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J. G. Mouser, D. M. Grzybowski, S. E. Katz, M. Criden; The Role of Vitamin A and Vitamin A Metabolites in the Pathogenesis of Idiopathic Intracranial Hypertension - A Pilot Study. Invest. Ophthalmol. Vis. Sci. 2007;48(13):924.
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Idiopathic Intracranial Hypertension (IIH) is a disabling disease that leads to intractable headache and loss of visual fields that can lead to total blindness. Transthyretin (TTR) and retinal binding protein (RBP), are BOTH critical transport proteins in blood and brain for Vitamin A. TTR is also a critical transport protein for thyroid hormone which is linked to obesity and important in controlling metabolism. Adipocytes are dynamically involved in retinoid storage and metabolism by storage of retinoid, and synthesis and secretion of retinol binding protein (RBP) which may be significant for the typical IIH patient with BMI of greater than 30. These increased levels of adipocytes, which can dynamically regulate vitamin A metabolism by altering gene expression, is critical in IIH. We propose to determine how these biologic mediators associated with obesity might contribute to the pathogenesis of chronically elevated intracranial pressure in obese women.
We prospectively determined serum and CSF levels of retinoic acid (RA), retinol, retinyl esters, retinol binding protein (RBP), and TTR in six women with IIH and six female controls matched for body mass index (BMI) and age.
Total CSF RA was statistically higher in the patient group (p=0.050) with means of 0.246 and 0.091 ng/mL. CSF 13-cis RA was significantly higher in patients (p=0.023), means of 0.146 for patients and 0.052 ng/mL for controls. There were no statistically significant differences in any of the measured serum variables.
Increased CSF RA levels may contribute to the pathogenesis of IIH. Abnormal elevated RA and subsequent formation of retinyl esters, which act as surfactants, and cause a toxic response in the arachnoid membrane, a major route for CSF outflow, causing improper brain water regulation leading to elevated CSF pressure (CSFP). In addition, the elevated levels of 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 also contributes to elevated CSFP.
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