Expression of 25-hydroxyvitamin D3-1α-hydroxylase in subcutaneous fat necrosis

Summary 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 ass...

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Bibliographic Details
Published inBritish journal of dermatology (1951) Vol. 160; no. 2; pp. 423 - 425
Main Authors Farooque, A., Moss, C., Zehnder, D., Hewison, M., Shaw, N.J.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.02.2009
Wiley-Blackwell
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Summary:Summary 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.
Bibliography:ark:/67375/WNG-PP21HGFX-F
ArticleID:BJD8844
istex:05710A5DC8CC3DA55B0BC37084E8D0324C4CD17F
Conflicts of interest
None declared.
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0007-0963
1365-2133
DOI:10.1111/j.1365-2133.2008.08844.x