0.42 PARENTERAL NUTRITION IN BONE MARROW TRANSPLANT RECIPIENTS. M Lough, R Watkins, 0 J Garden, K Carr, A K Burnett, A Shenkin, Departments of Biochemistry, Haematology, Dietetics and Surgery, Royal Infirmary, Glasgow, Scotland

There is controversy over the value of TPN in the nutritional support of patients undergoing bone marrow transplantation (BMT). We therefore performed a prospective study on 27 BMT patients, 13 of whom were randomised to receive TPN (8 allogeneic and 5 autologous recipients) and 14 who did not receive TPN (8 allogeneic and 6 autologous recipients). A standard regimen of TPN with 14 g of nitrogen and 2000 Kcal was commenced the day following marrow infusion, the median duration of administration being 11 days (range 4-17 days). Both groups of patients had free access to oral diet. Assessments were performed prior to , and at 3 weeks post transplantation.

TPN GROUP NON TPN GROUP PRE-TRANSPLANT POST-TRANSPLANT PRE-TRANSPLANT POST-TRANSPLANT

Weight (Median) (kg) Range (41.56f 73)

58.5 59.1 55.2 (39.5 - 64) (44.5 - 119.8) (40 - 115)

Albumin (g/l) 40.3 + 2.6 40.3 f 4.2 39.0 + 4.4 39.8 f 3.3

Mean f SD

No significant differences were observed between the groups for changes in weight or serum albumin, for days of sepsis (TPN group 9.5 f 4.3 days; non TPN-group 7.6 f 3.9 days (mean ? 1SD)) or for time to achieve 1000 WBC/mm3 (TPN group 19.9 + 4.3 days, non TPN group 17.9 * 6.4 days). Survival at 200 days post transplantation wasnotsignificantly different between the two groups (Chi-squared test), 10 of 13 patients surviving in the TPN group and 8 of 14 in the non TPN group. This study has therefore failed to demonstrate a significant benefit from the use of TPN during bone marrow transplantation.

0.43 BODY FUEL OXIDA'I'ION IN CANCER PATIENTS AND CON'TKOLS. D.T. Hansell, J.W.L. Davies, A. Shenkin, H.J.G. Burns. (University Departments of Surgery & Biochemistry, Royal Infirmary, Glasgow, Scotland).

In an attempt to define the mechanism of weight loss in cancer patients, fat and carbohydrate oxidation rates have been calculated in 70 patients with colorectal or gastric cancer and 23 patients with non-malignant illness. Twenty seven cancer patients and 13 control patients had lost more than 10% of their pre-illness body weight. Fat (FO) and carbohydrate (CO) oxidation rates were derived from measurements of oxygen consumption, carbon dioxide production and urinary nitrogen excretion using indirect calorimetry. Lean body mass (LBM) was derived from measurements of total body water using a tritium dilution technique.

Cancer Control

FG(g/kg/d) Weight stable Weight losing Weight stable Weight losing 1.39 + 0.08" 1.68 ? 0.12a

-- 1.07 i 0.16c 1.27 f o.14b

CO (g/kg/d) 1.79 ?r 0.20 1.54 + 0.22 2.10 r 0.33 2.38 + 0.47 REE(kcal/kgLBM/d) 28.0 f 1.0 29.3 + 0.8 26.0 + 1.6 28.2 + 0.5 mean t s.e.m. a v.b P<O.O2, a v.c PCO.01 (Mann-Whitney U test) When all cancer patients were compared with all controls, the cancer patients had higher fat oxidation rates (1.50 f 0.07 v. 1.18 i 0.10; P<O.Ol) and lower carbohydrate oxidation rates (1.69 + 0.14 v. 2.25 + 0.29; PcO.05) compared with controls. Cancer patients with liver metastases (n=14) had higher fat oxidation rates (1.89 ? 0.17 v. 1.40 + 0.07; P<O.Ol) and lower carbohydrate oxidation rates (1.04 + 0.28 v. 1.85 + 0.16; P<O.Ol) than patients with localised cancer. The presence of cancer appears to be associated with abnormal fat and carbohydrate metabolism. The increased rates of fat oxidation seen in cancer patients, especially those with weight loss or liver metastases, may be a significant factor in the development of cancer cachexia.

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