BACKGROUND: Acquired reactive perforating collagenosis (ARPC) is an uncommon itchy dermatosis of unknown etiology. OBJECTIVES: We aimed to study clinical features of ARPC and to characterize the expression profiles of proteins which are involved in extracellular matrix remodeling and wound repair. METHODS: Seventeen patients with ARPC were included in the study. Immunohistochemical analyses were performed for CD34, factor VIIIa, vascular endothelial growth factor, matrix metalloproteinase-1 (MMP-1), tissue inhibitor of metalloproteinase-1 (TIMP-1), transforming growth factor-beta3 (TGF-beta3), Smad-3, and Smad-7. RESULTS: Twelve patients (70.6%) had diabetes mellitus with disease duration of 14.6 +/- 13.1 years (mean +/- standard deviation). In all patients, chronic kidney disease was evident; two patients were receiving hemodialysis. Preexisting scabies infection was observed in 7 patients (41.2%). CD34 staining was significantly stronger in vessels of perilesional than those of lesional skin (P = .024). TGF-beta3, MMP-1, and TIMP-1 immunoreactivity was significantly stronger in lesional skin as compared with perilesional skin (P = .016, P = .0065, and P = .035, respectively). Although Smad-3 and Smad-7 immunoreactivity did not significantly differ in lesional and perilesional skin, there was a significant correlation between the protein expression of TGF-beta3 and Smad-3 (r = 0.56; P = .02), Smad-7 (r = 0.64; P = .006), and TIMP-1 (r = 0.56; P = .018) expression. LIMITATIONS: We did not perform polymerase chain reaction studies on mRNA expression. CONCLUSIONS: Our clinical data indicate that ARPC is etiopathogenetically linked to chronic kidney disease. Overexpression of TGF-beta3 and extracellular matrix proteins may represent antecedent tissue repair and therefore may be considered a significant event in the resolution of ARPC lesions.
BACKGROUND: Acquired reactive perforating collagenosis (ARPC) is an uncommon itchy dermatosis of unknown etiology. OBJECTIVES: We aimed to study clinical features of ARPC and to characterize the expression profiles of proteins which are involved in extracellular matrix remodeling and wound repair. METHODS: Seventeen patients with ARPC were included in the study. Immunohistochemical analyses were performed for CD34, factor VIIIa, vascular endothelial growth factor, matrix metalloproteinase-1 (MMP-1), tissue inhibitor of metalloproteinase-1 (TIMP-1), transforming growth factor-beta3 (TGF-beta3), Smad-3, and Smad-7. RESULTS: Twelve patients (70.6%) had diabetes mellitus with disease duration of 14.6 +/- 13.1 years (mean +/- standard deviation). In all patients, chronic kidney disease was evident; two patients were receiving hemodialysis. Preexisting scabies infection was observed in 7 patients (41.2%). CD34 staining was significantly stronger in vessels of perilesional than those of lesional skin (P = .024). TGF-beta3, MMP-1, and TIMP-1 immunoreactivity was significantly stronger in lesional skin as compared with perilesional skin (P = .016, P = .0065, and P = .035, respectively). Although Smad-3 and Smad-7 immunoreactivity did not significantly differ in lesional and perilesional skin, there was a significant correlation between the protein expression of TGF-beta3 and Smad-3 (r = 0.56; P = .02), Smad-7 (r = 0.64; P = .006), and TIMP-1 (r = 0.56; P = .018) expression. LIMITATIONS: We did not perform polymerase chain reaction studies on mRNA expression. CONCLUSIONS: Our clinical data indicate that ARPC is etiopathogenetically linked to chronic kidney disease. Overexpression of TGF-beta3 and extracellular matrix proteins may represent antecedent tissue repair and therefore may be considered a significant event in the resolution of ARPC lesions.
Authors: Stephan Schreml; Christian Hafner; Fabian Eder; Michael Landthaler; Walter Burgdorf; Philipp Babilas Journal: Case Rep Dermatol Date: 2011-09-29