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C Robey

Publications and source records attributed to C Robey.

3 recordsLinked to original sources

Effects of chronic peritoneal dialysis on thyroid function tests.

Peritoneal dialysis is associated with large losses of protein. In order to quantify thyroid hormone excretion in the dialysate and to examine the possibility that peritoneal dialysis may result in clinical hypothyroidism, nine endstage renal disease (ESRD) patients undergoing either continuous ambulatory peritoneal dialysis (CAPD) or chronic intermittent peritoneal dialysis (IPD) were studied. Total protein excretion in the peritoneal fluid was 21.5 +/- 2.1 g/24 h and did not vary with the mode of peritoneal dialysis. Thyroid binding globulin (TBG) excretion was 6.4 +/- 1.3 mg/24 h, higher than the values reported in the literature for urinary TBG excretion in patients with the nephrotic syndrome. Despite the higher TBG losses, serum TBG remained in the normal range. Mean peritoneal total T4 and T3 were 8.1 +/- 1.6 micrograms/24 h and 89.5 +/- 14.6 ng/24 h, and there was a significant correlation between peritoneal T4 and TBG (r = 0.69; P less than 0.01) and between peritoneal total proteins and T4 (r = 0.80; P less than 0.001). Despite the finding that large amounts of protein are lost in peritoneal fluid, T4 and T3 losses were relatively modest and remained below their daily production rates, and none of the patients were overtly hypothyroid. Serum thyroid stimulating hormone (TSH) was mildly elevated in three of nine patients and was consistent with early thyroid failure. The patients' serum iodine levels were higher than normal but did not predict the patients' thyroid status. We conclude that major protein losses could predispose patients undergoing CAPD to thyroid failure and that long-term follow-up of thyroid function is warranted in these patients.

Aged↗

Sorbinil partially prevents decreased erythrocyte deformability in experimental diabetes mellitus.

The ability of red blood cells (RBCs) to undergo an adaptation in shape that permits passage through the smallest vessels is reportedly impaired in diabetes. Several hypotheses have been proposed to explain decreased erythrocyte deformability, which has been implicated in the pathogenesis of microvascular complications, but the mechanisms responsible for this change have not been clearly delineated. In view of the fact that sorbitol accumulates in RBCs in diabetes and the postulate that increased sorbitol could alter deformability properties, we examined the influence of the aldose reductase inhibitor sorbinil on erythrocyte deformability. Erythrocyte deformability, determined as the volume of RBCs (VRBC) filtered per minute through 4.7-micron pore size filters, was significantly reduced in samples from diabetic rats compared with samples from controls (0.76 +/- 0.03 vs. 0.97 +/- .02 ml RBC/min; P less than .001). In contrast, deformability of RBCs from diabetic animals treated with sorbinil was significantly greater than in untreated diabetes, although not completely normalized (0.88 +/- 0.02; P less than .01 vs. diabetic, and P less than .02 vs. control). The reduced deformability characterizing cells from diabetic rats and its partial prevention by sorbinil persisted even when RBCs were washed to eliminate hyperglycemia and hyperviscous plasma. Thus, hyperviscosity per se is not responsible for the decreased deformability, and sorbinil can partially prevent this change despite persistent hyperglycemia. This effect may derive from sorbinil's action as an aldose reductase inhibitor and/or its ability to influence physicochemical properties of the erythrocyte membrane.

Animals↗

Thrombocytosis associated with acute osteomyelitis.

Thrombocytosis is rarely observed during infection. We are describing a patient with acute osteomyelitis and bacteremia who developed thrombocytosis. In the patient described the platelet count paralleled the activity of the infection and the response to therapy. The causes of thrombocytosis and its implications are briefly reviewed.

Female↗