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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 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

The choice of an optimal contraceptive method (OC) therapy is a significant problem in female SLE patients. In view of the influence of sex hormones on the evolution of SLE, oral contraceptive (OC) therapy has to be efficient, reversible and safe, without aggravating disease activity and causing metabolic and vascular side effects. Ethinyl estradiol-containing preparations, even at 30 micrograms/day, have been shown to trigger a crisis or unmask SLE, and they exert adverse metabolic and vascular effects. Therefore, combination estrogen-progestogen compounds must be avoided in women with SLE. Pure progestogen OC preparations do not stimulate SLE activity, but norsteroids have harmful metabolic effects and microprogestogens are not sufficiently reliable. In light of the decreased level of plasma androgens in female SLE patients, an attempt to modulate the hormonal milieu by lowering the estrogen to androgen ratio, while ensuring contraception was attempted using cyproterone acetate. This agent markedly lowered plasma estrogens and was effective and well tolerated, but its long-term effect on bone mineralization remains to be evaluated. Chlormadinone acetate, a 17-OH progesterone derivative, was proven effective and devoid of any metabolic or vascular side effects, and should be recommended as the safest routine OC therapy in women with SLE.
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PMID:[Hormonal contraception and lupus]. 169 73

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

In December, 1986, a 29 year old woman developed nephrosis due to systemic lupus erythematosus after taking oral contraceptives (OC) for 6.5 years. Hospitalized for 3 months, she received steroid treatment, which lowered albumin in urine. At the time of hospitalization, the following symptoms were noted. Edema on all her limbs, 4.5 g/dl of urine albumin per day, white blood cell count of 2600/mm, 640 time positive anti-nuclear antibodies, pseudo-positive response to syphilis via bentonite flocculation on particle (BFP). OC she had taken since 1980 were 0.5 mg of norgestrel day and 0/05 mg of ethinyl estradiol day. She had been routinely checked on her kidney function biannually and everything had been normal till then. For 2 months starting in December, 1987, at the patient's request, progesterone along (dydrogesterone 10 mg/day) was administered for contraception. No urine albumin was detected. It appears that autoimmune-type thyroid gland abnormality preceded systemic lupus erythematosus (SLE) which was triggered by the oral contraceptive use. Estrogen metabolism of SLE patients is characterized by estrogen active 16 alpha hydroxyestrone.
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PMID:[A case of systemic lupus erythematosus after taking oral contraceptives]. 276 93

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

Combined oral contraceptives (COCs) affect the skin 3 different ways. They decrease the amount of androgenic hormones produced in the ovaries and adrenal gland. They also limit the quantity of biologically active circulating testosterone. Finally, estrogen markedly decreases oil production in the sebaceous glands. Physicians should prescribe to women with acne a COC that is low in progestogen and high in estrogen. A biphasic pill with no more than 500 mcg norethisterone/day meets these requirements. If a woman is taking systemic antibiotics to treat acne, however, the physician should prescribe a biphasic pill containing 50 mcg ethinyl estradiol. Even though many believe that using COCs causes hair loss, there is little evidence to support it. Nevertheless, if a woman has indeed experienced hair loss, she should take a COC with a high estrogen to progestogen ratio. As in some pregnant women, cholasma may occur in women taking COCs when not protected from sunlight. Physicians need to prescribe the lowest possible dose of hormones in these women and counsel them to shield their face from sunlight. To err on the side of safety, women who have had a malignant melanoma should not use a hormonal contraceptive. In addition, women who have experienced many bouts of skin candidiasis should use an alternative contraceptive. Other skin disorders that they have been found to be more prevalent in women taking COCs include erythema nodosum, accelerated systemic lupus erythematosus, porphyria cutanea tarda, herpes gestationis, spider naevus, and telangiectasia. There also exists an association between dermatitis and barrier methods and spermicides. Some articles have suggested that copper containing IUDs have also cause a variety of skin disorders.
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PMID:Effect of contraceptives on the skin. 324 Jan 55

The susceptibility of women to autoimmune diseases is well-documented, of which systemic lupus erythematosus (SLE) is especially important. The use of oral contraceptives often activate SLE from a quiescent condition. The inductive effect of estrogen has been shown in animal studies indicating that female hormones can trigger autoimmune reaction. The effect of ethinyl estradiol, an estrogen (E), and d-norgestrel, a progesterone (P), on the mitogenic response of peripheral lymphocytes, and particularly on phytohemagglutinin (PHA)- and concanavalin-A (Con-A)-induced blastic transformation of lymphocytes (LBT) was studied in vitro. 25 patients with SLE and 27 healthy controls participated in the study. SLE was inactive in 16 patients, 7 took corticosteroids, and 3 also received 50 mg/day Imuran. 13 patients and 10 controls took contraceptives (Bisecurin, Infecundin, Ovidon, Rigevidon). The LBT value fell significantly in patients with active SLE, in contraceptive users, and the value was significantly lower in inactive patients than in those not using contraceptives. E and P separately or together significantly reduced LBT values. Contraceptives containing P only can be prescribed for women suffering from SLE, as its role in inducing the disease compared to E is negligible.
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PMID:[Effect of female sex hormones on blastic transformation of lymphocytes in systemic lupus erythematosus and in healthy women]. 332


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