reflected the protein status rather than the composition of the diet associated with the development of the deficiency state. Whitehead developed two simplified techniques, usable in the field, to relate the concentration of some non-essential amino acids to that of a group of essentials, the ratio beinq-3 directly correlated with the severity of protein deficiency, gauged in part by the serum albumin levels. Arroyave has proposed the ratios of several essential amino acids, indivi dually, to qlycine, as positively correlated with nutritional history and proteLn status (5). Both authors feel that these ratios or indices arc usuful for the recognition of marginal or pre-clinical cases of protein malnutrition. In marasmus, however, they do not serve as a gaucge of severity (8). The present report analyses the relationship between serum total protein, serum albumin and plasma amino acid concentrations in 41 severely malnourished infants and child ren, in an effort to assess their usefulness aq clinical or field tools. Materials and Methods The patients studied represent 41 nearly consecutive unselected cases of severe malnutrition admitted under our care to the British American Hospital in Lima, Peru. In most of them chronologic age was verified by examination of birth or baptismal certificates. Along with anthropometric mea surements, physical examination, routine hematologic studies, serum electrolytes, and appropriate cultures, the initial evaluation included serum total protein, serum albumin, and plasma free amino acid determinations. In all but one case (when it-was drawn 1.5 hours later, after partial rehydration) venous blood samples were obtained wiLhin the first hour after admission. Although we have no reliable data on the * Tyrosine and Cystine have also been included as essentials.

Neurologic findings characteristic of the impending hepatic coma syndrome occur in some cirrhotic patients treated with diuretic agents that may induce potassium losses (1-5). Even when diuretic agents are not employed, hypokalemia may be associated with this syndrome (6-8). Patients demonstrating these signs often improve after treatment with potassium salts. This result of therapy might indicate that potassium deficiency per se is a pathogenetic factor in the impending hepatic coma syndrome (9). Because of the extensive evidence relating abnormalities in nitrogen metabolism to hepatic coma (10), however, it seemed possible that some derangement of nitrogen metabolism might be associated with potassium deficiency.This hypothesis, relating potassium deficiency indirectly to the hepatic coma syndrome by an influence this cation has on ammonium metabolism, provided the rationale for undertaking this investigation. The relation of potassium to ammonium metabolism was studied in patients with cirrhosis of the liver and ascites rendered acutely potassium deficient by a diuretic regimen. The results of these studies demonstrate that metabolism of ammonium by the kidney is altered in potassium-deficient patients and that significant quantities of ammonium may be delivered to the cir-* A preliminary report of this investigation was included in the proceedings of the American Association for Study of Liver Disease, Chicago, 1959 (Gastroenterology 1960, 38, 803).

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