Serum 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D in dogs with sinonasal aspergillosis

Sinonasal aspergillosis (SNA) is a common cause of chronic nasal disease with a still poorly understood pathophysiology and which remains a challenge to treat. There is increasing evidence that vitamin D plays a role in both innate and adaptative immunity. A preliminary retrospective study showed that serum 25-hydroxyvitamin D concentration, measured by high performance liquid chromatography (HPLC), was significantly lower in dogs affected with SNA compared to healthy dogs. Objectives of this prospective study were 1) to compare serum 25(OH)D and 24,25(OH)2D concentrations in dogs with SNA to healthy control dogs and dogs with lymphoplasmacytic rhinitis (LPR) or nasal neoplasia; and 2) to determine if serum 25(OH)D and 24,25(OH)2D concentrations in dogs with SNA change from the time of diagnosis to when a cure is achieved. Twenty dogs with a novel diagnosis of SNA, 12 healthy control dogs, 9 dogs with LPR, 10 dogs with nasal neoplasia were included. Nine dogs with SNA were available for follow up until cure. Serum vitamin D concentrations were measured by liquid chromatography tandem mass spectrometry (LC-MS/MS) and compared: 1) among the different groups using a One-way ANOVA and 2) from diagnosis to cure with a paired t-test (significant p-value <0,05 for both tests). The vitamin D metabolite ratio (VMR) was calculated by dividing the 25(OH)D by the 24,25(OH)2D concentration. Serum 25(OH)D and 24,25(OH)2D were lower in dogs with SNA at the time of diagnosis (mean ± standard deviation = 23.5 ± 7,1 ng/ml – 10,5 ± 4,2 ng/ml, respectively) than in healthy dogs (34,1 ± 7,5 ng/ml; p=0,017 - 18,2 ± 5.4 ng/ml; p = 0,005) while there was no difference between healthy and dogs with tumor (27,8 ± 10,9 ng/ml – 15,4 ± 6,5 ng/ml) or LPR (27,4 ± 13,7 ng/ml – 14,3 ± 8,7 ng/ml). There was no significant difference in serum 25(OH)D and 24,25(OH)2D between dogs with SNA at the time of diagnosis and dogs achieving cure. The VMR was higher in SNA dogs (2,4 ± 0,7) than in control dogs (1,9 ± 0,3; p=0,031 t-test), indicating a decreased catabolic clearance of vitamin D in SNA dogs. These results further support the rationale that vitamin D could play a role in dogs with SNA as it does in human with aspergillosis. Whether hypovitaminosis D could contribute to the development of SNA or if oral supplementation could be a beneficial adjunctive therapy in affected dogs is unknown and warrants future investigations.