Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0409974 (lupus)
22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral contraceptive therapy has been reported to induce systemic lupus erythematosus (SLE) and rheumatic complaints with normal and abnormal serology. A case report is presented of a 23-year-old female in whom SLE developed 3 weeks after initiation of oral contraceptive (ethinyl estradiol 50 mg and norethisterone acetate 1 mg) usage, but who had experienced a chronic biological false positive (BFP) serological test for syphilis for 8 months prior to this. This implies that she had either a lupus diathesis or subclinical SLE which was unmasked by pill therapy rather than a de novo disease caused by this agent. A study of 134 patients with chronic BFP reactions found that 10 developed SLE, 4 developed discoid LE, and 6 developed a multiple sclerosis-like neuropathy probably due to SLE. BFP reaction is found in 10-20% of SLE patients. Other studies have found oral contraceptive therapy to exacerbate existing SLE and to induce serological markers (LE cells, antinuclear antibody, rheumatoid factor). In cases where SLE was exacerbated, the estrogen involved was either mestranol (0.5-1 mg) or ethinyloestradiol (0.5 mg). However, studies of women without symptoms have failed to show a significant association between oral contraceptive therapy, SLE serological markers, and rheumatic complaints. There is considerable evidence that female sex hormones play a role in determining SLE disease activity. There is a constant male:female ratio of 1:9, and the tendency to disease activity increases premenstrually, in pregnancy, and in the postpartum period.
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PMID:Oral contraceptive therapy and systemic lupus erythematosus. 31 Aug 87

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease affecting a variety of tissues and organs. The diagnosis of SLE can be made only after several related illnesses are considered and ruled out. The etiology of SLE is unclear, but hormonal factors, environmental toxins, infectious viruses, genetic predisposition, and certain medications have all been considered risk factors. Idiopathic SLE is seen predominantly in young women, with a female:male ratio of approximately 10:1. Each patient is unique and may suffer from a variety of signs and symptoms. The disease is highly unpredictable, and most patients experience flare-ups or fluctuations. The epidemiologic characteristics of medication-induced SLE (MI-SLE) are different from those of idiopathic SLE. Musculoskeletal symptoms predominate the clinical presentation of MI-SLE, while renal and central nervous system involvement is rare or absent. Moreover, a greater percentage of caucasian patients with no female predominance is evidenced in MI-SLE. Several medications can produce positive results on an antinuclear antibody test with or without evidence of clinical lupus. Hydralazine and procainamide are the most commonly recognized medications for inducing SLE. The onset of procainamide- and hydralazine-induced SLE occurs after 50 years of age, which is directly related to the age of the population using these medications. Estrogen-containing oral contraceptives and ibuprofen can exacerbate the symptoms of idiopathic SLE. Clinical judgment dictates the importance of careful patient monitoring and selection of therapy.
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PMID:Medication-induced systemic lupus erythematosus. 135 74

Estrogen is known to influence immune responses in healthy subjects in a dichotomous fashion. Thus, in number of previous studies we and others have demonstrated that B cell activities are augmented after exposure to estrogen whereas T cell reactivity is suppressed. Furthermore, it has been shown that this hormone has significant impact on the course of certain human and experimental autoimmune diseases. In this study we report that treatment with physiological doses of estradiol exerts dichotomous effects on different manifestations of the lupus disease in MRL/l mice. On one hand immune complex-mediated glomerulonephritis was significantly accelerated. This outcome was due to polyclonal B cell activation with increased production of antibodies to double-stranded DNA and formation of circulating immune complexes. In contrast, T cell-mediated lesions such as focal sialadenitis, renal vasculitis, and periarticular inflammation were all significantly ameliorated in MRL/l mice exposed to estrogen. Thus, we were able to demonstrate that, within one subject and even within one organ, administration of estrogen leads to differential outcome of SLE morbidity. We propose that the differential effect of estrogen on the manifestations of the autoimmune disease of MRL/l mice is due to its dichotomous effects on B and T cell-mediated immune responses.
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PMID:Estrogen accelerates immune complex glomerulonephritis but ameliorates T cell-mediated vasculitis and sialadenitis in autoimmune MRL lpr/lpr mice. 139 37

To evaluate effects of commonly used progestational estrogenic contraceptive steroids in a hormone-responsive model of lupus, we treated female NZB/W mice before clinical disease (6 wks of age) and after onset of lupus (24 wks of age) with doses of hormones titered to suppress reproduction. We report efficacy of norethindrone (NE) and norgestrel (NG), progestins derived from 19-nor-testosterone, in delaying expression of anti-DNA antibodies. Mice implanted with NG at 24 wks of age had prolonged lifespans. In contrast, the hydroxyprogesterone derivative, medroxyprogesterone acetate (MP), did not affect autoimmune disease. These observations suggest that prolonged administration of 19-nor-testosterone derivatives, in small doses adequate to suppress reproduction, may have ameliorative effects in systemic lupus erythematosus. Mice receiving ethinyl estradiol (EE) plus courses of tetracycline to suppress cystitis had active anti-DNA responses. In 60% of EE-treated mice, however, early deaths resulted from malignant lymphomas and complications of obstructive uropathy. Estrogen toxicity, rather than accelerated lupus, was the major cause of death in NZB/W mice treated with EE.
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PMID:Effects of prolonged administration of the 19-nor-testosterone derivatives norethindrone and norgestrel to female NZB/W mice: comparison with medroxyprogesterone and ethinyl estradiol. 166 44

Reported is the case of a 24-year-old Finnish woman who developed malignant hypertension while taking an oral contraceptive (OC) that contained 30 mcg of ethinyl estradiol. She presented with blurred vision, but reported no other remarkable signs or symptoms during the 5 months in which she had been using OCs. Laboratory tests at admission revealed incomplete systemic lupus erythematosus (SLE) with DNA antibodies and high levels of antiphospholipid antibodies. Her blood pressure was 220-140 mmHg. OC use was discontinued and antihypertensive treatment initiated, with good results. 2 years later, however, the patient developed epileptic seizures and an area of local atrophy in the cerebellum was identified through computerized tomography. In the 4-6th years after initial presentation, the patient experienced 3 miscarriages, all at 7-8 weeks of gestation. 1 year after presentation, the patient satisfied 4 of the criteria for SLE (positive DNA and antiphospholipid antibodies, thrombocytopenia, leukopenia, and proteinuria). At present, the patient's symptoms are being controlled with carbamazepine and metroprolol. The patient's older sister, who had never used OCs, had SLE. It appears that high levels of antiphospholipid antibodies are an additional risk factor for the development of vascular complications in OC users but are not induced by OCs. Similarly, while OCs are not believed to cause SLE, they can exacerbate the disease or unmask a lupus diathesis.
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PMID:Malignant hypertension and antiphospholipid antibodies as presenting features of SLE in a young woman using oral contraceptives. 174 6

Anti-histone antibodies have been reported in a number of human autoimmune diseases, most notably idiopathic and drug-induced lupus erythematosus. In the current study, anti-histone antibody activity was detected using ELISA and electroblotting techniques in sera from autoimmune NZB/W, MRL-lpr, and MRL-(+)/+ mice. Anti-histone activity increased with age, maturing earlier in females, in both NZB/W and MRL-lpr mice. Testosterone treatment decreased anti-histone activity in NZB/W mice and estrogen treatment from 2 weeks of age increased anti-histone activity in MRL-lpr mice, suggesting that gonadal hormones modified the expression of autoantibodies recognizing these protein antigens. Estrogen also increased serum IgG levels in MRL-lpr mice. Sex hormones affected expression of antibodies recognizing soy milk proteins but not ovalbumin in a similar manner. Nitrocellulose Western blots of SDS gels probed with sera from both types of autoimmune mice most often demonstrated reactivity with histone1. Some mice, usually mature females, also recognized histone4, histone3, and histone2.
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PMID:Anti-histone antibodies in the serum of autoimmune MRL and NZB/NZW1 F1 mice. 230 40

Oral contraceptives have been implicated in causing flares of systemic lupus erythematosus in humans, and studies of these agents in the NZB/W mouse model of lupus may help to elucidate mechanisms responsible for disease activation. To define doses which effectively suppress reproductive function in NZB/W mice, we implanted groups of NZB/W females with Silastic capsules containing increasing doses of four compounds: norethindrone (NE) 0.5-5.0 mg, norgestrel (NG) 1.0-7.5 mg, medroxyprogesterone (MP) 0.5-20.0 mg, and ethinyl estradiol (EE) 0.5-5.0 mg. Controls received empty implants. Serum concentrations of LH and FSH, uterine weight, endometrial proliferation, and luteal tissue were assessed after 3 weeks of treatment. Based upon these parameters, we determined that effective doses were 5.0 mg NE, 7.5 mg NG, and 0.5 mg EE given as single implants and 10.0 mg MP given in two 5.0-mg implants. This is the first dosing study of contraceptive steroids in a murine model of lupus. Effective, nontoxic doses of these drugs can now be employed in studies of interactions between gonadal hormones and autoimmunity.
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PMID:Suppression of reproductive function in autoimmune NZB/W mice: effective doses of four contraceptive steroids. 312 40

This is a case report of pulmonary hypertension in a woman with systemic lupus erythematosus who had taken an oral contraceptive. She was 16 yr old when diagnosed with SLE in July 1984, based on many clinical features and high DNA antibodies, RNP antibodies and CPK, and low complement. She improved slowly with prenisolone. She remained in remission for 7 months except for mild flare-ups involving synovitis, pleuritic chest pain and Raynaud's phenomenon. She began taking oral contraceptives 5 months later (30 mcg ethinyl estradiol and 150 mcg levonorgestrel). 7 months later she was readmitted with the same severe clinical and laboratory findings, but in addition exertional dyspnea. Pulmonary hypertension was evident, by x-ray, EKG, echocardiogram and right heart catheterization. Lupus anticoagulant and anticardiolipin antibodies were negative. She was treated with predniosolone, warfarin and nifedipine and remained stable for 6 months. She died of cardiac arrest after emergency surgery for ovarian cyst, complicated by shock and siezures. The author discussed the relationship between pulmonary hypertension and both oral contraception and SLE, since it is rare in either of these situations.
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PMID:Pulmonary hypertension, systemic lupus erythematosus, and the contraceptive pill: another report. 382 39

A case of acute diffuse lupus erythematosus in a 22-year-old woman who had been taking a contraceptive containing ethinyl estradiol and ethynodiol diacetate regularly for 2 years is reported. The course of the illness and the treatment are described in detail. This is regarded as a relatively rare possible side effect of oral contraceptives, although similar cases have been reported by other authors. The question of whether oral contraceptives are actually responsible for the development of such conditions is still the subject of heated debate, bu t it is concluded that in the case described there is an unquestionable correlation, because the subacute lupus erythematosus appeared suddenly, without being preceded by a chronic form of the disease, and especially because it coincided with thromboembolic accidents, which are much more frequently related to the use of oral contraceptives.
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PMID:[Lupic syndrome and estroprogestative drugs]. 412 Oct 19

Influence of oral contraceptive (OC) therapy on SLE activity was evaluated in 33 female patients with lupus nephropathy. Estroprogestative preparations containing either 50 mcg (18 cases) or 30 mcg (11 cases) of ethinyl estradiol were used in 29 courses in 28 patients. Onset or exacerbation of clinical SLE activity occurred within 3 months after beginning hormonal therapy in 13 cases, an overall incidence of lupus flareup of 44%, involving major renal histological lesions in 5 cases. In contrast, of 16 patients receiving pure progestogen contraceptive therapy with either discontinuous normal dosage progestogens (9 cases) or continuous low-dose norsteroids (7 cases), only 1 developed clinical or immunological evidence of lupus exacerbation within 3 months of hormonal therapy. We conclude that OC therapy using estrogens, even at a low dose, is associated with a high risk of SLE exacerbation. Pure progestogens, which have proven effective and devoid of such unfavorable effects, should be preferred in these patients when hormonal contraception is needed. (author's)
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PMID:[Effect of hormonal contraception on the course of lupus nephropathy]. 715 80


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