Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study of two cases of young patients with renal transplants who, successively and a few months after the procedure, presented a thrombophlebitis of the lower extremities (with or without pulmonary embolism), then an acute coronary insufficiency, without any encouraging or triggering factor, raises the hypothesis that this is not a mere coincidence. In fact, in the literature, numerous cardiovascular risk factors) inherent in complicated chronic renal failure, dialysis, steroid therapy and immuno-suppressive treatment (Azathioprime, under these circumstances) were demonstrated. In addition, abnormalities of the platelets aggregation, hemostasis and fibrinolysis, were at the origin of thrombo-embolic accidents. Besides any specific cardiovascular risk factor or any obvious biological anomaly, there is still a predisposition of patients with renal transplants, to arterial as well as venous thrombo-embolic accidents.
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PMID:[Arterial and venous thromboembolic complications in patients with renal transplants. Apropos of 2 cases]. 266 42

Tyrosine kinase inhibitors, represented by sunitinib, sorafenib, axitinib and pazopanib, are emerging molecules harbouring antitumoural efficacy in multiple neoplasia. We report the case of a 51-year-old woman with right thoracic sarcoma who developed fatal heart failure on pazopanib. The patient had no cardiovascular risk factor, except previous exposure to anthracycline, and her cardiac function was normally controlled before initiating the pazopanib. Despite a rapid tumour response, fatigue rapidly appeared, requiring treatment interruption 2 weeks after pazopanib introduction. After clinical improvement, the pazopanib was reintroduced at reduced dose; however, a few days later, our patient was admitted for worsening dyspnoea and fatigue. Pulmonary embolism was excluded as was pleuropericardial effusion. Brain natriuretic peptide was the only laboratory abnormality, and echocardiography revealed acute and severe heart failure. The patient died despite pazopanib arrest and inotropic support.
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PMID:Rapid and fatal acute heart failure induced by pazopanib. 2633 88

Age is an important cardiovascular risk factor. Among others, age is associated with an increased risk to develop thrombotic cardiovascular complications, both in the arterial (acute myocardial infarction, stroke) and the venous (deep vein thrombosis, pulmonary embolism) system, which cannot be explained by the age-associated increase in cardiovascular risk factors alone. A number of studies have demonstrated that the accumulation of senescent endothelial cells and specific phenotypic and functional alterations associated with endothelial cell senescence may play an important role during the development and progression of cardiovascular disease. Prevention of platelet aggregation and thrombosis as well as fibrinolysis are important functions of the endothelium lining the vasculature. Moreover, impaired proliferation and migration of local endothelial cells as well as exhaustion of endogenous endothelial repair mechanisms involving progenitor cells may also contribute to thrombosis and its complications with age by impairing re-endothelialisation. In this short review, we present and discuss important findings regarding the effects of the cardiovascular risk factor age on endothelial cell morphology and function including the senescence-associated secretory phenotype and altered expression of factors involved in thrombosis and fibrinolysis. We also summarize results from clinical and experimental studies in rodent and other models on the possible connection between endothelial senescence and thrombotic events. Furthermore, major mechanisms and pathways underlying endothelial cell senescence and models to study its pathomechanisms are presented. Finally, we briefly discuss potential targets and therapeutic options to prevent, postpone or treat endothelial senescence and thus the increased burden of thrombosis associated with age.
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PMID:Endothelial cell senescence and thrombosis: Ageing clots. 2766 26