Oxidative stress, inflammation, blood rheology, and microcirculation in adults with sickle cell disease: Effects of hydroxyurea treatment and impact of sickle cell syndrome.
hydroxyurea
inflammation
oxidative stress
sickle cell disease
vasoreactivity
Journal
European journal of haematology
ISSN: 1600-0609
Titre abrégé: Eur J Haematol
Pays: England
ID NLM: 8703985
Informations de publication
Date de publication:
Jun 2021
Jun 2021
Historique:
revised:
19
02
2021
received:
01
12
2020
accepted:
22
02
2021
pubmed:
26
2
2021
medline:
30
11
2021
entrez:
25
2
2021
Statut:
ppublish
Résumé
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.
Substances chimiques
Biomarkers
0
Hydroxyurea
X6Q56QN5QC
Types de publication
Clinical Trial
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
800-807Subventions
Organisme : European Regional Development Fund - European Commission
Organisme : GIRCI-APIDOM 2015
Organisme : Conseil Regional de la Guadeloupe
Informations de copyright
© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
Références
Pecker LH, Schaefer BA, Luchtman-Jones L. Knowledge insufficient: the management of haemoglobin SC disease. Br J Haematol. 2017;176(4):515-526.
Connes P, Alexy T, Detterich J, Romana M, Hardy-Dessources MD, Ballas SK. The role of blood rheology in sickle cell disease. Blood Rev. 2016;30(2):111-118.
Connes P, Renoux C, Romana M, et al. Blood rheological abnormalities in sickle cell anemia. Clin Hemorheol Microcirc. 2018;68(2-3):165-172.
Charlot K, Romana M, Moeckesch B, et al. Which side of the balance determines the frequency of vaso-occlusive crises in children with sickle cell anemia: Blood viscosity or microvascular dysfunction? Blood Cells Mol Dis. 2016;56(1):41-45.
Charache S, Terrin ML, Moore RD, et al. Effect of hydroxyurea on the frequency of painful crises in sickle cell anemia. Investigators of the Multicenter Study of Hydroxyurea in Sickle Cell Anemia. N Engl J Med. 1995;332(20):1317-1322.
Feeling-Taylor AR, Yau ST, Petsev DN, Nagel RL, Hirsch RE, Vekilov PG. Crystallization mechanisms of hemoglobin C in the R state. Biophys J. 2004;87(4):2621-2629.
Nagel RL, Fabry ME, Steinberg MH. The paradox of hemoglobin SC disease. Blood Rev. 2003;17(3):167-178.
Ballas SK, Larner J, Smith ED, Surrey S, Schwartz E, Rappaport EF. The xerocytosis of Hb SC disease. Blood. 1987;69(1):124-130.
Tripette J, Alexy T, Hardy-Dessources MD, et al. Red blood cell aggregation, aggregate strength and oxygen transport potential of blood are abnormal in both homozygous sickle cell anemia and sickle-hemoglobin C disease. Haematologica. 2009;94(8):1060-1065.
Mockesch B, Charlot K, Jumet S, et al. Micro- and macrovascular function in children with sickle cell anaemia and sickle cell haemoglobin C disease. Blood Cells Mol Dis. 2017;64:23-29.
Lemonne N, Lamarre Y, Romana M, et al. Impaired blood rheology plays a role in the chronic disorders associated with sickle cell-hemoglobin C disease. Haematologica. 2014;99(5):74-75.
Lionnet F, Hammoudi N, Stojanovic KS, et al. Hemoglobin sickle cell disease complications: a clinical study of 179 cases. Haematologica. 2012;97(8):1136-1141.
Beral L, Lemonne N, Romana M, et al. Proliferative retinopathy and maculopathy are two independent conditions in sickle cell disease: Is there a role of blood rheology?1. Clin Hemorheol Microcirc. 2019;71(3):337-345.
Conran N, Belcher JD. Inflammation in sickle cell disease. Clin Hemorheol Microcirc. 2018;68(2-3):263-299.
Nader E, Romana M, Connes P. The Red Blood Cell-Inflammation Vicious Circle in Sickle Cell Disease. Front Immunol. 2020;11:454.
van Beers EJ, van Wijk R. Oxidative stress in sickle cell disease; more than a DAMP squib. Clin Hemorheol Microcirc. 2018;68(2-3):239-250.
Hierso R, Waltz X, Mora P, et al. Effects of oxidative stress on red blood cell rheology in sickle cell patients. Br J Haematol. 2014;166(4):601-606.
Möckesch B, Connes P, Charlot K, et al. Association between oxidative stress and vascular reactivity in children with sickle cell anaemia and sickle haemoglobin C disease. Br J Haematol. 2017;178(3):468-475.
Antwi-Boasiako C, Dankwah GB, Aryee R, Hayfron-Benjamin C, Donkor ES, Campbell AD. Oxidative Profile of Patients with Sickle Cell Disease. Med Sci (Basel). 2019;7(2).
Ajibola KA, Adedokun KA, Oduola T, Oparinde DP, Ayelagbe OG, Ojokuku HO. Assessment of iron status and interplay between lipid peroxidation and antioxidant capacity in common hemoglobin variants in Osun State, southwestern Nigeria. Kaohsiung J Med Sci. 2019;35(6):358-364.
Torres LS, Okumura JV, Silva DGH, et al. Inflammation in Sickle Cell Disease: Differential and Down-Expressed Plasma Levels of Annexin A1 Protein. PLoS One. 2016;11(11):e0165833.
Guarda CC, Silveira-Mattos PSM, Yahouédéhou SCMA, et al. Hydroxyurea alters circulating monocyte subsets and dampens its inflammatory potential in sickle cell anemia patients. Sci Rep. 2019;9(1):14829.
Lanaro C, Franco-Penteado CF, Albuqueque DM, Saad ST, Conran N, Costa FF. Altered levels of cytokines and inflammatory mediators in plasma and leukocytes of sickle cell anemia patients and effects of hydroxyurea therapy. J Leukoc Biol. 2009;85(2):235-242.
Zahran AM, Nafady A, Saad K, et al. Effect of Hydroxyurea Treatment on the Inflammatory Markers Among Children With Sickle Cell Disease. Clin Appl Thromb Hemost. 2020;26:1076029619895111.
Nader E, Grau M, Fort R, et al. Hydroxyurea therapy modulates sickle cell anemia red blood cell physiology: Impact on RBC deformability, oxidative stress, nitrite levels and nitric oxide synthase signalling pathway. Nitric Oxide. 2018;81:28-35.
Torres LDS, Silva DGHd, Junior EB, et al. The influence of hydroxyurea on oxidative stress in sickle cell anemia. Rev Bras Hematol Hemoter. 2012;34(6):421-425.
Baskurt OK, Boynard M, Cokelet GC, et al. New guidelines for hemorheological laboratory techniques. Clin Hemorheol Microcirc. 2009;42(2):75-97.
Hardeman MR, Dobbe JG, Ince C. The Laser-assisted Optical Rotational Cell Analyzer (LORCA) as red blood cell aggregometer. Clin Hemorheol Microcirc. 2001;25(1):1-11.
Witko-Sarsat V, Friedlander M, Capeillère-Blandin C, et al. Advanced oxidation protein products as a novel marker of oxidative stress in uremia. Kidney Int. 1996;49(5):1304-1313.
Skinner SC, Diaw M, Pialoux V, et al. Increased Prevalence of Type 2 Diabetes-Related Complications in Combined Type 2 Diabetes and Sickle Cell Trait. Diabetes Care. 2018;41(12):2595-2602.
Roustit M, Cracowski JL. Non-invasive assessment of skin microvascular function in humans: an insight into methods. Microcirculation. 2012;19(1):47-64.
Boignard A, Salvat-Melis M, Carpentier PH, et al. Local hyperemia to heating is impaired in secondary Raynaud's phenomenon. Arthritis Res Ther. 2005;7(5):R1103-1112.
Lemonne N, Charlot K, Waltz X, et al. Hydroxyurea treatment does not increase blood viscosity and improves red blood cell rheology in sickle cell anemia. Haematologica. 2015;100(10):e383-386.
Ware RE. How I use hydroxyurea to treat young patients with sickle cell anemia. Blood. 2010;115(26):5300-5311.
Lopes FC, Traina F, Almeida CB, et al. Key endothelial cell angiogenic mechanisms are stimulated by the circulating milieu in sickle cell disease and attenuated by hydroxyurea. Haematologica. 2015;100(6):730-739.
Wong BJ, Fieger SM. Transient receptor potential vanilloid type-1 (TRPV-1) channels contribute to cutaneous thermal hyperaemia in humans. J Physiol. 2010;588(Pt 21):4317-4326.
Wallengren J, Hakanson R. Effects of substance P, neurokinin A and calcitonin gene-related peptide in human skin and their involvement in sensory nerve-mediated responses. Eur J Pharmacol. 1987;143(2):267-273.
Medow MS, Aggarwal A, Baugham I, Messer Z, Stewart JM. Modulation of the axon-reflex response to local heat by reactive oxygen species in subjects with chronic fatigue syndrome. J Appl Physiol (1985). 2013;114(1):45-51.
Lemaire C, Lamarre Y, Lemonne N, et al. Severe proliferative retinopathy is associated with blood hyperviscosity in sickle cell hemoglobin-C disease but not in sickle cell anemia. Clin Hemorheol Microcirc. 2013;55(2):205-212.
Luchtman-Jones L, Pressel S, Hilliard L, et al. Effects of hydroxyurea treatment for patients with hemoglobin SC disease. Am J Hematol. 2016;91(2):238-242.
Miller MK, Zimmerman SA, Schultz WH, Ware RE. Hydroxyurea therapy for pediatric patients with hemoglobin SC disease. J Pediatr Hematol Oncol. 2001;23(5):306-308.