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Critical Care

Open Access

Platelet membrane potential: unable to pull the plug on sepsis

Critical Care201418:428

Published: 12 May 2014


Reactive Oxygen SpeciesPlatelet CountThrombocytopeniaNeurodegenerative DiseaseEnvironmental Agent

In a recent issue of Critical Care, we read with interest the work of Gründler and colleagues [1] regarding platelet mitochondrial depolarization reflecting disease severity in patients with sepsis. It has been established that, regardless of the source of sepsis, microcirculatory dysfunction with increased permeability and increased reactive oxygen species is similar among pathogens and leads to multi-organ dysfunction [2].

The microcirculatory response in patients with sepsis clearly influences clinical outcome, and biomarkers to reliably assess this response have been difficult to elucidate. Interestingly, the authors in this study were able to show a correlation between platelet membrane potential and Acute Physiology and Chronic Health Evaluation II and Sepsis-related Organ Failure Assessment scores and Simplified Acute Physiology Score II.

Several confounders such as neurodegenerative diseases and exposure to environmental agents such as cigarette smoke are known to affect platelet mitochondrial function [3]. It is difficult to control for patients with these confounders, and this could have biased the results of this study.

It is unclear what testing for platelet membrane potential adds to our ability to predict overall clinical outcome. Thrombocytopenia is already an established correlate to poor outcome in sepsis, and a platelet count, unlike the platelet membrane potential, is almost always readily available [4]. The authors did not control for thrombocytopenia, and it is unclear whether membrane potential would predict mortality, independent of platelet count.

We feel that this biomarker will not be useful in the clinical realm, but this work will add to our overall understanding of the microcirculatory physiologic response in sepsis.


Authors’ Affiliations

Internal Medicine Division, Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, USA
Pulmonary and Critical Care Division, Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, USA
Division of Nephrology, Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, USA


  1. Gründler K, Angstwurm M, Hilge R, Baumann P, Annecke T, Crispin A, Sohn HY, Massberg S, Kraemer BF: Platelet mitochondrial membrane depolarization reflects disease severity in patients with sepsis and correlates with clinical outcome. Crit Care 2014, 18: R31. 10.1186/cc13724PubMedPubMed CentralView ArticleGoogle Scholar
  2. Legrand M, Klijn E, Payen D, Ince C: The response of the host microcirculation to bacterial sepsis: does the pathogen matter? J Mol Med 2010, 88: 127-133. 10.1007/s00109-009-0585-6PubMedPubMed CentralView ArticleGoogle Scholar
  3. Smith PR, Cooper JM, Govan GG, Harding AE, Schapira AH: Smoking and mitochondrial function: a model for environmental toxins. Q J Med 1993, 86: 657-660. 10.1093/qjmed/86.10.657PubMedView ArticleGoogle Scholar
  4. Strauss R, Wehler M, Mehler K, Kreutzer D, Koebnick C, Hahn EG: Thrombocytopenia in patients in the medical intensive care unit: bleeding prevalence, transfusion requirements, and outcome. Crit Care Med 2002, 30: 1765-1771. 10.1097/00003246-200208000-00015PubMedView ArticleGoogle Scholar


© Schaer et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.