Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004364 (autoimmune disease)
 24,845 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four cases are described of multi-system immunologically-mediated disease (systemic lupus erythematosus (two cases), polymyositis, and sarcoidosis) in association with thyroid autoimmunity. In all patients there was evidence of T lymphocyte deficiency, namely poor response of peripheral blood lymphocytes (PBL) to T cell mitogens (four cases) and failure or decreased ability to become sensitized to dinitrochlorobenzene (three cases), although two patients were ill and two were being treated with steroids. There was also evidence of B lymphocyte deficiency since PBL of no patient responded normally to pokeweed mitogen, a B and T lymphocyte mitogen. In two patients there was evidence of cell-mediated immunity to human thyroid antigens. Although thyroid stimulating antibody was not detected in the one patient with Graves' disease tested, significant titres of thyroid antibodies were detected in all cases. Possible relationships between T lymphocyte deficiency, organ-specific autoimmune disease and immunologically-mediated multi-system disorders are discussed.
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PMID:Multi-system immunologically mediated disease: T lymphocyte deficiency and thyroid immunologic disease--a report of four cases. 30 99

We studied a 57-year old woman with severe myasthenic syndrome predominantly proximal. There was no therapeutic effect using cholinesterase inhibitors. Clinical findings, electromyography, whole body scanning and biopsy revealed polymyositis. Thirteen years before the patient was operated of a benign thymoma. The history of the patient showed numerous life threatening episodes of viral and fungal infections. Autoimmune anemia was diagnosed. Investigations of the immune system in vivo and in vitro revealed severe qualitative and quantitative defects in the lymphocyte population spontaneously forming rosettes with sheep red blood cells (SRBC). Thymoma, autoimmune disorder, such as polymyositis and myasthenia gravis, unspecifically elevated antibody titers, multiple severe viral and fungal infections and the defect of the cell-mediated immunity suggest a T-lymphocyte effector- and regulatory dysfunction in this patient.
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PMID:Polymyositis, myasthenic syndrome and thymoma in a patient with defective cell-mediated immunity. 31 78

Autoimmune diseases are characterized by an alteration of the body's defense mechanism, designed for protection against infections and toxic injuries, which for unknown reasons attacks and destroys normal tissue. Some evidence strongly suggests that such diseases are the result of hydrolytic enzymes that escape from lysosomes whose membranes have been damaged by lipid peroxidation or other causes and that combine with and denature normal tissue proteins--in effect converting them into foreign proteins--to which the body then reacts by producing antibodies. During the past ten years, in a private dermatologic practice, we have conducted clinical investigations on the possible therapeutic value of vitamin E in the management of a number of disabling skin diseases of unknown etiology as well as several muscular disorders. Among the diseases that were successfully controlled were a number in the autoimmune category, including scleroderma, discoid lupus erythematosus, porphyria cutanea tarda, several types of vasculitis, and polymyositis. Since vitamin E is a physiologic stabilizer of cellular and lysosomal membranes, and since some autoimmune diseases respond to vitamin E, we suggest that a relative deficiency of vitamin E damages lysosomal membranes, thus initiating the autoimmune process.
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PMID:Is vitamin E involved in the autoimmune mechanism? 34 98

Although there is good evidence that D-penicillamine can induce polymyositis, the exact pathogenic mechanism remains unclear. We report two patients with psoriatic arthritis and primary biliary cirrhosis respectively, who developed polymyositis while receiving D-penicillamine treatment for their primary diseases. Whether D-penicillamine treatment was the sole cause of polymyositis or acted as a trigger for the development of a secondary autoimmune disease is discussed.
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PMID:Polymyositis complicating D-penicillamine treatment. 177 10

Paraneoplastic neurological syndromes are of two types: some are more often seen without than with cancers and may therefore be called "occasionally para neoplastic" (e.g. chronic sensorimotor polyneuropathy and polymyositis), while others are fairly regularly associated with cancers, and particularly with small cell lung carcinoma. In this category falls subacute encephalomyelitis, an entity of broad anatomico-clinical spectrum including limbic encephalitis and subacute sensory neuronopathy; the patient's serum and cerebrospinal fluid may contain neuronal antinuclear antibodies. One type of subacute cerebellar degeneration is characterized by the presence of antibodies specifically directed against Purkinje cell cytoplasmic antigens, and it is associated with ovarian and mammary cancers. The other type shows no antibodies or different antibodies and sometimes neuronal antinuclear antibodies; the latter case may represent the cerebellar form of subacute encephalopathy. Because it may be either a true autoimmune disease or a true paraneoplastic syndrome, Lambert-Eaton myasthenic syndrome, caused by autoantibodies that block the voltage-dependent calcium channels, stands out as the most convincing argument in support of the autoimmune paraneoplastic syndrome theory. The theory, which refers to cross-antigenicity, cannot be extended to the other syndromes without reservation: there is no evidence that autoantibodies are neurotoxic, and specific autoantibodies in high levels are sometimes detected in patients with cancer but without any neurological symptom. Nevertheless, the finding of circulating antineuronal antibodies in patients with a suggestive clinical syndrome should prompt investigations for cancer perhaps at an early stage.
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PMID:[Paraneoplastic neurologic syndromes]. 182 23

Several reports have linked the presence of certain serum autoantibodies with particular clinical manifestations of autoimmune disease. For example, the Jo-1 antibody is now established as a marker for fibrosing alveolitis in polymyositis. To investigate the possible association of further autoantibodies or idiotypes with fibrosing alveolitis in autoimmune rheumatic disease a panel of autoantibodies was measured in serum samples from 28 patients with systemic lupus erythematosus (SLE) (10 with and 18 without lung involvement), 21 patients with scleroderma (12 with fibrosing alveolitis and nine without), and 41 patients with 'lone' fibrosing alveolitis. Antibodies measured were IgM and IgG anti-dsDNA and anti-ssDNA antibody; IgG and IgM anticardiolipin antibody; anti-poly (ADP-ribose) antibody; antibodies to two common idiotypes of anti-DNA antibodies, designated 134 and 16/6; and IgM, IgG, and IgA isotypes of rheumatoid factor. None of these antibodies was specifically associated with lung involvement in SLE or scleroderma, but a trend was found towards an increase in all autoantibodies in association with lung disease in SLE, while the reverse trend was seen in scleroderma.
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PMID:Autoantibody and idiotype profile of lung involvement in autoimmune rheumatic disease. 232 27

The classification of inflammatory muscle disorders is at best confusing owing to the wide spectrum of clinical, histological and serological findings within this group of patients. Although it is generally agreed that most cases reflect an autoimmune disorder with skeletal muscle as the primary target tissue, additional features of the more common form of the disease in juvenile patients, dermatomyositis, have suggested that it may differ in aetiology and pathogenesis from other forms of inflammatory muscle disease. Some adults may also be included within this category. In this study, we have divided patients with inflammatory muscle disease into two groups, 8 adult patients with 'pure' polymyositis and 13 children with dermatomyositis, and compared their in vitro lymphocyte function. Abnormal proliferative responses to T-cell mitogens were shown by peripheral blood mononuclear cells (PBM) from adult patients. PBM from the children gave values similar to normal control children. In vitro immunoglobulin production by cells from adult patients was comparable with appropriate controls both in the presence and absence of pokeweed mitogen. Childhood controls responded similarly to normal adults. PBM from the juvenile patients with dermatomyositis, however, produced significantly elevated levels of immunoglobulin spontaneously, with little or no increase for most patients following mitogen stimulation. This defective response was shown to be a consequence of activated T- and B-cells present in their peripheral blood and was not related to clinical parameters or drug therapy.
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PMID:A comparative study of in vitro proliferative responses to mitogens and immunoglobulin production in patients with inflammatory muscle disease. 246 36

A prospective study of IgG and IgM isotypes of anticardiolipin antibodies (aCL) was performed in a series of 167 patients with various autoimmune diseases, including rheumatic and nonrheumatic disorders, and in a group of 100 healthy blood donors. The IgG aCL serum was regarded as positive if a binding index (BI) greater than 2.85 (3.77 SD) was detected and a BI greater than 4.07 (3.90 SD) was defined as positive for IgM aCL. Forty patients (24%) were found to be positive for IgG and/or IgM aCL. IgG aCL were detected in 23% of patients with systemic lupus erythematosus (SLE), in 9% with idiopathic thrombocytopenic purpura, in 7% with progressive systemic sclerosis, and in 6% with dermatomyositis-polymyositis. IgM aCL were present in 43% patients with primary biliary cirrhosis, in 33% with rheumatoid arthritis, in 22% with SLE, and in 8% with giant-cell arteritis. IgG aCL were found to have a significant association with thrombosis and thrombocytopenia, and IgM and aCL with haemolytic anaemia and neutropenia, in SLE but not in the other autoimmune diseases. The identification of these differences in the aCL isotype associations, depending on the autoimmune disorder, may improve the clinical usefulness of these tests.
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PMID:Anticardiolipin antibodies in patients with autoimmune diseases: isotype distribution and clinical associations. 261 16

Genetic factors may be important in the development of autoimmune disease. We describe the development of fulminant systemic lupus erythematosus in a patient 5 years after recovery from polymyositis. The successive unfolding of different autoimmune diseases in the same individual is suggestive of sequential gene activation.
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PMID:Successive unfolding of two different collagen vascular diseases in the same patient. 278 96

Murine polymyositis (PM) induced by coxsackievirus B1 (CVB1) has been used as a model of human PM. Our study was undertaken to investigate the role of T cells in CVB1 induced PM by examining disease development in neonatally thymectomized mice. Clinical weakness and histological inflammatory myositis occurred in 42.7% of sham operated animals but only 7.7% of thymectomized mice. These experiments demonstrate the importance of T cells in the pathogenesis of this virus induced autoimmune disorder.
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PMID:T cells are required for coxsackievirus B1 induced murine polymyositis. 283 72


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