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Recent development in research and management of cancer anorexia-cachexia syndrome

机译:癌症厌食症综合征癌症研究与管理的最新发展

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Cachexia is among the most debilitating and life-threatening aspects of cancer, and is more common in children and elderly patients. Associated with anorexia, fat and muscle tissue wasting, psychological distress, and a lower quality of life, cachexia arises from a complex interaction between the cancer and the host. This process results from a failure of the adaptive feeding response seen in simple starvation and includes cytokine production, release of lipid-mobilizing and proteolysis-inducing factors, and alterations in intermediary metabolism. Cytokines play a pivotal role in long-term inhibition of feeding by mimicking the hypothalamic effect of excessive negative feedback signaling from leptin, a hormone secreted by adipose tissue, which is an integral component of the homeostatic loop of body weight regulation. This could be done by persistent inhibition of feeding-stimulatory circuitry including neuropeptide Y. Cachexia should be suspected in patients with cancer if an involuntary weight loss of greater than five percent of premorbid weight occurs within a 3-6-month period. The two major options for pharmacological therapy have been either progestational agents or corticosteroids. However, knowledge of the mechanisms of cancer anorexia-cachexia syndrome has led to, and continues to lead to, effective therapeutic interventions for several aspects of the syndrome. These include antiserotonergic drugs, gastroprokinetic agents, branched-chain amino acids, eicosapentanoic acid, cannabinoids, melatonin, and thalidomide-all of which act on the feeding-regulatory circuitry to increase appetite and inhibit tumor-derived catabolic factors to antagonize tissue wasting and/or host cytokine release. The outcomes of drug studies in cancer cachexia should focus on the symptomatic and quality-of-life advantages rather than simply on nutritional end points, since the survival of cachexia cancer patients may be limited to weeks or months due to the incurable nature of the underlying malignancy. Communication among physicians and other health care professionals provides the patient with a multidisciplinary approach to care. The patient record will be an excellent resource to document a plan of care and patient responses to treatment. Psychological distress and psychiatric disorders are common among cancer patients. These problems are also as common among the family members of people with cancer. The use of psychological and behavioral interventions in cancer is increasing, and recent studies have suggested that some of these techniques may affect quality of life and, perhaps, survival rates. Evaluations of relaxation, hypnosis, and short-term group psychotherapy have suggested some benefit with regard to anorexia and fatigue, although the population most likely to benefit from these interventions has not yet been determined. Because weight loss shortens the survival time of cancer patients and decreases performance status, effective therapy would extend patient survival and improve quality of life.
机译:恶病质是最衰弱和癌症危及生命的方面之一,是在儿童和老年患者中更常见。厌食,脂肪和肌肉组织萎缩,心理困扰,生活质量较低有关,恶病质起因于癌症和主机之间复杂的相互作用。从自适应馈送响应的故障该过程导致见于简单饥饿和包括细胞因子产生,脂质动员和蛋白水解诱导因子的释放,并且在中间代谢的改变。细胞因子在通过模仿过度负反馈信令的从瘦素,由脂肪组织,这是体重调节的稳态循环的整体部件分泌的激素下丘脑作用馈送的长期抑制发挥关键作用。这可以通过馈送刺激电路,包括神经肽Y.恶病质的持久抑制应在癌症患者如果不自主体重减轻更大的比病前重量的百分之五的3-6个月的期间内发生被怀疑来完成。对于药物治疗两大选项已要么促孕剂或皮质类固醇。然而,癌症厌食 - 恶病质综合征的机制的认识已经导致,并继续导致,有效的治疗干预综合征的几个方面。这些包括抗5药物,gastroprokinetic剂,支链氨基酸,二十碳五烯酸,大麻素,褪黑激素,和衍生的肿瘤的沙利度胺,所有这些作用在进食调节电路,以增加食欲和抑制分解因子拮抗组织消瘦和/或主机细胞因子释放。药物研究的癌症恶病质的成果应着眼于有症状和质量寿命的优点,而不是简单地对营养的终点,因为恶病质癌症患者的生存可能仅限于几个星期或几个月,由于潜在的无法治愈的性质恶性肿瘤。医生和其他医疗专业人士之间的沟通提供了一个多学科的方法来照顾病人。病人记录将记录的保健和患者的反应计划,以处理一个很好的资源。心理痛苦和精神疾病是癌症患者常见。这些问题也都是癌症患者的家庭成员之间一样普遍。使用在癌症的心理和行为干预的不断增加,以及最近的研究表明,其中的一些技术可能影响生活质量,也许,存活率。放松,催眠,短期集体心理评估,提出关于厌食和疲劳一些好处,虽然人口最有可能从这些措施受益尚未确定。因为减肥缩短癌症患者的生存时间和降低性能状态,有效的治疗将延长患者生存期,提高生活质量。

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