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PubMed1986

Susceptibility genetics of systemic lupus erythematosus.

The etiology of systemic lupus erythematosus (SLE) is determined in part by genetic factors which influence susceptibility to the disease. These factors presumably have a major role in determining the clinical and laboratory manifestations of SLE. Certain newer observations which may pertain to an understanding of the genetic basis of SLE will be critically reviewed in this chapter. These observations are based on advances in the analysis of human SLE and the increased knowledge provided by various murine models of human autoimmune processes. However, the specific genes involved and the mechanisms by which they exert their effect are at present still unknown. Special attention will be given newer insights into the role of genes of the major histocompatibility complex (MHC) and their relationship to the genes encoding the T cell antigen receptor. The role of classic immunoglobulin genes as well as more complex mechanisms involving preferential maternal or paternal genetic effects are also discussed. The contribution of genes encoding complement and complement receptors toward the expression of the disease state are discussed in brief.

Animals↗

PubMed1989

Drug-induced mononucleosis-like hepatic injury in a patient with systemic lupus erythematosus.

A case of systemic lupus erythematosus (SLE) with mononucleosis-like hepatic injury was described. An emergent cesarean section was performed in a 25 yr-old house wife at 34 weeks gestation, followed by administration of several antibiotics. After the surgery she complained of high fever, hepatomegaly and dull right hypochondralgia, and mild liver dysfunction was also found. The liver biopsy showed prominent mononuclear cell infiltration in the sinusoids with minimum hepatocellular necrosis and mild triaditis, resembling hepatic lesion in infectious mononucleosis (mononucleosis-like injury). There were no clinical and serological features suggestive of infectious mononucleosis. This hepatic lesion was thought to be a manifestation of allergic reaction to drugs to which the lymphocyte stimulation test was found to be positive. Immunological abnormalities inherent in SLE might be related to occurrence of such allergic drug reaction.

Adult↗

PubMed2007

Autoimmune hepatitis with raised alpha-fetoprotein level as the presenting symptoms of systemic lupus erythematosus: a case report.

Systemic lupus erythematosus (SLE) and autoimmune hepatitis are distinct clinical disorders, which rarely occur, in the same patient. We describe a 59-year-old woman with coexistence of both conditions. Photosensitivity, arthritis, positive ANA, and extreme elevation of anti-dsDNA concluded the diagnosis of SLE. Hyperbilirubinemia, high serum value of liver function, and elevation of alpha-fetoprotein were also prominent. By a review of pertinent literature, clinical investigation, calculation of autoimmune hepatitis score, and pathology of liver biopsy specimen, we were in favor of autoimmune hepatitis. Awareness of this rare presentation may be beneficial to clinicians in identifying and treating patients with both SLE and autoimmune hepatitis.

Diagnosis, Differential↗

PubMed2004

Association analyses of DNA methyltransferase-1 (DNMT1) polymorphisms with systemic lupus erythematosus.

The etiology of systemic lupus erythematosus (SLE) is very complex, and genetic factors appear to play a significant role in susceptibility to SLE, in determining the disease expression, and in the autoantibody profiles of individuals with SLE. DNA methyltransferase-1 (DNMT1) is a major enzyme that determines genomic methylation patterns and both maintains methyltransferase and exhibits de novo DNA methylation activity in vivo. In order to clarify the association of DNMT1 polymorphisms with SLE, we scrutinized the genetic polymorphisms in exons and their boundaries of DNMT1, including the -1,500 bp promoter region, by direct sequencing in 24 Korean individuals. Twenty-nine sequence variants were identified: two in 5'UTR, six in exons, and 21 in introns. Eight of these polymorphisms were selected for a larger-scale genotyping (n=680) by considering their allele frequencies, haplotype-tagging status, and linkage disequilibrium coefficiencies (LDs) among polymorphisms. The associations between DNMT1 polymorphisms and the clinical profiles of SLE were analyzed. No significant associations with the risk of SLE were detected. However, further analyses of association with autoantibody production among SLE patients revealed that one nonsynonymous SNP, +14463G>C (V120L) in exon 4, was weakly associated with an increased risk of anti-La antibody production (P=0.04), although the significance could not be retained after correction of multiple tests. The DNMT1 variations and haplotypes clarified in this study would provide valuable information for future genetic studies of other autoimmune diseases.

Chromosome Mapping↗

PubMed2000

Circulating endothelial cells and vascular injury in systemic lupus erythematosus.

In flares of systemic lupus erythematosus (SLE), endothelial cells activated by immune stimuli are potential participants in the inflammatory processes, which contribute to injury. Elevated levels of circulating endothelial cells (CEC) may be a proxy for vascular injury, as demonstrated in patients with sickle cell anemia during acute crises. In active SLE, CEC levels in peripheral blood are elevated (vs healthy controls and correlate with plasma C3a). CEC may reflect widespread unrecognized, ongoing injury despite the absence of clinical stigmata of vasculitis in patients with SLE.

Biomarkers↗

PubMed1975

Clinical features of chorea associated with systemic lupus erythematosus.

Neurologic complications of systemic lupus erythematosus (SLE) are common, but chorea is rare. Three cases of chorea associated with SLE are presented as well as a review of 28 cases from the world literature. Chorea may be the first and at times the only sign prior to the establishment of diagnosis of SLE. Under such conditions the establishment of the correct diagnosis is difficult, and the chorea may be attributed to a more common etiology, Also the SLE-related chorea may recur in the same subject during the course of the disease. Finally, the chorea associated with SLE can be brought under control by use of haloperidol (HALDAL).

Adult↗

PubMed1981

Studies of the pathogenesis of interstitial cystitis, obstructive uropathy, and intestinal malabsorption in a patient with systemic lupus erythematosus.

A patient with systemic lupus erythematosus (SLE) is described who displayed the unusual extraglomerular syndromes of interstitial cystitis with obstructive uropathy and severe secretory-type diarrhea with intestinal malabsorption. Pathologic investigations into the nature of these events revealed immunofluorescent deposits in blood vessel walls of the small intestine and urinary bladder. The patient's malabsorption state and cystitis with urinary obstruction regressed with therapy of the SLE. We are postulating that immune complexes from the circulation may deposit in blood vessel walls, and may be responsible for tissue injury in these sites and the clinical manifestations of this patient.

Adult↗

PubMed1992

Laryngeal involvement in systemic lupus erythematosus.

Laryngeal involvement in systemic lupus erythematosus (SLE) can range from mild ulcerations, vocal cord paralysis, and edema to necrotizing vasculitis with airway obstruction. In this report, four cases showing the range of severity of this disease manifestation are presented, accompanied by a comprehensive review of the literature. The clinical course of 97 patients with laryngeal involvement with SLE are reviewed, of whom 28% had laryngeal edema and 11% had vocal cord paralysis. In the majority of cases, symptoms such as hoarseness, dyspnea, and vocal cord paralysis resolved with corticosteroid therapy. Other, less common causes of this entity included subglottic stenosis, rheumatoid nodules, inflammatory mass lesions, necrotizing vasculitis, and epiglottitis. The clinical presentation of laryngeal involvement in patients with SLE follows a highly variable course, ranging from an asymptomatic state to severe, life-threatening upper airway compromise. With its unpredictable course and multiple causations, this complication remains a diagnostic and therapeutic challenge to physicians involved in the care of patients with SLE.

Adult↗

PubMed1994

Hypoprothrombinemia in childhood systemic lupus erythematosus.

Three children with systemic lupus erythematosus who developed hemorrhagic tendencies as a consequence of a clotting factor II (prothrombin) deficiency are described. All three responded rapidly to treatment with corticosteroids. A literature review added 25 case reports, with the following findings. First, factor II deficiency occurs in the presence of the lupus anticoagulant, although the interrelationship between the two is not understood. Second, the deficiency is presumed to be secondary to rapid clearing of the antigen/antibody factor II complex in the liver. Finally, most cases respond to corticosteroid therapy with or without the coadministration of vitamin K or fresh frozen plasma. In corticosteroid-dependent patients, the addition of antimetabolites such as azathioprine has enabled reduction in steroid doses.

Adolescent↗

PubMed1990

HLA-DP+ T cells and deficient interleukin-2 production in patients with systemic lupus erythematosus.

In patients with systemic lupus erythematosus (SLE), frequency of the T cells positive for HLA-DP, one of the major histocompatibility complex (MHC) class II molecules, was markedly increased in peripheral blood lymphocytes (PBL), in association with an increase in the amount of specific cytoplasmic transcript of the HLA-DP gene segment. Cell cycle analysis showed that HLA-DP is an early activation marker of T cells and that the high ratios of HLA-DP+ T cells from SLE patients are associated with high frequency of T cells at early activation phases, mainly of G1A. Initial high ratios of HLA-DP+ T cells decreased to a great extent during 4 days of in vitro culture, in the absence of mitogens. This event was associated with decreases in the amount of HLA-DP transcript and the disappearance of activated T cells. Studies on the interleukin 2 (IL-2) production of T cells from patients with SLE demonstrated that while the PBL rich in HLA-DP+ T cells show a markedly low production of IL-2, preculture of these PBL restores the ability to produce IL-2. Thus, it appears that the T cells in patients with SLE are essentially intact with regard to the capacity to produce IL-2 and that T cell activation events continuously occurring in SLE patients are related to a deficiency in IL-2 production. The possible underlying mechanisms are discussed.

Adolescent↗

PubMed1992

Genetic and immunological mechanisms in the pathogenesis of systemic lupus erythematosus.

Recent research in systemic lupus erythematosus and animal models of lupus has provided new insight into the pathogenesis of this complex autoimmune disease. Progress has been made towards understanding the genetic contributions to disease susceptibility and induction, as well as towards elucidation of the lymphocyte abnormalities involved in pathogenic autoantibody production.

Animals↗

PubMedDate not supplied

Olanzapine-induced agranulocytosis in systemic lupus erythematosus: a case report.

Systemic lupus erythematosus (SLE) patients may have psychiatric manifestations during the illness course. Psychotropic agents are indicated in treating these symptoms. Second-generation antipsychotics, such as risperidone, olanzapine and quetiapine, have been thought to be safer than clozapine with regard to the side effect of neutropenia or agranulocytosis. We report a case of SLE who developed agranulocytosis during the treatment with olanzapine for the SLE-related psychiatric symptoms.

Adult↗

PubMed2005

Respiratory changes in a murine model of spontaneous systemic lupus erythematosus.

The pathophysiology of systemic lupus erythematosus (SLE) has been very well described in many organs. However, the relation between extracellular matrix changes and lung dynamic mechanical behaviour deserves elucidation. To that end, pulmonary mechanics, lung morphometry and the amount of collagen and elastic fibres in the alveolar septa were analysed in mice with SLE [NZB/W (New Zealand Black/White) F1] and non-diseased NZW mice (control). Static (E(st)) and dynamic (E(dyn)) elastances, difference between dynamic and static elastances (DeltaE), airway resistance (R(aw)) and viscoelastic/inhomogeneous pressure (DeltaP(2)) were determined by the end-inflation occlusion method. Lungs were removed and prepared for histology. E(st), E(dyn), DeltaE and DeltaP(2) were higher in SLE than in control group, while R(aw) was similar in both groups. SLE group showed alveolar collapse and increased amount of elastic and collagen fibres. In conclusion, SLE mice showed an increase in elastic and viscoelastic/inhomogeneous pressures that was accompanied by deposition of collagen and elastic fibres in the alveolar septa.

Animals↗

PubMed1976

Plasmapheresis in the management of acute systemic lupus erythematosus?

Eight patients with systemic lupus erythematosus (S.L.E.) have been treated with plasmapheresis. In four patients in whom immunochemical studies indicated high levels of circulating immune complexes, the removal of 5-8 litres of plasma weekly produced a striking clinical and immunochemical improvement. The four other patients, with only minor complement disturbances and no direct evidence of circulating immune complexes, could not be shown to benefit from plasmapheresis and one patient in this group died of cerebral lupus despite intensive treatment with cytotoxic drugs. It is concluded that plasmapheresis may be of value as an adjuvant to the treatment of acute S.L.E.

Acute Disease↗

PubMed1995

Prevention of relapses in systemic lupus erythematosus.

Many relapses of systemic lupus erythematosus (SLE) are preceded by a rise in antibodies against double-stranded DNA (anti-dsDNA). We investigated whether these relapses can be prevented by giving prednisone when a rise in anti-dsDNA occurs. 156 patients with SLE were studied. Anti-dsDNA was measured by Farr assay monthly. When a rise in anti-dsDNA was found, patients were randomly assigned either conventional treatment or 30 mg prednisone added to the current daily dose and tapering off to baseline over 18 weeks. A rise in anti-dsDNA was detected in 46 patients (24 assigned conventional treatment and 22 prednisolone). The relapse rate was higher in the conventional group than in the prednisolone group (20 vs 2, p < 0.001). Although rises in anti-dsDNA in the prednisone group were treated with additional prednisone, the cumulative oral doses of prednisone in the two groups did not differ significantly (p = 0.025). 7 major relapses requiring additional cytotoxic immunosuppressive treatment occurred in the conventional group versus 2 in the prednisone group. Treatment with prednisone as soon as a significant rise in anti-dsDNA occurs prevents relapse in most cases, without increasing the cumulative dose of prednisdone given.

Adult↗

PubMed1984

Hyporeninemic hypoaldosteronism in two patients with systemic lupus erythematosus.

Two patients with systemic lupus erythematosus (SLE) and hyperkalemia were studied. The hyperkalemia was disproportionate to the degree of renal excretory impairment. The usual causes of hyperkalemia were excluded. Basal levels of plasma renin activity (PRA) and plasma aldosterone (PAC) were low. The responses of PRA and plasma aldosterone to the combined stimulus of ambulation and furosemide were blunted. Plasma levels of 18-hydroxycorticosterone (18-OH-B) were normal. The hyperkalemia in both patients could be attributed to hyporeninemic hypoaldosteronism (HH). In one patient, the hyperkalemia was corrected by the administration of fludrocortisone. In the second patient, treatment of lupus nephritis with azathioprine, prednisone, and plasmapheresis normalized both the serum creatinine and the serum potassium.

18-Hydroxycorticosterone↗

PubMed2001

Treatment of systemic lupus erythematosus.

The treatment of systemic lupus erythematosus (SLE) is mainly based on a number of "traditional" drugs such as corticosteroids, antimalarials, azathioprine and cyclophosphamide. However, this scenario is rapidly changing due to the introduction of new compounds. Some of these new agents have been successfully used in other diseases, while others are being specifically designed to interfere with the immune abnormalities seen in SLE. As our knowledge on the mechanisms of immune response increases, new drugs that can interfere with T and B cell interaction and activation, production of anti-dsDNA autoantibodies, immune-complexes deposition and cytokine activation have been developed and some of these are now under investigation in SLE. Although initial data regarding their safety and efficacy are encouraging, caution must be taken before these drugs are considered as the treatment of choice for specific SLE manifestations. Specifically, controlled clinical trials with sufficient number of patients are necessary. If the promising results already available are confirmed, the use of these drugs might represent the keystone in the future management of SLE and other autoimmune diseases.

Adjuvants, Immunologic↗

PubMed2006

Onset of systemic lupus erythematosus during pregnancy.

When systemic lupus erythematosus (SLE) is first suspected during pregnancy, though rare, the diagnostic criteria are not different from those for nonpregnant women. The pregnancy outcome is good if treatment with adequate immunosuppressive agents starts as soon as the diagnosis is made. There are 4 cases in this report who had SLE onset during pregnancy. Although 2 of them suffered from preeclampsia, all 4 pregnancies resulted in favorable outcomes after the lupus was controlled by medical treatment.

Adult↗