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To the Editor: It is often assumed that sclerodermatous (thickened) skin in patients with systemic sclerosis (SSc) is hypoxic. This is because many of the clinical features of the disease, e.g., digital ulceration and/or pitting, are attributed to ischemic atrophy, and hypoxia activates a number of genes implicated in the SSc disease process, e.g., transforming growth factor-s and endothelin-11. Studies have shown that hypoxia induces several extracellular matrix proteins in both SSc and healthy dermal fibroblasts2. However, there is very little direct evidence that sclerodermatous skin is hypoxic. Silverstein, et al showed a skin thickness-related reduction in transcutaneous oxygen pressures3. Valentini, et al subsequently reported reduced transcutaneous oxygen pressure in both sclerotic and nonsclerotic skin of patients with SSc at 44°C but not at 37°C4. We tested the hypothesis that skin of patients with SSc is hypoxic, especially where the skin is abnormal. The hypoxic cell marker pimonidazole can be detected and quantified using immunohistochemistry on formalin-fixed, paraffin-embedded biopsies. Although there are many examples of pimonidazole being used to quantify hypoxia in … Address correspondence to Dr. A.L. Herrick, University of Manchester, Salford Royal NHS Foundation Trust, Manchester, UK M6 8HD. E-mail: ariane.herrick{at}manchester.ac.uk

Testing for Hypoxia in Forearm Skin of Patients with Systemic Sclerosis, Assessed by Pimonidazole