131I effective half-life and dosimetry in thyroid cancer patients.

UNLABELLED: (131)I treatment in thyroid cancer patients may induce side effects, including extrathyroidal cancer and leukemia. There are still some uncertainties concerning parameters that may influence the effective half-life of (131)I and the absorbed doses by extrathyroidal organs. METHODS: Whole-body retention of radioiodine was measured in 254 patients, and repeated quantitative whole-body scans and measurements of the urinary excretion of (131)I were performed on 30 of these patients. RESULTS: The mean effective half-life (10.5 h) was shorter by 31%, with little difference between patients, in the 36 patients who received recombinant human thyroid-stimulating hormone than in the 218 patients who underwent thyroid hormone withdrawal (15.7 h). The residence times in the stomach and in the rest of the body were significantly shorter in patients who received recombinant human thyroid-stimulating hormone than in patients who underwent withdrawal, but the residence times were similar in the colon and bladder. CONCLUSION: In patients who undergo thyroid hormone withdrawal, the longer mean effective half-life is mainly due to delayed renal excretion of (131)I and results in dose estimates higher than the data in report 53 of the International Commission on Radiological Protection, which were obtained from healthy, euthyroid subjects.

Evidence for impairment of hepatic energy homeostasis in head-injured rat.

Traumatic brain injury (TBI) is known to induce a metabolic adaptation characterized by a nitrogen transfer from the periphery to the liver. However, the consequences of TBI on liver energy status are poorly documented. We evaluated the consequences of TBI on liver energy homeostasis in rats. In a first set of experiments, rats were randomized into two groups: a TBI group traumatized by fluid percussion, and an ad libitum fed group (AL) of healthy rats. The rats were sacrificed at 2, 3, or 4 days (D2, D3, and D4, respectively to determine the kinetic of hepatic energy changes). Since TBI leads to a profound anorexia, in a second set of experiments TBI rats received enteral nutrition (TBI-EN group) for 4 days to specifically assess the role of anorexia in the hepatic disturbances. TBI led to a decrease in hepatic glycogen (D2: TBI 3.9 +/- 1.9 vs. AL 18.9 +/- 2.6 mg/g, p < 0.05) and ATP (D2: TBI 540 +/- 57 vs. AL 850 +/- 44 nmol/g, p < 0.05) contents. These effects were not linked to anorexia, since they were observed when rats were fed using continuous enteral nutrition. Interestingly, there was no adaptation of the mitochondrial oxidative capacity to compensate for the increase in energy requirements (cytochrome C oxidase activity: AL, 82 +/- 5; TBI, 82 +/- 4; and TBI-EN, 87 +/- 3 micromol/min/g, NS). These findings demonstrate that TBI is responsible for an impairment of liver energy homeostasis. Moreover, these alterations are related neither to anorexia nor to decreased mitochondrial oxidative capacity.

Arginine-enriched diet limits plasma and muscle glutamine depletion in head-injured rats.

OBJECTIVE: Injury is associated with a depletion in glutamine (GLN) pools, which may contribute to impairment of immune and nutritional statuses. Total parenteral nutrition enriched with arginine (ARG) is able to generate GLN in surgical patients. We hypothesized that this same concept may be applicable to enteral administration and could be extended to muscle GLN reserves. This study investigated the ability of an enteral formula enriched with ARG to restore the GLN pools in an experimental model of head injury. METHODS: Twenty-five male Sprague-Dawley rats were randomized into 4 groups: ad libitum access to food, head injury plus free access to nutrition, head injury plus standard enteral nutrition (Sondalis), and an immune-enhancing diet (IED). The two enteral diets were adjusted to be isocaloric (290 kcal.kg(-1).d(-1)) and isonitrogenous (3.29 g.kg(-1).d(-1)) and were delivered for 4 d (24 h/24 h). After sacrifice, plasma and muscle amino acids were determined. RESULTS: Head injury was associated with a large depletion of muscle and plasma GLN pools that were restored by IED administration but not by the standard diet. Moreover, the IED but not the standard diet improved or normalized ornithine and glutamate pools, suggesting that the modification of GLN pools is related to ARG administration. CONCLUSION: In our model of head injury, our IED, a diet without free GLN, is efficient in restoring the plasma and muscle pools of GLN, probably due to its high ARG content.

Impairment of lymphocyte function in head-injured rats: effects of standard and immune-enhancing diets for enteral nutrition.

BACKGROUND: The metabolic response to head injury (HI) is characterized by a dysimmunity which may be a risk factor of a septic state. The use of immune enhancing diets (IEDs) could be a promising approach to improve immune functions. The aim of the study was to investigate the consequences of HI on lymphocyte function and to determine the effects of an enteral IED comparatively to a standard enteral nutrition. METHOD: A rat model of HI by fluid percussion was used. Twenty-five male Sprague-Dawley rats were randomized into 4 groups: rats receiving standard chow diet ad libitum (AL), rats sustaining HI and receiving standard chow diet and enteral saline (HI), rats receiving the enteral standard diet Sondalis HP (HIS), and rats receiving the IED Crucial (HIC). The two enteral diets were infused continuously during 4 days after the HI and were isocaloric, isonitrogenous and isovolumic. RESULTS: HI induced a thymus atrophy (HI vs. AL, P<0.05), and an impairment in lymphocyte CD25 receptor density responsiveness to stimulation. The IED blunted thymus atrophy and allowed to preserve the stimulation of blood and Peyer patches lymphocytes (HIC: Stimulated vs. Basal, P<0.05). CONCLUSION: IED seems more adapted for preserving lymphocyte function than standard diet in HI patients.