We compared two methods of calcium gluconate infusion to maintain plasma ionized calcium ([Ca ]) during therapeutic plasma exchange (TPE) performed using the Spectra Optia Apheresis System. Method A, our legacy method, consisted of adding 5 mL of 10% calcium gluconate to each 500 mL bottle of 5% albumin replacement fluid. Method B used an accessory IV infusion of calcium gluconate (2 g in 50 mL of 0.9% NaCl starting at 25 mL/h). Plasma [Ca ] was measured at 20-minute intervals, and symptoms of hypocalcemia were recorded during TPE. Baseline [Ca ] was the same (P = 0.616), as was total acid citrate dextrose Formula A used (P = 0.865), with either method. TPE with method A used 2.62 ± 0.52 g of calcium gluconate vs 1.13 ± 0.27 g with method B (P < 0.001). [Ca2+] remained stable with method A (P = 0.251), but fell on average by 5% with method B (P < 0.05). Hypocalcemic symptoms were reported in 0 of 23 TPE with method A and 2 of 24 TPE with method B. We conclude that both methods A and B prevent a symptomatic fall in plasma [Ca ] during TPE. Method B requires significantly less calcium gluconate than does method A.
Hypocalcemic toxicity, because of return of citrate anion to the donor, is the major toxicity of apheresis platelet donation. Oral calcium carbonate, given prophylactically at the start of donation, has shown limited ability to alleviate this toxicity. We examined whether repeated prophylactic doses of calcium carbonate, or of a liquid preparation containing calcium citrate, calcium phosphate, and vitamin D 3 , would be more effective at preventing symptoms of hypocalcemic toxicity. Symptoms were reported by 48% of donors who received no prophylaxis and 60% of donors who received 1000 mg of oral calcium carbonate at the start of, and every 20 minutes during, donation (P 5 0.711). Only 19.2% of donors who received the liquid preparation (1000 mg calcium, 1000 IU vitamin D 3 ) reported symptoms (P 5 0.040 versus no prophylaxis, P 5 0.039 versus calcium carbonate). This difference was not because of gender, weight, age, or blood volume of the donor. Neither calcium preparation prevented a measurable fall in plasma ionized calcium during donation. We conclude that liquid calcium citrate/calcium phosphate/vitamin D 3 provides effective prophylaxis against hypocalcemic toxicity during platelet donation, however it does not prevent a fall in plasma ionized calcium. K E Y W O R D Sblood donor, paresthesia, plateletpheresis, side effects | I NT ROD UCTI ONHypocalcemic toxicity is a common adverse effect of apheresis platelet donation. [1][2][3] It is caused by the return to the donor of plasma carrying a citrate-based anticoagulant, and may limit the blood flow rate and component yield during collection procedures. 3,4 Prophylactic administration of 1-2 g of oral calcium carbonate has been shown to have a distinct but modest effect on plasma ionized calcium ([Ca 21 ]) during platelet donation with only very modest effects on overall symptom development in the donors. 5,6 Gastrointestinal absorption and bioavailability of calcium carbonate is relatively limited compared to some other calcium salts such as calcium citrate, 7-9 and little is known about the effects of repetitive prophylactic dosing of calcium during platelet donation. We therefore undertook to examine alternative approaches to oral prophylaxis for hypocalcemic toxicity in apheresis platelet donation.
Sirolimus is an immunosuppressant used to prevent graft versus host disease in allogeneic hematopoietic stem cell transplant recipients. It has a large volume of distribution (12 ± 7.5 l/kg) and within the intravascular space ∼95% of it is bound to red blood cells. Because of potential toxic effects at high trough levels, therapeutic drug monitoring is recommended for sirolimus. We present a case of severe hepatic dysfunction due to Hepatitis B and sirolimus toxicity, in a 51-year-old male stem cell transplant recipient. An automated red cell exchange decreased his blood sirolimus level from 22.6 to 10.3 ng/ml (55% reduction) and improved his liver enzymes. Re-equilibration of sirolimus from other compartments to the blood necessitated a series of four red cell exchanges, after which the sirolimus level was 4.7 ng/ml. Although the patient ultimately succumbed to multiorgan failure, red cell exchange may be considered for acute removal of sirolimus in selected patients.
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