Nutritional status was investigated in 10 patients who had previously undergone total gastrectomy without evidence of malignancy. The ability of these patients to ingest and absorb adequate amounts of nutrients was examined. Metabolic balance studies were also performed to discover how effectively these patients could accumulate and use the absorbed nutrients. In the controlled hospital situation, the amount of food ingested was greater than the amount required for maintenance of Ideal Body Weight. Although mild malabsorption of fat and nitrogen was documented, weight gain and positive nitrogen balance occurred. In direct contrast, food intake significantly decreased when the patients returned to their home environment. While severe malabsorption may contribute to malnutrition in the individual patient, the most common mechanism responsible for postoperative malnutrition was inadequate intake. In the occasional patient with severe malabsorption, the universal demonstration of jejunal anaerobic bacterial overgrowth offers important therapeutic implications. The relative importance of pancreatico-biliary insufficiency in promoting malabsorption remains to be determined. Construction of a Hunt-Lawrence jejunal pouch was not found to favorably affect caloric intake, weight gain, degree of malabsorption, or dumping symptoms. Although some degree of malnutrition does result from total gastric resection, in most cases it is mild and potentially correctable. Avoidance of indicated total gastrectomy due to fears of progressive postoperative malnutrition is unwarranted.

by adding 5 mg of cortisol/liter to P900, the fluid can be infused through peripheral veins. P900 is intermediate in nutritional value between P400 and C1,800. P900 without oral supplement prevents negative balance of all elements except Ca. P900 + daily oral intake of 670-1700 cal is nutritionally equivalent to C1,800.

To evaluate the role of tyramine in hepatic disorders, we used a radioimmunoassay to study plasma concentration of tyramine in eight healthy subjects, 20 hospitalized patients without liver disease, and 13 cirrhotic patients of whom seven had hepatic encephalopathy. The effect of increasing dietary protein on tyramine level of cirrhotic patients was also assessed. No significant difference in plasma tyramine concentration was seen between normal subjects, 1.3 +/- 0.1 ng per milliliter (average +/- S.E.), hospitalized patients without hepatic disease (1.4 +/- 0.1 ng per milliliter) and cirrhotic patients without encephalopathy (2.7 +/- 0.5 ng per milliliter). However, the tyramine level in cirrhotic patients with encephalopathy, 6.4 +/- 0.1 ng per milliliter, was significantly (P less than 0.001) higher than in normal subjects or in cirrhotic patients without encephalopathy. Increasing dietary protein from 40 to 80 g per day raised fasting tyramine concentration by 30 to 70 per cent within three days in both encephalopathic and non-encephalopathic cirrhotic patients. Concentration of plasma tyramine in cirrhotic subjects was significantly correlated with that of plasma tyrosine (P less than 0.001).

Measurement of venous plasma NH3 in normal subjects by the ion-exchange method of Forman [Clin. Chem. 10, 497 (1964)] in a hospital clinical laboratory gave a mean value of 640 mug/liter (range, 300-1320 mug/liter; intraassay, intra-individual, and inter-individual coefficients of variation, 8, 47, and 47%, respectively). The following conditions adversely affect the reproducibility of the test: pollution of laboratory atmosphere and glassware by NH3-containing detergents; smoking by patient or analyst; delay, turbulence, or use of heparin lock in venipuncture; delay or warming of plasma above degrees C before mixing it with resin; and delay in colorimetric analysis of resin eluate. When these sources of error were eliminated, the mean value for normals was reduced to 330 mug/liter, the range was narrowed to 220-470 mug/liter, and the above-mentioned CV's were 5, 16, and 17%, respectively. With the precautions cited, furthermore, the intra-assay and intra-individual CV's for fasting NH3 concentration in cirrhotic patients were similarly reduced. An NH3 tolerance test was done by administering a standard dose of NH4Cl to patients and measuring venous plasma NH3 at 0, 15, 30, 60, and 90 min; the NH3 tolerance was quantified from the area under the curve relating concentration to time (mug - min/liter). As measured in the clinical laboratory, NH3 tolerance of cirrhotic patients showed intra-assay and intra-individual CV's of 50 to 90%. When the tolerance tests were repeated in the same subjects with the laboratory precautions listed above, these CV's were reduced to 8-15%.

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