Assuntos
Diabetes Mellitus/etiologia , Diabetes Mellitus/imunologia , Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia , Linfócitos T Reguladores/efeitos dos fármacos , Envelhecimento/imunologia , Envelhecimento/metabolismo , Doenças Cardiovasculares/prevenção & controle , Diabetes Mellitus/classificação , Humanos , Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico , Fatores de Risco , Linfócitos T Reguladores/fisiologia , Terminologia como AssuntoAssuntos
Diabetes Mellitus Tipo 2/terapia , Obesidade/terapia , Sobrepeso/terapia , Comportamento de Redução do Risco , Diabetes Mellitus Tipo 2/complicações , Diabetes Mellitus Tipo 2/mortalidade , Humanos , Obesidade/complicações , Obesidade/mortalidade , Sobrepeso/complicações , Sobrepeso/mortalidade , Resultado do TratamentoRESUMO
Although the cholesterol-heart hypothesis is often regarded as a dogmatic belief, controversy continues to surround the aetiology and pathogenesis of atherosclerosis. In fact, lowering cholesterol with statin drugs has been shown to reduce cardiovascular risk. However, statins have pleiotropic effects independent of their capacity to lower cholesterol. We highlight that statin drugs exert an important action on iron metabolism, which in turn may prevent progression and destabilization of atherosclerotic plaque. If it is found that the effect of statins on iron metabolism is a mechanism of their beneficial action, this consequence of statin use can be clinically replicated by other methods, such as controlled reduction of body iron stores. This might allow the use of lower doses or even obviate the use of statins in primary cardiovascular prevention, and therefore avoid the side effects and expense of these drugs.
Assuntos
Aterosclerose/tratamento farmacológico , Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia , Ferro/metabolismo , Relação Dose-Resposta a Droga , Custos de Cuidados de Saúde , Hemossiderose/tratamento farmacológico , Humanos , Inibidores de Hidroximetilglutaril-CoA Redutases/efeitos adversos , Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêuticoAssuntos
Antígeno Prostático Específico/metabolismo , Neoplasias da Próstata/metabolismo , Inibidores de 5-alfa Redutase/efeitos adversos , Animais , Neoplasias da Mama/metabolismo , Feminino , Humanos , Masculino , Camundongos , Prognóstico , Antígeno Prostático Específico/efeitos dos fármacos , Hiperplasia Prostática/tratamento farmacológico , Neoplasias da Próstata/etiologiaRESUMO
It is well-known that cancer surgery can actually promote the growth of some tumors by a variety of mechanisms. There are observational data suggesting that surgery per se can increase the risk of cancer among individuals without a history of clinical cancer. Occult microscopic cancers are exceedingly common in the general population and are held in a dormant state by a balance between cell proliferation and cell death and also an intact host immune surveillance. The catecholamine surge from the stress of surgery and resulting ß(2)-adrenergic signaling culminates in a transient and robust increased vascular endothelial growth factor expression locally and systemically that is enough to start tumor angiogenesis and end dormancy. The same catecholamine surge and ß(2)-adrenergic signaling impairs cell-mediated immunity at a crucial time. Elegant animal studies have demonstrated that perioperative nonselective ß-blockade abrogates surgical stress-induced angiogenesis and tumor growth. Prospective human trials are desperately needed and clinical implications are discussed.