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)

The influence of a 2-h neuropsychological stress test on plasma catecholamines, cortisol, and on the distribution of lymphocyte subpopulations was studied in 14 patients with systemic lupus erythematosus (SLE), 10 patients on prednisone treatment (without collagenosis), and 14 sex-and-age-matched healthy controls. Psychological stress induced comparably significant increases in plasma adrenaline and noradrenaline levels as compared with baseline values (P less than 0.05) in all three groups, whereas plasma cortisol remained unchanged. The rise in plasma catecholamines was accompanied by a significant cell mobilization in healthy subjects and prednisone-treated patients, but not in patients with SLE. CD19+ cells increased significantly in number from baseline in healthy subjects and prednisone-treated controls (P less than 0.05), while remaining unchanged in SLE patients. In conclusion, SLE patients showed a reduced cell mobilization due to psychological stress despite hormonal alterations paralleling those of healthy subjects or prednisone-treated patients without collagenosis.
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PMID:Influence of prolonged neuropsychological testing on immunoregulatory cells and hormonal parameters in patients with systemic lupus erythematosus. 141 Oct 82

Physical and psychological stress in healthy subjects leads to characteristic alterations of plasma hormone concentrations and the lymphocyte subset distribution. After short-term bicycle ergometry or acoustic stress, and after a 2-h-long neuropsychological examination, a rise in B- and T-suppressor/cytotoxic lymphocytes and a decrease in T-helper lymphocytes has been shown to occur. This cell mobilization was accompanied by an elevation in plasma catecholamines. Although the rise in catecholamine levels was similar in patients with systemic lupus erythematosus (SLE) and in healthy subjects, the alterations in the lymphocyte subsets were less pronounced in SLE patients after bicycle ergometry as well as after psychological testing than in healthy subjects, patients with sarcoidosis, and patients without collagenosis under treatment with corticosteroids. Differences between short-term physical exercise and the acoustic stress test on the one hand, and the 2-h-long neuropsychological test on the other, were observed only for the absolute lymphocyte count. After short-term stress, a rise in the leukocyte and lymphocyte count was noted, whereas after long-term testing, only an increase in leukocytes and a decrease in lymphocytes could be found. In conclusion, sympathomimetic stimulation by bicycle ergometry or by psychological stress led to a characteristic cell mobilization in all the groups investigated. The extent of cell mobilization was attenuated in SLE patients despite the fact that comparable increases of plasma catecholamines were observed.
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PMID:Modulation of the immune response to stress in patients with systemic lupus erythematosus: review of recent studies. 145 82

It is now established that communication between the CNS and the immune system is bidirectional, that endocrine factors can alter immune function and that immune responses can alter both endocrine and CNS responses. In many respects CNS and endocrine responses to acute inflammation are similar to the changes associated with acute stress exposure. In contrast, during chronic inflammation associated with adjuvant induced arthritis (AA), although circulating levels of corticosterone are increased, the peptidergic regulation of the hypothalamus is different from that seen during acute stress. As the disease progresses, a paradoxical reduction occurs in CRH mRNA in the paraventricular nucleus (PVN), whereas PVN AVP mRNA increases. These data suggest that there is increased expression of AVP mRNA within the CRH cells of the PVN with an increased emphasis on AVP regulation of HPA output. Additionally, HPA function is altered during chronic inflammation such that responses to psychological stress (i.e. restraint) are significantly dampened, while responses to further inflammatory challenges are maintained. These data suggest that alterations in PVN peptide colocalization may be important in regulating the progression of peripheral inflammatory responses and that the effects of inflammation on the hypothalamus alter stress-responsive systems. In addition to the AA model, we have similarly observed alterations in PVN peptide mRNA expression with disease onset in the murine MRL lpr/lpr and MRL +/+ model of SLE. Disease onset in murine SLE is spontaneous and does not rely on exogenous application of adjuvant; however, decreased levels of CRH in the PVN were observed from early disease onset in this animal model. It is suggested that alterations in CRH regulation in response to either acute or chronic inflammation may contribute as etiological factors to both psychiatric (i.e. neuropsychiatric SLE) and stress-related disease.
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PMID:Inflammatory disease as chronic stress. 962 87

Clinical observations suggest that psychological stress induces exacerbation of disease activity in patients with systemic lupus erythematosus (SLE). In order to determine whether SLE patients differ from healthy controls in their stress response, we analyzed heart rate, blood pressure, catecholamine concentration, lymphocyte subpopulations, natural killer (NK) cell activity, and expression of beta-adrenoceptors on PBMC before, immediately after, and 1 h after a public speaking task in 15 SLE patients and 15 healthy subjects. Both groups demonstrated similar psychological, cardiovascular, and neuroendocrine responses to acute stress. However, natural killer (CD16(+)/CD56(+)) cell numbers transiently increased after stress exposure, with significantly less pronounced changes in SLE patients. In addition, NK activity increased in healthy controls (n = 8) but not in SLE patients (n = 4) after acute stress. Furthermore, the number of beta(2)-adrenoceptors on PBMC significantly increased only in healthy subjects (n = 8) after stress but not in SLE patients (n = 7). These data indicate that SLE patients differ from healthy controls in stress-induced immune responses.
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PMID:Patients with systemic lupus erythematosus differ from healthy controls in their immunological response to acute psychological stress. 1060 Feb 17

Mental stress has an enormous impact on physical health. This impact commonly manifests as headache, muscle tension, acne, peptic ulcer disease, or a compromised immune system. Stress is also associated with more serious adverse effects, such as cardiovascular disease and exacerbations of rheumatoid arthritis and systemic lupus erythematosus. As these effects are far-reaching, it is important for primary care physicians to identify and manage the symptoms of mental stress in their patients. This is increasingly possible with office-based mental stress testing, which uses cardiovascular markers to identify patients who are overresponders to mental stress, and, thus, at risk for stress-induced disorders. Mental stress in this population can be managed with nonpharmacologic and pharmacologic interventions to improve patients' responses to stress and decrease morbidity and mortality associated with this condition.
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PMID:Evaluating the impact of stress on systemic disease: the MOST protocol in primary care. 1277 65

Psychological stress is believed to be one of the predisposing factors for systemic lupus erythematosus (SLE), whereas physical stress such as exercise has never been reported to be related. We measured the circulating levels of antibodies (IgM, IgG, anti-dsDNA IgG), Th1 (IFN-gamma), Th2 (IL-4, IL-6), and of pro-inflammatory (TNF-alpha, IL-1beta) and anti-inflammatory (TGF-beta) cytokines of C4(-l-) female mice at rest, after acute exercise and after exercise training, using an antibody-capture ELISA. Prior to the exercise, the C4(-l-) mice had higher levels of IgG and anti-dsDNA IgG but lower levels of IFN-gamma, IL-1beta, IL-6 and IL-4 than wild-type C57BL/6 (B6) mice. A single bout of exercise to exhaustion increased serum IgG, TNF-alpha, IL-1beta and TGF-beta in the B6 mice but only TGF-beta in the C4(-l-) mice was increased. We conclude that exhaustive or moderate exercise has no effect on the levels of serum antibodies and cytokines and is thus unlikely to promote the onset of SLE.
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PMID:Serum antibodies and cytokines in C4-deficient mice and their responses to exercise. 2023 74

Prolactin (PRL) is not only a pituitary hormone with important role in the reproduction but it also acts as a cytokine involved in the immune response. Prolactin is produced by many immune system cells that express the prolactin receptor (PRL-R). PRL is then able to affect local microenvironment of the immune system organs and contribute to maturation as well as functioning of the immune system cells. The role of PRL in the immune reactions is stimulating; its presence significantly increases the ability of the immune cells to proliferate and produce cytokines such as TNF-alpha, IFN-gamma, IL-12, IL-1 beta. This effect results from activation of a number of intracellular pathways (Jak2/STAT, Ras/Raf/MAPK etc.) and activation of the genes linked to apoptosis and proliferation (Bcl-XL, Bcl-2, pim, XIAP) or transcription factors (IRF-1). Interestingly, PRL itself is unable to initiate an immune reaction; it is more a factor maintaining balance within immune reactions, contra-regulatory to glucocorticoids, which effect is manifested under critical circumstances of physical or psychological stress. Intensified immunosuppression during stress, combined with a lack of prolactin, has surprisingly been identified during experiments on mice and is also found in human medicine. On the other hand, increased prolactin serum levels were described in several systemic as well as organ-specific autoimmune diseases. PRL levels elevation in these diseases might result from several factors: an increased release of prolactin from the anterior pituitary due to inflammatory cytokines or reduced production of suppressive dopamine, or, alternatively, an increased production of prolactin in immune system cells. In some of these diseases, such as celiac disease and systemic lupus erythematosus (SLE), the PRL level correlates with the disease activity. This supports the hypothesis that PRL oversupply shifts the balance in the immune response towards higher activity of the immune system cells and initiation of the immune reaction. For example, in SLE, prolactin prolongs the life cycle of autoreactive B-lymphocytes and their ability to produce pathogenic autoantibodies. Further research into the effects of PRL and monitoring of patients with hyperprolactinaemia and autoimmune diseases will provide guidance on how to best utilize the possibly so far hidden prolactin potential. It is questionable whether pharmacotherapy could be used to decrease serum PRL levels in the treatment ofautoimmune diseases. However, the currently running studies suggest it might be possible to use PRL level detection as a marker of a disease activity.
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PMID:[A review of the effects of prolactin hormone and cytokine on the development and pathogenesis of autoimmune diseases]. 2057 90

Gulf War syndrome (GWS) is a multi-symptom condition comprising a variety of signs and symptoms described in the literature, which not been fully resolved. The various symptoms of the condition include muscle fatigue and tiredness, malaise, myalgia, impaired cognition, ataxia, diarrhoea, bladder dysfunction, sweating disturbances, headaches, fever, arthralgia, skin rashes, and gastrointestinal and sleep disturbances. In addition, excessive chemical sensitivity and odour intolerance is reported. The aetiology of the condition is unclear, but many reviews and epidemiological analyses suggest association with pyridostigmine bromide (PB), certain vaccination regimes, a variety of possible chemical exposures, including smoke from oil-well fires or depleted uranium from shells, as well as physical and psychological stress. Recently, Shoenfeld et al. suggested that four conditions--siliconosis, macrophagic myofaciitis (MMF), GWS and post-vaccination phenomena--that share clinical and pathogenic resemblances, may be incorporated into common syndrome called 'Autoimmune (Autoinflammatory) Syndrome induced by Adjuvants' (ASIA). Symptoms and signs of the four conditions described by Shoenfeld et al. show that at least eight out of ten main symptoms are in correlation in all four conditions. Namely, myalgia, arthralgias, chronic fatigue, neurological cognitive impairment, gastrointestinal symptoms, respiratory symptoms, skin manifestations and appearance of autoantibodies. Regardless of the aetiology of GWS, be it exposure to environmental factors or chemical drugs, vaccinations or the adjuvants in them, GWS fits well with the definition of ASIA and is included as part of 'Shoenfeld's syndrome'.
Lupus 2012 Feb
PMID:Gulf War syndrome as a part of the autoimmune (autoinflammatory) syndrome induced by adjuvant (ASIA). 2223 52

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

Insulin resistance (IR) is a general phenomenon of many physiological states, disease states, and diseases. IR has been described in diabetes mellitus, obesity, infection, sepsis, trauma, painful states such as postoperative pain and migraine, schizophrenia, major depression, chronic mental stress, and others. In arthritis, abnormalities of glucose homeostasis were described in 1920; and in 1950 combined glucose and insulin tests unmistakably demonstrated IR. The phenomenon is now described in rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, polymyalgia rheumatica, and others. In chronic inflammatory diseases, cytokine-neutralizing strategies normalize insulin sensitivity. This paper delineates that IR is either based on inflammatory factors (activation of the immune/ repair system) or on the brain (mental activation via stress axes). Due to the selfishness of the immune system and the selfishness of the brain, both can induce IR independent of each other. Consequently, the immune system can block the brain (for example, by sickness behavior) and the brain can block the immune system (for example, stress-induced immune system alterations). Based on considerations of evolutionary medicine, it is discussed that obesity per se is not a disease. Obesity-related IR depends on provoking factors from either the immune system or the brain. Chronic inflammation and/or stress axis activation are thus needed for obesity-related IR. Due to redundant pathways in stimulating IR, a simple one factor-neutralizing strategy might help in chronic inflammatory diseases (inflammation is the key), but not in obesity-related IR. The new considerations towards IR are interrelated to the published theories of IR (thrifty genotype, thrifty phenotype, and others).
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PMID:Insulin resistance, selfish brain, and selfish immune system: an evolutionarily positively selected program used in chronic inflammatory diseases. 2560 58


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