Pathogenesis and Treatment of Infant Skin Strawberry Hemangiomas

Abstract

Corticosteroid treatment of infant strawberry hemangiomas produced premature regression of growing lesions in patients less than a year of age, but not in patients with cavernous or port-wine hemangiomas. Abnormally elevated serum estradiol-17 beta levels were found in strawberry hemangiomas, fourfold higher than in control, cavernous, and port-wine hemangiomas which were adjusted for age and sex of the patients. Specific estradiol-17 beta receptor binding activity was studied in biopsy tissues obtained from normal prepubertal skin and skin from various kinds of hemangiomas. Minimal specific estradiol-17 beta binding activity was detected in tissues of normal skin and involuting strawberry, cavernous, or port-wine hemangiomas. Abnormally high levels of specific estradiol-17 beta binding sites were demonstrated by receptor assays and by in vitro tissue culture technique in nine tissue samples obtained from strawberry hemangiomas, seven of which responded definitely or probably to corticosteroid therapy. The in vitro estradiol-17 beta binding activity in these tissue explants was inhibited by low (5 micrograms/ml) and high (100 micrograms/ml) doses of cortisone. The present data seem to suggest that there may be a causal relationship between the presence of elevated serum E2 and specific estradiol-17 beta receptors in the pathogenesis of strawberry hemangiomas and in response to corticosteroid treatment of the hormone-sensitive hemangiomas.