[Skin diseases and immune system].
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Most immunologic diseases are caused by the derailment of the humoral or cellular pathways of the immunologic defense system. This derailment results from numerous factors such as the inability of the patient to remove the pathogen; the consumption, defect, or deficiency in any component of these pathways, and the overproduction of any of the components. To diagnose these immunologic disorders one has to detect the pathogen and the reactions caused by it and to determine the cause of its nonclearance. The immunofluorescence techniques has been invaluable in detecting both the antigen that causes the disease and the reactions initiated by the antigen, such as the production of antibodies and the activation of the complement system. The immunoperoxidase technique has also been used for these purposes in certain instances. For detecting the circulating immune complexes which occur as intermediates in the chain of reactions initiated by the antigen, various physiochemical and biologic techniques have been used. However, none of these tests seems to be totally reliable for determining whether circulating immune complexes are present. The consumption of complement was detected by hemolytic estimations and radial immunodiffusion or rocket electrphoresis. These techniques were also useful in detecting the hereditary deficiencies in immunoglobulins and components of classical and alternative pathways of complement activation. Since these techniques cannot be used to estimate IgE, the radioallergosorbent test was used to measure such levels in the atopic patients. Cellular hypersensitivity was detected with skin tests together with methods which assess the ability of lymphocytes to produce mediators in response to antigen. Many of these mediator assays, however, are not suitable for this purpose. A satisfactory substitute appears to be to determine the factor in antigen-stimulated, lymphocyte culture supernatants which activates macrophages to take up radiolabeled colloidal gold or radiolabeled glucosamine. In contact allergic dermatitis, an increase in the IgD-bearing lymphocytes and granulocytes has also been correlated with cellular hypersensitivity. Lymphocytes and polymorphonuclear leukocytes coated with antibodies mainly directed against nuclear antigens of the basal layer cells of the noninvolved epidermis have invariably been encountered in psoriasis. The use of these findings for diagnostic purposes and for understanding the mechanisms of certain diseases is being explored.
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The classical division of the immune reactions into an immediate humoral type and a cellular late type is left in favour of a classification in 4 forms of reaction according to Gell and Coombs. This classification allows of a by far more reasonable coordination of the diagnostic measures as well as aimed therapeutic conclusions. In detail are differed: type I as anaphylaxis and reagin type (mediator-substance-type), example-anaphylactic shock and asthma; type II as cytotoxic type (cytotoxic antibodies), example-Coombs-positive haemolytic anaemia; type III as immune complex type, examples-serum disease, Arthus-reaction, glomerulonephritis; type IV as type of the cellular immune reactions. Combinations and transitions are possible in the same way as a further sub-classification of the types. It is demonstrated as by the combination of in-vitro-tests, skin tests and, perhaps, bioptic investigations the type is to be determined as far as possible. Only this allows an aimed and reasonable therapy.
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Using a research network of general practitioners (Resomed 44) representing the 20th of all GP's in the Loire Atlantique region and distributed at random according to district, age and sex made it possible to evaluate the respective prevalences of temporal arteritis (TA) and polymyalgia rheumatica (PMR) in all the systemic immune diseases listed. Among these diseases, rheumatoid arthritis was the most frequent (35.39%). TA (18.8%) and PMR (18.54%) had about the same prevalence. For each of these diseases the year/physician prevalence was evaluated at 0.11, which means that the probability for each GP to see 1 TA and 1 RP at once in 10 years. At the time of the survey, 52.9% of TA patients and 78.8% of PMR patients were surviving. GP's alone follow up more TA's and PMR's than the other systemic immune diseases.
Trophoblastic tumours form a spectrum of disease from the borderline malignancy of HM to highly aggressive choriocarcinoma. Their management requires the integration of the information derived from serial hCG estimations, the clinical history and pattern of spread of the disease, so that our understanding of the prognostic variables can be applied appropriately. This maximizes the patient's chances of complete remission from her disease with the minimum of toxicity. Given our knowledge of this group of diseases and an integrated approach to management, it should be uncommon for any woman to die from her trophoblastic tumour.
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It has been reported previously that HgCl2 chronically injected in the BN rat induced a biphasic renal disease. During the first stage, anti-glomerular basement membrane antibodies appeared and during the second stage, an immune-complex type glomerulonephritis was observed. In the present study, a systemic immune disease is described. During the first stage, antibasement membrane antibodies were observed in various extrarenal structures. Their localization has been found to depend mainly on the characteristics of the endothelium. During the second stage, immune-complex type deposits containing IgG and C3 were found in most vascular structures. Their localization did not apparently depend on the endothelial characteristics. Among the organs tested the lung was most often spared. The occurrence of immune complex deposits was found to depend on the dose of HgCl2 injected: deposits were absent in some high dose HgCl2-injected rats but they were very numerous in low dose HgCl2-injected rats. These deposits probably have a pthogenic role although no major histological lesion could be found. This model may help to explain immune complex type deposits in systemic diseases.
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The main symptom in immunologic diseases of the gut is diarrhea. This is true for heterosensitization as well as for autosensitization, for local as well as for generalized diseases. Since the immunopathogenetic mechanism is connected with the presence of the antigen, the manifestation is depending on its local and temporal persistence. Elimination of the antigenic factor terminates the diarrhea. In autosensitization this is not possible; therefore an antiphlogistic and immunosuppressive therapy is necessary.