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)

A 21-year-old woman suffering from bipolar affective disorder developed systemic lupus erythematosus (SLE) with characteristic laboratory findings, 18 months after starting carbamazepine maintenance treatment. SLE receded after withdrawal of carbamazepine and treatment with anti-inflammatory drugs. Although both the spontaneous occurrence of SLE and the psychosis as a sign of CNS involvement of SLE cannot be excluded, SLE could be considered as an adverse effect of carbamazepine.
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PMID:Carbamazepine-induced systemic lupus erythematosus. 139 48

Magnetic resonance imaging (MRI) examinations were made on 9 high-risk fetuses (poor fetal growth, 3; maternal manic-depressive psychosis, 1; maternal systemic lupus erythematosus, 1; habitual intrauterine fetal death, 1; twin pregnancy with 1 fetus in distress, 1; fetal hydrocephalus, 1), ranging from 29 to 36 weeks of gestation. T1 weighting sequences were better than T2 weighting sequences for in utero fetal imaging. Fetal movement significantly degraded the imaging quality. In all fetuses, cerebrum, cerebellum, heart, lung, liver, stomach, bladder and extremities were identified and in 1 fetus, even the cochlea was seen. In 2, the four-chamber view of the heart was evident. The signal intensity of the lung was lower than that of the liver in T1 weighting imaging. In the case of maternal lupus erythematosus, a cavum veli interpositi was noted. In the fetus with hydrocephalus, clear images of the intracranial structure were obtained. Similarly, location of the placenta was clearly depicted. MRI is currently less than satisfactory to determine the fetal anatomy, however, it does provide unique and characteristic information that complements the superior anatomic imaging by ultrasonography.
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PMID:Magnetic resonance imaging of the fetus: initial experience. 236 32

Drug-induced psychosis resulted from the administration of quinacrine hydrochloride at a dosage of 100 mg twice daily for the treatment of discoid lupus. After two weeks of drug treatment, the patient exhibited symptoms similar to those seen in the manic phase of bipolar affective disorder. Although the incidence of antimalarial psychosis is unclear and perhaps small, we recommend close observation of patients for behavioral changes suggesting the development of antimalarial psychosis. Astute observation, leading to the early detection of behavioral changes, may help avert the development of a costly and disabling complication of drug therapy.
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PMID:Antimalarial psychosis revisited. 672 43

Manic-depressive illness is recently named as a mood disorder according to the ICD-10 or DSM-III R diagnostic criteria. It consists of two opposite states, manic state and depressive state. Typical manic symptoms include a pathologic delightful mood, flight of ideas, heightened level of activity and sexual interest. Grandiosity, rapid and pressured speech, increased energy and decreased need for sleep are also frequently seen. On the other hand, depressive symptoms are characterized by prolonged depressive mood, inhibition of thought, lowered level of activity, depressive ideas or delusions and various somatic dysfunctions such as loss of appetite and sleep disturbance. Mood disorders are often seen in association with organic brain diseases, collagen diseases such as SLE, some endocrinological diseases and medication. Diagnosis of manic or depressive states is usually carried out by careful psychiatric interviews. No specific somatic symptoms or signs have been identified for manic-depressive illness. Many rating scales, for instance Zung's SDS or HDSR, have been utilized as diagnostic aids. Rating scales and the symptomatology and diagnosis of manic-depressive illness are described in general.
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PMID:[Symptomatology and diagnosis of manic-depressive illness]. 800 80

Complex diseases arise from a combination of heritable and environmental factors. The contribution made by environmental factors may be mediated through epigenetics. Epigenetics is the study of changes in gene expression that occur without a change in DNA sequence and are meiotically or mitotically heritable. Such changes in gene expression are achieved through the methylation of DNA, the post-translational modifications of histone proteins, and RNA-based silencing. Epigenetics has been implicated in complex diseases such as cancer, schizophrenia, bipolar disorder, autism and systemic lupus erythematosus. The prevalence and severity of these diseases may be influenced by factors that affect the epigenotype, such as ageing, folate status, in vitro fertilization and our ancestors' lifestyles. Although our understanding of the role played by epigenetics in complex diseases remains in its infancy, it has already led to the development of novel diagnostic methods and treatments, which augurs well for its future health benefits.
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PMID:Epigenetic mechanisms in the context of complex diseases. 1745 2

In recent years, the field of epigenetics has grown dramatically and has become one of the most dynamic and fast-growing branches of molecular biology. The amount of diseases suspected of being influenced by DNA methylation is rising steadily and includes common diseases such as schizophrenia, bipolar disorder, Alzheimer's disease, diabetes, atherosclerosis, cancer, major psychosis, lupus and Parkinson's disease. Due to cellular heterogeneity of methylation patterns, epigenetic analyses of single cells become a necessity. One rationale is that DNA methylation profiles are highly variable across individual cells, even in the same organ, dependent on the function of the gene, disease state, exposure to environmental factors (e.g. radiation, drugs or nutrition), stochastic fluctuations and various other causes. Using a polymerase chain reaction (PCR)-slide microreaction system, we present here a methylation-sensitive PCR analysis, the restriction enzyme-based single-cell methylation assay (RSMA), in the analysis of DNA methylation patterns in single cells. This method addresses the problems of cell heterogeneity in epigenetics research; it is comparably affordable, avoids complicated microfluidic systems and offers the opportunity for high-throughput screening, as many single cells can be screened in parallel. In addition to this study, critical principles and caveats of single cell methylation analyses are discussed.
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PMID:A high-throughput DNA methylation analysis of a single cell. 2126 84

Recently, an increasing number of susceptibility variants have been identified for complex diseases. At the same time, the concern of "missing heritability" has also emerged. There is however no unified way to assess the heritability explained by individual genetic variants for binary outcomes. A systemic and quantitative assessment of the degree of "missing heritability" for complex diseases is lacking. In this study, we measure the variance in liability explained by individual variants, which can be directly interpreted as the locus-specific heritability. The method is extended to deal with haplotypes, multi-allelic markers, multi-locus genotypes, and markers in linkage disequilibrium. Methods to estimate the standard error and confidence interval are proposed. To assess our current level of understanding of the genetic basis of complex diseases, we conducted a survey of 10 diseases, evaluating the total variance explained by the known variants. The diseases under evaluation included Alzheimer's disease, bipolar disorder, breast cancer, coronary artery disease, Crohn's disease, prostate cancer, schizophrenia, systemic lupus erythematosus (SLE), type 1 diabetes and type 2 diabetes. The median total variance explained across the 10 diseases was 9.81%, while the median variance explained per associated SNP was around 0.25%. Our results suggest that a substantial proportion of heritability remains unexplained for the diseases under study. Programs to implement the methodologies described in this paper are available at http://sites.google.com/site/honcheongso/software/varexp.
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PMID:Evaluating the heritability explained by known susceptibility variants: a survey of ten complex diseases. 2137 18

Lamotrigine, as a new generation anticonvulsant, has been widely used in treating epilepsy. It is also a mood stabilizer for bipolar disorder. Common adverse effects include nausea and vomiting, dyspepsia, insomnia, somnolence, and rash. However, drug-induced lupus (DIL) due to lamotrigine has been rarely reported. We report a case of lupus-like syndrome associated with lamotrigine. A 39-year-old male developed arthralgias and positive serum antinuclear antibody repeatedly with introductions of lamotrigine. The strong temporal relationship between the rheumatological features and drug exposure is illustrative of the disease course of DIL. Two hitherto reported lamotrigine-related DIL cases are compared with our case.
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PMID:Lamotrigine-induced lupus-like syndrome: a case report and literature review. 2301 Nov 69

The neurotransmitter norepinephrine (NE) participates in a broad range of physiological functions, both in the brain and in the periphery, where it is a principal output molecule of the sympathetic nervous system. NE receptors are present in nearly all, if not all, organs of the body, which may allow this molecule to play a role in a variety of disease processes. This paper examines the hypothesis elevated NE signaling, through genetics and/or environmental factors, is an etiological factor in a variety of diseases outside of the brain, including age-related macular degeneration, systemic lupus erythematosus, atrial fibrillation, and metabolic syndrome. Lines of evidence presented to assess the hypothesis include: (1) studies of noradrenergic drugs modulating the four diseases; (2) association of these diseases with bipolar disorder, hypertension, and obesity, where the latter three conditions may involve elevated NE signaling; and (3) association with psychological stress, since NE is released in response to stress. Many of the studies cited tend to support the hypothesis, or are at least consistent with it. If the hypothesis is correct, perhaps a large number of individuals would benefit from chronically taking drugs that systemically diminish noradrenergic signaling, thereby helping prevent or treat a wide variety of diseases.
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PMID:Elevated norepinephrine may be an etiological factor in a wide range of diseases: age-related macular degeneration, systemic lupus erythematosus, atrial fibrillation, metabolic syndrome. 2341 Apr 97

Use of electroconvulsive therapy (ECT) has been infrequently described in patients with systemic lupus erythematosus and is most commonly used in patients with catatonia. In this report, we describe the use of ECT in a young adolescent girl who had bipolar affective disorder associated with systemic lupus erythematosus and was treated with ECT for the depressive episode. The patient achieved remission with a course of 6 ECT treatments.
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PMID:Use of electroconvulsive therapy in an adolescent with systemic lupus erythematosus for management of depression. 2396 11


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