Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is now known that human exposure to certain chemicals e.g. benzene, halocarbons, ketones, nitrosamines, etc. can result in adverse health effects that are often not easily recognised as manifestations of chemical toxicity. These are inflammatory states, such as hepatitis, nephritis, scleroderma, and lupus, due to production of reactive oxygen species (ROS) through activation of cytochrome P4502E1 by the chemical, or by metabolism of the chemical to reactive intermediates and neoantigens which initiate immunotoxic effects. Intracellular glutathione (GSH), vitamins C, E and A protect against this ROS toxicity and inflammation; fasting and consumption of alcohol exacerbate it. Chronic inflammatory states may subsequently develop, including rheumatoid disease, atherosclerosis, diabetes, infertility and birth defects, multiple system organ failure (MSOF), Alzheimer's disease, and cancer.
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PMID:Chemical-induced inflammation and inflammatory diseases. 897 63

Bloom syndrome (BS) is a rare autosomal recessive genetic disorder characterized by lupus-like erythematous telangiectasias of the face, sun sensitivity, stunted growth infertility and immunodeficiency. In addition, BS patients are highly predisposed to cancers. Although recently the causative gene of BS (BLM) was identified as a DNA helicase homologue, the function of BLM in DNA replication has not been elucidated. In this study, p53 mutation and microsatellite instability in B-cell lymphomas originating from 2 sibling BS patients were investigated. In the originally developed tumor of both patients, no p53 mutation was detected. In one patient, however, after treatment by ionizing radiation the B-cell lymphoma recurred, showing a 9-bp deletion in exon 7. In lymphoma cells and an EB-virus-transformed cell line from BS lymphocytes of this patient, microsatellite instability was also detected from the reduced length of microsatellite DNA markers, although in the other patient microsatellite instability was not detected. Thus, 2 B-cell lymphomas, despite having the same BLM mutation, showed different phenotypes in terms of p53 mutation and microsatellite instability.
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PMID:Microsatellite instability in B-cell lymphoma originating from Bloom syndrome. 898 Feb 51

To describe the prevalence of antiphospholipid antibodies in women undergoing in-vitro fertilization (IVF) and to determine if heparin and aspirin affect implantation rates, 191 women with a history of infertility undergoing IVF were prospectively tested for antiphospholipid antibodies. This was a two-centre, non-randomized comparison of women with positive antiphospholipid antibodies receiving heparin and aspirin versus standard treatment. An enzyme-linked immunosorbent assay, with referenced standards and known positive and negative sera on each plate, was utilized to measure antibodies to cardiolipin, phosphatidylinositol, phosphatidylglycerol, phosphatidylserine and phosphatidylethanolamine. Statistical analyses of results included analysis of variance and Fisher's two-tailed exact test. Antiphospholipid antibodies were detected in 18.8% of patients undergoing IVF compared with only 5.5% in the 200 normal controls, 26% in 200 women with recurrent pregnancy loss, and 32% in 200 women with systemic lupus erythematosus. In conclusion, antiphospholipid antibodies were found more frequently in women undergoing IVF than in the normal control population. Although implantation rates appeared higher in the group of women treated with heparin and aspirin, no statistically significant differences were detected in implantation, pregnancy and ongoing pregnancy rates between those who received standard therapy and those treated with heparin and aspirin.
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PMID:Effect of antiphospholipid antibodies in women undergoing in-vitro fertilization: role of heparin and aspirin. 922 95

Infertility represents one of the main remote sequelae of cytotoxic chemotherapy given for various malignant diseases. The impairment of gonadal function after cytotoxic chemotherapy is more frequent in the male than in the female. Because dividing cells are more sensitive to the cytotoxic effects of alkylating agents than are cells at rest, it has been hypothesized that inhibition of the pituitary-gonadal axis by gonadotropin-releasing hormone (GnRH) agonists would render the germinal epithelium less susceptible to the cytotoxic effects of chemotherapy. This hypothesis has not been thoroughly clinically tested until recently, although several investigators have demonstrated that GnRH-agonistic analogues (GnRH-a) inhibit chemotherapy-induced ovarian follicular depletion in the rat and Rhesus monkeys. Based on this rationale, we have undertaken a prospective evaluation to determine whether GnRH-a administration during combination chemotherapy for Hodgkin's and non-Hodgkin's lymphoma could prevent posttreatment ovarian damage in women by inducing a temporary prepubertal hormonal milieu. While over 93% of the surviving patients in the GnRH-a and chemotherapy group resumed spontaneous ovulation and menses, less than 40% of the women in the control group of chemotherapy without the GnRH-a cotreatment resumed normal ovarian cyclic activity. More than 60% of the women experienced premature ovarian failure (POF) in the chemotherapy alone group. Our preliminary results suggest that GnRH-a cotreatment protects against POF during cytotoxic chemotherapy. The GnRH-a and chemotherapy cotreatment may be also suggested for young women treated by cyclophosphamide pulse therapy or other gonadotoxic treatments for systemic lupus erythematosus, organ transplantation and other autoimmune diseases. The technology of cryopreservation of human ova for future fertility in these patients awaits clinical validation and substantiation. This review discusses possibilities to prevent gonadal damage induced by cytotoxic therapy and presents the clinical data currently available.
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PMID:Prevention of gonadal damage during cytotoxic therapy. 924 Jun 25

The authors investigated antiphospholipid antibodies (APA) against phosphatidic acid, ph-ethanolamine, ph-DL-glycerol, ph-inositol, ph-L-serine and cardiolipine in isotypes IgG and IgM in various diagnoses associated with reproduction. They found that the most varied pattern of high levels of these antibodies is in particular in patients with the diagnosis of intractable infertility (in 26.5% women IgG against cardiolipine, in 24.5% patients IgG against ph-inositol and ph-DL-glycerol, in 17.6% women IgG against ph-ethanolamine, in 20.6% women IgG against phosphatidic acid antigens). Intractable infertility, repeated failures of IVF and patients with a basic autoaggressive disease were followed up and their antiphospholipid antibodies were assessed. In one patient follow up of APA revealed SLE before the patient developed clinical symptoms of the disease.
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PMID:[Profile of antiphospholipid antibodies in various diagnoses associated with reproduction]. 941 Apr 25

Bloom syndrome (BS) is a rare autosomal recessive genetic disorder characterized by lupus-like erythematous telangiectasia of the face, sun sensitivity, infertility and stunted growth. Upper respiratory tract and gastrointestinal infections are commonly associated with the decreased immunoglobulin levels found in BS patients. Chromosomal abnormalities are hallmarks of the disorder, and high frequencies of sister chromatid exchanges and quadriradial configurations in lymphocytes and fibroblasts are virtually diagnostic. Recently, the causative gene for BS (BLM) has been identified. We encountered and defined a family with a nonsense mutation in BLM. The brother and sister were homozygous for the mutation and both developed B-cell malignant lymphoma in their twenties. These findings indicate the importance of prenatal diagnosis and the detection of BS carriers based on molecular genetic analysis.
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PMID:Two Japanese siblings with Bloom syndrome gene mutation and B-cell lymphoma. 947 37

The prognosis of systemic lupus erythematosus (SLE) has greatly improved during the last two decades, now allowing most patients to have a very long survival including a satisfactory quality of life. Initially considered contraindicated in SLE due to its overwhelming risks, pregnancy is nowadays allowed in a majority of patients, and fair results are usually obtained under appropriate management (1-3). Consequently, patients thought to have infertility ask the question of a possible therapy, i.e. ovulation induction (OI) associated or not with in vitro fertilization (IVF). Considering the importance of estrogens in the pathogenesis of the disease, the use of such procedures raise several questions in SLE. Though data remain to date extremely scarce, the theoretical and practical aspects of OI in SLE will be briefly reviewed here.
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PMID:Can we advise ovulation induction in patients with SLE? 975 34

Some clinicians are convinced that antiphospholipid antibodies, including antibodies to any one of five-to-seven phospholipid antigens, are associated with infertility. Additionally, some clinicians recommend that infertile women who have antiphospholipid antibodies and are undergoing in-vitro fertilization should be treated with heparin to improve the rate of pregnancy. However, experts disagree regarding the relationship between antiphospholipid antibodies and infertility. There is also substantial evidence that treatment with heparin does not alter the rate of pregnancy following in-vitro fertilization. Why the confusion? Probable culprits include variation in study design and the selection of infertile patients. Another important problem is that assays for antiphospholipid antibodies other than anticardiolipin are not standardized. Before the real relationship between antiphospholipid antibodies and infertility is discovered, assays for antiphospholipid antibodies other than anticardiolipin must be standardized and properly designed studies conducted. Randomized, controlled trials must be done to determine if heparin should be recommended as an adjunctive treatment for in-vitro fertilization in women with antiphospholipid antibodies.
Lupus 1998
PMID:Antiphospholipid antibodies and infertility: fact or fallacy. 981 81

Systemic lupus erythematosus (SLE) is a multisystemic disease characterized by alterations in the regulation of both cellular and humoral immune responses. B cell hyperactivity and genetic aberrations lead to formation of compliment-fixing IgG autoantibodies including anti-DNA and anti-nucleosome antibodies. Pathological T cell clones that recognize double-stranded DNA and nucleosomes further drive B cell production of DNA autoantibodies. Deposition of autoantibodies within the skin, kidney, brain, and other organ systems contributes to the pathophysiology and clinical manifestations of SLE. A growing body of experimental evidence indicates that DNA antibodies contribute to the histological changes observed in lupus nephritis. The binding of anti-DNA and other autoantibodies to basement membranes and other cellular structures within the glomerulus results in activation of compliment and recruitment of inflammatory cells into the glomerulus. The use of high-dose steroid hormones and cytotoxic agents have improved patient and renal survival, but are associated with major infection, infertility, osteoporosis, and secondary malignancies. New pharmacological approaches to the treatment of lupus nephritis will include drugs that deplete specific B cell clones involved in the synthesis of nephritogenic autoantibodies as well as the blocking of signal transduction pathways required for antigen-dependent antibody synthesis. Novel clonal-specific approaches to immunosuppression in patients with SLE offer the potential for precise targeting of the disease pathogenesis and for reducing toxic complications of treatment.
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PMID:Lupus nephritis: novel immunosuppressive modalities and future directions. 995 82

Autoimmune disease occurs when the immune system attacks self-molecules as a result of a breakdown of immunologic tolerance to autoreactive immune cells. Many autoimmune disorders have been strongly associated with genetic, infectious, and/or environmental predisposing factors. Comprising multiple disorders and symptoms ranging from organ-specific to systemic, autoimmune diseases include insulin-dependent diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus, scleroderma, thyroiditis, and multiple sclerosis. There are also implications of autoimmune pathology in such common health problems as arteriosclerosis, inflammatory bowel disease, schizophrenia, and certain types of infertility. Largely of unknown etiology, autoimmune disorders affect approximately 3% of the North American and European populations, > 75% of those affected being women. This discussion provides a brief introduction to the immune system and tolerance maintenance, an overview of selected autoimmune diseases and possible mechanisms of immune autoreactivity, and a review of experimental autoimmune models.
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PMID:Introduction to immunology and autoimmunity. 1050 28


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