Low-dose propranolol for infantile haemangioma
Related Experiment Videos
Swee T Tan1, Tinte Itinteang, Philip Leadbitter
1Centre for the Study & Treatment of Vascular Birthmarks, Wellington Regional Plastic, Maxillofacial & Burns Unit, Hutt Hospital, Wellington, New Zealand. swee.tan@huttvalleydhb.org.nz
Insights
Propranolol effectively treats problematic infantile haemangioma at a minimal dosage of 1.5-2.0 mg kg(-1) day(-1). Treatment duration until complete involution or 12 months ensures safety and efficacy.
Area of Science:
- Dermatology
- Pediatric Medicine
- Pharmacology
Background:
- Infantile haemangioma treatment is empirical, lacking defined dosage and duration protocols.
- The mechanism of propranolol's efficacy in infantile haemangioma involution remains unknown.
Observation:
- Propranolol was serendipitously found to accelerate infantile haemangioma involution in 2008.
- This study investigated the minimal effective dosage and duration for problematic infantile haemangioma.
Findings:
- A minimal dosage of 1.5-2.0 mg kg(-1) day(-1) of propranolol achieved accelerated involution.
- Treatment maintained until complete involution or 12 months of age showed no rebound growth in most patients.
- No significant complications were observed in the treated cohort.
Implications:
- Propranolol at 1.5-2.0 mg kg(-1) day(-1) is a safe and effective treatment for problematic infantile haemangioma.
- Establishing clear dosage and duration guidelines can optimize treatment outcomes.
- Further large-scale studies are warranted to confirm safety and efficacy, potentially broadening treatment indications.
Abstract:
In 2008, propranolol was serendipitously observed to cause accelerated involution of infantile haemangioma. However, the mechanism by which it causes this dramatic effect is unknown, the dosage empirical and the optimal duration of treatment unexplored. This study determines the minimal dosage and duration of propranolol treatment to achieve accelerated involution of problematic infantile haemangioma. Consecutive patients with problematic proliferating infantile haemangioma treated with propranolol were culled from our prospective vascular anomalies database. The patients were initially managed as inpatients and commenced on propranolol at 0.25 mg kg(-1) twice daily, and closely monitored. The dosage was increased to 0.5 mg kg(-1) twice daily after 24 h, if there was no cardiovascular or metabolic side effect. The dosage was increased further by 0.5 mg kg(-1) day(-1) until a visible effect was noticed or up to a maximum of 2 mg kg(-1) day(-1), and was maintained until the lesion had fully involuted or the child was 12-months old. A total of 15 patients aged 3 weeks to 8.5 months (mean, 11 weeks) underwent propranolol treatment for problematic proliferating infantile haemangioma, which threatened life (n=1) or vision (n=2) or nasal obstruction (n=3) and/or caused ulceration (n=6) and/or bleeding (n=2) and/or significant tissue distortion (n=12). The minimal dosage required to achieve accelerated involution was 1.5-2.0 mg kg(-1) day(-1). Rebound growth occurred in the first patient when the dose was withdrawn at 7.5 months of age requiring reinstitution of treatment. No rebound growth was observed in the remaining patients. No other complications were observed. Propranolol at 1.5-2.0 mg kg(-1) day(-1), administered in divided doses with gradual increase in the dose, is effective and safe for treating problematic proliferating infantile haemangioma in our cohort of patients. Treatment should be maintained until the lesion is completely involuted or the child is 12-months old. Larger scale studies confirming the safety and efficacy of propranolol may broaden the indications of treatment of proliferating infantile haemangioma.
Related Concept Videos
Adrenergic Antagonists: Pharmacological Actions of β-Receptor Blockers
Adrenergic Antagonists: ɑ and β-Receptor Blockers
Antihypertensive Drugs: Types of β-Blockers
Drug Dosing: Infants and Children
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Antihypertensive Drugs: Vasodilators