Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

;Primary' pulmonary hypertension, which is rare in western countries, was found to be relatively common in Ceylon. The clinical and haemodynamic features were studied. There were two distinct types of the disease, malignant and benign. Patients with the malignant form of the disease had a rapidly progressive illness of short duration and an invariably fatal outcome. Those with the benign form gave a long history and, in spite of severe pulmonary hypertension, were only slightly disabled. They seemed to tolerate the disease better. An important factor which determined the clinical course of the disease was the patency of the foramen ovale. This appeared to act as a safety valve permitting a right-to-left shunt in times of stress. The foramen ovale was closed in all patients with the malignant type. The therapeutic implications of this need further study. Many patients with ;primary' pulmonary hypertension had an unusually high eosinophil count (normal range for Ceylon, 0-500 per cu.mm.). Patients in hospitals often have higher counts ranging from 0-1000 per cu.mm. due to intestinal parasitic infestation. Patients with ;primary' pulmonary hypertension were found to have a significantly higher mean eosinophil count than age-matched, sex-matched controls admitted to the Cardiology Unit with chronic rheumatic heart disease and congenital heart disease. The higher count was not due to intestinal parasitic infestation, and none of the other known causes of a raised eosinophil count were present. Four patients had eosinophil counts over 3,000 per cu.mm., the range commonly associated with tropical pulmonary eosinophilia, a disease caused by filariasis. These patients did not manifest any of the symptoms of tropical pulmonary eosinophilia. Patients with ;primary' pulmonary hypertension were examined for evidence of filariasis (clinical, haematological, and serological). Volunteers from among patients with tropical pulmonary eosinophilia and symptom-free patients positive for Wuchereria bancrofti microfilaria were similarly tested and also catheterized for evidence of pulmonary hypertension. The results of these investigations and their significance are discussed. The geographical incidence of ;primary' pulmonary hypertension and filariasis was similar. Filarial worms are known to cause pulmonary hypertension in animals. There is sufficient evidence to suspect that the same may be true in humans. This may explain the high incidence of the disease in Ceylon and its unusually high prevalence among men.
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PMID:"Primary" pulmonary hypertension, eosinophilia, and filariasis in Ceylon. 543 14

It has been shown that chronic African endomyocardial fibrosis (E.m.f.) is most likely the burnt-out phase of parasite-induced hypereosinophilia. It has also been shown that African E.m.f. and Loffler's heart disease are pathologically identical. The mechanism by which these parasites and/or eosinophilia are associated with endomyocardial damage remains, however, unknown. The parasites which have been associated with induction of eosinophilia in E.m.f. include filariasis; trichinosis; ascariasis and hookworm and schistosomiasis. These parasites are known to produce neurologic, cardiac, pneumonic, hepatic and dermal damage during the migration of their larvae; at which time eosinophilia is usually most severe. The tissue damage induced by larval migration of these parasites appears comparable to findings seen in the hypereosinophilic syndrome. The evidence from our observations and this review suggests that the cardiac damage induced by larval migration, like the neurologic, pneumonic and dermal damage, is allergic in nature. Endomyocardial fibrosis has previously been shown to be an allergic heart disease. It appears reasonable to regard African endomyocardial fibrosis as representing the most intense, non-specific cardiac allergic reaction to helminthic larvae.
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PMID:Helminthiasis, the hypereosinophilic syndrome and endomyocardial fibrosis: some observations and an hypothesis. 632 49

On epidemiological basis EMF behaves like a vector transmitted disease. The cardiac pathologies of EMF and HES are identical. In some cases of HES, hypereosinophilia may return to normal, leaving residual heart disease that is exactly like EMF. Most temporary residents from Europe and North America who developed EMF while resident in the endemic areas of Africa had hypereosinophilia that was induced by helminths. In our case studies from the EMF endemic areas of Nigeria, most children with acute idiopathic myocarditis associated with helminth induced hypereosinophilia, developed clinical EMF on follow up. We showed also that the rate of decline in the incidence of hypereosinophilia in EMF cases was significantly related to the duration of symptoms. Our studies and other observations show that EMF, like HES is a multiple system disease with similar organ damage. The morphologic evolution of cardiac damage in EMF appears similar to that reported for HES; with a stage of myocarditis/pericarditis, followed by a stage of cardiac necrosis, a stage of thrombosis and by the chronic fibrotic stage. Also during larval migration, all the helminths associated with EMF induce the same spectrum of damage in the central and peripheral nervous system, in the lungs, kidneys and skin, as are reported for HES. The cardiovascular damage reported for these worms (which include hypersensitivity vasculitis, acute myocarditis/ pericarditis) are also similar to what is reported for HES. Acute endomyocardial necrosis and thrombosis that are similar to what is found in HES, have been documented in Trichinella Spiralis and in filariasis. Increased cerium concentrations have been documented in the endocardium of EMF cases from South India. It remains to be established whether cerium excess, which is known to stimulate collagen synthesis does accelerate the process of endomyocardial fibrosis, following cardiac necrosis (which may have been triggered by helminths and the associated hypereosinophilia).
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PMID:Aetiology of endomyocardial fibrosis (EMF). 1192 51