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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied a patient with systemic lupus erythematosus and type B insulin resistance, who progressed from extreme insulin resistance to fasting hypoglycemia. The plasma insulin level was 63.3 +/- 20.9 pmol/L in the fasting state and rose above 1440 pmol/L postprandially. Intravenous administration of human insulin caused almost no decline in plasma glucose. Therefore, it was concluded that the patient was still resistant to insulin and that plasma insulin did not play a crucial role in the development of hypoglycemia. Immunoglobulin G from this patient did not inhibit insulin binding to the insulin receptor; rather, it enhanced [125I]insulin binding in both the immunoprecipitate and the in vitro binding assay to intact cells. Antiinsulin receptor antibodies strongly inhibited insulin internalization in human adipocytes, slowed down the dissociation of [125I]insulin from receptors and failed to induce down-regulation of surface insulin receptors in both the presence and absence of insulin. Finally, autoantibodies mimicked the insulin stimulatory effect on human fat cell lipogenesis even after long term exposure, but inhibited the metabolic potency of insulin when added simultaneously with the natural ligand. We conclude that antiinsulin receptor antibodies induce fasting hypoglycemia, through their continuous receptor stimulatory action, and insulin resistance, possibly by a conformational perturbation of the receptor protein, which, in turn, uncouples insulin receptor binding from receptor function.
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PMID:Insulin resistance and hypoglycemia in a patient with systemic lupus erythematosus: description of antiinsulin receptor antibodies that enhance insulin binding and inhibit insulin action. 187 39

A 59-year-old woman with systemic lupus erythematosus was found to have marked hyperglycemia, extreme insulin resistance and abnormally high plasma immunoreactive insulin. Her circulating erythrocytes displayed a dramatic decrease of 125I-labeled insulin binding. Both the whole serum and purified IgG fraction strongly inhibited the binding of radiolabeled insulin to control erythrocytes. These results suggested, although indirectly, the existence of antibodies to insulin receptors in the serum of the patient. To directly investigate this issue, we used an enzyme-linked solid-phase immunoassay which allows the detection and enumeration of lymphocytes secreting antibodies towards insulin receptors. Peroxidase-conjugated anti-human immunoglobulin is used to reveal the binding of antibodies to insulin receptor-coated dishes. We demonstrated that the patient's mononuclear cells, when briefly incubated in Petri dishes with partially purified insulin receptor, were able to secrete immunoglobulins of G class specifically directed to the antigen. Moreover, only a fraction of the whole population of anti-insulin receptor antibodies was directed towards the insulin binding region of the receptor, seemingly corresponding to the auto-antibodies detected with conventional binding-inhibition assay.
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PMID:Extreme insulin resistance due to anti-insulin receptor antibodies: a direct demonstration of autoantibody secretion by peripheral lymphocytes. 219 Jul 81

An elderly woman with unexplained episodic fasting hypoglycemia was hospitalized for ascites. Evaluation revealed polyserositis, arthritis and immunologic abnormalities that suggested the diagnosis of systemic lupus erythematosus (SLE). Antibodies to insulin receptor with insulin binding inhibitory activity were detected in her serum. Treatment with prednisone was accompanied by resolution of hypoglycemic episodes and disappearance of the antireceptor antibodies. Autoantibody mediated alterations in serum glucose may be included in the growing list of autoimmune phenomena in SLE. Antiinsulin receptor antibodies should be sought in patients with SLE and idiopathic hypoglycemia.
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PMID:Hypoglycemia due to antiinsulin receptor antibodies in systemic lupus erythematosus. 229 Jan 67

A 52-year-old black woman presented with clinical features of systemic lupus erythematosus (SLE) and severe fasting hypoglycemia. Hypoglycemia was secondary to autoantibodies to the insulin receptor that were detected in the patient's serum. There were no anti-insulin antibodies, and other causes of hypoglycemia were excluded. Treatment with high-dose glucocorticoids resulted in restoration of euglycemia associated with resolution of circulating anti-receptor antibodies and parallel improvement in clinical and laboratory features of SLE. This case is compared with other cases of autoimmune hypoglycemia due to anti-receptor antibodies.
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PMID:Autoantibodies to the insulin receptor as a cause of autoimmune hypoglycemia in systemic lupus erythematosus. 304 73

We report a young woman with systemic lupus erythematosis (SLE) who developed diabetes secondary to extreme insulin resistance, associated with severe hyperandrogenism and acanthosis nigricans. Her insulin resistance was found to be associated with high titers of insulin receptor antibodies. The hyperandrogenism has been favourably influenced by cyclical treatment with cyproterone acetate and ethinyl oestradiol, but the insulin resistance and acanthosis nigricans have remained unmodified after 15 months of follow up.
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PMID:Hyperandrogenism, insulin resistance, acanthosis nigricans, and systemic lupus erythematosis associated with insulin receptor antibodies. 338 33

An 82-year-old woman developed symptomatic reactive hypoglycemia in the same year she developed a lupus-like syndrome, probably secondary to the administration of procainamide or hydralazine. Reactive hypoglycemia was confirmed by an oral glucose tolerance test, in which plasma glucose decreased from a fasting level of 87 mg/dL to 32 mg/dL at 3 hours and 23 mg/dL at 4 hours, the last value being associated with loss of consciousness. The patient awoke after the intravenous administration of dextrose. Sensitivity to exogenous insulin was normal or increased. Attempts to measure plasma insulin levels led to the finding of anti-insulin antibodies in the patient's serum; these antibodies were of relatively low titer, were IgG, and not associated with antibodies to the insulin receptor. The patient had no history of exogenous insulin use. Her reactive hypoglycemia appeared due to the autoimmune insulin syndrome, which developed in association with drug-induced lupus erythematosus.
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PMID:Reactive hypoglycemia and insulin autoantibodies in drug-induced lupus erythematosus. 634 54

Since Kahn et al. reported in 1976 insulin resistant diabetes due to anti-insulin receptor antibodies, an unusual form of diabetes mellitus (type B) has been found in many countries. We had two diabetic patients with anti-insulin receptor antibodies, associated with either acanthosis nigricans or systemic lupus erythematosus. Remission occurred 15 months after the onset of insulin resistant diabetes. One patient unfortunately died of acute pneumonia and the other has been followed up. The anti-insulin receptor antibodies were measured according to the method of Omori and Hirata by using the pellet of human placental membrane. The anti-insulin receptor antibodies in both cases diminished as remission occurred. Reverse hemolytic plaque assay (PFG) detected immunoglobulin-producing cells. In Case 2, the plaque forming cells were twenty times as many as the normal value. Immunosuppressive therapy with cyclophosphamide reduced the immunoglobulin secreting cells as remission occurred. The patients with insulin resistance (type B) should be treated with enough insulin inspite of the presence of insulin resistance. Besides, cyclophosphamide, 6-mercaptopurine and prednisolone should be used with caution. Plasma exchange is a treatment to be tried. It is important to note that spontaneous remission may occur more than half a year after the onset of insulin resistant diabetes.
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PMID:Remission of insulin resistant diabetes in two patients with anti-insulin receptor antibodies. 675 1

The New Zealand Obese (NZO) mouse was studied as a potential model for autoimmune diabetes. NZO mice develop obesity, glucose intolerance, and insulin resistance, and have low-titer IgM antibodies to the insulin receptor. It is shown that they have circulating antibodies to both native DNA and denatured, single-stranded DNA. The antibody levels are higher in females, and, up to 6 mo of age, are comparable to those found in the related NZB X NZW F1 (NZB/W) mouse, a model for systemic lupus erythematosus. After 6 mo of age the antibody levels in NZO mice fall toward normal, in contrast to the persistently elevated levels in NZB/W mice. NZB/W mice are known to succumb to immune complex-mediated proliferative glomerulonephritis before 1 yr of age, whereas NZO mice survive. NZO kidneys exhibit light microscopic features of both diabetic and lupus nephropathies: glomerular proliferation, mesangial deposits, mild basement membrane thickening, glomerulosclerosis, eosinophilic nodules in some glomeruli, occasional hyalinization of the glomerular arterioles, and healing arteriolar inflammation. These changes are associated with glomerular deposition of immunoglobulin, especially IgM, in a granular pattern on fluorescent staining. The NZO mouse, therefore, has evidence of a generalized immune disorder and provides a model for studying the relationship between autoimmunity, obesity, and diabetes.
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PMID:Diabetes is associated with autoimmunity in the New Zealand obese (NZO) mouse. 700 65

Gestational diabetes resistant to insulin therapy occurring in association with insulin receptor antibodies has not been reported previously. A patient developed diabetes mellitus at 21 weeks' gestational age and had a previous history of thrombotic thrombocytopenia purpura, then in remission. She developed life-threatening diabetic ketoacidosis that was severely resistant to insulin treatment despite the usage of adjunct therapy, including plasmapheresis, and intravenous cyclophosphamide and steroids. She also had lupus nephropathy. Termination of the pregnancy at 22 weeks' gestation resulted in a rapid resolution of both the diabetes and lupus nephropathy.
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PMID:Gestational diabetes mellitus with profound insulin resistance. A case report. 816 28

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


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