Geisen, V., K. Weber, et al. (2009). "Vitamin D-Dependent Hereditary Rickets Type I in a Cat." Journal of Veterinary Internal Medicine 23(1): 196-199.
A 5-month-old female domestic short hair cat was examined for a short history of generalized pain. The cat weighed 1.8 kg and had a sibling in the household that was healthy and weighed 2.6 kg. The cat was increasingly reluctant to move and had also developed constipation. Radiographs indicated reduced skeletal mineralization. A serum biochemistry profile indicated such abnormalities as hypocalcemia, hyperphosphatemia, plus elevated alkaline phosphatase and creatine kinase values. Hypocalcemia, hyperphosphatemia, and skeletal abnormalities are indicative of rickets. Rickets can develop after prolonged feeding of a diet deficient in calcium or vitamin D. Cats cannot synthesize vitamin D in the skin so sunlight does not contribute to their vitamin D supply. A board certified nutritionist analyzed the diet fed to both cats and determined it was not deficient. Parathyroid hormone was measured and found to be high. Calcium gluconate and a vitamin D metabolite (1,25-dihydroxycholecalciferol) were started as a therapeutic regimen. Radiographs were taken 4 months after starting treatment and bone structure, while still abnormal, showed marked improvement. Vitamin D-dependent rickets Type I (VDDRI) is caused by a defect in the gene encoding the enzyme 25-hyproxyvitamin D-1-alpha hydroxylase (CYP27B1). This is an autosomal recessive disorder. The affected cat had genetic sequencing performed and two mutations were found that affect the CYP27B1 transcript. These results along with the clinical findings of rickets and hyperparathyroidism confirmed a case of VDDR1. The patient was continued on oral 1,25dihydroxycholecalciferol to maintain calcium homeostasis and will need to be continued lifelong with frequent rechecks of serum calcium concentrations. [VT]
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