Donor and Procedural Factors Associated With Citrate Toxicity During Plateletpheresis
7 affiliations
- 1Department of Transfusion Medicine, Ahsania Mission Cancer and General Hospital, Dhaka, BGD
- 2Department of Transfusion Medicine, Dhaka Medical College Hospital, Dhaka, BGD
- 3Department of Transfusion Medicine, Bangladesh Institute of Health Sciences General Hospital, Dhaka, BGD
- 4Department of Transfusion Medicine, Meherpur 250 Bedded General Hospital, Meherpur, BGD
- 5Department of Transfusion Medicine, Rangpur Medical College Hospital, Rangpur, BGD
- 6Department of ENT and Head-Neck Surgery, Cumilla Medical College Hospital, Cumilla, BGD
- 7Department of Pharmacology and Therapeutics, Ibrahim Medical College and Bangladesh Institute of Research and Rehabilitation in Diabetes, Endocrine and Metabolic Disorders (BIRDEM) General Hospital, Dhaka, BGD
Abstract
Background
Citrate anticoagulation during plateletpheresis can reduce ionized calcium and cause neuromuscular or gastrointestinal symptoms. Identifying donor and procedure-related factors may support earlier recognition and prevention. This study assessed factors associated with clinically identified citrate toxicity among plateletpheresis donors.
Methods
This analytical observational cross-sectional study included 60 plateletpheresis donors at Dhaka Medical College and Hospital, Bangladesh. Citrate toxicity was defined by any prespecified symptom or sign during the donation encounter. Crude and adjusted prevalence ratios (PRs) were estimated using modified Poisson regression with robust variance. The parsimonious adjusted model included pre-procedure oral calcium exposure, body mass index (BMI), pre-donation platelet count, and anticoagulant citrate dextrose solution A (ACD-A) volume. Calcium administration was non-randomized, and total and ionized calcium were not measured.
Results
All 60 donors were male; 28 (46.7%) developed citrate toxicity. Compared with donors without toxicity, affected donors had lower mean BMI (24.03 versus 25.56 kg/m2; p=0.020), lower pre-donation platelet count (2.53 versus 3.23×1011/L; p<0.001), and greater mean ACD-A exposure (333.39 versus 259.13 mL; p<0.001). In adjusted analysis, absence of pre-procedure calcium was associated with higher toxicity prevalence (adjusted PR {aPR} 4.42, 95% CI: 2.59-7.56), each 1 kg/m2 higher BMI with lower prevalence (aPR: 0.91, 95% CI: 0.85-0.98), and each 50 mL higher ACD-A volume with higher prevalence (aPR: 1.65, 95% CI: 1.24-2.18). Pre-donation platelet count was not independently associated after adjustment (aPR: 0.79 per 0.5×1011/L, 95% CI: 0.56-1.12).
Conclusions
Clinical citrate toxicity was common and was associated with absence of pre-procedure calcium, lower BMI, and greater ACD-A volume. These findings identify potential monitoring markers but do not establish causality because procedural factors and symptoms were recorded within the same encounter and ionized calcium was not measured. The calcium association should be interpreted as exploratory and hypothesis-generating, rather than as evidence of prophylactic efficacy.
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BibTeX
@article{shishir2026donor,
title = {{Donor and Procedural Factors Associated With Citrate Toxicity During Plateletpheresis}},
author = {Abrar Kabir Shishir and A B M Al-Mamun and Ummea Sayeba Hassan and Sadiya Nahar Shorna and M M Zahidul Islam and Md Zubayer Ferdous and Ferdousy Binte Ali Borna and Md. Faizul Ahasan and Kashfia Islam and Shanaz Karim},
journal = {Cureus},
year = {2026},
month = sep,
doi = {10.7759/cureus.117188},
url = {https://europepmc.org/article/PMC/PMC13720392},
note = {CC BY},
}
RIS
TY - JOUR
TI - Donor and Procedural Factors Associated With Citrate Toxicity During Plateletpheresis
AU - Abrar Kabir Shishir
AU - A B M Al-Mamun
AU - Ummea Sayeba Hassan
AU - Sadiya Nahar Shorna
AU - M M Zahidul Islam
AU - Md Zubayer Ferdous
AU - Ferdousy Binte Ali Borna
AU - Md. Faizul Ahasan
AU - Kashfia Islam
AU - Shanaz Karim
PY - 2026
DA - 2026/09/29
JO - Cureus
DO - 10.7759/cureus.117188
UR - https://europepmc.org/article/PMC/PMC13720392
AB - Background Citrate anticoagulation during plateletpheresis can reduce ionized calcium and cause neuromuscular or gastrointestinal symptoms. Identifying donor and procedure-related factors may support earlier recognition and prevention. This study assessed factors associated with clinically identified citrate toxicity among plateletpheresis donors. Methods This analytical observational cross-sectional study included 60 plateletpheresis donors at Dhaka Medical College and Hospital, Bangladesh. Citrate toxicity was defined by any prespecified symptom or sign during the donation encounter. Crude and adjusted prevalence ratios (PRs) were estimated using modified Poisson regression with robust variance. The parsimonious adjusted model included pre-procedure oral calcium exposure, body mass index (BMI), pre-donation platelet count, and anticoagulant citrate dextrose solution A (ACD-A) volume. Calcium administration was non-randomized, and total and ionized calcium were not measured. Results All 60 donors were male; 28 (46.7%) developed citrate toxicity. Compared with donors without toxicity, affected donors had lower mean BMI (24.03 versus 25.56 kg/m2; p=0.020), lower pre-donation platelet count (2.53 versus 3.23×1011/L; p<0.001), and greater mean ACD-A exposure (333.39 versus 259.13 mL; p<0.001). In adjusted analysis, absence of pre-procedure calcium was associated with higher toxicity prevalence (adjusted PR {aPR} 4.42, 95% CI: 2.59-7.56), each 1 kg/m2 higher BMI with lower prevalence (aPR: 0.91, 95% CI: 0.85-0.98), and each 50 mL higher ACD-A volume with higher prevalence (aPR: 1.65, 95% CI: 1.24-2.18). Pre-donation platelet count was not independently associated after adjustment (aPR: 0.79 per 0.5×1011/L, 95% CI: 0.56-1.12). Conclusions Clinical citrate toxicity was common and was associated with absence of pre-procedure calcium, lower BMI, and greater ACD-A volume. These findings identify potential monitoring markers but do not establish causality because procedural factors and symptoms were recorded within the same encounter and ionized calcium was not measured. The calcium association should be interpreted as exploratory and hypothesis-generating, rather than as evidence of prophylactic efficacy.
SN - 2168-8184
ER -