Abstract：
:Sickle cell disease (SCD) describes a group of disorders associated with a point mutation in the beta chain of hemoglobin. The mutation leads to the creation of sickle hemoglobin (HbS) and causes distortion of erythrocytes through polymerization under low oxygen, resulting in characteristic sickle red blood cells. Vaso-occlusion episodes caused by accumulation of sRBCs results in ischemia-reperfusion injury, reduced oxygen supply to organs, oxidative stress, organ damage and severe pain that often requires hospitalization and opioid treatment. Further, many patients suffer from chronic pain, including hypersensitivity to heat and cold stimuli. Progress towards the development of novel strategies for both acute and chronic pain in patients with SCD has been impeded by a lack of understanding the mechanisms underlying pain in SCD. The purpose of this review is to highlight evidence for the contribution of peripheral and central sensitization that leads to widespread, chronic pain and hyperalgesia. Targeting the mechanisms that initiate and maintain sensitization in SCD might offer effective approaches to manage the severe and debilitating pain associated with this condition.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Uhelski ML,Simone DAdoi
10.1016/j.neulet.2019.04.013subject
Has Abstractpub_date
2019-07-13 00:00:00pages
20-26eissn
0304-3940issn
1872-7972pii
S0304-3940(19)30247-2journal_volume
705pub_type
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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