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)

Insulin antibodies (IAA) can be detected in the serum of the majority of newly diagnosed IDDM patients prior to insulin therapy. In first degree relatives of IDDM patients, IAA are associated with an increased risk of development of IDDM. However, the disease specificity of IAA, detected by radiobinding assays, has not been addressed. We thus tested sera from patients with autoimmune disease for IAA. One of 29 (3%) patients with Graves' disease and five of 27 (19%) patients with SLE had IAA levels exceeding the range for normal controls. IAA were not detected in sera from 29 patients with Addison's disease, 15 patients with pernicious anaemia or 10 patients with increased gamma globulins. Non-specific binding of 125I-labelled insulin was increased in serum from 14 (21%) samples from patients with Graves' disease, 10 (37%) patients with SLE, one (3.2%) of 29 patients with Addison's disease and two (13%) of 15 patients with pernicious anaemia. The increased non-specific binding most likely relates to immunoglobulin binding as it was also found in eight of 10 patients with oligoclonal or polyclonal increase in gamma globulins. Our findings suggest that moderate elevations of IAA are not uncommon in patients with SLE, in whom increased non-specific binding of insulin is also common. This observation is of importance in preclinical diabetes screening studies.
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PMID:Insulin autoantibodies in patients with autoimmune diseases. 147 50

The authors report the case of a 22-year-old Guatemalan in whom lupus was diagnosed 8 months after a second pregnancy. The diagnosis of lupus met the criteria of the ARA: Raynaud's syndrome, alopecia, arthralgia, thrombophlebitis, facial erythema, antinuclear factor at 1/100, Farr at 75 p. 100 and immunofluorescent demonstration of IgM binding in healthy skin. Two months after the beginning of the lupus, there was onset of insulin-resistant ketosic diabetes without overweight. The serum insulin was 1.140 mu U/ml. Acanthosis nigricans was noted and confirmed by a biopsy. Insulin-resistance can be attributed to anti-membrane receptor antibodies titrating at 1/200 (R. Khan). The short-term progress of the disease was favorable on corticosteroid treatment. Insulin could be stopped, but high insulin serum levels persisted. This case meets criteria for type B as defined by Flier, Khan and Roth, and is the first European case of lupus with a complete presentation. Short-term progress was favorable, and there is no evidence to affirm that there will be a tardive progression towards hypoglycemia which is, however, possible due to the persistence of elevated serum insulin levels.
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PMID:[Lupus, insulin-resistant diabetes and acanthosis nigricans (author's transl)]. 723 1

Insulin dependent diabetes (IDD) is considered to be an immune endocrinopathy as in such patients a disorder of the immune system is involved; however, up to now no data are available on the occurrence of antiphospholipid antibodies (aPL) in IDD pregnant women and on possible correlation between the presence of aPL and the high fetomaternal morbidity reported in these patients. The presence of lupus anticoagulant (LA) and of anticardiolipin antibodies (ACA) was monthly evaluated. In 35 IDD pregnant women referring within the 7 degrees week of pregnancy to the High Risk Pregnancy Medical Unit. Levels of D-dimer, fibrin degradation product, were also assayed. Twelve IDD pregnant women resulted to be aPL positive with a markedly high prevalence of positivity (34%). aPL positive did not significantly differ from aPL negative women in age, duration and severity of diabetes and in metabolic control throughout pregnancy. Pregnancy induced hypertension (PIH) and intrauterin growth retard (IUGR) were observed in 6/12 aPL positive and in only 2/23 aPL negative patients (p < 0.02). A pathological increase in D-dimer levels occurred in 6/12 aPL positive patients and in none aPL negative (p < 0.03). The high frequency of aPL positivity and its strict relation to pregnancy complications strongly support a major role for an autoimmune pathogenetic mechanism in the occurrence of feto-maternal morbidity in IDD pregnant women. The identification of this subgroup at risk for complications may be clinically relevant.
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PMID:Antiphospholipid antibodies and pregnancy disorders in women with insulin dependent diabetes. 873 24

Acanthosis nigricans, insulin receptor antibody, and systemic lupus erythematosus are associated in the potentially lethal syndrome of type B insulin resistance. Hyperpigmentation has been reported rarely, while glucose intolerance is common in these patients. We report an adolescent girl with acanthosis nigricans, hyperpigmentation, insulin receptor antibody, and systemic lupus erythematosus without glucose intolerance. Insulin resistance may be mild or transient in some patients with type B insulin resistance. Resolution of skin lesions was noted during therapy of SLE, and was associated with disappearance of insulin receptor antibody.
Lupus 1997
PMID:Systemic lupus erythematosus with acanthosis nigricans, hyperpigmentation, and insulin receptor antibody. 910 36

It has been suggested that neuroendocrine regulation plays an important role in the pathogenesis and activation of autoimmune diseases. The aim of this investigation was to clarify the hypothalamic-pituitary response to a well-defined stimulus under standardised conditions in patients with SLE. Plasma concentrations of prolactin (PRL), growth hormone (GH) and cortisol were determined in venous blood drawn through an indwelling cannula during insulin-induced hypoglycaemia (0.1 U/kg b.w., i.v.) in ten patients and in 12 age-, gender- and weight-matched healthy subjects. Basal PRL concentrations were higher in patients vs healthy controls (12 vs 6 ng/ml, P < 0.01), though still within the physiological range. Insulin-induced plasma PRL and GH were significantly increased both in patients and healthy subjects; however, the increments or areas under the curves were not different in the two groups. Plasma cortisol response showed moderate attenuation in patients. Sensitivity of pituitary lactotrothrops to thyrotropin-releasing hormone (TRH) administration (200 microg, i.v.) was the same in patients and control subjects. In SLE patients with low activity of the disease the sensitivity of pituitary PRL release to TRH administration remained unchanged. The hypothalamic response to stress stimulus (hypoglycaemia) was comparable in patients and healthy subjects.
Lupus 1998
PMID:The hypothalamic-pituitary response in SLE. Regulation of prolactin, growth hormone and cortisol release. 973 25

In systemic lupus erythematosus, plasma concentrations of tumor necrosis factor alpha (TNF alpha) and other pro-inflammatory cytokines are elevated and those of transforming growth factor beta (TGF beta) are decreased. TNF alpha prevents lupus nephropathy whereas increased concentration of TGF beta causes glomerulosclerosis. Insulin inhibits TNF alpha and enhances TGF beta production, augments nitric oxide synthesis and blocks superoxide anion generation. Polyunsaturated fatty acids (PUFAs) also have actions similar to insulin. Hence, it is suggested that a combination of insulin (in the form of glucose-insulin-potassium) and PUFAs may be of benefit in lupus and other inflammatory conditions.
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PMID:Hypothesis: can glucose-insulin-potassium regimen in combination with polyunsaturated fatty acids suppress lupus and other inflammatory conditions? 1154 28

A 22-year-old woman was admitted in August 2001 for loss of consciousness due to hypoglycemia. Her serum insulin level during the hypoglycemic episode was high at 121 mU/l (normal range: 5-25 mU/l). She had never received an insulin injection. Insulin antibodies by radioimmunoassay were positive. During hospitalisation, the patient presented clinical and biological features of systemic lupus erythematosus (SLE). Treatment with high-dose corticosteroids and cyclophosphamide resulted in restoration of euglycemia associated with resolution of circulating anti-insulin antibodies and parallel improvement in clinical and laboratory features of SLE.
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PMID:[Insulin autoimmune syndrome revealing systemic lupus erythematosus]. 1274 60

We previously reported that systemic lupus erythematosus (SLE) patients have a higher risk of insulin resistance and abnormal insulin secretion. Recent studies demonstrated that interleukin (IL)-18, a novel pro-inflammatory cytokine, may be involved in triggering the inflammatory processes in SLE and the concentrations of circulating IL-18 in SLE patients were significantly higher than those in healthy subjects. IL-12 has a synergistic effect with IL-18, and both cytokines are inducers of interferon (IFN)-gamma. The objective of this study was to identify the effect of fasting insulin levels on circulating concentrations of IL-18, IL-12 and IFN-gamma in patients with SLE. Plasma levels of proinflammatory Th-1 cytokines were determined by enzyme-linked immunosorbent assay in a total of 70 female SLE patients and 34 age-matched healthy females. Insulin resistance (IR) and secretion were evaluated by homeostasis model assessment (HOMA). All patients were further classified into subgroups based on the quartiles of fasting insulin levels. SLE patients with fasting insulin levels in the top quartile compared with other quartiles had significantly higher plasma levels of IL-18. The presence of insulin auto-antibodies (IAA) in SLE patients had no influence on plasma levels of IL-18. In addition, fasting insulin levels and HOMA IR were positively correlated with IL-18 in all SLE patients, respectively. In conclusion, elevated circulating IL-18 concentrations corresponded with increases in fasting insulin levels and the status of insulin resistance in patients with SLE.
Lupus 2006
PMID:Elevation of plasma interleukin-18 concentration is associated with insulin levels in patients with systemic lupus erythematosus. 1668 59

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

Kidney biopsy remains the mainstay of Lupus Nephritis (LN) diagnosis and prognostication. The objective of this study is to identify non-invasive biomarkers that closely parallel renal pathology in LN. Previous reports have demonstrated that serum Insulin-like growth factor binding protein 4 (IGFBP-4) was increased in diabetic nephropathy in both animal models and patients. We proceeded to assess if IGFBP4 could be associated with LN. We performed ELISA using the serum of 86 patients with LN. Normal healthy adults (N = 23) and patients with other glomerular diseases (N = 20) served as controls. Compared to the healthy controls or other glomerular disease controls, serum IGFBP-4 levels were significantly higher in the patients with LN. Serum IGFBP-4 did not correlate well with systemic lupus erythematosus disease activity index (SLEDAI), renal SLEDAI or proteinuria, but it did correlate with estimated glomerular filtration rate (R = 0.609, P < 0.0001). Interestingly, in 18 patients with proliferative LN whose blood samples were obtained at the time of renal biopsy, serum IGFBP-4 levels correlated strongly with the chronicity index of renal pathology (R = 0.713, P < 0.001). IGFBP-4 emerges a potential marker of lupus nephritis, reflective of renal pathology chronicity changes.
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PMID:Insulin-Like Growth Factor Binding Protein-4 as a Marker of Chronic Lupus Nephritis. 2701 56


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