Expression of 25-hydroxyvitamin D3-1α-hydroxylase in subcutaneous fat necrosis
Farooque, A., Moss, C., Zehnder, Daniel, Hewison, M. and Shaw, N.J.. (2009) Expression of 25-hydroxyvitamin D3-1α-hydroxylase in subcutaneous fat necrosis. British Journal of Dermatology, Vol.160 (No.2). pp. 423-425. ISSN 0007-0963Full text not available from this repository.
Official URL: http://dx.doi.org/10.1111/j.1365-2133.2008.08844.x
Background The most serious complication of subcutaneous fat necrosis (SCFN), a rare condition of the newborn characterized by indurated purple nodules, is hypercalcaemia. However, the mechanism for this hypercalcaemia remains unclear.
Objectives To determine whether the hypercalcaemia associated with SCFN involves expression of the vitamin D-activating enzyme 25-hydroxyvitamin D3-1α-hydroxylase (1α-hydroxylase) in affected tissue.
Methods Skin biopsies from two male patients with SCFN and hypercalcaemia were taken. The histological specimens were assessed using a polyclonal antibody against 1α-hydroxylase.
Results Histology in both cases showed strong expression of 1α-hydroxylase protein (brown staining) within the inflammatory infiltrate associated with SCFN. This was consistent with similar experiments in other granulomatous conditions.
Conclusions Hypercalcaemia in SCFN appears to be due to abundant levels of 1α-hydroxylase in immune infiltrates associated with tissue lesions. This is consistent with previous observations of extrarenal 1α-hydroxylase in skin from other granulomatous conditions such as sarcoidosis and slack skin disease.
|Item Type:||Journal Article|
|Subjects:||R Medicine > R Medicine (General)|
|Divisions:||Faculty of Medicine > Warwick Medical School > Translational & Systems Medicine > Metabolic and Vascular Health
Faculty of Medicine > Warwick Medical School
|Journal or Publication Title:||British Journal of Dermatology|
|Publisher:||Wiley-Blackwell Publishing Ltd.|
|Official Date:||February 2009|
|Page Range:||pp. 423-425|
|Access rights to Published version:||Restricted or Subscription Access|
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