sclerosis (scleroderma) and primary Sjögren's syndrome. The typical fibromyalgia findings encountered in these diseases were examined. METHODS: We enrolled 250 consecutive outpatients: 100 with systemic lupus erythematosus, 50 with systemic sclerosis, 100 with primary Sjögren's syndrome and 2 control groups (30 healthy subjects and 75 patients with primary fibromyalgia). Fibromyalgia features were evaluated by algometry, VAS for pain, Mc Gill Pain Questionnaire and Fibromyalgia Impact Questionnaire. RESULTS: Fibromyalgia has been found in 1 case (1%) with systemic lupus erythematosus, 1 case with systemic sclerosis (2%), 22 cases (22%) with primary Sjögren's syndrome and in 1 (3.3%) of the healthy controls. The number of tender points was significantly higher (p<0.01) in the patients with Sjögren's syndrome in comparison with the other groups. Fibromyalgic findings were similar in the patients with primary fibromyalgia and Sjögren's syndrome with fibromyalgia, unless for both poor sleep and low algometric thresholds which were more frequently found in primary fibromyalgia (respectively p<0.001 and p=0.05). CONCLUSIONS: Our study suggests that fibromyalgia is relatively frequent in primary Sjögren's syndrome, while in systemic lupus and systemic sclerosis its prevalence is not different from that found in the healthy controls. Typical fibromyalgia findings, except algometric values, were similar between the cases with Sjögren's syndrome plus fibromyalgia and fibromyalgia alone.

Case-Control Studies↗

PubMed2001

The role of Epstein-Barr virus in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a devastating autoimmune disease with no known cure. Lupus patients suffer from a myriad of clinical symptoms which variably include arthritis, pleuritis, pericarditis, vasculitis, and nephritis. The underlying mechanisms behind these clinical findings and the etiologic events preceding and causing disease onset, however, remain largely unknown. For many years, investigators have suspected that Epstein-Barr virus might somehow be involved in the etiology and/or pathogenesis of systemic lupus. Numerous studies have examined this possibility from various angles and have arrived at different conclusions. This work reviews these historical papers in the context of new results and presents a hypothetical role for this virus as an etiological environmental trigger for SLE.

Antibodies, Viral↗

PubMed2002

Fcgamma receptor IIIA polymorphism in Korean patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is characterized by the presence of various autoantibodies and the deposition of immune complex, which is cleared by Fcgamma receptors. Genotype analysis was done to investigate whether the FcgammaRIIIA-176F/V polymorphism is a risk factor for SLE in Koreans. We genotyped 145 Korean SLE patients and 75 control subjects for FcgammaRIIIA-176F/ V. After amplifying a 1.7-kb fragment containing the Fcgamma/RIIIA-176F/V polymorphic site using two FcgammaRIIIA gene-specific primers, we performed a nested polymerase chain reaction (PCR) for allele-specific genotyping at position 559 in FcgammaRIIIA. FcgammaRIIIA genotype or allele distribution was not significantly different between lupus patients and controls, and also between lupus nephritis patients and healthy controls. Neither creatinine clearance, 24 h urine proteinuria, number of American College of Rheumatology (ACR) criteria, nor the Systemic Lupus International Collaborating Clinics (SLICC)/ACR damage index was different according to the genotype. In conclusion, FcgammaRIIIA-176F/V polymorphism is not associated with SLE in Koreans.

Asian People↗

PubMed1989

Acute visual loss in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) often presents as a multisystem disease that can be difficult to diagnose. Although ocular symptoms are infrequent, actual acute visual loss has been reported. A review of four cases of acute visual loss from a lupus clinic revealed that two patients had visual loss as a presenting sign of SLE. One had bilateral occipital lobe infarctions, the other multiple cotton wool spots and an attenuated retinal vascular system. Of the two patients with documented SLE prior to the onset of visual problems, one presented with a coincidental retinal tear and the other with retinal phlebitis.

Adult↗

PubMed2001

Genetics and systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a complex, multifactorial autoimmune disease. Genetic factors are believed to contribute to its pathogenesis. There have been numerous recent advances in the study of murine and human lupus genetics. In well-defined, experimental, transgenic or gene-knockout mouse models, the development of lupus-like disease has implicated specific genes and pathways in the disease pathogenesis. Linkage analyses have mapped multiple susceptibility loci and disease suppressive loci using inbred strains of mice that spontaneously develop lupus-like disease. Elegant genetic dissection has demonstrated that a component phenotype of SLE is displayed by each congenic strain carrying a single susceptibility locus on a resistant genetic background, whereas polycongenic strains exhibit fatal lupus nephritis. These studies suggest that genes in separate pathways can interact to augment or suppress the initiation and progression of systemic autoimmunity. In association studies of human lupus, the contributions of the MHC loci, Fcg receptors, various cytokines, components of the complement cascade, and proteins involved in apoptosis have been explored. Most recently, linkage analyses have been performed and provide many chromosomal regions for further exploration for susceptibility genes. Studies to identify the genes in the susceptibility regions are underway. An understanding of the genes involved in the development of lupus should provide targets for more focused therapy in lupus.

Animals↗