Jacob Stewart1, Donald A Glass 2nd2. 1. Department of Dermatology, UT Southwestern Medical Center, Dallas, TX. 2. McDermott Center for Human Growth and Development, UT Southwestern Medical Center.
Abstract
INTRODUCTION: Keloidal scarring is associated with hypertension and its pathogenesis remains poorly understood. The role of angiotensin-converting enzyme (ACE) in both hypertensive and fibrotic conditions suggests ACE may be a common mechanism for the pathogenesis of both hypertension and keloids. OBJECTIVE: This paper aims to investigate the possible underlying role of ACE in keloid pathogenesis. MATERIALS AND METHODS: Plasma samples were collected from participants with and without keloids. Enzyme-linked immunosorbent assays were then performed to determine ACE levels in the plasma samples. The plasma ACE levels of patients with and without keloid scarring were compared, while controlling for hypertension. RESULTS: The 78 samples (39 keloid participants, 39 controls) were divided into 4 cohorts of either 18 (hypertensive) or 21 (normotensive) participants. The mean ± standard deviation ACE levels were 77.9 ± 31.2 ng/mL for the hypertensive keloid group (n = 18), 69.2 ± 18.8 ng/mL for the normotensive keloid group (n = 21), 72.7 ± 21.5 ng/mL for the hypertensive control group (n = 18), and 77.6 ± 18.5 ng/mL for the normotensive control group (n = 21). No significant differences in the mean plasma ACE levels were found between any of the 4 groups. CONCLUSIONS: Although the data showed no significant correlation between plasma ACE levels, keloids, and hypertension, additional studies may be pursued to determine the possible underlying role of ACE in keloid pathogenesis.
INTRODUCTION: Keloidal scarring is associated with hypertension and its pathogenesis remains poorly understood. The role of angiotensin-converting enzyme (ACE) in both hypertensive and fibrotic conditions suggests ACE may be a common mechanism for the pathogenesis of both hypertension and keloids. OBJECTIVE: This paper aims to investigate the possible underlying role of ACE in keloid pathogenesis. MATERIALS AND METHODS: Plasma samples were collected from participants with and without keloids. Enzyme-linked immunosorbent assays were then performed to determine ACE levels in the plasma samples. The plasma ACE levels of patients with and without keloid scarring were compared, while controlling for hypertension. RESULTS: The 78 samples (39 keloid participants, 39 controls) were divided into 4 cohorts of either 18 (hypertensive) or 21 (normotensive) participants. The mean ± standard deviation ACE levels were 77.9 ± 31.2 ng/mL for the hypertensive keloid group (n = 18), 69.2 ± 18.8 ng/mL for the normotensive keloid group (n = 21), 72.7 ± 21.5 ng/mL for the hypertensive control group (n = 18), and 77.6 ± 18.5 ng/mL for the normotensive control group (n = 21). No significant differences in the mean plasma ACE levels were found between any of the 4 groups. CONCLUSIONS: Although the data showed no significant correlation between plasma ACE levels, keloids, and hypertension, additional studies may be pursued to determine the possible underlying role of ACE in keloid pathogenesis.