Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymphocytes from patients with insulin-dependent diabetes mellitus (IDDM), a chronic autoimmune disease, have recently been shown to have decreased surface expression of MHC class I antigens. Since IDDM and other autoimmune diseases share a strong genetic association with MHC class II genes, which may in turn be linked to genes that affect MHC class I expression, we studied other autoimmune diseases to determine whether MHC class I expression is abnormal. Fresh PBLs were isolated from patients with IDDM, Hashimoto's thyroiditis, Graves' disease, systemic lupus erythematosis, rheumatoid arthritis, and Sjogren's syndrome. Nondiabetic and non-insulin-dependent diabetes mellitus patients served as controls. MHC class I expression was measured with a conformationally dependent monoclonal antibody, W6/32. Freshly prepared PBLs from the autoimmune diseases studied and the corresponding fresh EBV-transformed B cell lines had decreased MHC class I expression compared with PBLs from normal volunteers and non-insulin-dependent (nonautoimmune) diabetic patients. Only 3 of more than 180 donors without IDDM or other clinically recognized autoimmune disease had persistently decreased MHC class I expression; one patient was treated with immunosuppressive drugs, and subsequent screening of the other two patients revealed high titers of autoantibodies, revealing clinically occult autoimmunity. Patients with nonautoimmune inflammation (osteomyelitis or tuberculosis) had normal MHC class I expression. Autoimmune diseases are characterized by decreased expression of MHC class I on lymphocytes. MHC class I expression may be necessary for self-tolerance, and abnormalities in such expression may lead to autoimmunity.
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PMID:Defective major histocompatibility complex class I expression on lymphoid cells in autoimmunity. 848 90

This study was undertaken to determine if there is an association between increased titers of five different antiphospholipid antibodies (aPLA) in young patients' sera and the occurrence of acute myocardial infarction (AMI). Antibodies to anticardiolipin (aCL), anti-phosphatidylserine (aPS), antiphosphatidylinositol (aPI), anti-phosphatidylcholine (aPC), and anti-phosphatidylethanol amine (aPEA) were measured in 214 patients (102 patients, 102 healthy controls and 10 patients with antiphospholipid syndrome). These antibodies were measured twice (within 4h of onset of acute myocardial ischemic chest pain and 3 months after the myocardial infarction) by enzyme linked immunosorbent assay (ELISA). Elevated titers of four different aPLA were detected in 6.9% of all patients with AMI on hospitalization. Titers of aPLA in AMI were elevated in the younger age group < 50 years old (P < 0.001) and in men only (not statistically significant). No correlation was found between the presence of aPLA and cardiovascular risk factors (smoking, hypertension, diabetes mellitus and hyper-cholesterolemia). Three of the seven patients with increased titers of aPLA did not have any other cardiovascular risk factors. The titers of aPLA were within normal range 3 months after AMI. Evidence of significantly elevated titers of different aPLA at the early stage of AMI suggests that these autoantibodies are present before the AMI and are not secondary to them. The disappearance of the elevated aPLA 3 months after AMI may be due to an absorption effect or possibly a cyclic phenomenon similarly found in other autoimmune diseases. aPLA may be an additional risk factor for AMI, and should especially be considered in a patient of the younger age group without apparent cardiovascular risk factors.
Lupus 1995 Aug
PMID:The presence of antiphospholipid antibodies in acute myocardial infarction. 852 29

Vitamin D has been discovered at the beginning of this century. 7-Dehydrocholesterol is converted to vitamin D3 in the skin and after several hydroxylations it is further converted to the active hormonal form, 1 alpha,25-(OH)2D3. Vitamin D stimulates the absorption of calcium and phosphate and is an essential link in bone resorption and formation and calcium metabolism. 1 alpha,25-(OH)2D3 acts through a vitamin D receptor. These receptors are not only present in clinical target organs (kidney, gut, liver) but can also be found in a wide variety of "non-classical" tissues (keratinocytes, cells belonging to the immune system). Moreover, numerous cells (keratinocytes, macrophages) can locally synthetize or can be induced to synthetize 1 alpha,25-(OH)2D3 and these cells are responsive to its action. When these data are combined, a possible paracrine function of 1 alpha,25-(OH)2D3 can be suspected. Via this paracrine function 1 alpha,25-(OH)2D3 can suppress the cellular and humoral immunity. Based on the discovery of these effects on immune cells in vitro it became clear that 1 alpha,25-(OH)2D3 might be an interesting molecule to prevent autoimmune diseases and organ transplantation. This has already been shown in several animal models (Heymann nephritis, diabetes mellitus, experimental allergic-encephalomyelitis, lupus). 1 alpha,25-(OH)2D3 demonstrates however some side-effects (hypercalciuria, hypercalcemia, bone resorption) and for this reason 1 alpha,25-(OH)2D3-analogs are developed with dissociated effects i.e. an activity profile that allows a specific action on non-classical tissues without calcemic effects. Some chemical modifications of the side chain, A and/or CD-ring results in "superanalogs" with 10 to 100-fold more activity on cell differentiation and the immune system then 1 alpha,25-(OH)2D3 but with less calcemic activity in vivo. These biological effects can be explained by differences in pharmacokinetics (low affinity for the plasma vitamin D-binding protein and short extracellular half-life) and increased intracellular activation and gen transactivation. Preclinical research must still be done to select the most potent superanalogs and to find the exact protocols for the prevention and treatment of autoimmune diseases and rejection of transplanted organs.
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PMID:[Immune modulation by vitamin D analogs in the prevention of autoimmune diseases]. 857 69

A 38 year-old man with a 12-year history of noninsulin-dependent diabetes mellitus with rapidly progressive diabetic complications presented with microangiopathic hemolytic anemia and thrombocytopenia. He had no disorders that could induce microangiopathic hemolytic anemia other than diabetic microangiopathy. In addition, there was a significant negative correlation between serum lactate dehydrogenase levels and peripheral platelet counts, which suggested that the hemolysis and thrombocytopenia occurred through the same mechanism. Activated partial thromboplastin time was slightly prolonged, and lupus anticoagulant and antiphospholipid immunoglobulin G antibodies were positive. Both the hemolysis and the thrombocytopenia spontaneously improved after the initiation of hemodialysis. This is a unique case of diabetic microangiopathic hemolytic anemia and thrombocytopenia in which antiphospholipid syndrome also may be involved.
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PMID:Case report: diabetic microangiopathic hemolytic anemia and thrombocytopenia with antiphospholipid syndrome. 861 92

A superficial (dermal) granuloma annulare (GA) of the eyelid developed in a 69-year-old woman who initially had no evidence of precipitating causes, including trauma, tuberculosis, octopus bite, lupus vulgaris, actinic damage, sarcoidosis, diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus, or rheumatic fever. She later developed complete bilateral nasolacrimal duct obstruction that led to dacryocystorhinostomy on the right side. Systemic workup showed evidence of a lupus-like syndrome. Although deep, subcutaneous GAs have been reported in the periocular tissues, episclera, and orbit in children and young adults, a superficial dermal GA of the eyelid in an elderly patient is distinctly rare. The characteristic histopathologic feature of both superficial and deep GAs is a necrobiotic granuloma in which necrotic collagen is surrounded by a zone of histiocytes and fibroblasts. This case demonstrates that superficial GA of the eyelid may be associated with an underlying lupus-like syndrome. This case also raises the question of whether GA of the eyelid and lupus erythematosus may be associated with bilateral nasolacrimal duct obstruction.
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PMID:Granuloma annulare of the eyelid. 872 83

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

Thermoregulation involves a long term adaptation system with hormonal processes and an immediate regulation system by extrapyramidal tracts, sympathetic part of autonomic nervous system and cortical integration of body temperature changes. Both system are under control of a hypothalamic center. Prolonged accidental exposure to intense cold and myxoedematous coma are the best known etiologies of hypothermia. However milder and often misdiagnosed hypothermia can occur at home in patients without endocrinologic disease. In these cases, hypothermia is due to dysfunction of immediate thermregulation under neuronal control, especially somatomotor and autonomic system. We report four cases of hypothermia of this kind. Two patients had an inhibition of peripherical mechanisms of protecting against cold (cutaneous vasoconstriction, shivering) and had dampened perception of cold: one was 73, had diabetes mellitus and took different drugs, the other one suffered from systemic lupus with myelopathy. The two other patients probably had a disorder of the thermoregulation hypothalamic center: one had Wernicke's encephalopathy and the other multiple sclerosis. From these cases and a review of the literature, we describe the different etiologies of hypothermia and their pathophysiology.
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PMID:[Hypothermia and the nervous system. Review of the literature apropos of 4 cases]. 876 Jun 89

The cause of toxic oil syndrome (TOS) has not yet been definitively determined, but some genetic susceptibility factors (certain HLA antigens and female sex) have been identified in 236 patients. Similarities with genetic factors for scleroderma and hydralazine-induced lupus (i.e. in TOS female sex and HLA-A24, Pcorrected = 0.00001 and DR4, Pcorrected = 0.04, respectively) may provide a clue to the responsible xenobiotic and its pathogenesis, and may also help in understanding the basis of the related eosinophilia-myalgia syndrome associated with tryptophan ingestion. In this paper it is also established that a human class I antigen (HLA-A24) and, independently, an HLA class II haplotype (DR4-DQ8, Pcorrected = 0.04) and arginine 52 in the alpha-DQ chains (Pcorrected = 0.03) are associated with TOS susceptibility, similarly to insulin-dependent diabetes. This further supports the classification of TOS as an autoimmune disease. Also, the increased frequency of a particular set of low-frequency HLA class I antigens in chronic TOS patients (i.e. B27, B37, B38 and B49) and the probable decrease in the frequency of HLA-B homozygotes in surviving patients (Pcorrected = 0.008) may provide an objective model to explain the maintenance of the HLA polymorphism: less frequent HLA alleles may be more advantageous in the event of unexpected human contact with unusual xenobiotics (not only microbes); however, other mechanisms working together to preserve and generate HLA polymorphism may coexist.
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PMID:Frequencies of HLA-A24 and HLA-DR4-DQ8 are increased and that of HLA-B blank is decreased in chronic toxic oil syndrome. 880 34

Hydroxychloroquine is used by 35% of SLE patients enrolled in the Baltimore Lupus Cohort. Eighty per cent of patients who took hydroxychloroquine at cohort entry remain on it six years later. In addition to its role for disease manifestations of lupus, hydroxychloroquine may be indicated for the prevention of disease or treatment-induced complications, including hyperlipidemia, diabetes mellitus, liver function test elevation and thrombosis.
Lupus 1996 Jun
PMID:Hydroxychloroquine use in the Baltimore Lupus Cohort: effects on lipids, glucose and thrombosis. 880 5

Membranous lipodystrophy, an uncommon disorder, was described by Nasu et al. in 1973 as a form of regressive degeneration or localized destruction of the adipose tissue. Clinical features of the lesions with membranous fat necrosis are variable and the condition can only be diagnosed histopathologically. These peculiar changes in fat tissue have been associated with many local and systemic diseases including lupus erythematosus, diabetes mellitus, erythema nodosum, stasis dermatitis, morphoea and trauma, but occasionally no underlying disease is found. Even though various hypotheses concerning the pathogenesis of membranous lipodystrophy have been proposed, the exact causes are still in dispute. We reviewed 22 patients having membranous lipodystrophy confirmed by biopsy and discuss the pathogenetic mechanisms which have been suggested by many authors.
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PMID:A clinical and histopathological study of 22 patients with membranous lipodystrophy. 895 96


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