School of Medicine and Health Sciences Poster Presentations
Scleroderma Wounds Exhibit Slower Healing than Wounds from Other Etiologies
Poster Number
4
Document Type
Poster
Publication Date
3-2016
Abstract
Introduction: Scleroderma is an autoimmune disease characterized by inflammation, vasculopathy, and fibrosis of skin, vasculative and internal organs. Delayed wound healing is a known complication of scleroderma. The purpose of this study was to investigate whether chronic wounds in scleroderma patients heal more slowly than chronic wounds of other etiology.
Methods: This research was conducted through the Wound Etiology and Healing Study (WE-HEAL Study). The WE-HEAL Study is a biospecimen and data repository approved by the George Washington University IRB (041408). Subjects gave written informed consent for collection of their data. Scleroderma cases with wounds (n=25) and age and sex matched control patients with chronic wounds from other etiologies (n=25) were selected for analysis. Baseline demographics, comorbidities, wound size, time to healing, and pain score were compared between the two groups. Scleroderma wounds were further analyzed based on scleroderma classification (localized vs. systemic; limited vs. diffuse). Statistical tests including T-test, Fisher’s Exact and Chi Square were performed using GraphPad Prism 5.0.
Results: While baseline total wound surface area (tWSA) was unchanged between the scleroderma and chronic wound groups, the tWSA at the last visit was significantly larger in the scleroderma group 24.80cm2 54.18 compared to the chronic wound group 0.18cm2 0.71 (p=0.028). Scleroderma wounds were significantly less likely to ultimately heal 52% compared to 84% (p=0.015). Pain scores tended to be higher in the subjects with scleroderma, but this did not reach statistical significance (4.08 ± 3.73 compared to 2.68 ± 2.90, p=0.145). Limited scleroderma wounds took longer to heal compared to wounds in patients with diffuse scleroderma suggesting the mechanisms of delayed wound healing in scleroderma may be more related to vasculopathy than ongoing inflammation.
Conclusion: Scleroderma patients exhibit delayed wound healing compared to patients with wounds from other etiologies. Scleroderma wounds are significantly less likely to ultimately heal than chronic wounds of other etiologies. There is an unmet need to further investigate the etiology of delayed wound healing in patients with scleroderma.
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Open Access
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Scleroderma Wounds Exhibit Slower Healing than Wounds from Other Etiologies
Introduction: Scleroderma is an autoimmune disease characterized by inflammation, vasculopathy, and fibrosis of skin, vasculative and internal organs. Delayed wound healing is a known complication of scleroderma. The purpose of this study was to investigate whether chronic wounds in scleroderma patients heal more slowly than chronic wounds of other etiology.
Methods: This research was conducted through the Wound Etiology and Healing Study (WE-HEAL Study). The WE-HEAL Study is a biospecimen and data repository approved by the George Washington University IRB (041408). Subjects gave written informed consent for collection of their data. Scleroderma cases with wounds (n=25) and age and sex matched control patients with chronic wounds from other etiologies (n=25) were selected for analysis. Baseline demographics, comorbidities, wound size, time to healing, and pain score were compared between the two groups. Scleroderma wounds were further analyzed based on scleroderma classification (localized vs. systemic; limited vs. diffuse). Statistical tests including T-test, Fisher’s Exact and Chi Square were performed using GraphPad Prism 5.0.
Results: While baseline total wound surface area (tWSA) was unchanged between the scleroderma and chronic wound groups, the tWSA at the last visit was significantly larger in the scleroderma group 24.80cm2 54.18 compared to the chronic wound group 0.18cm2 0.71 (p=0.028). Scleroderma wounds were significantly less likely to ultimately heal 52% compared to 84% (p=0.015). Pain scores tended to be higher in the subjects with scleroderma, but this did not reach statistical significance (4.08 ± 3.73 compared to 2.68 ± 2.90, p=0.145). Limited scleroderma wounds took longer to heal compared to wounds in patients with diffuse scleroderma suggesting the mechanisms of delayed wound healing in scleroderma may be more related to vasculopathy than ongoing inflammation.
Conclusion: Scleroderma patients exhibit delayed wound healing compared to patients with wounds from other etiologies. Scleroderma wounds are significantly less likely to ultimately heal than chronic wounds of other etiologies. There is an unmet need to further investigate the etiology of delayed wound healing in patients with scleroderma.
Comments
Presented at: GW Research Days 2016