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Background Elevated levels of retinoic acid (RA) may cause dynamic vitamin A metabolic and genetic transcriptional changes that will lead to decreased cellular viability, proliferation, cellular remodeling, adhesion changes and a resultant decrease in permeability, which contributes to elevated CSFP. RA and subsequent formation of retinyl esters, which act as surfactants may cause a toxic response in the arachnoid membrane leading to elevated CSFP.

The role of vitamin A and its CSF metabolites in supporting a novel mechanism of idiopathic intracranial hypertension