Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients infected with the human immunodeficiency virus (HIV) appear to have a high risk of ischaemic cerebral events. We observed two cases of cerebral infarction in patients with acquired immune deficiency syndrome (AIDS). In the first case, a 38-year-old homosexual with no cardiovascular risk other than smoking presented with rapidly progressive hemiparesia. Brain CT-scan visualized two infarcts in the territory of the right sylvian artery and the arteriography an occlusion of the internal carotid artery. In the second, a 37-year-old homosexual, hospitalization was required for a left-sided pure sensitive epilepsy seizure. There was no cardiovascular risk other than smoking. Magnetic resonance imaging showed parietal ischaemia and thrombus in the left atrium without atrial hypertrophy was seen at transoesophageal echocardiography. In both cases, there was no evidence of endocarditis, dissection of the neck vessels or disseminated intravascular coagulation nor of associated viral or bacterial infectious complication of AIDS. Angiographic findings eliminated cerebral vascularitis. Among the perturbed haemostasis factors previously reported in HIV+ patients, we observed free proteins S deficiency (68 and 43%) and heparin cofactor II deficiency (54 and 40%). Serum albumin was 33 and 32 g/l respectively. Outcome was favourable in both cases with anticoagulant therapy. These coagulation anomalies would not appear sufficient to explain cerebral infarction. Other mechanisms including immune complexed deposition, direct HIV toxicity for endothelial cells or the effect of cytokines on smooth muscles fibres and fibroblasts are probably more important causal factors.
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PMID:[Cerebral infarction in human immunodeficiency virus infection]. 763 44

Cardiovascular diseases are the leading cause of death worldwide. Conceptually, endothelial dysfunction, inflammatory status and oxidative stress are at the forefront in the onset and development of most cardiovascular diseases, particularly coronary artery disease and heart failure. Serum albumin, the most abundant plasma protein, has many physiological properties, including anti-inflammatory, antioxidant and antiplatelet aggregation activity. It also plays an essential role in the fluid exchange across the capillary membrane. Definite evidence is that hypo-albuminemia is a powerful prognostic marker in the general population as well as in many pathological settings. In the more specific context of cardiovascular diseases, serum albumin is independently associated with the development of a variety of deleterious conditions such as coronary artery disease, heart failure, atrial fibrillation and stroke. Serum albumin has also emerged as a powerful prognostic parameter in patients with coronary artery disease, heart failure, congenital heart disease, infective endocarditis, cardiovascular surgery and stroke, regardless of usual prognostic markers. This prognostic value probably refers mainly to the malnutrition-inflammation syndrome and the severity of comorbidities. Nevertheless, hypo-albuminemia may act as an unknown and modifiable risk factor that contributes to the emergence and the pejorative evolution of cardiovascular diseases, mainly by exacerbation of inflammation, oxidative stress and platelet aggregation, and by pulmonary and myocardial edema. This article provides an overview of the physiological properties of serum albumin, the prevalence, causes, prognostic value and potential contribution to the emergence and aggravation of cardiovascular disease of hypoalbuminemia, as well as its clinical implications.
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PMID:[Serum albumin and cardiovascular diseases: A comprehensive review of the literature]. 2990 49