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Background The pathogenesis of infantile haemangioma ( IH) is unknown. Several mechanisms have been proposed, including hypoxia, which triggers upregulation and stabilization of hypoxia-inducible factor ( HIF)1α. HIF1α stimulates downstream transcription of target genes that enhance angiogenesis. Aim To identify possible involvement of hypoxia in the pathogenesis of IH, as hypoxia signalling constitutes a potential therapeutic target. Methods IH tissue samples collected during the period 1991-2011 (preserved in paraffin wax) were immunohistochemically analysed for HIF1α and the known HIF1α targets: BCL2/adenovirus E1B kD-interacting protein family member 3 (BNIP3), carbon anhydrase (CA)-IX, glucose transporter (GLUT)-1, phosphorylated protein kinase B ( pAKT), phosphorylated S6 protein ( pS6) and vascular endothelial growth factor (VEGF). Four observers independently assessed the findings. Results Of the 10 IH samples, 2 appeared to be in the growth phase. In all samples, GLUT-1, BNIP3, pAKT and VEGF were positive, CA-IX was weakly positive, and HIF1α was negative. pS6 was positive in 9/10 cases and negative in 1/10. Conclusions Several factors implicated in hypoxia-induced angiogenesis may be involved in IH development. However, the small sample size and retrospective approach of the study preclude definitive conclusions. Prospective studies are needed to conclusively determine which of the factors involved in the (hypoxia) cascade are required for an IH to grow, and could thus be a possible target of drugs for IH treatment. [ABSTRACT FROM AUTHOR]

The article describes the case of a 63-year-old Moroccan woman who developed soft, yellowish papules on the neck. Melanophages and a mild perivascular lymphocytic infiltration in the superficial dermis were identified, and fragmentation of elastic fibers in the reticular dermis and loss of elastic fibers in the papillary dermis were observed. The patient was diagnosed with Pseudoxanthoma elasticum-like papillary dermal elastolysis (PXE-PDE), a rare dermatological disorder.