PROTEIN-LOSING ENTEROPATHY IN HUMANS

摘要

In healthy individuals, loss of protein through the gut epithelium plays only a minor role in total protein metabolism; daily enteric loss of serum proteins accounts for approximately 1-2% of the entire serum protein pool and enteric loss of albumin accounts for less than 10% of total albumin (1). Indeed, most endogenous proteins found within the gut are from secretions and sloughed enterocytes. Protein-losing enteropathy (PLE) is characterized by a loss of serum protein into the gastrointestinal (GI) tract resulting in hypoproteinemia, which can be complicated by edema, ascites, pleural and pericardial effusions and malnutrition. GI protein loss in PLE has been reported to involve up to 60% of the total albumin pool. This excessive protein loss across the gut epithelium can be due to either mucosal injury, resulting in increased mucosal permeability, or to lymphatic obstruction resulting in direct leakage of protein-rich lymph. The serum protein levels most affected by this process are those withlimited ability to rapidly respond to such losses and generally have longer half-lives such as albumin, most immunoglobulins and ceruloplasmin. Hepatic protein synthesis is maintained or slightly increased in patients with PLE and this is reflected by normal or increased levels of rapid-turnover proteins such as prealbumin, also known as transthyretin (2). Lower serum concentrations of other substances such as lipids, iron and other trace elements are also occasionally encountered in PLE as is lymphopenia, particularly in the setting of lymphatic obstruction.