الفهرس 
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Abstract
Congenital vascular lesions have been, and still rem am poorly understood. Prior to 1980s, the study of congenital vascular lesions was confusing. The lack of a uniformly accepted classification and clear understanding of their natural history were in part to blame. A renaissance with the biological classification proposed by Mulliken and Glowachi, 1982, was a giant step forward. It was the first trial not only to diagnose congenital vascular lesions, but to understand their natural history as well (Achauer et ai, 1998). Haemangioma is the most common benign tumour during infancy. It represents about 10-12٪ of tumours in all children and 22٪ in pre-term infants with a reported racial variation. Although haemangioma is not believed to be familial, about 10% of affected infants have positive family history (Laverdiere et ai, 2008). This is despite of the controversial results regarding the influence of hereditary factors that could be attributed in the aetiology of haemangiomas (Mulliken et ai, 2000; Willenberg and Baumgartner, 2008). Haemangioma commonly appears soon after birth, although about 30٪ of lesions may already be present since birth (Mulliken, 1988). It typically proliferates during 1 st year of life and then involutes later during childhood period. Although considerable variations are seen regarding rate of proliferation and involution, these two features are constant and distinguish haemangiomas from congenital vascular malformations that neither proliferate nor involute. There are missing links between the rare rapidly involuting congenital haemangiomas (RICH), non-involuting congenital haemangiomas (NICH), congenital non-progressive haemangioma and the common infantile haemangiomas (Baselga et ai, 2008; Ethunandan and Melior, 2006; Mulliken and Enjolras, 2004; North et al 2001a). During proliferative phase of haemangioma, tubules of plump proliferating endothelial cells with frequent mitosis are dominant histopathological features. Afterward, mast cells become more abundant with less active endothelial cell proliferation. Recently, mesenchymal stem cells (MSCs) were recognized as a novel cellular constituent in infantile haemangioma. These MSCs may contribute to adipogenesis during haemangioma involution (Yu et ai, 2006). The pathogenesis of haemangioma is not clear. Growth factor, hormonal and mechanical factors have been thought to affect the abnormal growth of endothethial cells in haemangioma. However, these influences may secondly represent the response to an underlying primary molecular event leading to the development of haemangioma (Blei et ai, 1998). Several hypotheses have been put forth concerning the process of haemangiogenesis, including the role of somatic mutation in one or ore components of vascular growth-regulatory pathways (Waiter et ai, 2002). Although haemangioma do present in most organs, the majority is found in or just deep to the skin. Cutaneous haemangiomas at or superficial to the papillary dermis are referred to as superficial haemangiomas, while those within the reticular dermis or subcutaneous tissue are known as deep haemangiomas. On occasion, both superficial and deep components could be present simultaneously resulting into a lesion that is called compound or mixed haemangioma (Ethunandan and Melior, 2006; Jackson et ai, 1993). Certain dogmas are still persisted however; chief of which was the notion that most of haemangiomas involute completely and therefore they require no management. Accordingly, the policy of benign neglect had been the standard protocol for many years. However, this policy deprives the patients from recent technological advances. This; in addition to the reported adverse sequelae of haemangioma, made interventions are frequently indicated (Werner et ai, 1998). Several modalities could be used for treatment of haemangioma. Presently, all treatment modalities can be considered among four main categories. These include; pharmacotherapy, laser photocoagulation, surgical excision and image- guided intervention procedures. The reported success rates of these treatment modalities are variable. In the best interests of patients, it is imperative to establish H protocol of management based on what is the best treatment modality for the patient rather than what are the most familial with (Frieden, 1997)