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1.
Br J Clin Pharmacol ; 76(4): 560-72, 2013 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-23110527

RESUMEN

The complex relationships between cardiovascular, renal, and bone disease are increasingly recognized but not yet clearly understood. Vascular calcification (VC) represents a common end point between these interlinked systems. It is highly prevalent in chronic kidney disease (CKD) and may be responsible for some of the excess cardiovascular events seen in this condition. There is much interest in developing therapeutic agents to stop its development or reverse its progression. Traditionally considered to be due to abnormalities in calcium and phosphate metabolism alone, VC is now known to be the product of active, dynamic processes within the vessel wall. Primary prevention of VC is possible through successful prevention or reversal of progressive renal dysfunction, hypertension and hyperlipidaemia, but is challenging given the increasing global prevalence of these risk factors. Secondary prevention of VC through tight control of calcium and phosphate, can be achieved by dietary or pharmacological means. Both the modification of haemodialysis duration or methods and the use of renal transplantation have an effect. Novel drugs such as cinacalcet were hoped to halt calcification but results have been mixed, and no intervention has yet been shown to reverse calcification reliably. A new range of experimental targets involved in the putative mediatory pathways between bone and vascular disease has emerged. Aiming to manipulate the active mechanisms involved in calcium deposition, these hold hope for reversal of calcification, but are still theoretical or in early animal or human experimentation.


Asunto(s)
Enfermedades Cardiovasculares/prevención & control , Insuficiencia Renal Crónica/terapia , Calcificación Vascular/prevención & control , Animales , Calcio/metabolismo , Enfermedades Cardiovasculares/etiología , Enfermedades Cardiovasculares/metabolismo , Cinacalcet , Humanos , Naftalenos/administración & dosificación , Naftalenos/uso terapéutico , Fosfatos/metabolismo , Prevención Primaria/métodos , Diálisis Renal/efectos adversos , Diálisis Renal/métodos , Insuficiencia Renal Crónica/complicaciones , Insuficiencia Renal Crónica/tratamiento farmacológico , Insuficiencia Renal Crónica/metabolismo , Prevención Secundaria/métodos , Calcificación Vascular/etiología , Calcificación Vascular/metabolismo
4.
BMJ Case Rep ; 20092009.
Artículo en Inglés | MEDLINE | ID: mdl-21691400

RESUMEN

Large bowel obstruction is an important surgical emergency. The cause of obstruction may be benign or malignant, and include large bowel volvulus, polyps, intraperitoneal adhesions, strictures and neoplastic growths. Large bowel obstruction caused by gallstone(s) is a very rare phenomenon and not many cases are reported in the English literature. The present report describes a case of large bowel obstruction and faecal peritonitis caused by a gallstone perforating sigmoid colon. A database search (PubMed) did not locate any cases of large bowel perforation by a gallstone in the English literature, and hence this case report may be the first on this subject.

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