Introduction
Hypoxic-ischemic encephalopathy is a major cause of infant mortality and
morbidity with long-term neurological sequelae. Hypoxic brain injury is
an evolving process that results from an initial insult and extends
during the reperfusion phase of injury.1,2 It is
characterized by symptoms such as seizure, difficulty in starting and
maintaining respiration, circulatory impairment, abnormal muscular
tonus, and a decrease in reflexes.3 Transient ischemia
of the cerebral vasculature followed by reperfusion leads to a secondary
cascade of pathophysiological events, characterized by a complex
inflammatory response.4 In particular, it activates
immune cells in hypoxia-ischemia-induced cell damage or cell death,
microglia, and astrocytes. These activated cells lead to the synthesis
and production of pro-inflammatory cytokines such as interleukin 1b,
interleukin 6, and tumor necrosis factor-a. Pro-inflammatory cytokines
increase the expression of mediators that induce vascular permeability,
the migration of leukocytes, and promote local inflammatory
reactions.5-7 The production of leukocytes and the
number of circulating neutrophils increase. Cell damage occurs due to
the production of reactive and toxic metabolites such as hydrogen
peroxide, superoxide anion, and hypochlorous acid from
neutrophils.8 Thrombocytes play a fundamental role in
hemostasis. However, recent studies have revealed that thrombocytes also
play an essential role in infection and
inflammation.9,10 Mean platelet volume (MPV) is a
value that indicates thrombocyte activation and can be used as a
biomarker in inflammation. Changes in the MPV have been studied in many
diseases.11-13 Therapeutic hypothermia constitutes one
of the most important therapies providing neuroprotection, and has been
reported to reduce brain damage by reducing the production of
inflammatory cells and inflammatory cytokines.14
The aim of this study was to investigate the inflammatory cell response
in NE before and during TH.