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Vascular Anomalies Center, La Paz Hospital, University of Madrid, P° de la Castellana 261, Madrid, 28046 Spain
(Email: queminfantil.hulp{at}salud.madrid.org).
With regard to Onat and colleagues' recent publication [1] some considerations must be stated as follows:
Accurate diagnosis of the chest wall vascular anomalies remains a challenge for thoracic surgeons. Tremendous confusion exists with regard to the classification and treatment of vascular lesions [2, 3]. Vascular anomalies have been categorized using inconsistent terminology and a significant number of patients receive ineffective and potentially harmful treatment based on misclassification.
In 1996, the International Society for the Study of Vascular Anomalies (ISSVA) approved a classification system to establish a common language for the many different medical specialists involved in the management of these lesions:
Vascular tumors: Infantile hemangioma, rapidly involuting congenital hemangioma, noninvoluting congenital hemangioma, kaposiform hemangioendothelioma and tufted angioma.
Vascular malformations: Arteriovenous malformation, venous malformation, lymphatic malformation, lymphatic-venous malformation, and capillary malformation. Clinical, histologic, histochemical, and biochemical differences, and radiographic imaging findings support this classification.
A wide variety of vascular anomalies are incorrectly referred to as the "hemangioma" in the medical literature. The natural history of hemangioma has been well documented. They proliferate at a rapid rate in the first 6 months of life and they involute before puberty. Disappearance occurs progressively being replaced by fibrous fatty tissue by 10 years of age.
The histopathology of hemangioma is characterized by cellular markers. The glucose transporter (GLUT-1) is found at all phases in hemangiomas and can be extremely helpful in their differentiation from other vascular tumors [4, 5].
According with the current ISSVA classification, hemangioma is a pediatric disorder not to be considered in the adult patient.
Venous malformations consist of dysplastic vessels and are present on a lifelong basis. Unlike hemangiomas, there is no proliferation phase. Venous malformations seem to grow because the vessels progressively dilate; they are not multiplying and dividing. Conversely, there is no regression phase. Phlebolits are a very common finding and have been observed in patients as young as 2 years.
After close examination of the "hemangioma" reported case, we support the diagnosis of sternum venous malformation.
Significant differences must be taken into consideration before deciding any surgical approach on hemangiomas and venous malformations of the sternum. Although pain is the most common symptom of both hemangiomas and venous malformations, treatment differs. Pharmacologic inhibition of angiogenesis with propranolol or steroids is the mainstay of hemangioma therapy. Percutaneous vascular obliteration is extremely useful in treating vascular malformations. Sclerotherapy is clearly the first option to consider for sternal venous malformations. Surgical excision should be reserved as a procedure when pain and enlargement is out of control, despite several sclerosis attempts [6, 7].
In conclusion, biologic classification of vascular anomalies distinguishing vascular tumors from vascular malformations is clinically useful and forms the framework for our understanding of vascular anomalies [8].
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S. Onat, R. Ulku, A. Avci, C. Ozcelik, and B. Mizrak Reply Ann. Thorac. Surg., July 1, 2009; 88(1): 353 - 354. [Full Text] [PDF] |
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