Infantile hemangioma is a benign vascular tumor that involutes spontaneously by 5 to 7 years of age. Approximately 10 percent of these tumors are problematic.
For function- and life-threatening hemangiomas, the first-line medical treatment is corticosteroid, followed by vincristine or interferon.1–3 Corticosteroid results in regression in 40 percent, stabilization in 30 percent, and no response in 30 percent of cases. Corticosteroid complications have been well described in the literature; all disappear after the treatment is stopped.4 The effect on blood pressure has not been studied. We report the effect of acebutolol (β-blocking agent), 10 mg/kg/day, in four infants with proliferating phase hemangioma.
The first patient had a parotid hemangioma diagnosed at 6 weeks of age. Initially, he was treated with corticosteroid (prednisolone, 2 mg/kg/day) and developed high blood pressure that necessitated acebutolol given at 10 mg/kg/day. The effect of this drug on the hemangioma was immediately visible; the color and bulk decreased. The corticosteroid was tapered progressively until the child was 5 months old. We attempted to stop acebutolol at 4 months but noticed that the hemangioma swelled each time we discontinued the drug. Acebutolol was maintained until the age of 1 year, when the hemangioma stabilized.
We treated two other 2-month-old patients with hemifacial hemangioma. One of these had ocular occlusion. Corticosteroid (prednisolone, 2 mg/kg/day) was given immediately. Because there was no response after 15 days of treatment, we began acebutolol at 10 mg/kg/day. The corticosteroid dosage was decreased slowly over 3 months and acebutolol was stopped at 1 year of age. The hemangioma regressed and the ocular occlusion improved during administration and after discontinuation of the corticosteroid (Fig. 1).
The fourth child was 13 months old and had a perineal hemangioma complicated by cutaneous ulcerations. We did not give corticosteroids; instead, acebutolol (10 mg/kg/day) was given, and we observed decreased vascularity and thickness and healing of cutaneous lesions over 1 month. He is always treated by acebutolol.
Acebutolol is a selective β-adrenergic receptor–blocking agent. We propose that it reduces blood flow to the hemangioma either by blocking the vasodilator response to β-adrenergic stimulation or by diminishing heart rate.
Acebutolol was administered to treat corticosteroid hypertension and induced an effectiveness on the proliferating phase hemangioma. The dose given was always minimal for hypertension. We had no complications during this treatment and no hypotension. The only contraindications were bronchial asthma and cardiac insufficiency. We plan a prospective clinical and Doppler sonographic study (corticosteroid versus acebutolol) to evaluate the possible effectiveness of acebutolol.
Michele Bigorre, M.D.
Department of Orthopedic and Plastic Pediatric Surgery
Aurelie Khau Van Kien, M.D.
Department of Vascular Medicine
Saint Eloi Hospital
Huguette Valette, M.D.
Arnaud de Villeuneuve Hospital
1. Boon LM, Bataille AC, Bernier V, Vermylen C, Verellen G. Medical treatment of juvenile hemangiomas (in French). Ann Chir Plast Esthet.
2. Enjolras O, Brevière GM, Roger G, et al. Vincristine treatment for function- and life-threatening infantile hemangioma (in French). Arch Pediatr.
3. Ezekowitz RA, Mulliken JB, Folkman J. Interferon alfa-2a therapy for life-threatening hemangiomas of infancy. N Engl J Med.
4. Boon LM, MacDonald DM, Mulliken JB. Complications of systemic corticosteroid therapy for problematic hemangioma. Plast Reconstr Surg.
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