Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with procainamide lupus erythematosus had a large pericardial effusion. As in other reported cases histology revealed a fibrinous mononuclear pericarditis and the pericardial fluid was a serosanguinous inflammatory exudate with a high LDH level and normal glucose concentration. The ANF and LE cell preparation were positive in the fluid but the C3 complement was normal. The frequency of pericarditis is similar in systemic and drug-induced lupus erythematosus yet low complement levels need not occur. Complement activation may therefore be unnecessary for the development of either type of lupus pericarditis.
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PMID:Procainamide-induced lupus erythematosus: report of a case with a large pericardial effusion and fluid analysis. 52 1

Proteins from U1 and U2 small nuclear ribonucleoprotein (snRNP) particles, which are common targets of autoantibodies found in some rheumatic diseases, were analysed for the presence of glycans. A glycan detection assay revealed that the U1-specific proteins 68K and A and the U2-specific protein B" are glycosylated. However, none of the Sm proteins, which are common to all the major snRNP particles, showed a detectable level of glycosylation. With the use of specific lectins, an analysis of the particular carbohydrate(s) attached to the U1 snRNP 68K protein demonstrated the presence of at least one N-linked oligosaccharide chain. Lectin detection of galactose, glucose, mannose and N-acetylglucosamine on 68K was confirmed by chemical analysis of the carbohydrates. The glycopeptide nature of these antigens may be important for understanding the role of autoantigens in the pathogenesis of autoimmune disorder.
Lupus 1992 Feb
PMID:Small nuclear ribonucleoprotein particles contain glycoproteins recognized by rheumatic disease-associated autoantibodies. 130 63

The central nervous system (CNS) is clinically involved in approximately 40% of all systemic lupus erythematosis (SLE) patients. Minor psychiatric symptoms and abnormalities on neuropsychological testing are being detected with increasing frequency. This review summarizes current thinking concerning the diagnosis and pathogenesis of CNS lupus. The main symptoms of CNS lupus can be diffuse (generalized seizures, psychosis) or focal (stroke, peripheral neuropathies). Neuropsychiatric symptoms often occur in the first year of SLE, but are rarely the presenting symptoms of the disease. In studies on the pathology of CNS lupus, vasculopathy, infarcts and haemorrhages are often observed, whereas vasculitis is rare. Endocardial lesions and mural thrombi have also been reported in 33-50% of CNS lupus patients. In diagnostic imaging of the CNS, magnetic resonance imaging (MRI) scans often provide evidence for edema or small infarcts, both in focal and diffuse CNS lupus, whereas computerized tomography (CT) scans only show gross abnormalities. The first reports on position emission tomography (PET) scans in CNS lupus patients show decreased glucose uptake in the brain. The cerebral blood flow decreases during active diffuse and focal CNS lupus. The blood-brain barrier is somewhat more frequently impaired in diffuse CNS lupus. Intrathecal IgG and IgM production is observed in 25-66% of all CNS lupus patient. Various specificities of autoantibodies have been observed in CNS lupus. Of these, anticardiolipin (ACA) antibodies show a well-documented association with focal involvement of the CNS in SLE. These antibodies could cause thrombosis by interfering with the protein C pathway of fibrinolysis. In addition, they are associated with endocardial and valvular heart disease, which is often observed in SLE and which could cause embolism. The relation between ACA and diffuse CNS lupus is not yet clear. Low-avidity anti-DNA antibodies are also found in CNS lupus, possibly because of their cross-reaction with cardiolipin. Antineuronal antibodies and lymphocytotoxic antibodies have been associated with diffuse CNS lupus and abnormalities on neuropsychological testing. However, the population of these antibodies is rather heterogeneous and it has not been possible to assess a common target antigen. Therefore, it is still obscure whether there is also a second immune-mediated mechanism responsible for the development of the diffuse form of CNS lupus.
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PMID:Diagnosis and pathogenesis of CNS lupus. 186 69

A 47-year-old man with Graves' disease suffered from a feeling of hunger and sweating in the night, polyarthralgia and fever one month after the start of treatment with methimazole. The above symptoms were ascribed to the side effects of methimazole; insulin autoimmune syndrome and lupus-like syndrome. The change in the antithyroid drug to propylthiouracil caused an amelioration of the symptoms. In addition to an anti-insulin antibody with a high binding capacity, hyperglucagonemia (260 pg/ml with a plasma glucose level of 61 mg/dl) was observed, which returned to normal in parallel with the decrease in the insulin binding capacity of the plasma one month after beginning the treatment with propylthiouracil. A normal decrease in the plasma glucagon level due to exogenous insulin (2 mU/kg/min) was observed with the euglycemic clamp. However, the plasma glucagon level was not suppressed by the oral glucose loading and elicited a poor response to the arginine infusion. Taking previous reports into account, this basal hyperglucagonemia seems to be a characteristic finding in the insulin autoimmune syndrome, while a sluggish response of glucagon to oral glucose or arginine infusion might be ascribed to hyperthyroidism. This is the first case report concerning a kinetical study of the glucagon secretion in insulin autoimmune syndrome with Graves' disease.
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PMID:Hyperglucagonemia of insulin autoimmune syndrome induced by methimazole in a patient with Graves' disease. 265 8

During a survey period of 28 years a total of 449 patients suffering respectively from pemphigus, systemic lupus erythematous and chronic nephritis was admitted to the hospital. Of the 286 patients who received glucocorticoid treatment 28 were found to have steroid diabetes (9.8%). The incidences of steroid diabetes in these diseases were as follows: pemphigus 20% (7/35), systemic lupus erythematous 12.5% (14/112), chronic nephritis 5% (7/139). Two thirds of the diabetic subjects appeared asymptomatic, while the remainder showed polydipsia and polyuria. Renal glucosuria was seen in 3 cases and hyperosmolar hyperglycemia in 4. Blood glucose level in 10 out of the 21 remaining cases was 8.9 +/- 1.5 mmol/L and in the other 11 cases 14.8 +/- 2.4 mmol/L. Generally, the treatment of steroid diabetes is not intricate. Satisfactory improvement was seen in about 80% of the patients if a strict line of therapy against primary diabetes was oriented. In this series 18 patients did well under the treatment either with reduction of steroid or with use of oral hypoglycemic agents or insulin or both. Their blood glucose levels returned to normal and urine sugar disappeared rapidly. Four of the 5 deaths were caused by their primary diseases. One died of pemphigus complicated with infection and shock exhibiting an ante mortem blood glucose level as high as 31.7 mmol/L, obviously hyperosmolar status being the predisposing factor. Due to the fact that most of the steroid diabetic patients were clinically asymptomatic, delayed or misbranded diagnosis was not infrequently seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Steroid diabetes: an analysis of 28 cases]. 280 46

Four patients with central nervous system lupus erythematosus (SLE), were studied with nuclear magnetic resonance imaging (NMRI) and positron emission tomography (PET) to assess cerebral blood flow and glucose metabolism. The NMRI showed brain atrophy and demyelinating defects. The PET scan showed cerebral blood flow and metabolic abnormalities that improved in one patient after neuropsychiatric recovery. These preliminary findings demonstrate cerebral derangements in patients with SLE cerebritis.
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PMID:Cerebral involvement in systemic lupus erythematosus. 326 Jul 88

Autoantibodies in sera from newly diagnosed insulin-dependent diabetes mellitus (IDDM) patients recognize a 64,000 Mr human islet cell antigen. The incidence of these antibodies was 86% in 28 insulin-dependent diabetes mellitus patients, 100% in seven first-degree relatives with abnormal glucose tolerance, 6% in 34 healthy individuals, 17% in 29 patients with Hashimoto's or Graves' disease, and 0% in five systemic lupus erythematosis patients. It is suggested that the 64,000 Mr human islet cell protein is the major target antigen of islet cell autoantibodies in insulin-dependent diabetes mellitus.
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PMID:Immunoreactivity to a 64,000 Mr human islet cell antigen in sera from insulin-dependent diabetes mellitus patients and individuals with abnormal glucose tolerance. 352 81

In the studies reported here we demonstrate that bombesin decreases food intake in wolf (Canis lupus) pups without altering glucose or insulin levels. A high dose of cholecystokinin-octapeptide (CCK, 5 micrograms/kg) decreased food intake. CCK produced a transient increase in insulin, without altering glucose. Glucagon (0.5 mg/kg) failed to decrease food intake despite producing a marked hyperglycemia and hyperinsulinemia. Calcitonin was ineffective at decreasing food intake, although it did decrease the time spent feeding. These studies suggest a potential role for peripheral peptides in food regulation in the wolf.
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PMID:The effect of peripheral administration of peptides on food intake, glucose and insulin in wolf pups. 355 Jul 28

The frequency of various autoimmune features in 14 patients with insulin-resistant diabetes mellitus (type B) was reviewed. Twelve patients had leukopenia, high titers of antinuclear antibodies (speckled pattern), and hypoalbuminemia; 11 had elevated serum levels of IgG and high erythrocyte sedimentation rates; 7 had proteinuria and high serum levels of antibodies to DNA; and 5 had alopecia and elevated serum levels of IgA. Lupus erythematosus preparations were negative in all patients. Eight patients met the conventional criteria for the diagnosis of systemic lupus erythematosus. Three patients developed renal involvement while under care at the National Institutes of Health. Kidney tissue samples showed proliferative and membranous glomerulonephritis, tubulointerstitial nephritis, and electron-dense deposits similar to those of lupus nephritis. The lupus nephritis in these 3 patients appeared to be independent of the level of insulin-receptor antibody and glucose dysmetabolism. This study documents the presence of systemic lupus erythematosus in a large proportion of patients with insulin resistance due to autoantibodies to insulin receptors and emphasizes that careful monitoring of such patients for major complications of lupus nephritis is warranted.
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PMID:Lupus nephritis and other autoimmune features in patients with diabetes mellitus due to autoantibody to insulin receptors. 396 55

22 nonneoplastic, noninflammatory effusions (cirrhosis and congestive heart failure), 12 non-neoplastic inflammatory effusions (tuberculosis, lupus erythematosus, rheumatoid arthritis, and idiopathic pleuropericarditis), and 58 neoplastic effusions (cancer of lung, breast, ovary, and pancreas, and lymphoma) were analyzed by radial immunodiffusion for orosomucoid concentration. The average concentration +/-SE was 35+/-4, 65+/-17, and 130+/-13 mg/100 ml in the three types of effusion, respectively. By gel filtration and ion exchange chromatography, orosomucoid was isolated from 12 nonmalignant and 14 malignant fluids. The orosomucoid preparations reacted as single components in acrylamide gel electrophoresis at pH 9.0, and in immunodiffusion and immunoelectrophoresis against antisera to human serum and to human plasma orosomucoid. In radial immunodiffusion, the slope of the line relating concentration to the square of the diameter of the precipitate area was identical for orosomucoid isolated from normal human plasma and from nonneoplastic effusions, but was subnormal for orosomucoid isolated from neoplastic fluids. All orosomucoid preparations had normal amino acid composition. Orosomucoid from the nonmalignant effusions had normal carbohydrate content. 11 of 14 samples of orosomucoid isolated from neoplastic fluids had abnormalities in carbohydrate composition, consisting of subnormal content of sialic acid (11 of 14), hexose (10 of 14), and hexosamine (3 of 14), and abnormally high content of hexosamine (4 of 14). Discriminant analysis showed that concentration of orosomucoid distinguished between neoplastic and nonneoplastic noninflammatory effusions more effectively than concentration of total protein, albumin, alpha(1), alpha(2), beta, or gamma-globulin.
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PMID:Orosomucoid content of pleural and peritoneal effusions. 420 34


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