Cachexia, the metabolic component of neoplastic diseases.
Cachexia, the metabolic component of neoplastic diseases.
复制标题
恶病质，肿瘤疾病的代谢成分。
作者：
G. Costa
肿瘤的生长导致宿主器官和功能的深刻改变。总的结果是恶病质，一种主要以虚弱、厌食和宿主成分的消耗和重新分配为特征的综合征。恶病质是解剖学改变、食物摄入或吸收减少以及代谢改变的结果。在癌症患者中，解剖学上的改变总是存在的。然而，反复观察到，恶病质的程度与肿瘤负荷、肿瘤细胞类型或受累解剖部位没有简单的相关性。食物摄入或食物吸收受损的后果是癌症患者总体发病率的主要因素。蛋白质和/或脂肪储备的消耗、维生素缺乏症和微量元素浓度的降低，以各种不同的方式组合在一起，导致几乎与营养不良或消瘦症相同的状态。最近为癌症患者制定了明确的识别这些状态的指导方针。这些综合征的认识是巨大的临床重要性，因为它们是潜在的可逆的现代技术的高营养。同样重要的是要认识到由肿瘤产生的代谢作用，并且独立于解剖改变或营养物质的输送不足。非内分泌肿瘤产生的内分泌综合征就是这种影响的例证，这种影响在概念上具有重要意义，因为它们意味着肿瘤分泌的有毒物质作用于远离解剖受累部位的部位。对这些缺陷的研究很可能为理解癌症侵袭的机制铺平道路。
Summary The growth of cancer leads to profound alterations of host organs and functions. The overall result is cachexia, a syndrome characterized primarily by weakness, anorexia, and the depletion and redistribution of host components. Cachexia is the consequence of anatomical alterations, decreased food intake or absorption, and altered metabolism. Anatomical alterations are always present in a cancer patient. It has been repeatedly observed, however, that the degree of cachexia bears no simple correlation to tumor burden, tumor cell type, or anatomical site of involvement. The consequences of impaired food intake or food absorption are a major contributor to the overall morbidity of the cancer patient. Depletion of protein and/or fat stores, hypovitaminoses, and decrease in the concentration of trace elements, variously combined, lead to states nearly identical to kwashiorkor or marasmus. Clear guidelines for recognition of these states have been set recently for cancer patients. Awareness of these syndromes is of enormous clinical importance since they are potentially reversible by the modern techniques of hyperalimentation. It is also important to recognize metabolic effects produced by tumors and independent of either anatomical alterations or insufficient delivery of nutrients. Such effects, exemplified by the endocrine syndromes produced by nonendocrine tumors, are of substantial conceptual importance inasmuch as they imply secretion by the tumor of toxic substances that act at sites distant from the sites of anatomic involvement. The study of such defects might well pave the way to understanding of the mechanisms of cancer aggression.