Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011633 (dermatomyositis)
4,181 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum FDPs were investigated in 30 healthy and 95 patients with pulmonary thrombembolia, not-stabilized angina pectoris, myocardial infarction, rheumatism, rheumatoid arthritis, lupus erythematodes and dermatomyositis. FDPs are determined by hemagglutination inhibition according to Merskey. They are found in the sera of the healthy in average values of 3.73 mkgr/ml. The highest average values in the first 24 h were found in case of pulmonary thrombembolia up to 106.64 mkgr/ml, followed by rheumatoid arthritis 26.3 mkgr/ml, myocardial infarction with complication 22.4 mkgr/ml, rheumatism +5.58 mkgr/ml, not-stabilized angina pectoris 5.5 mkgr/ml; and noncomplicated myocardial infarction 4.3 mkgr/ml. By the third day of the disease FDP in pulmonary thrombembolia decreased, whereas a negligible elevation was observed in case of non-complicated myocardial infarction. The results were interpreted as well as the cause for the presence of the mentioned products in those groups of diseases. FDP determination is recommended as a routine method in case of: diagnosis of pulmonary thrombembolia, differentiation of myocardial infarction with or without complications, differentiation of pulmonary thrombembolia from myocardial infarction in emergency states, progressing with chest pain, collapse phenomena, dyspnea and establishment of the activity of the process of rheumatoid arthritis. FDP determination in stenocardia and rheumatism is not expedient.
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PMID:[Level of fibrinogen/fibrin degradation products (F/FDP) in certain internal diseases]. 49 29

Seventy-one children with the diagnosis of systemic lupus erythematosus (SLE) (39 cases), dermatomyositis (25 cases), or scleroderma (7 cases) were studied retrospectively. The children with SLE were much sicker than those with the other two diseases and were found to have a poorer prognosis than adults with SLE. In general, the earlier the age of onset, the poorer the prognosis. Early gastrointestinal bleeding, abnormal renal findings, and cardiac abnormalities heralded early death from SLE. The peak incidence of SLE near the time of puberty suggests hormonal influence on this disorder in children. Survival rates and morbidity improved as the treatment improved. Corticosteroids were the main therapeutic agents. The patients with scleroderma also received varying doses of vitamin E, penicillamine, chloroquine hydrochloride, and salicylates. The antimetabolites were used to treat SLE starting in the late 1960s.
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PMID:Collagen disease in children. A review of 71 cases. 57 42

Myoglobin was detected in the sera of patients with dermatomyositis, polymyositis, scleroderma, and systemic lupus erythematosus (LE) with active myopathy. Overall, myoglobinemia was detected in 74.1% of sera taken from patients with active myositis before therapy, with slightly greater frequency in the groups with dermatomyositis and polymositis. With steroid therapy, this frequency fell to 43.4% and to 9.5% in patients in clinical remission not requiring therapy. Serum enzyme (creatine phosphokinase, lactic dehydrogenase, and SGOT) activity was higher in samples containing myoglobin, but there was considerable overlap between those with and without myoglobinemia. Sequential serum determinations in six patients demonstrated rapid reduction in the levels of serum myoglobin with therapy, usually before enzyme values had returned to normal. In one patient followed up for 30 months, myoglobinemia correlated with clinically observed exacerbations of rash and weakness to a greater degree than did enzyme determinations.
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PMID:Myoglobinemia in inflammatory myopathies. 57 36

Lupus erythematodes is related to the vegetative nervous system in Raynaud's disease, the butterfly distribution in the face, the involvement of the lateral part of the eyebrows (Hertoghe) and in cerebral attacks. Involvement of peripheral and central animal nervous systems is common and produces primary and secondary syndromes. Prominent are polymyositis or lupus-myopathy, in the brain mainly functional psychoses, epileptiform attacks, and a variety of focal, often very massive, signs. There are very clear differences from the neurologic signs of dermatomyositis, less so from arteritis nodosa and even less from progressive sclerodermia. Peripheral neurologic syndromes in lupus erythematosus are less common and more subtle than in arteritis nodosa. Bio-electric parameters of the petitmal-trias have been found. The relative absence of collagenoses from the spinal cord is also noticed in lupus erythematosus. Signs of involvement here appear to be limited and often subacute. Differential diagnosis has to consider many neurologic diseases, a special problem when MS is simulated just as in sclerodermia. Since cerbral attacks appear early in about 5%, the use of anticonvulsive drugs, particularly of the hydantoin group, provides special problems. Signs of myasthenia demand further attention. The neuropathologic changes are known in essential points and can obviously hardly be mistaken for inflammatory processes due to other causes. Certain basic facts appear to apply to other collagenoses. All 4 "grand" or "classic" collagen diseases are very similar and have much in common, but also show more or less definite differences. This is true for their clinical and anatomical appearance and last but not least to their neurologic aspects. The "roof-concept" of Collagenosis" is once more proved to be justified. As far as is known today the autonomic system plays a decisive and obligatory role only is sclerodermia. This syndrome is also the only one which contains the odd phenomenon of atrophy of which the best-known form is facial hemia-atrophy.
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PMID:[Erythematodes and nervous system (author's transl)]. 58 95

The study included 19 children with dermatomyositis. All showed frequently atypical cutaneous disords which in most cases were the initial manifestation. In every case there was some clinical evidence of proximal myopathy. Arthralgias were frequently found and sinusal tachycardia was present in 10 cases. The correct diagnosis was made from the beginning only in 6 cases. Systemic lupus erythematosus was the main cause of confusion. The differential diagnosis between these two entities cannot be made only by the presence or not of nephropathy, even if this disease was evident in 42% of patients with dermatomyositis. The most useful laboratory tests for the diagnosis and management were CPK, aldose and serum TGO. Electromyography was abnormal in every case where it was practiced. Muscular biopsy was valuable in 15 of the 19 patients. All were treated with prednisone and in most cases with good results.
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PMID:[Dermatomyositis in pediatrics]. 62 32

Sera of children with juvenile rheumatoid arthritis and other connective tissue diseases were tested for antibodies to native DNA by a radiolabeled-binding assay. Normal values were obtained in 130 children with JRA, including 28 with uveitis and 14 with selective IgA deficiency. Normal values were also found in sera from children with dermatomyositis, scleroderma, polyarteritis, ankylosing spondylitis, and a variety of other nonconnective tissue diseases. The only sera with elevated DNA-binding assays were from children with systemic lupus erythematosus. On the basis of these data, increased levels of antibodies to native DNA distinguished patients with active SLE from children with JRA.
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PMID:Diagnostic significance of antibody to native deoxyribonucleic acid in children with juvenile rheumatoid arthritis and other connective tissue diseases. 69 Jul 54

Frequency and type of pulmonary and pleural involvement in collagen disease (rheumatoid arthritis, progressive systemic scleroderma, polymyositis-dermatomyositis and lupus erythematodes are analysed on the basis of literature and of own cases with particular regard to the roentgenographic appearance.
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PMID:[Lung and pleural involvement in collagen disease (author's transl)]. 84 23

The Leucocyte-Migration-Inhibition-Test was performed to examine 10 patients with Systemic Lupus Erythematosus (SLE), 10 patients with Discoid Lupus Erythematosus (DLE) and 4 patients with Dermatomyositis for evidence of cell-mediated immunity to RNA, DNA, human muscle antigen and collagen human type I. Our results support, that cell-mediated immunity plays a pathogenic role in both diseases. Patients with SLE show a correlation between activity of disease, Leucocyte-Migration-Inhibition to DNA and DNA-binding-activity of serum. Muscle-antigen is an obvious relevant partner of reaction of cellular immunity in patients with Dermatomyositis.
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PMID:[Leukocyte migration inhibition test in lupus erythematosus and dermatomyositis]. 91 May 38

The clinical and radiological features in 100 patients with collagen diseases (rheumatoid arthritis, lupus, sclerodermia, dermatomyositis, and panarteritis nodosa) were compared with respiratory performance. 56 patients were drawn from the series of Pende et Al. and 44 from a personal series. The results are set out in tables and graphs. It was found that lung lesions due to collagen disease have no special clinical and radiological features. Respiratory performance is that of a restrictive syndrome that gradually progresses from A.R. to E.S., S. and P.M., accompanied by obstruction of the large airways, as shown by hyperinsufflation in sclerodermia and reduced specific conductance in rheumatoid arthritis.
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PMID:[Clinico-radiological and functional aspects of respiratory syndromes caused by collagen diseases]. 99 94

Immunosupprissive therapy was carried out using steroids, azathiprine and antilymphocyte globulin in one patient with systemic lupus erythematosus (SLE) and four with dermatomyositis. Response to treatment was based upon clinical evaluation. The patients with SLE and two of the four with dermatomyositis responded favourably to the regime. It is suggested that this preliminary study is sufficiently promising to warrant the creation of a rigidly controlled investigation.
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PMID:The treatment of connective tissue diseases with antilymphocyte globulin. 99 82


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