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Biomedical subjects

J D Ansley

Publications and source records attributed to J D Ansley.

29 records · Page 2Linked to original sources
PubMed1979

Hyperalimentation in alcoholic hepatitis.

Enteral hyperalimentation in four patients with severe alcoholic hepatitis and anorexia increased spontaneous food intake, increased their nitrogen balance and the patients improved clinically. Seven patients with alcoholic hepatitis, who were clinically ill and able to eat only 410-1,100 calories per day, were given a 900 mosM/l. parenteral "hyperalimentation" solution by a peripheral vein (P-900). The intravenous nutrition provided daily 51.6-77.4 gm. amino acids in addition to oral intake. All patients improved. None developed detectable encephalopathy after 16-42 days of P-900 therapy. Five additional patients had ascites and alcoholic hepatitis. The daily infusion of 2,000 ml. P-900 was not associated with hyponatremia, renal failure or encephalopathy in four of these five patients who improved and continued their diuresis. P-900 therapy was discontinued in one because of progressive hyponatremia. The observations indicate that over and above the maximum tolerable oral nutrition, intravenous nutrition can be effectively utilized by clinically ill, jaundiced patients with alcoholic hepatitis without precipitating encephalopathy or interference with standard therapy of ascites.

Hepatitis, Alcoholic↗
PubMed1978

Decarboxylation to tyramine: an important route of tyrosine metabolism in dogs with experimental hepatic encephalopathy.

Tyrosine metabolism via decarboxylation to tyramine was evaluated in dogs with functional end-to-side portacaval shunt. It was found that the endogenous plasma levels of both tyrosine and tyramine increased steadily after the construction of the shunt. These elevations became more pronounced when the dogs manifested symptoms of hepatic encephalopathy. In encephalopathic dogs, average endogenous plasma tyrosine and tyramine concentrations were 110.1 mumoles per liter and 7.6 ng per ml as compared to 55.4 and 1.2 in control dogs, respectively. The pattern of plasma concentrations of tyrosine and tyramine after an oral dose of L-tyrosine (50 mg per kg) was also investigated in control and shunted dogs. There was a progressive rise in peak levels of tyramine (to about 50-fold increase, at 6 weeks) after the construction of the shunt, as compared to levels obtained in pre- and at 1 and 4 weeks postoperatively (70.6 versus 1.20, 3.9, and 8.11 ng per ml). Similar observations were made with levels of plasma tyrosine. Six weeks after portacaval shunt, mean peak levels of plasma tyrosine, achieved at 5 hr after dose administration, were 450 as compared to 85 mumoles per liter obtained in preshunted dogs. These studies demonstrated a correlation between abnormalities in tyrosine metabolism and postshunt hepatic encephalopathy.

Amino Acids↗
PubMed1977

Management of liver trauma in children.

The charts of 203 consecutive children undergoing emergency laparotomy for management of an acute liver injury were reviewed. Although drainage was all that was required in the majority of cases, massive hemorrhage, usually arising from disrupted hepatic veins, appeared to demand liver resection (as performed in 17 children, with a mortality of 18%) during earlier years of the survey. Control of exsanguinating bleeding from such liver wounds by packing with viable autogenous tissue (pedicled omentum) subsequently eliminated almost entirely the need for resection. Fatalities resulting from either hemorrhagic shock or loss of liver substance then became relatively rare. Additional significant problems were associated organ injuries, postoperative wound and intra-abdominal sepsis, bleeding diatheses, and late instances of hemobilia. The overall mortality was 6%.

Adolescent↗
PubMed1977

Deficiency of carnitine in cachectic cirrhotic patients.

Carnitine is synthesized from lysine and methionine. In the rat, inadequate intake of either of these essential amino acids causes carnitine depletion. Inasmuch as protein deficiency is common in the hospital population, we have investigated the possible occurrence of nosocomial carnitine deficiency. Fasting serum carnitine concentration was measured in 16 normal and 247 patients in 16 disease groups. Normal range of carnitine was 55-103 muM. Only the cirrhotic group showed significant (P < 0.05) hypocarnitinemia. 14 of 36 hospitalized cirrhotics had subnormal values for serum carnitine. The creatinine/height index, midarm muscle circumference, and triceps skin-fold thickness indicated protein-calorie starvation in the 14 hypocarnitinemic liver patients. In six of the hypocarnitinemic cirrhotics (average serum level 50% of normal), spontaneous dietary intakes of carnitine, lysine, and methionine were measured and found to be only 5-15% as great as in six normocarnitinemic, healthy controls. When these six cirrhotic and six normal subjects were given the same lysine-rich, methionine-rich, and carnitine-free nutritional intake, the normals maintained normal serum carnitine levels and excreted 100 mumol/day, whereas the cirrhotics' serum level fell to 25% of normal, and urinary excretion declined to 15 mumol/day. Seven hypocarnitinemic cirrhotics died. Postmortem concentrations of carnitine in liver, muscle, heart, kidney, and brain averaged only one-fourth to one-third those in corresponding tissues of eight normally nourished nonhepatic patients who died after an acute illness of a 1-3-day duration. THESE DATA SHOW THAT CARNITINE DEPLETION IS COMMON IN PATIENTS HOSPITALIZED FOR ADVANCED CIRRHOSIS, AND THAT IT RESULTS FROM THREE FACTORS: substandard intake of dietary carnitine; substandard intake of lysine and methionine, the precursors for endogenous carnitine synthesis; and loss of capacity to synthesize carnitine from lysine and methionine.

Adult↗
PubMed1976

Technical pitfalls in measurement of venous plasma NH3 concentration.

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%.

Adolescent↗