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The balance between the rates of formation and disposition of a protein determines its plasma concentration, and it is now believed that protein disposition, particularly of albumin, takes place largely in the gastrointestinal tract. In 1933, Moschowitz suggested that the hypoproteinemia of an enteric inflammation such as ulcerative colitis was due to excessive protein loss into the gut. Fourteen years later, Citrin et al proved that the hypoalbuminemia seen with giant gastric rugal hypertrophy results from excessive albumin loss into the stomach. That idiopathic hypoproteinemia, a rare condition presenting as edema without obvious cardiac, hepatic, or renal disease, could be similarly explained was not appreciated until 1959 when Gordon demonstrated an abnormal leak of large molecules from the blood into the gastrointestinal tract of patients with this disorder. Since then Jarnum and his colleagues have contributed significantly to our understanding of the pathophysiology and clinical consequences of proteinlosing gastroenteropathy.
Laster L. Protein-losing Gastroenteropathy. JAMA. 1964;187(8):622. doi:10.1001/jama.1964.03060210072030