Biomedical subjects
Publications and source records attributed to J Powell-Tuck.
1. Whole-body protein turnover was measured using the [15N]glycine tracer technique in 10 post-absorptive healthy volunteers during normal daily activities and a period of bed rest. 2. Bed rest reduced whole-body protein turnover (25%), synthesis (26%) and breakdown (25%), but short-term urinary nitrogen excretion remained unchanged.
OBJECTIVE: To examine the relationship between weight gain, changes in body composition and physiological characteristics of fitness during the recovery from anorexia nervosa. DESIGN: Longitudinal over eight weeks of intensive inpatient re-feeding (Wk 0-8). SETTING: The London Hospital Medical College. SUBJECTS: Ten female patients who agreed to participate. Seven completed the protocol. INTERVENTIONS: Dual-energy X-ray absorptiometry (dexa) and skinfold thickness measures at Wk 0 and 8. Weekly measures of peak expiratory flow rate and cycle ergometry (several variables relating to aerobic work recorded at rest and during cycling at low loads (0-60 W)). Blood samples for lactate and potassium measures, taken during cycling at Wk 0, 4 and 8 only. RESULTS: (1) Body composition: Mean weight gain over eight weeks was 9.6 kg, dexa and skinfold measures showing fat gain to contribute 62% and 54%, respectively. Both methods showed significant changes in percentage body fat with refeeding (P < 0.01 and P < 0.001, respectively), however there were significant differences in results between methods before (P < 0.01) but not after (P = 0.2) refeeding. (2) Physiological function: Between weeks 0 and 8, mean peak expiratory flow rate rose to 85% of predicted values, cycle ergometry performance improved in six subjects (three never reached 60 W load), mean respiratory exchange ratio (RER) during cycling fell at 0 W and 20 W loads (both P < 0.05), and oxygen pulse increased at rest and 0 W load cycling (both P < 0.05), Wk 8 values being well below normal. Oxygen uptake at rest and all loads increased in line with body weight gain only. No significant changes were seen in heart rate or blood lactate and potassium levels. CONCLUSIONS: (1) Lean body and fat mass increased significantly during eight weeks of refeeding. The methodological difference in initial body fat measurements requires further investigation. (2) The women had severely impaired physiological function. Variables studied were only slowly improving with refeeding, and work capacity was still well below normal.
Studies using stable isotopes to determine the effect of insulin on whole-body protein turnover have given conflicting results. The precursor approach to studying healthy subjects in a postabsorptive state shows reductions in breakdown and oxidation; with end product methods in parenterally fed patients no such changes are seen. To explain these discrepancies, we measured protein turnover with and without euglycemic hyperinsulinemic clamping postabsorptively in nine healthy subjects by using single-dose [15N]glycine with calculations based on ammonia and urea end product excretion. With and without clamping, respectively, insulin reduced nitrogen (22.1 and 48.2 mg.kg-1.9 h-1, P < 0.01) and urea (15.8 and 37.5 mg.kg-1.9 h-1, P < 0.05) but increased ammonia (7.7 and 5.0 mg.kg-1.9 h-1, P < 0.05) excretion. Although the urea end product method suggested that insulin tended to reduce both protein breakdown and synthesis, the protein metabolism changes detected with the ammonia end product method tended to be in the opposite direction. The [15N]glycine ammonia end-product method may be inappropriate for studies during insulin infusion because of insulin's effect on ammonia excretion.
Malnutrition is common and undiagnosed in the majority of affected hospital patients; it is associated with impaired organ function, morbidity, and increased length of hospital stay. Artificial nutritional support in malnourished patients leads to improvement in nutritional status and clinical outcome. Nutritional support is required in malnourished patients, patients who are unable to take normal diet and patients with intestinal failure. Gastroenterologists are required to supervise patients with intestinal failure, to insert endoscopic feeding devices, and increasingly to participate in, or lead, nutritional support teams. Major developments in nutrient delivery have included percutaneous endoscopic feeding devices, the recognition that enteral feeding is possible in patients with gastric stasis, and that nutrient needs can be met by peripheral parenteral nutrition. There is much interest in the use of new substrates, or substrates delivered in pharmacological doses such as glutamine and arginine, to manipulate the response to disease. Many hospitals lack an organized approach to artificial nutritional support. Patients continue to suffer from a lack of treatment or the consequences of inappropriate or inadequate treatment. This article reviews the current status of artificial nutritional support and provides guidelines for patient management.
Various methods for the diagnosis of malnutrition, and some of the physical signs commonly associated with it, are discussed. The incidence and possible causes of malnutrition and its effects are then addressed. Finally, the indications for nutritional support, using either the enteral or the parenteral route, are examined.
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One of the well known complications of radical neck dissection is a chylous fistula, which results from injury to the thoracic duct as it enters the left subclavian vein. Such fistulae may cause considerable increased morbidity to a patient who is already debilitated by malignancy and by the increased catabolic response to surgery. Further surgery may be appropriate for those with a high fistula output but conservative therapy is normally advocated for the remainder. Nutritional and electrolyte support for these patients is essential and poses potential problems in management. We present three such patients. One was fed parenterally and two enterally and in all cases the fistulae closed spontaneously. We examine the known physiological stimuli to chyle production and conclude that the enteral feedings of these patients with fat or an isomolar enteral feed does not, contrary to current belief, increase chyle flow or delay the healing of these fistulae.
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Whole-body protein turnover measurements using the single dose 15N-glycine technique have been made in a patient completely paralysed by the Guillaine-Barré syndrome. Variation (difference x 100/mean) between the results of the studies was better than 0.75 per cent for protein flux, better than 0.85 per cent for protein breakdown, and better than 5 per cent for protein synthesis.
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The effect of varying the calorie source of parenteral feeding from an all glucose source to a high fat source has been studied in seven patients with normal liver function by randomised crossover trial. 'Intralipid' used as the major non-nitrogen calorie source (except for 400 kcal as glucose) was associated with significantly lower plasma concentrations of insulin and glucose, significantly higher plasma concentrations of the three branched chain amino acids, and a significantly higher urinary excretion of sodium. If these effects of a high fat parenteral feed were repeatable in patients with liver failure and portasystemic encephalopathy they might be of therapeutic benefit.
In a prospective, randomised clinical trial, 47 patients with severe, acute, non-infective colitis treated with 60 mg intravenous prednisolone daily, received either bowel rest with parenteral nutrition or oral diet. Although those who received 'bowel rest' experienced a reduction in daily stool weight, there were no differences in the operation or mortality rates between the groups. Fourteen of the 27 patients with ulcerative colitis, but none of the 16 patients with Crohn's disease required urgent surgery. Bowel rest did not affect the outcome in severe ulcerative colitis treated with intravenous prednisolone. Ulcerative colitis and Crohn's colitis behaved differently in the acute attack.
Major loss of body protein mass in inflammatory bowel disease is much less common than weight loss, which is often attributable to losses of other body, particularly water and fat. It does occur, however, in a few patients, especially in those with compromised food intake. It is due principally to the combined effects of diminished intake and excessive intestinal losses of amino nitrogen. Nitrogen metabolism is influenced not only by protein nutritional state and net nitrogen intake but also by disease activity. There is some evidence for abnormally low secretion of growth hormone in adolescents with inflammatory bowel disease and growth failure. Low serum albumin concentrations are not necessarily related to protein undernutrition and are the combined result of relatively reduced albumin synthesis, increased intestinal losses, and maldistribution between intravascular and extravascular spaces. Concentrations in the plasma of IgG and acute phase reactants may be raised despite increased losses into the bowel lumen. The prevention of total body protein depletion is achieved principally by maintaining adequate and often not supranormal intakes of a balanced source of amino nitrogen in a balanced diet given orally, enterally, or parenterally, combined with a medical or surgical approach to reduce disease activity: supranormal energy intakes are not beneficial.