Levitt David G, Levitt Michael D
Department of Integrative Biology and Physiology, University of Minnesota.
Research Service, Veterans Affairs Medical Center, Minneapolis, MN, USA.
Int J Gen Med. 2016 Jul 15;9:229-55. doi: 10.2147/IJGM.S102819. eCollection 2016.
Serum albumin concentration (CP) is a remarkably strong prognostic indicator of morbidity and mortality in both sick and seemingly healthy subjects. Surprisingly, the specifics of the pathophysiology underlying the relationship between CP and ill-health are poorly understood. This review provides a summary that is not previously available in the literature, concerning how synthesis, catabolism, and renal and gastrointestinal clearance of albumin interact to bring about albumin homeostasis, with a focus on the clinical factors that influence this homeostasis. In normal humans, the albumin turnover time of about 25 days reflects a liver albumin synthesis rate of about 10.5 g/day balanced by renal (≈6%), gastrointestinal (≈10%), and catabolic (≈84%) clearances. The acute development of hypoalbuminemia with sepsis or trauma results from increased albumin capillary permeability leading to redistribution of albumin from the vascular to interstitial space. The best understood mechanism of chronic hypoalbuminemia is the decreased albumin synthesis observed in liver disease. Decreased albumin production also accounts for hypoalbuminemia observed with a low-protein and normal caloric diet. However, a calorie- and protein-deficient diet does not reduce albumin synthesis and is not associated with hypoalbuminemia, and CP is not a useful marker of malnutrition. In most disease states other than liver disease, albumin synthesis is normal or increased, and hypoalbuminemia reflects an enhanced rate of albumin turnover resulting either from an increased rate of catabolism (a poorly understood phenomenon) or enhanced loss of albumin into the urine (nephrosis) or intestine (protein-losing enteropathy). The latter may occur with subtle intestinal pathology and hence may be more prevalent than commonly appreciated. Clinically, reduced CP appears to be a result rather than a cause of ill-health, and therapy designed to increase CP has limited benefit. The ubiquitous occurrence of hypoalbuminemia in disease states limits the diagnostic utility of the CP measurement.
血清白蛋白浓度（CP）是患病和看似健康的受试者发病和死亡的一个非常有力的预后指标。令人惊讶的是，人们对CP与健康不良之间关系背后的病理生理学细节了解甚少。本综述总结了白蛋白的合成、分解代谢以及肾脏和胃肠道清除是如何相互作用以实现白蛋白稳态的，这在以前的文献中未曾有过，重点关注影响这种稳态的临床因素。在正常人体内，白蛋白周转时间约为25天，反映出肝脏白蛋白合成速率约为10.5克/天，由肾脏（约6%）、胃肠道（约10%）和分解代谢（约84%）清除率保持平衡。脓毒症或创伤导致的低白蛋白血症急性发展是由于白蛋白毛细血管通透性增加，导致白蛋白从血管重新分布到间质空间。慢性低白蛋白血症最容易理解的机制是在肝脏疾病中观察到的白蛋白合成减少。白蛋白产生减少也解释了低蛋白和正常热量饮食时出现的低白蛋白血症。然而，热量和蛋白质缺乏的饮食并不会降低白蛋白合成，也与低白蛋白血症无关，且CP不是营养不良的有用标志物。在大多数非肝脏疾病状态下，白蛋白合成正常或增加，低白蛋白血症反映白蛋白周转速率加快，这要么是由于分解代谢速率增加（一种了解甚少的现象），要么是白蛋白向尿液（肾病）或肠道（蛋白丢失性肠病）的丢失增加。后者可能与细微的肠道病变有关，因此可能比普遍认为的更为常见。临床上，CP降低似乎是健康不良的结果而非原因，旨在提高CP的治疗益处有限。疾病状态下普遍存在的低白蛋白血症限制了CP测量的诊断效用。
