Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
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An allergic disease may develop in any organ or system. The respective etiological factors include foreign proteins, infectious agents such as various microbes, viruses, moulds, parasites, chemical compounds often in the form of drugs usually designated as haptens, polysaccharides, benign and malignant neoplasms. Of the factors operating in the causal pathogenesis of such diseases the most important one is an exaggerated formation of antibodies, which appears to be uncontrolled and occurring irrespective of the demands of the organism. The essential morphological features in allergic inflammation are rather variegated, their diagnostic value differing in a wide range but being never absolute. The above features include eosinophilic leucocytes, allergic arteritis and phlebitis, fibrinoid necrotic glomerulonephritis, histiocytic granulomatous inflammation or histiocytic granuloma. Granulomatous capsulitis and trabeculitis affecting the spleen and lymph nodes are believed to be of major diagnostic significance. The immunofluorescent and immunoperoxidase methods and electron microscopy are important diagnostic tools. It has been generally acknowledged that many drugs operate as antigens. They may cause death of the respective patient, but allergic manifestations may subside after withdrawal of such drugs. On occasion they operate as a trigger mechanism with the allergy progressing even after treatment had been interrupted. Therefore they have been receiving extreme attention. Our collection of cases a case of giant-cell myocarditis following sulfamethoxypyridazine, anaphylactic shock has been reported to occur after intravenous administration of novocaine, and generalized cutaneous vasculitis developed in the same patient during the subsequent phase. A similar cutaneous finding was reported to have developed after penicillin injection, granulomatous inflammation developed owing to sulfonamide treatment. Allergic tumour-like lymphadenitis developed after administration of anti-anthracic serum; an anticonvulsive syndrome developed after hydantoinate administration. The latter consisted of generalized exanthema, hepatomegaly, splenomegaly and generalized lymphadenopathy. The lymph nodes showed tumour-like lymphadenitis mimicking lymphogranuloma or reticulosis. Allergic diseases appear as either isolated organ lesions or systemic diseases. Thus, isolated and systemic polyarteritis nodosa, isolated nasal, pulmonary or systemic Wegener's granulomatosis have been recognized. Temporal arteritis has been recognized as a localized form of systemic giant-cell arteritis. The haemolytic-uraemic syndrome appears to be a milder variety of thrombotic thrombocytopenic purpura. Allergic diseases or manifestations occasionally affect two or more organs or systems.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathology of allergic diseases. 248 27

Venous thrombophilia is the result of clotting changes namely of a hypercoagulable state together with blood flow and vessel wall changes. There is no need for all these components to be present in order for thrombosis to occur. As the matter of fact, thrombosis may occur even if only one of these conditions is present. In clinical practice a combination of factors is usualy seen. In comparison with arterial thrombophilia, clotting changes and blood flow seen to play a major role in venous thrombosis. Venous thrombophilia may remain asynptomatic or may result in a series of clinical syndromes. The commonest of these are: 1. Superficial vein thrombosis, 2. Deep vein thrombosis of legs, 3. Deep vein thrombosis of arms, 4. Caval veins thrombosis, 5. Portal vein thrombosis, 6. Hepatic veins thrombosis, 7. Renal vein thrombosis, 8. Cerebral sinuses thrombosis, 9. Right heart thrombosis, 10. Miscellaneous (ovarian, adrenal veins thrombosis, etc.). Since the first two are widely and easily recognized, these is no need for an extensive discussion. Deep vein thromboses of upper limbs are not as frequent as those of lower limbs or of superficial phlebitis but they can still be recognized on clinical grounds and non invasive techniques. The remaining 7 syndromes are less common and therefore less frequently suspected and recognized. Of particular interest, among these less common manifestations of venous thrombophilia are hepatic vein and renal vein thrombosis. Hepatic veins thrombosis, sometimes part of inferior vena cava thrombosis is most frequently due to an isolated occlusion of hepatic veins thereby causing a form of venocclusive disease. Occasionally diagnosis may be difficult because of slow onset of symptoms (hepatomegaly, right flank pain, fever, ascites etc.). The same is true for renal vein thrombosis which may also be of difficult diagnosis since it causes proteinuria and flank pain. The proteinuria is often interpreted as due to a nephrotic syndrome which, incidentally, may cause by its turn renal vein thrombosis. Portal vein thrombosis and cerebral sinuses thrombosis on the contrary are more easily suspected because of ascites, adominal pain, jaundice or headache, eye proptosis, vomiting. Right heart thrombosis should be suspected in cases of recurrent pulmonary embolization. Ovarian or adrenal veins thrombosis are rare. The competent physician should always consider, given certain congenital or acquired conditions, the possibility to be facing a special form of venous thrombosis or a venous thrombosis in unusual sites. An early diagnosis, as often in medicine, is of paramount importance for a prompt treatment and a satisfactory outcome.
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PMID:Clinical aspects of venous thrombophilia. 1367 53