Around 20 years, ago a biological classification system for paediatric vascular anomalies based on physical findings, natural history and histopathological features was published. In this system, vascular anomalies were essentially divided into two broad categories of haemangiomas and vascular malformations. Haemangiomas represented tumours, characterised by rapid growth during infancy followed by gradual involution, their underlying pathophysiology being abnormal endothelial cell proliferation. By contrast, malformations represent lesions present at birth (although not necessarily clinically apparent at this time), which grow proportionally with the child and do not spontaneously regress, their pathophysiological basis being dysplastic vascular channel formation. Vascular malformations have subsequently been further subcategorised according to the predominant type of vascular channel (capillary, venous, arterial, lymphatic or a combination) and their haemodynamic features (low or high blood flow).
In 1996, the classification of Mulliken and Glowaki was adopted and expanded by the International Society for the Study of Vascular Anomalies (ISSVA;http://www.ISSVA.org). In this revised classification, vascular anomalies are similarly divided into tumours and malformations, thus reflecting the awareness of other vascular lesions that are also characterised histologically by endothelial cell proliferation, such as lobular capillary haemangiomas and tufted angiomas (table 2). However, the term “haemangioma of infancy” or “infantile haemangioma” has replaced the classic “haemangioma” described in the original classification and is now included in the group of tumours. Further, it has now also been reported that the erythrocyte glucose transporter protein 1 (GLUT1) is strongly and diffusely expressed in the lesional endothelial cells of infantile haemangiomas during all stages of their natural history but not in other vascular tumours or malformations and this finding has also been incorporated into the ISSVA classification.
1. J Clin Pathol 2006;59:1278-1282 doi:10.1136/jcp.2006.038240