Impact of pneumatic tube vs. bicycle courier transport on platelet aggregation: influence of sex and diabetes

TL;DR

The study compares how pneumatic tube and bicycle courier transport affect platelet aggregation, finding that transport method and patient characteristics like sex and diabetes influence results.

Contribution

The study provides novel comparative data on platelet aggregation differences between pneumatic tube and bicycle courier transport, highlighting sex and diabetes as modifying factors.

Findings

Bicycle courier transport caused small but significant reductions in platelet aggregation for ADP, arachidonic acid, ristocetin, and collagen agonists compared to pneumatic tube transport.

Female patients and individuals with diabetes showed more pronounced reductions in collagen-induced aggregation, suggesting increased platelet mechanosensitivity in these groups.

Epinephrine-induced aggregation was unaffected by transport mode, and antiplatelet drugs inhibited aggregation for ADP, arachidonic acid, and epinephrine but not for collagen or ristocetin.

Abstract

Pneumatic tube (PT) transport can impact platelet function, often altering platelet aggregation. Consequently, manual transport is frequently recommended to mitigate preanalytical effects on platelet function tests. However, comparative data between PT and bicycle courier (BC) transport remain limited, and it is unclear whether different agonist pathways or specific patient characteristics, such as sex and diabetes, modify transport-related effects.

In this study, two S-Monovette® 3.2% citrate syringes of whole blood were collected from 96 participants (43 female participants, 53 male participants; median age: 63 years). Samples were transported simultaneously by PT or BC to the Central Laboratory of University Hospital Heidelberg. Platelet function was assessed through light transmission aggregometry (LTA) using five diagnostically established agonists, including ADP, arachidonic acid, ristocetin, collagen, and epinephrine.

BC transport was associated with small but statistically significant reductions in platelet aggregation compared with PT for several agonists: ADP (−2.5%, p = 0.02), arachidonic acid (−1.0%, p = 0.006), ristocetin (−2.0%, p = 0.003), and collagen (−3.0%, p = 0.002), while epinephrine-induced aggregation was unaffected (p = 0.58). These reductions were more pronounced in female patients and individuals with diabetes, particularly for collagen-induced aggregation (up to −3.5%, p = 0.02). Epinephrine-induced aggregation was unaffected by transport mode (p = 0.58). Females patients showed higher aggregation responses overall, especially to arachidonic acid (p = 0.02 vs. males). Among participants, antiplatelet drugs markedly inhibited ADP, arachidonic acid, and epinephrine-induced aggregation but did not meaningfully affect collagen or ristocetin responses.

PT transport resulted in minor increases in platelet aggregation compared with BC transport, which are unlikely to be clinically relevant for the majority of patients but may influence interpretation in selected subgroups, particularly in individuals with heightened platelet reactivity or borderline test results. The observed transport-related differences in female patients and individuals with diabetes suggest increased platelet mechanosensitivity in these groups and warrant confirmation in larger, dedicated studies.

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