News on infantile haemangioma. Part 2: therapy and evaluation

Abstract

Infantile haemangioma (IH) is the most frequently occurring tumour of childhood. While benign, in more than half of the cases, less or more severe sequelae can be observed. In Part 1 of this review, we discussed the clinical course and pathomechanism of IHs. In Part 2 of this state-of-the-art review, we will discuss the current management of IH and focus on the working mechanism of b-blockers in IHs. Furthermore, we will discuss options for the evaluation of patients and their families (quality of life and family burden), as well as for the evaluation of IHs by healthcare providers, such as assessments of activity and severity. This review will update the reader on the working mechanism of propranolol in IHs and offer an oversight of tools (questionnaires and scoring systems) that can be used in clinical practice or for research.

IADVL SIG pediatric dermatology (academy) recommendations on Hemangioma of Infancy (HOI)

“…The relevance of such a classification is to screen for extra-cutaneous manifestations in segmental hemangiomas involving the face or perineal region associated with syndrome complex, mid-line hemangiomas involving the lumbosacral region associated with occult spinal dysraphism and other mid-line anomalies, and multi-focal hemangiomas >5 associated with hepatic hemangiomas and hypothyroidism. [ 10 , 26 - 29 ] These patients should undergo a thorough physical examination to look for associated defects and mid-line lesions and undergo investigations to rule out syndromic associations. The extra-cutaneous manifestations and complications associated with infantile hemangioma and the screening protocol are summarized in Table 2 .…”

A Systematic Review on the Role of Adrenergic Receptors in Angiogenesis Regulation in Health and Disease

“…In in vivo mouse models of lung cancer, chemical depletion of norepinephrine delays tumor growth, which seems to result from a decrease in the percentage of polarized M2 macrophages compared to M1 macrophages, as well as a decrease in the concentration of VEGFA in the tumors. Following stimulation with epinephrine or norepinephrine, M2 polarized macrophages secrete VEGFA and enhance angiogenesis in vitro, effects that are prevented by their pretreatment with propranolol [75]. Similarly, in a mouse model of breast cancer, stress-induced epinephrine and norepinephrine lead to the polarization of macrophages to the M2 phenotype and increased tumor weight and volume.…”