Oxidative stress, inflammation, blood rheology, and microcirculation in adults with sickle cell disease: Effects of hydroxyurea treatment and impact of sickle cell syndrome
Inflammation and oxidative stress play a key role in the pathophysiology of sickle cell disease (SCD). However, the potential influence of different sickle genotypes, or hydroxyurea (HU) treatment, on these factors remains poorly documented. The present study compared several plasma markers of infla...
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| Veröffentlicht in: | European journal of haematology 2021-06, Vol.106 (6), p.800-807 |
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| creator | Connes, Philippe Möckesch, Berenike Tudor Ngo Sock, Emilienne Hardy‐Dessources, Marie‐Dominique Reminy, Karen Skinner, Sarah Billaud, Marie Nader, Elie Tressieres, Benoit Etienne‐Julan, Maryse Guillot, Nicolas Lemonne, Nathalie Hue, Olivier Romana, Marc Antoine‐Jonville, Sophie |
| description | Inflammation and oxidative stress play a key role in the pathophysiology of sickle cell disease (SCD). However, the potential influence of different sickle genotypes, or hydroxyurea (HU) treatment, on these factors remains poorly documented. The present study compared several plasma markers of inflammation and oxidative stress, as well as microvascular function, between patients with sickle SC disease (HbSC, n = 19) and patients with sickle cell anemia (HbSS) under hydroxyurea (HU) treatment (n = 16), or not (n = 13). Hemorheological parameters and levels of inflammatory (IL‐6, IL‐8, IFN‐γ, MCP‐1, MIP‐1β, TNF‐α) and oxidative stress (AOPP, MDA, MPO) markers were determined. Peripheral microcirculatory cutaneous blood flow and immediate microvascular response to local heat were evaluated using laser Doppler flowmetry. Oxidative stress and inflammation were lower in HbSC patients and HbSS patients under HU therapy compared to HbSS patients not treated with HU. Blood viscosity was higher in HbSC than in HbSS patients treated with or not with HU. Vasodilation response of the cutaneous microcirculation to heat stress was higher in HbSS patients receiving HU treatment. Our results clearly established that both sickle cell genotype and HU treatment modulate inflammation and oxidative stress. |
| doi_str_mv | 10.1111/ejh.13607 |
| format | Article |
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However, the potential influence of different sickle genotypes, or hydroxyurea (HU) treatment, on these factors remains poorly documented. The present study compared several plasma markers of inflammation and oxidative stress, as well as microvascular function, between patients with sickle SC disease (HbSC, n = 19) and patients with sickle cell anemia (HbSS) under hydroxyurea (HU) treatment (n = 16), or not (n = 13). Hemorheological parameters and levels of inflammatory (IL‐6, IL‐8, IFN‐γ, MCP‐1, MIP‐1β, TNF‐α) and oxidative stress (AOPP, MDA, MPO) markers were determined. Peripheral microcirculatory cutaneous blood flow and immediate microvascular response to local heat were evaluated using laser Doppler flowmetry. Oxidative stress and inflammation were lower in HbSC patients and HbSS patients under HU therapy compared to HbSS patients not treated with HU. Blood viscosity was higher in HbSC than in HbSS patients treated with or not with HU. Vasodilation response of the cutaneous microcirculation to heat stress was higher in HbSS patients receiving HU treatment. Our results clearly established that both sickle cell genotype and HU treatment modulate inflammation and oxidative stress.</description><identifier>ISSN: 0902-4441</identifier><identifier>EISSN: 1600-0609</identifier><identifier>DOI: 10.1111/ejh.13607</identifier><identifier>PMID: 33629431</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Blood flow ; Doppler effect ; Genotypes ; Hematology ; Human health and pathology ; Hydroxyurea ; Inflammation ; Interferon ; Life Sciences ; Microvasculature ; Oxidative stress ; Rheology ; Sickle cell disease ; Tumor necrosis factor ; Vasodilation ; vasoreactivity</subject><ispartof>European journal of haematology, 2021-06, Vol.106 (6), p.800-807</ispartof><rights>2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><rights>Copyright © 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3877-8de948fe520ad883a9379990625c31319e6bea4643db8ddfc9f1d252f3041f6c3</citedby><cites>FETCH-LOGICAL-c3877-8de948fe520ad883a9379990625c31319e6bea4643db8ddfc9f1d252f3041f6c3</cites><orcidid>0000-0003-0691-2177 ; 0000-0002-9232-0268 ; 0000-0002-6054-2456 ; 0000-0002-2155-0816</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fejh.13607$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fejh.13607$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33629431$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.univ-antilles.fr/hal-03265316$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Connes, Philippe</creatorcontrib><creatorcontrib>Möckesch, Berenike</creatorcontrib><creatorcontrib>Tudor Ngo Sock, Emilienne</creatorcontrib><creatorcontrib>Hardy‐Dessources, Marie‐Dominique</creatorcontrib><creatorcontrib>Reminy, Karen</creatorcontrib><creatorcontrib>Skinner, Sarah</creatorcontrib><creatorcontrib>Billaud, Marie</creatorcontrib><creatorcontrib>Nader, Elie</creatorcontrib><creatorcontrib>Tressieres, Benoit</creatorcontrib><creatorcontrib>Etienne‐Julan, Maryse</creatorcontrib><creatorcontrib>Guillot, Nicolas</creatorcontrib><creatorcontrib>Lemonne, Nathalie</creatorcontrib><creatorcontrib>Hue, Olivier</creatorcontrib><creatorcontrib>Romana, Marc</creatorcontrib><creatorcontrib>Antoine‐Jonville, Sophie</creatorcontrib><title>Oxidative stress, inflammation, blood rheology, and microcirculation in adults with sickle cell disease: Effects of hydroxyurea treatment and impact of sickle cell syndrome</title><title>European journal of haematology</title><addtitle>Eur J Haematol</addtitle><description>Inflammation and oxidative stress play a key role in the pathophysiology of sickle cell disease (SCD). However, the potential influence of different sickle genotypes, or hydroxyurea (HU) treatment, on these factors remains poorly documented. The present study compared several plasma markers of inflammation and oxidative stress, as well as microvascular function, between patients with sickle SC disease (HbSC, n = 19) and patients with sickle cell anemia (HbSS) under hydroxyurea (HU) treatment (n = 16), or not (n = 13). Hemorheological parameters and levels of inflammatory (IL‐6, IL‐8, IFN‐γ, MCP‐1, MIP‐1β, TNF‐α) and oxidative stress (AOPP, MDA, MPO) markers were determined. Peripheral microcirculatory cutaneous blood flow and immediate microvascular response to local heat were evaluated using laser Doppler flowmetry. Oxidative stress and inflammation were lower in HbSC patients and HbSS patients under HU therapy compared to HbSS patients not treated with HU. Blood viscosity was higher in HbSC than in HbSS patients treated with or not with HU. Vasodilation response of the cutaneous microcirculation to heat stress was higher in HbSS patients receiving HU treatment. 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| source | Wiley Online Library All Journals |
| subjects | Blood flow Doppler effect Genotypes Hematology Human health and pathology Hydroxyurea Inflammation Interferon Life Sciences Microvasculature Oxidative stress Rheology Sickle cell disease Tumor necrosis factor Vasodilation vasoreactivity |
| title | Oxidative stress, inflammation, blood rheology, and microcirculation in adults with sickle cell disease: Effects of hydroxyurea treatment and impact of sickle cell syndrome |
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