Hypercalciuria in patients receiving total parenteral nutrition

Hypercalciuria in patients receiving total parenteral nutrition

F75EFFECTS OF 1.25 DIHYDROXYVITAMIN D ON CALCIUM METABOLISM IN PARENTERALLY NOURISHED RATS A. Gueho, J. Combet, F. Durr, G. Llorca, B. Lauras, B. Desc...

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F75EFFECTS OF 1.25 DIHYDROXYVITAMIN D ON CALCIUM METABOLISM IN PARENTERALLY NOURISHED RATS A. Gueho, J. Combet, F. Durr, G. Llorca, B. Lauras, B. Descos, A. Frederich. Laboratoire de pharmacologic, Faculte Medicine Lyon Nord, 8 avenue Rockefeller, 69373 Lyon Cedex 2. France Patients receiving long term pare&era1 nutrition may develop hypercalciuria and metabolic bone disease with loss of skeletal calcium, impaired mineralisation and patchy osteomalacia. This patients have a serum level of 1.25 dihydroxyvitamin D (1.25 (OH) 2D) reduced. This study evaluates the effects of intravenous administration of 1.25 (OH)2D in normal rats and depleted vitamin D rats feeding by total parenteral nutrition. In normal rats, after a single high dose (500ng/rat), calciuria increases (from 7mg/day to 20mg/day) and calcium retention decreases. The peak of urinary calcium excretion is obtained after 3 days. After a single low dose (5ng/rat), more physiologic, calciuria rises less(from 7mg/day to 14,5mg/day) and the peak of urinary calcium excretion is obtained after 7 days. In depleted rats, initial calciuria is low, but increases also after administration of 1.25 (OH)2D (for 500ng/rat from 4mg/day to 15mg/day). This present experiment demonstrated that 1.25 (OH)2D increases calciuria in rats This principal metabolite of vitamin D not during total parenteral nutrition. improve the calcium balance in depleted vitamin D rat with unfunctional small intestine. This study suggests that the 1.25 (OH)2D is not a preventive or curative treatment of hypercalciuria and metabolic bone disease observed during long term total parenteral nutrition in man.

F76 HYPERCALCIURIA IN PATIENTS RECEIVING TOTAL PARENTERAL NUTRITION A.Allan, D. Gordon, A.J.W. Sim, A. Shenkin. Surgical Nutritional Advisory Group, Depts. of Biochemistry and Surgery, Royal Infirmary, Glasgow, Great Britain Hypercalciuria in association with metabolic bone disease has been reported in patients receiving long-term parentera nutrition (TPN). This study examines hypercalciuria arising in patients receiving TPN for short periods in general surgical practice. 28 patients fed intravenously with a standard dextrose/amino acid/fat emulsion regimen have been studied for a minimum of 14 consecutive days. 12 patients received 3.75 mmol calcium per day intravenously and 16 received a total of 8.75 mmol calcium per day. All patients received 15 mmol phosphate per day (excluding phospholipid) and vitamin supplements which included 3 g Vit D/day. Urine calcium, phosphate, nitrogen, sodium and glucose, and serum phosphate and albumin were measured in all patients. 13 patients calcium, developed hypercalciuria ( 6mmo1/24hr) within. 2 weeks of starting TPN. The incidence fell thereafter, hypercalciuria occurring in only 2 patients out of 14 at week 4 and 1 patient out of 12 at week 5. No patient developed hypercalciuria after the second week. No difference was detected in development of hypercalciuria between the groups on the two different levels of intake of calcium supplements. Urine phosphate was significantly lower (p 0.05) in the normocalciuric group prior to TPN (mean + SD; 5.1 + 3.4 mmol/i!4 hr) compared to the group who developed hypercalciuria (il.1 + &8mmol/vol). However, by the end of the first week phosphate excretion in the-two groups was similar. No differences were detectable between the groups in any of the other parameters measured. Development of hypercalciuria was not related to clinical outcome. Hypercalciuria is therefore common in patients receiving short-term TPN, particularly in the first two weeks, and is unlike the hypercalciuria reported during longer TPN, in that it does not persist and does not constitute a clinical problem.

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