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- W1973928886 abstract "Within a few years of the serendipitous discovery of its remarkable effects on proliferating infantile haemangiomas (IH) in 2008,1 the nonselective beta‐adrenergic antagonist propranolol has become the first‐line therapy for complicated haemangiomas worldwide. As evidenced in large case series and meta‐analyses,2 3 4 the response rate to oral propranolol (2–3 mg kg−1 per day for 6 months) is 96–98%; reported side‐effects were reversible and mostly benign. Propranolol has thus virtually replaced oral corticosteroids, laser surgery or interferon and vincristine, which in former years (and for decades) were used to treat infants with obstructive, ulcerative or disfiguring IH. Unlike ‘new’ agents, propranolol is a generic, off‐patent and readily available drug, and was used for the treatment of IH at the discretion of the prescribing physician long before randomized controlled studies5 or official recommendations6 were published. Its mode of action, however, is incompletely understood so far. In this issue of BJD, two articles shed new light on the effects of propranolol. Ji et al.7 summarize current knowledge about mechanisms potentially underlying the antiproliferative effect of propranolol in IH. Beta‐adrenergic blockade targets endothelial cells, pericytes and haemangioma stem cells, initially resulting in vasoconstriction, followed by long‐term tumour regression that is likely due to inhibition of both vasculogenesis and angiogenesis. This is a result of suppression of de novo growth of blood vessels from stem cells and interference with proliferation of existing vessels." @default.
- W1973928886 created "2016-06-24" @default.
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- W1973928886 date "2015-01-01" @default.
- W1973928886 modified "2023-10-17" @default.
- W1973928886 title "Propranolol for infantile haemangiomas: certain chances, potential risks" @default.
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- W1973928886 doi "https://doi.org/10.1111/bjd.13535" @default.
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