Fibroblast growth factor-23 in patients with homozygous familial hypercholesterolemia

Abstract

Patients with homozygous familial hypercholesterolemia (HoFH) develop significant vascular calcification early in life, the cause of which is not yet fully understood. Patients with chronic kidney disease have similar vascular calcification, with fibroblast growth factor-23 (FGF23) implicated in these patients. To determine whether there was a difference in FGF23 between patients with HoFH and age- and gender-matched controls and whether there is a correlation between FGF23 and serum low-density lipoprotein, total cholesterol, and carotid intima-media thickness in patients with HoFH. The study was a cross-sectional review involving 30 patients with HoFH attending the Charlotte Maxeke Johannesburg Academic Hospital Lipid Clinic in Parktown, South Africa, as well as 30 age- and gender-matched healthy controls. FGF23, fasting lipid profiles, calcium, and phosphate were measured. B-mode ultrasonography of the carotid arteries was done to assess the extent and severity of arterial calcification. There was no difference in mean FGF23 between the patient and control groups (62.07±26.42 pg/mL vs 63.69±19.84 pg/mL; P=.4621) nor was there any correlation between FGF23 and low-density lipoprotein cholesterol (P=.9483 and .8474) or total cholesterol (P=.9261 and .859). In the HoFH patients, FGF23 did not correlate significantly with any cardiovascular disease. Serum FGF23 is not elevated in patients with HoFH when compared to non-familial hypercholesterolemia age- and gender-matched controls, and there is no correlation between serum FGF23 and cardiovascular disease in patients with HoFH. FGF23 does not appear to be a major factor for arterial calcification in HoFH.