| dc.relation.references |
Prefeitura do Município de São Paulo. Secretaria Municipal da Saúde. Manual de padronização de curativos. São Paulo: Secretaria Municipal da Saúde, 2021.
ABDUL-HUSSEIN, H. K.; AL-MAMMORI, H. S.; HASSAN, M. K. Evaluation of the expression of red blood cell CD36, interleukin-6 and interleukin-8 in sickle cell anemia pediatric patients. Cytokine, [s. l.], v. 143, p. 155534, 2021.
AL GHAZAL, P. et al. Evaluation of the Essen Rotary as a new technique for bacterial swabs: results of a prospective controlled clinical investigation in 50 patients with chronic leg ulcers. International Wound Journal, [s. l.], v. 11, n. 1, p. 44–49, 2014.
ALDALLAL, S. M. Mini review: leg ulcers - a secondary complication of sickle cell disease. International Journal of General Medicine, [s. l.], v. 12, p. 279–282, 2019.
ALLISON, A. C. Protection Afforded by Sickle-cell Trait Against Subtertian Malarial Infection. British Medical Journal, [s. l.], v. 1, n. 4857, p. 290–294, 1954.
ALMAGRO-MOLTO, M.; EDER, W.; SCHUBERT, S. Bordetella trematum in chronic ulcers: report on two cases and review of the literature. Infection, [s. l.], v. 43, n. 4, p. 489–494, 2015.
ALOUI, C. et al. The Signaling Role of CD40 Ligand in Platelet Biology and in Platelet Component Transfusion. International Journal of Molecular Sciences, [s. l.], v. 15, n. 12, p. 22342–22364, 2014.
ALTMAN, I. A. et al. A treatment algorithm to identify therapeutic approaches for leg ulcers in patients with sickle cell disease. International Wound Journal, [s. l.], v. 13, n. 6, p. 1315–1324, 2016.
ANTWI-BOASIAKO, C. et al. A study of the geographic distribution and associated risk factors of leg ulcers within an international cohort of sickle cell disease patients: the CASiRe group analysis. Annals of Hematology, [s. l.], v. 99, n. 9, p. 2073–2079, 2020.
ASHCROFT, G. S. et al. TNFα is a therapeutic target for impaired cutaneous wound healing. Wound Repair and Regeneration, [s. l.], v. 20, n. 1, p. 38–49, 2012a.
ASHCROFT, G. S. et al. Tumor necrosis factor-alpha (TNF-α) is a therapeutic target for impaired cutaneous wound healing. Wound Repair and Regeneration, [s. l.], v. 20, n. 1, p. 38–49, 2012b.
ATARASHI, K. et al. Rolling of Th1 cells via P-selectin glycoprotein ligand-1 stimulates LFA-1-mediated cell binding to ICAM=1. Journal of Immunology, [s. l.], v. 174, n. 3, p. 1424–1432, 2005.
AYOOLA, O. O. et al. Intima-media thickness of the common femoral artery as a marker of leg ulceration in sickle cell disease patients. Blood Advances, [s. l.], v. 2, n. 22, p.
90
3112–3117, 2018.
AZBELL, R. C. G.; DESAI, P. C. Treatment dilemmas: strategies for priapism, chronic leg ulcer disease, and pulmonary hypertension in sickle cell disease. Hematology. American Society of Hematology. Education Program, [s. l.], v. 2021, n. 1, p. 411–417, 2021.
BABALOLA, O. A. et al. Haematological indices of sickle cell patients with chronic leg ulcers on compression therapy. African Journal of Laboratory Medicine, [s. l.], v. 9, n. 1, p. 1037, 2020a.
BABALOLA, O. A. et al. Haematological indices of sickle cell patients with chronic leg ulcers on compression therapy. African Journal of Laboratory Medicine, [s. l.], v. 9, n. 1, 2020b. Disponível em: http://www.ajlmonline.org/index.php/AJLM/article/view/1037. Acesso em: 27 abr. 2025.
BALLAS, S. K.; MOHANDAS, N. Pathophysiology of vaso-occlusion. Hematology/Oncology Clinics of North America, [s. l.], v. 10, n. 6, p. 1221–1239, 1996.
BELCHER, J. D. et al. The BACH1 inhibitor ASP8731 inhibits inflammation and vaso-occlusion and induces fetal hemoglobin in sickle cell disease. Frontiers in Medicine, [s. l.], v. 10, 2023. Disponível em: https://www.frontiersin.org/journals/medicine/articles/10.3389/fmed.2023.1101501/full. Acesso em: 8 out. 2024.
BELISÁRIO, A. R. et al. Association between inflammatory molecules, nitric oxide metabolites and leg ulcers in individuals with sickle cell anemia. Hematology, Transfusion and Cell Therapy, [s. l.], v. 44, n. 2, p. 169–176, 2022.
BERGANT SUHODOLČAN, A.; LUZAR, B.; KECELJ LESKOVEC, N. Matrix metalloproteinase (MMP)-1 and MMP-2, but not COX-2 serve as additional predictors for chronic venous ulcer healing. Wound Repair and Regeneration, [s. l.], v. 29, n. 5, p. 725–731, 2021.
BILLETT, H. H.; PATEL, Y.; RIVERS, S. P. Venous insufficiency is not the cause of leg ulcers in sickle cell disease. American Journal of Hematology, [s. l.], v. 37, n. 2, p. 133–134, 1991.
BISWAL, S. et al. Oxidative stress, antioxidant capacity, biomolecule damage, and inflammation symptoms of sickle cell disease in children. Hematology, [s. l.], v. 24, n. 1, p. 1–9, 2019.
BLOCK, H.; ROSSAINT, J.; ZARBOCK, A. The Fatal Circle of NETs and NET-Associated DAMPs Contributing to Organ Dysfunction. Cells, [s. l.], v. 11, n. 12, p. 1919, 2022.
BOOTHBY, I. C.; COHEN, J. N.; ROSENBLUM, M. D. Regulatory T cells in Skin Injury: At the Crossroads of Tolerance and Tissue Repair. Science immunology, [s. l.], v. 5, n. 47, p. eaaz9631, 2020a.
BOOTHBY, I. C.; COHEN, J. N.; ROSENBLUM, M. D. Regulatory T cells in Skin Injury: At the Crossroads of Tolerance and Tissue Repair. Science immunology, [s. l.], v. 5, n. 47, p. eaaz9631, 2020b.
91
BOWERS, A. S. et al. Blood Viscosity and the Expression of Inflammatory and Adhesion Markers in Homozygous Sickle Cell Disease Subjects with Chronic Leg Ulcers. PLOS ONE, [s. l.], v. 8, n. 7, p. e68929, 2013.
BOWERS, A. S.; PEPPLE, D. J.; REID, H. L. Optimal haematocrit in subjects with normal haemoglobin genotype (HbAA), sickle cell trait (HbAS), and homozygous sickle cell disease (HbSS). Clinical Hemorheology and Microcirculation, [s. l.], v. 47, n. 4, p. 253–260, 2011.
BRANCATO, S. K.; ALBINA, J. E. Wound Macrophages as Key Regulators of Repair: Origin, Phenotype, and Function. The American Journal of Pathology, [s. l.], v. 178, n. 1, p. 19–25, 2011.
BRITO, L. S. et al. DA SUPERPROTEÇÃO AO ESTIGMA: RELAÇÕES FAMILIARES DE PESSOAS COM ÚLCERA DE PERNA E DOENÇA FALCIFORME. Revista Baiana de Enfermagem , [s. l.], v. 35, 2021. Disponível em: https://periodicos.ufba.br/index.php/enfermagem/article/view/37793. Acesso em: 15 ago. 2024.
BRUNI, E. et al. The healing process of diabetic ulcers correlates with changes in the cutaneous microbiota. Scientific Reports, [s. l.], v. 14, p. 27628, 2024.
BUECHLER, C. et al. Detection and Characterization of Clinical Bordetella trematum Isolates from Chronic Wounds. Pathogens, [s. l.], v. 10, n. 8, p. 966, 2021.
BURIAN, E. A. et al. A simplified method for monitoring cytokines in wound fluid. Wound Repair and Regeneration: Official Publication of the Wound Healing Society [and] the European Tissue Repair Society, [s. l.], v. 31, n. 1, p. 47–55, 2023.
BURIAN, E. A. et al. Cytokines and Venous Leg Ulcer Healing—A Systematic Review. International Journal of Molecular Sciences, [s. l.], v. 23, n. 12, p. 6526, 2022.
BYEON, J. et al. Insights into the skin microbiome of sickle cell disease leg ulcers. Wound Repair and Regeneration: Official Publication of the Wound Healing Society [and] the European Tissue Repair Society, [s. l.], v. 29, n. 5, p. 801–809, 2021.
CACKOVIC, M. et al. Leg Ulceration in the Sickle Cell Patient. Journal of the American College of Surgeons, [s. l.], v. 187, n. 3, p. 307, 1998.
CANÇADO, R. D. et al. Estimated mortality rates of individuals with sickle cell disease in Brazil: real-world evidence. Blood Advances, [s. l.], v. 7, n. 15, p. 3783–3792, 2023.
CARVALHO, M. O. S. et al. Inflammatory mediators in sickle cell anaemia highlight the difference between steady state and crisis in paediatric patients. British Journal of Haematology, [s. l.], v. 182, n. 6, p. 933–936, 2018.
CATELLA, J. et al. Controversies in the pathophysiology of leg ulcers in sickle cell disease. British Journal of Haematology, [s. l.], v. 205, n. 1, p. 61–70, 2024.
CHOI, Y. et al. Co-occurrence of Anaerobes in Human Chronic Wounds. Microbial Ecology, [s. l.], v. 77, n. 3, p. 808–820, 2019.
CHONG, K. K. L. et al. Enterococcus faecalis Modulates Immune Activation and Slows
92
Healing During Wound Infection. The Journal of Infectious Diseases, [s. l.], v. 216, n. 12, p. 1644–1654, 2017.
CHONG, D. L. W. et al. Platelet-derived transforming growth factor-β1 promotes keratinocyte proliferation in cutaneous wound healing. Journal of Tissue Engineering and Regenerative Medicine, [s. l.], v. 14, n. 4, p. 645–649, 2020.
CISZEK-LENDA, M. et al. Pseudomonas aeruginosa biofilm is a potent inducer of phagocyte hyperinflammation. Inflammation Research, [s. l.], v. 68, n. 5, p. 397–413, 2019.
COGNASSE, F. et al. Platelets as Key Factors in Inflammation: Focus on CD40L/CD40. Frontiers in Immunology, [s. l.], v. 13, 2022. Disponível em: https://www.frontiersin.orghttps://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.825892/full. Acesso em: 24 abr. 2025.
CONNES, P. et al. Vascular pathophysiology of sickle cell disease. Presse Medicale (Paris, France: 1983), [s. l.], v. 52, n. 4, p. 104202, 2023.
DA SILVA, R. R. et al. Evaluation of Th17 related cytokines associated with clinical and laboratorial parameters in sickle cell anemia patients with leg ulcers. Cytokine, [s. l.], v. 65, n. 2, p. 143–147, 2014.
DAVENPECK, K. L. et al. Activation of human leukocytes reduces surface P-selectin glycoprotein ligand-1 (PSGL-1, CD162) and adhesion to P-selectin in vitro. Journal of Immunology (Baltimore, Md.: 1950), [s. l.], v. 165, n. 5, p. 2764–2772, 2000.
DE CATERINA, R. et al. Nitric oxide decreases cytokine-induced endothelial activation. Nitric oxide selectively reduces endothelial expression of adhesion molecules and proinflammatory cytokines. The Journal of Clinical Investigation, [s. l.], v. 96, n. 1, p. 60–68, 1995.
DEPREZ, K. N.; FERGUSON, J. Endobronchial Infection and Bacterial Lymphadenitis by Gemella morbillorum Leading to Airway Perforation and a Bronchopleural Fistula. Case Reports in Pulmonology, [s. l.], v. 2024, n. 1, p. 8850287, 2024.
DESMOULIÈRE, A. et al. Transforming growth factor-beta 1 induces alpha-smooth muscle actin expression in granulation tissue myofibroblasts and in quiescent and growing cultured fibroblasts. The Journal of Cell Biology, [s. l.], v. 122, n. 1, p. 103–111, 1993.
DEVARAJ, S.; JIALAL, I. C-Reactive Protein Polarizes Human Macrophages to an M1 Phenotype and Inhibits Transformation to the M2 Phenotype. Arteriosclerosis, Thrombosis, and Vascular Biology, [s. l.], v. 31, n. 6, p. 1397–1402, 2011.
DHAMODHARAN, U. et al. Genetic association of IL-6, TNF-α and SDF-1 polymorphisms with serum cytokine levels in diabetic foot ulcer. Gene, [s. l.], v. 565, n. 1, p. 62–67, 2015.
DIXIT, R. et al. Folate supplementation in people with sickle cell disease. The Cochrane Database of Systematic Reviews, [s. l.], v. 3, n. 3, p. CD011130, 2018.
DOMINGOS, I. F. et al. High levels of proinflammatory cytokines IL-6 and IL-8 are associated with a poor clinical outcome in sickle cell anemia. Annals of Hematology, [s. l.], v. 99, n. 5, p. 947–953, 2020.
93
DUNYACH-REMY, C. et al. Pressure ulcers microbiota dynamics and wound evolution. Scientific Reports, [s. l.], v. 11, n. 1, p. 18506, 2021.
ELALFY, M. S. et al. Immunological role of CD4+CD28null T lymphocytes, natural killer cells, and interferon-gamma in pediatric patients with sickle cell disease: relation to disease severity and response to therapy. Immunologic Research, [s. l.], v. 66, n. 4, p. 480–490, 2018.
ELLIS, S.; LIN, E. J.; TARTAR, D. Immunology of Wound Healing. Current Dermatology Reports, [s. l.], v. 7, n. 4, p. 350–358, 2018a.
ELLIS, S.; LIN, E. J.; TARTAR, D. Immunology of Wound Healing. Current Dermatology Reports, [s. l.], v. 7, n. 4, p. 350–358, 2018b.
ESCOPY, S.; CHAIKOF, E. L. Targeting the P-selectin/PSGL-1 pathway: discovery of disease-modifying therapeutics for disorders of thromboinflammation. Blood Vessels, Thrombosis & Hemostasis, [s. l.], v. 1, n. 3, p. 100015, 2024.
FASOLA, F. A. et al. The Effect of Alpha Thalassemia, HbF and HbC on Haematological Parameters of Sickle Cell Disease Patients in Ibadan, Nigeria. Mediterranean Journal of Hematology and Infectious Diseases, [s. l.], v. 14, n. 1, p. e2022001, 2022.
FORTUNA, V. et al. Enhancing Sickle Cell Leg Ulcer Healing with Combined Photodynamic and Photobiomodulation Therapies: a pilot experience. Journal of Tissue Viability, [s. l.], p. 100879, 2025.
FRENETTE, P. S. et al. P-Selectin Glycoprotein Ligand 1 (Psgl-1) Is Expressed on Platelets and Can Mediate Platelet–Endothelial Interactions in Vivo. The Journal of Experimental Medicine, [s. l.], v. 191, n. 8, p. 1413–1422, 2000.
GHOSH, S. et al. P-selectin plays a role in haem-induced acute lung injury in sickle mice. British journal of haematology, [s. l.], v. 186, n. 2, p. 329–333, 2019.
GLADWIN, M. et al. Divergent Nitric Oxide Bioavailability in Men and Women With Sickle Cell Disease. Circulation, [s. l.], v. 107, p. 271–278, 2003.
GOMES, I. C. P. et al. Levels of inflammatory markers are differentially expressed in sickle cell anemia and sickle cell trait. eJHaem, [s. l.], v. 4, n. 3, p. 705–709, 2023.
GRANJA, P. D. et al. Úlceras de perna em pacientes com anemia falciforme. Jornal Vascular Brasileiro, [s. l.], v. 19, p. e20200054, 2020.
GRÖNWALL, C. et al. In vivo VL-targeted microbial superantigen induced global shifts in the B cell repertoire. Journal of Immunology (Baltimore, Md.: 1950), [s. l.], v. 189, n. 2, p. 850–859, 2012.
GUPTA, P.; KUMAR, R. Nitric oxide: A potential etiological agent for vaso-occlusive crises in sickle cell disease. Nitric Oxide, [s. l.], v. 144, p. 40–46, 2024.
HALABI-TAWIL, M. et al. Sickle cell leg ulcers: a frequently disabling complication and a marker of severity. The British Journal of Dermatology, [s. l.], v. 158, n. 2, p. 339–344, 2008.
94
HAN, Y.-P. et al. Transforming Growth Factor-β- and Tumor Necrosis Factor-α- mediated Induction and Proteolytic Activation of MMP-9 in Human Skin. The Journal of biological chemistry, [s. l.], v. 276, n. 25, p. 22341–22350, 2001.
HELVACI, M. et al. Acute painful crises may be causes of sudden deaths in sickle cell diseases. [s. l.], 2023.
HENRY, E. R. et al. Allosteric control of hemoglobin S fiber formation by oxygen and its relation to the pathophysiology of sickle cell disease. Proceedings of the National Academy of Sciences of the United States of America, [s. l.], v. 117, n. 26, p. 15018–15027, 2020.
HEO, S. C. et al. Tumor necrosis factor-α-activated human adipose tissue-derived mesenchymal stem cells accelerate cutaneous wound healing through paracrine mechanisms. The Journal of Investigative Dermatology, [s. l.], v. 131, n. 7, p. 1559–1567, 2011.
HIGDON, A. N. et al. Hemin causes mitochondrial dysfunction in endothelial cells through promoting lipid peroxidation: the protective role of autophagy. American Journal of Physiology. Heart and Circulatory Physiology, [s. l.], v. 302, n. 7, p. H1394-1409, 2012.
HINES, P. C. et al. Flow adhesion of whole blood to P-selectin: a prognostic biomarker for vaso-occlusive crisis in sickle cell disease. British Journal of Haematology, [s. l.], v. 194, n. 6, p. 1074–1082, 2021a.
HINES, P. C. et al. Flow adhesion of whole blood to P‐selectin: a prognostic biomarker for vaso‐occlusive crisis in sickle cell disease. British Journal of Haematology, [s. l.], v. 194, n. 6, p. 1074–1082, 2021b.
HINZ, B. Formation and Function of the Myofibroblast during Tissue Repair. Journal of Investigative Dermatology, [s. l.], v. 127, n. 3, p. 526–537, 2007.
HODDE, J. P.; HILES, M. C.; METZGER, D. W. Characterization of the local wound environment following treatment of chronic leg ulcers with SIS wound matrix. Journal of Tissue Viability, [s. l.], v. 29, n. 1, p. 42–47, 2020.
HOSSEINI, M. et al. Skin biomechanics: a potential therapeutic intervention target to reduce scarring. Burns & Trauma, [s. l.], v. 10, p. tkac036, 2022.
HOU, K. et al. Microbiota in health and diseases. Signal Transduction and Targeted Therapy, [s. l.], v. 7, n. 1, p. 1–28, 2022.
HUANG, Y. et al. Rapid microbiological diagnosis based on 16S rRNA gene sequencing: A comparison of bacterial composition in diabetic foot infections and contralateral intact skin. Frontiers in Microbiology, [s. l.], v. 13, 2022. Disponível em: https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2022.1021955/full. Acesso em: 31 mar. 2025.
INGRAM, V. M. A specific chemical difference between the globins of normal human and sickle-cell anaemia haemoglobin. Nature, [s. l.], v. 178, n. 4537, p. 792–794, 1956.
ISHIDA, Y. et al. CCL2-Mediated Reversal of Impaired Skin Wound Healing in Diabetic Mice by Normalization of Neovascularization and Collagen Accumulation. Journal of Investigative Dermatology, [s. l.], v. 139, n. 12, p. 2517-2527.e5, 2019.
95
ITOKUA, K. E. et al. Albuminuria, serum antioxidant enzyme levels and markers of hemolysis and inflammation in steady state children with sickle cell anemia. BMC Nephrology, [s. l.], v. 17, n. 1, p. 178, 2016.
JANCIAUSKIENE, S.; VIJAYAN, V.; IMMENSCHUH, S. TLR4 Signaling by Heme and the Role of Heme-Binding Blood Proteins. Frontiers in Immunology, [s. l.], v. 11, 2020. Disponível em: https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2020.01964/full. Acesso em: 15 ago. 2024.
JANG, D. et al. The Role of Tumor Necrosis Factor Alpha (TNF-α) in Autoimmune Disease and Current TNF-α Inhibitors in Therapeutics. International Journal of Molecular Sciences, [s. l.], v. 22, n. 5, p. 2719, 2021.
JANSEN, E. E. et al. Platelet-Therapeutics to Improve Tissue Regeneration and Wound Healing—Physiological Background and Methods of Preparation. Biomedicines, [s. l.], v. 9, n. 8, p. 869, 2021.
JNANA, A. et al. Microbial Community Distribution and Core Microbiome in Successive Wound Grades of Individuals with Diabetic Foot Ulcers. Applied and Environmental Microbiology, [s. l.], v. 86, n. 6, p. e02608-19, 2020.
JOHNSON, B. Z. et al. The Role of IL-6 in Skin Fibrosis and Cutaneous Wound Healing. Biomedicines, [s. l.], v. 8, n. 5, p. 101, 2020.
JOLIBOIS, J. et al. Targeting TXNIP in endothelial progenitors mitigates IL-8-induced neutrophil recruitment under metabolic stress. Stem Cell Research & Therapy, [s. l.], v. 15, n. 1, p. 225, 2024.
JURK, K.; KEHREL, B. E. Platelets: Physiology and Biochemistry. Seminars in Thrombosis and Hemostasis, [s. l.], v. 50, n. 5, p. 794–803, 2024.
KALAN, L. R. et al. Strain- and Species-Level Variation in the Microbiome of Diabetic Wounds Is Associated with Clinical Outcomes and Therapeutic Efficacy. Cell Host & Microbe, [s. l.], v. 25, n. 5, p. 641-655.e5, 2019.
KALIYADAN, F. et al. Prevalence and Predictive Factors for Leg Ulcers in Sickle Cell Disease Patients in Saudi Arabia: A Cross-Sectional Observational Study. Cureus, [s. l.], v. 12, n. 10, p. e11280, 2020.
KANDHWAL, M. et al. Role of matrix metalloproteinase in wound healing. American Journal of Translational Research, [s. l.], v. 14, n. 7, p. 4391–4405, 2022.
KARTIKA, R. W. et al. The role of VEGF, PDGF and IL-6 on diabetic foot ulcer after Platelet Rich Fibrin + hyaluronic therapy. Heliyon, [s. l.], v. 7, n. 9, 2021. Disponível em: https://www.cell.com/heliyon/abstract/S2405-8440(21)02037-5. Acesso em: 30 mar. 2025.
KATO, G. J. et al. Lactate dehydrogenase as a biomarker of hemolysis-associated nitric oxide resistance, priapism, leg ulceration, pulmonary hypertension, and death in patients with sickle cell disease. Blood, [s. l.], v. 107, n. 6, p. 2279–2285, 2006.
KATO, G. J. et al. Sickle cell disease. Nature Reviews. Disease Primers, [s. l.], v. 4, p.
96
18010, 2018.
KOSHY, M. et al. Leg ulcers in patients with sickle cell disease [see comments]. Blood, [s. l.], v. 74, n. 4, p. 1403–1408, 1989.
KOTTNER, J. et al. Pressure ulcer/injury classification today: An international perspective. Journal of Tissue Viability, [s. l.], v. 29, n. 3, p. 197–203, 2020.
KUNIMITSU, M. et al. Relationship between healing status and microbial dissimilarity in wound and peri-wound skin in pressure injuries. Journal of Tissue Viability, [s. l.], v. 32, n. 1, p. 144–150, 2023.
L. BOWLING, F.; U. DISSANAYAKE, S.; B. JUDE, E. Opportunistic Pathogens in Diabetic Foot Lesions. Current Diabetes Reviews, [s. l.], v. 8, n. 3, p. 195–199, 2012.
LADIZINSKI, B. et al. Sickle Cell Disease and Leg Ulcers. Advances in Skin & Wound Care, [s. l.], v. 25, n. 9, p. 420, 2012a.
LADIZINSKI, B. et al. Sickle cell disease and leg ulcers. Advances in Skin & Wound Care, [s. l.], v. 25, n. 9, p. 420–428, 2012b.
LAI, Y. et al. Commensal bacteria regulate TLR3-dependent inflammation following skin injury. Nature medicine, [s. l.], v. 15, n. 12, p. 1377–1382, 2009.
LANARO, C. et al. Altered levels of cytokines and inflammatory mediators in plasma and leukocytes of sickle cell anemia patients and effects of hydroxyurea therapy. Journal of Leukocyte Biology, [s. l.], v. 85, n. 2, p. 235–242, 2009.
LANDÉN, N. X.; LI, D.; STÅHLE, M. Transition from inflammation to proliferation: a critical step during wound healing. Cellular and Molecular Life Sciences, [s. l.], v. 73, n. 20, p. 3861–3885, 2016.
LEID, J. G. et al. The Exopolysaccharide Alginate Protects Pseudomonas aeruginosa Biofilm Bacteria from IFN-γ-Mediated Macrophage Killing1. The Journal of Immunology, [s. l.], v. 175, n. 11, p. 7512–7518, 2005.
LI, Y. et al. Sequence analysis of microbiota in clinical human cases with diabetic foot ulcers from China. Heliyon, [s. l.], v. 10, n. 14, 2024. Disponível em: https://www.cell.com/heliyon/abstract/S2405-8440(24)10399-4. Acesso em: 26 mar. 2025.
LI, D. et al. Single-Cell Analysis Reveals Major Histocompatibility Complex II‒Expressing Keratinocytes in Pressure Ulcers with Worse Healing Outcomes. Journal of Investigative Dermatology, [s. l.], v. 142, n. 3, p. 705–716, 2022.
LIGI, D. et al. Chronic venous disease – Part I: Inflammatory biomarkers in wound healing. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, [s. l.], v. 1862, n. 10, p. 1964–1974, 2016.
LIMA, K. T. L. L. et al. Qualidade de vida dos portadores de doença falciforme. Rev. enferm. UFPE on line, [s. l.], p. 424–430, 2019.
LIN, M.-H. et al. Enhancing wound healing in recalcitrant leg ulcers with aminolevulinic
97
acid-mediated antimicrobial photodynamic therapy. Photodiagnosis and Photodynamic Therapy, [s. l.], v. 33, p. 102149, 2021.
LIN, S. et al. Heme activates TLR4-mediated inflammatory injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage. Journal of Neuroinflammation, [s. l.], v. 9, n. 1, p. 46, 2012.
LITTIG, J. P. B. et al. Increased Population of CD40+ Fibroblasts Is Associated with Impaired Wound Healing and Chronic Inflammation in Diabetic Foot Ulcers. Journal of Clinical Medicine, [s. l.], v. 11, n. 21, p. 6335, 2022.
LIU, X. et al. Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c. Cell, [s. l.], v. 86, n. 1, p. 147–157, 1996.
LOBO, C. L. de C. et al. Mortality in children, adolescents and adults with sickle cell anemia in Rio de Janeiro, Brazil. Revista Brasileira De Hematologia E Hemoterapia, [s. l.], v. 40, n. 1, p. 37–42, 2018.
LOOMIS, K. H. et al. A mixed community of skin microbiome representatives influences cutaneous processes more than individual members. Microbiome, [s. l.], v. 9, n. 1, p. 22, 2021.
MAHESWARY, T.; NURUL, A. A.; FAUZI, M. B. The Insights of Microbes’ Roles in Wound Healing: A Comprehensive Review. Pharmaceutics, [s. l.], v. 13, n. 7, p. 981, 2021.
MAHMOUD, N. N. et al. Investigating Inflammatory Markers in Wound Healing: Understanding Implications and Identifying Artifacts. ACS Pharmacology & Translational Science, [s. l.], v. 7, n. 1, p. 18–27, 2024a.
MAHMOUD, N. N. et al. Investigating Inflammatory Markers in Wound Healing: Understanding Implications and Identifying Artifacts. ACS Pharmacology & Translational Science, [s. l.], v. 7, n. 1, p. 18–27, 2024b.
MANZO MARGIOTTA, F. et al. Monoclonal Antibodies in the Management of Inflammation in Wound Healing: An Updated Literature Review. Journal of Clinical Medicine, [s. l.], v. 13, n. 14, p. 4089, 2024.
MAROTTA, C. A. et al. Human beta-globin messenger RNA. III. Nucleotide sequences derived from complementary DNA. The Journal of Biological Chemistry, [s. l.], v. 252, n. 14, p. 5040–5053, 1977.
MATHEUS, G. G. et al. Understanding the pathophysiology of Pseudomonas aeruginosa colonization as a guide for future treatment for chronic leg ulcers. Burns & Trauma, [s. l.], v. 13, p. tkae083, 2025.
MCCARTY, S. M.; PERCIVAL, S. L. Proteases and Delayed Wound Healing. Advances in Wound Care, [s. l.], v. 2, n. 8, p. 438–447, 2013.
MCDONALD, B. et al. Intravascular Danger Signals Guide Neutrophils to Sites of Sterile Inflammation. Science, [s. l.], v. 330, n. 6002, p. 362–366, 2010.
MCMAHON, T. J. et al. Nitric oxide loading reduces sickle red cell adhesion and
98
vaso-occlusion in vivo. Blood Advances, [s. l.], v. 3, n. 17, p. 2586–2597, 2019.
MENDONÇA, R.; SILVEIRA, A. A. A.; CONRAN, N. Red cell DAMPs and inflammation. Inflammation Research, [s. l.], v. 65, n. 9, p. 665–678, 2016.
MIKOSIŃSKI, J. et al. Longitudinal Evaluation of Biomarkers in Wound Fluids from Venous Leg Ulcers and Split-thickness Skin Graft Donor Site Wounds Treated with a Protease-modulating Wound Dressing. Acta Dermato-Venereologica, [s. l.], v. 102, p. adv00834, 2022.
MINNITI, C. P. et al. The impact of voxelotor treatment on leg ulcers in patients with sickle cell disease. American Journal of Hematology, [s. l.], v. 96, n. 4, p. E126–E128, 2021a.
MINNITI, C. P. et al. The impact of voxelotor treatment on leg ulcers in patients with sickle cell disease. American Journal of Hematology, [s. l.], v. 96, n. 4, p. E126–E128, 2021b.
MINNITI, C. P. et al. Vasculopathy, inflammation, and blood flow in leg ulcers of patients with sickle cell anemia. American journal of hematology, [s. l.], v. 89, n. 1, p. 1–6, 2014.
MINNITI, C. P.; KATO, G. J. Critical Reviews: How we treat sickle cell patients with leg ulcers. American Journal of Hematology, [s. l.], v. 91, n. 1, p. 22–30, 2016.
MOFFATT, C. J. et al. Prevalence of leg ulceration in a London population. QJM: An International Journal of Medicine, [s. l.], v. 97, n. 7, p. 431–437, 2004.
MONDORO, T. H. et al. Biological action of nitric oxide donor compounds on platelets from patients with sickle cell disease. British Journal of Haematology, [s. l.], v. 112, n. 4, p. 1048–1054, 2001.
MONFORT, J.-B.; SENET, P. Leg Ulcers in Sickle-Cell Disease: Treatment Update. Advances in Wound Care, [s. l.], v. 9, n. 6, p. 348–356, 2020.
MORIKIS, V. A. et al. Targeting Neutrophil Adhesive Events to Address Vaso-Occlusive Crisis in Sickle Cell Patients. Frontiers in Immunology, [s. l.], v. 12, 2021. Disponível em: https://www.frontiersin.orghttps://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2021.663886/full. Acesso em: 27 abr. 2025.
MUÑOZ-CALLEJAS, A. et al. Low P-Selectin Glycoprotein Ligand-1 Expression in Neutrophils Associates with Disease Activity and Deregulated NET Formation in Systemic Lupus Erythematosus. International Journal of Molecular Sciences, [s. l.], v. 24, n. 7, p. 6144, 2023.
MURPHY, E. C. et al. Identification of molecular mechanisms used by inegoldia magna to penetrate and colonize human skin. Molecular Microbiology, [s. l.], v. 94, n. 2, p. 403–417, 2014.
NADER, E.; ROMANA, M.; CONNES, P. The Red Blood Cell-Inflammation Vicious Circle in Sickle Cell Disease. Frontiers in Immunology, [s. l.], v. 11, p. 454, 2020.
NG, C. T. et al. Interferon-Gamma Increases Endothelial Permeability by Causing Activation of p38 MAP Kinase and Actin Cytoskeleton Alteration. Journal of Interferon & Cytokine Research: The Official Journal of the International Society for Interferon and Cytokine
99
Research, [s. l.], v. 35, n. 7, p. 513–522, 2015.
OBEAGU, E. I. et al. An Update on Interferon Gamma and C Reactive Proteins in Sickle Cell Anaemia Crisis. [s. l.], 2022. Disponível em: http://hdl.handle.net/20.500.12493/14519. Acesso em: 27 abr. 2025.
OKPALA, I. et al. Relationship between the clinical manifestations of sickle cell disease and the expression of adhesion molecules on white blood cells. European Journal of Haematology, [s. l.], v. 69, n. 3, p. 135–144, 2002.
OLATUNYA, O. S. et al. Evaluation of sociodemographic, clinical, and laboratory markers of sickle leg ulcers among young nigerians at a tertiary health institution. Nigerian Journal of Clinical Practice, [s. l.], v. 21, n. 7, p. 882–887, 2018.
OLIVEIRA, F. M. de. Caracterização do microbioma em úlcera de perna de pacientes com Doença Falciforme. 2023a. text - Universidade de São Paulo, [s. l.], 2023. Disponível em: https://www.teses.usp.br/teses/disponiveis/5/5134/tde-29052023-163729/. Acesso em: 23 set. 2024.
OLIVEIRA, F. M. de. Caracterização do microbioma em úlcera de perna de pacientes com Doença Falciforme. [S. l.], 2023b.
PAULING, L. et al. Sickle Cell Anemia, a Molecular Disease. Science, [s. l.], v. 110, n. 2865, p. 543–548, 1949.
PIIPPONEN, M.; LI, D.; LANDÉN, N. X. The Immune Functions of Keratinocytes in Skin Wound Healing. International Journal of Molecular Sciences, [s. l.], v. 21, n. 22, p. 8790, 2020a.
PIIPPONEN, M.; LI, D.; LANDÉN, N. X. The Immune Functions of Keratinocytes in Skin Wound Healing. International Journal of Molecular Sciences, [s. l.], v. 21, n. 22, p. 8790, 2020b.
PUKSTAD, B. S. et al. Non-healing is associated with persistent stimulation of the innate immune response in chronic venous leg ulcers. Journal of Dermatological Science, [s. l.], v. 59, n. 2, p. 115–122, 2010.
QIAN, L.-W. et al. Exacerbated and prolonged inflammation impairs wound healing and increases scarring. Wound Repair and Regeneration, [s. l.], v. 24, n. 1, p. 26–34, 2016.
RAFFETTO, J. D. et al. Why Venous Leg Ulcers Have Difficulty Healing: Overview on Pathophysiology, Clinical Consequences, and Treatment. Journal of Clinical Medicine, [s. l.], v. 10, n. 1, p. 29, 2021.
RAZIYEVA, K. et al. Immunology of Acute and Chronic Wound Healing. Biomolecules, [s. l.], v. 11, n. 5, p. 700, 2021.
RIDIANDRIES, A.; TAN, J. T. M.; BURSILL, C. A. The Role of Chemokines in Wound Healing. International Journal of Molecular Sciences, [s. l.], v. 19, n. 10, p. 3217, 2018.
RIFKIND, J. M.; MOHANTY, J. G.; NAGABABU, E. The pathophysiology of extracellular hemoglobin associated with enhanced oxidative reactions. Frontiers in Physiology, [s. l.], v.
100
5, p. 500, 2014.
SALOMONE, F. et al. Unconjugated bilirubin, a potent endogenous antioxidant, is decreased in patients with non-alcoholic steatohepatitis and advanced fibrosis. Journal of Gastroenterology and Hepatology, [s. l.], v. 28, n. 7, p. 1202–1208, 2013.
SANTOS, E. do C. et al. Leg Ulcers in Sickle Cell Disease: A Multifactorial Analysis Highlights the Hemolytic Profile. Hematology Reports, [s. l.], v. 15, n. 1, p. 119–129, 2023.
SCHECHTER, A. N. Sickle cell anaemia therapy in 2025. British Journal of Haematology, [s. l.], v. 206, n. 3, p. 842–845, 2025.
SCHULTZ, G. S. et al. Principles of Wound Healing. In: FITRIDGE, R.; THOMPSON, M. (org.). Mechanisms of Vascular Disease: A Reference Book for Vascular Specialists. Adelaide (AU): University of Adelaide Press, 2011. Disponível em: http://www.ncbi.nlm.nih.gov/books/NBK534261/. Acesso em: 16 ago. 2024.
SERJEANT, G. R. Leg Ulceration in Sickle Cell Anemia. Archives of Internal Medicine, [s. l.], v. 133, n. 4, p. 690–694, 1974.
SERJEANT, G. R. et al. Leg ulceration in sickle cell disease: medieval medicine in a modern world. Hematology/Oncology Clinics of North America, [s. l.], v. 19, n. 5, p. 943–956, viii–ix, 2005.
SERRA, R. et al. Extracellular matrix assessment of infected chronic venous leg ulcers: role of metalloproteinases and inflammatory cytokines. International Wound Journal, [s. l.], v. 13, n. 1, p. 53–58, 2014.
SHARMA, C. et al. The role of matrix metalloproteinase-9 and its inhibitor TIMP-1 in burn injury: a systematic review. International Journal of Burns and Trauma, [s. l.], v. 11, n. 4, p. 275–288, 2021.
SHETTY, P.; DSOUZA, R.; KUMAR B, V. Matrix Metalloproteinase-9 as a Predictor of Healing in Diabetic Foot Ulcers. Cureus, [s. l.], 2024. Disponível em: https://www.cureus.com/articles/323401-matrix-metalloproteinase-9-as-a-predictor-of-healing-in-diabetic-foot-ulcers. Acesso em: 30 mar. 2025.
SIMKA, M. Delayed healing of chronic leg ulcers can result from impaired trafficking of bone marrow-derived precursors of keratinocytes to the skin. Medical Hypotheses, [s. l.], v. 69, n. 3, p. 637–641, 2007.
SINGH, A. P.; MINNITI, C. P. Leg Ulceration in Sickle Cell Disease: An Early and Visible Sign of End‐Organ Disease. In: LEG ULCERATION IN SICKLE CELL DISEASE, 2016. (B. P. D. Inusa, Org.)Anais [...]. [S. l.]: InTech, 2016. Disponível em: http://www.intechopen.com/books/sickle-cell-disease-pain-and-common-chronic-complications/leg-ulceration-in-sickle-cell-disease-an-early-and-visible-sign-of-end-organ-disease. Acesso em: 31 mar. 2025.
SMITH, B. et al. Chronic Edema Management of the Lower Extremities. Cureus, [s. l.], 2024. Disponível em: https://www.cureus.com/articles/261171-chronic-edema-management-of-the-lower-extremities. Acesso em: 9 maio 2025.
101
SMITH, K. et al. One step closer to understanding the role of bacteria in diabetic foot ulcers: characterising the microbiome of ulcers. BMC Microbiology, [s. l.], v. 16, n. 1, p. 54, 2016.
SOUZA, V. R. de et al. Factors Associated with Leg Ulcers in Adults with Sickle Cell Disease in Brazil. [s. l.], 2023. Disponível em: https://observatorio.fm.usp.br/handle/OPI/53116. Acesso em: 16 ago. 2024.
SPIRA, J. A. O. et al. Doença falciforme: cuidado com pessoas com úlcera da perna nos serviços de atenção à saúde. Revista Enfermagem UERJ, [s. l.], v. 32, p. e79186–e79186, 2024.
SPIRA, J. A. O. et al. Estimated costs in treating sickle cell disease leg ulcer. Revista da Escola de Enfermagem da USP, [s. l.], v. 54, p. e03582, 2020.
SPIRA, J. A. O. et al. Prevalence of people with sickle cell disease and leg ulcers in Brazil: Socioeconomic and clinical overview. PloS One, [s. l.], v. 17, n. 9, p. e0274254, 2022.
STODDARD, K.; SOHAL, M.; BEDSON, R. Anaesthetic management of patients with sickle cell disease in obstetrics. BJA Education, [s. l.], v. 22, n. 3, p. 87–93, 2022.
STOJADINOVIC, O. et al. Deregulation of keratinocyte differentiation and activation: a hallmark of venous ulcers. Journal of Cellular and Molecular Medicine, [s. l.], v. 12, n. 6b, p. 2675–2690, 2008.
TAN, J. et al. Tissue and urinary haemosiderin in chronic leg ulcers. European Journal of Vascular and Endovascular Surgery: The Official Journal of the European Society for Vascular Surgery, [s. l.], v. 34, n. 3, p. 355–360, 2007.
TANAKA, T.; NARAZAKI, M.; KISHIMOTO, T. IL-6 in Inflammation, Immunity, and Disease. Cold Spring Harbor Perspectives in Biology, [s. l.], v. 6, n. 10, p. a016295, 2014.
TELES, W. et al. Frequência de casos de anemia falciforme, transfusão e tratamento – Experiência de um centro de hemoterapia em uma região do nordeste brasileiro / Frequency of sickle cell anemia cases, transfusion and treatment - Experience of a hemotherapy center in a region of northeastern Brazil. Brazilian Journal of Health Review, [s. l.], v. 4, p. 20426–20441, 2021.
THOMSON, A. M. et al. Global, regional, and national prevalence and mortality burden of sickle cell disease, 2000–2021: a systematic analysis from the Global Burden of Disease Study 2021. The Lancet Haematology, [s. l.], v. 10, n. 8, p. e585–e599, 2023.
TOYGAR, I.; SIMSIR, I. Y.; CETINKALP, S. Evaluation of three different techniques for measuring wound area in diabetic foot ulcers: a reproducibility study. Journal of Wound Care, [s. l.], v. 29, n. 9, p. 518–524, 2020.
TSIOUMPEKOU, M. et al. The Role of Cytokines in Neutrophil Development, Tissue Homing, Function and Plasticity in Health and Disease. Cells, [s. l.], v. 12, n. 15, p. 1981, 2023.
UBEROI, A.; MCCREADY-VANGI, A.; GRICE, E. A. The wound microbiota: microbial mechanisms of impaired wound healing and infection. Nature Reviews Microbiology, [s. l.], v. 22, n. 8, p. 507–521, 2024a.
102
UBEROI, A.; MCCREADY-VANGI, A.; GRICE, E. A. The wound microbiota: microbial mechanisms of impaired wound healing and infection. Nature Reviews Microbiology, [s. l.], v. 22, n. 8, p. 507–521, 2024b.
VALENZUELA, N. M. IFNγ, and to a Lesser Extent TNFα, Provokes a Sustained Endothelial Costimulatory Phenotype. Frontiers in Immunology, [s. l.], v. 12, p. 648946, 2021.
VAN LOO, G.; BERTRAND, M. J. M. Death by TNF: a road to inflammation. Nature Reviews Immunology, [s. l.], v. 23, n. 5, p. 289–303, 2023.
VELUSAMY, P. et al. IL-6 Contributes to Impaired Nitric Oxide and Increased Mitochondrial ROS Production in Human Aortic Endothelial Cells. Physiology, [s. l.], v. 39, n. S1, p. 2062, 2024.
VICARI, P. et al. Interleukin-1β and interleukin-6 gene polymorphisms are associated with manifestations of sickle cell anemia. Blood Cells, Molecules & Diseases, [s. l.], v. 54, n. 3, p. 244–249, 2015.
VOUILLARMET, J. et al. Advanced glycation end products assessed by skin autofluorescence: a new marker of diabetic foot ulceration. Diabetes Technology & Therapeutics, [s. l.], v. 15, n. 7, p. 601–605, 2013.
WADUD, R. et al. Yoda1 and phosphatidylserine exposure in red cells from patients with sickle cell anaemia. Scientific Reports, [s. l.], v. 10, n. 1, p. 20110, 2020.
WANG, Y. et al. [Protein expressions of matrix metalloproteinase-9 and its inhibitor and their ratio changes in wound healing of patients with stages Ⅲ and Ⅳ pressure ulcers]. Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns, [s. l.], v. 35, n. 10, p. 746–751, 2019.
WEINZWEIG, N. et al. Lower Limb Salvage by Microvascular Free-Tissue Transfer in Patients with Homozygous Sickle Cell Disease. Plastic and Reconstructive Surgery, [s. l.], v. 96, n. 5, p. 1154, 1995.
WILLENBORG, S.; INJARABIAN, L.; EMING, S. A. Role of Macrophages in Wound Healing. Cold Spring Harbor Perspectives in Biology, [s. l.], v. 14, n. 12, p. a041216, 2022.
WOOD, S. et al. Pro-Inflammatory Chemokine CCL2 (MCP-1) Promotes Healing in Diabetic Wounds by Restoring the Macrophage Response. PLOS ONE, [s. l.], v. 9, n. 3, p. e91574, 2014.
XU, Q. et al. Neutrophil reverse migration. Journal of Inflammation (London, England), [s. l.], v. 19, p. 22, 2022.
YAHOUÉDÉHOU, S. C. M. A. et al. Sickle Cell Anemia: Variants in the CYP2D6, CAT, and SLC14A1 Genes Are Associated With Improved Hydroxyurea Response. Frontiers in Pharmacology, [s. l.], v. 11, 2020. Disponível em: https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2020.553064/full. Acesso em: 15 ago. 2024.
YOUNESI, F. S. et al. Fibroblast and myofibroblast activation in normal tissue repair and fibrosis. Nature Reviews Molecular Cell Biology, [s. l.], v. 25, n. 8, p. 617–638, 2024.
103
YOUSIF, T. Y. E. Impact of Abnormal Leukocyte Count in the Pathophysiology of Sickle Cell Anemia. Journal of Blood Medicine, [s. l.], v. 13, p. 673–679, 2022.
ZHANG, L.; LEVY, A.; RIFKIND, J. M. Autoxidation of hemoglobin enhanced by dissociation into dimers. The Journal of Biological Chemistry, [s. l.], v. 266, n. 36, p. 24698–24701, 1991.
ZHENG, D. et al. ROS-triggered endothelial cell death mechanisms: Focus on pyroptosis, parthanatos, and ferroptosis. Frontiers in Immunology, [s. l.], v. 13, p. 1039241, 2022.
ZHU, Y. et al. Preventive effect of cluster nursing on pressure ulcers in orthopedic patients and predictive value of serum IL-6 and TNF-α for the occurrence of pressure ulcers. American Journal of Translational Research, [s. l.], v. 15, n. 2, p. 1140–1149, 2023.
ŽIBERNA, L.; JENKO-PRAŽNIKAR, Z.; PETELIN, A. Serum Bilirubin Levels in Overweight and Obese Individuals: The Importance of Anti-Inflammatory and Antioxidant Responses. Antioxidants, [s. l.], v. 10, n. 9, p. 1352, 2021.
ZILLMER, R. et al. Duration of wound fluid secretion from chronic venous leg ulcers is critical for interleukin-1α, interleukin-1β, interleukin-8 levels and fibroblast activation. Archives of Dermatological Research, [s. l.], v. 303, n. 8, p. 601–606, 2011a.
ZILLMER, R. et al. Duration of wound fluid secretion from chronic venous leg ulcers is critical for interleukin-1α, interleukin-1β, interleukin-8 levels and fibroblast activation. Archives of Dermatological Research, [s. l.], v. 303, n. 8, p. 601–606, 2011b. |
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