Previous studies reported the prevalence of vitamin D deficiency in chronic spinal cord injured patients(Reference Flueck and Perret1). Vitamin D deficiency has been implicated as an etiologic factor responsible for osteoporosis and various skeletal and extra-skeletal issues in spinal cord injured patients(Reference Waliullah, Kumar and Kumar2). However, few data were available regarding vitamin D status in patients with acute spinal cord injury or immediately assessed at hospital admission. This retrospective study aimed to evaluate vitamin D status (indicated by serum 25(OH)D concentration) in spinal cord injured patients at admission to a UK spinal cord injury centre during January-December 2017 and to assess the characteristics of vitamin D deficiency in this patient group.
Patients with serum 25(OH)D concentration records at admission were recruited. Vitamin D status was categorised as severe deficiency, deficiency, insufficiency and sufficiency, defined by serum 25(OH)D < 25 nmol/L, 25–50 nmol/L, 51–75 nmol/L, and >75 nmol/L respectively that most studies with spinal cord injured patients adopted(Reference Flueck and Perret1). Various categorical and blood test parameters were retrieved from the patients’ profiles. Data were presented as percentage or mean ± SD. Pearson Chi-Square, correlation, single linear regression, Mann Whitney U test and Kruskal Wallis were used to analyse the data.
Among 196 eligible patients, 74% were males vs 26% females, 92% were white Caucasians vs 8% non-white, 57% were traumatic vs 43% non-traumatic, and 42% were complete vs 58% incomplete spinal cord injury. The age was 50.5 ± 18.6 y (18–90 y). The body mass index was 25.7 ± 5.9 kg/m2 (16–46 kg/m2). The results found that 57% of the patients had vitamin D deficiency (serum 25(OH)D < 50 nmol/L), and 24% were severe vitamin D deficiency (serum 25(OH)D<25 nmol/L), similar to the prevalence of severe vitamin D deficiency in the general population in the UK (23%)(Reference Calame, Street and Hulshof3). However male patients, patients admitted in wintertime (December-May), and patients with hyponatremia (serum sodium<135 mEq/L) or caused by non-traumatic conditions had significant worse vitamin D status than their counterparts (28% males vs 11.8% females, P = 0.019; 30.2% in winter vs 12.9% in summer, P = 0.007; 32.1% non-traumatic vs 17.6% traumatic, P = 0.025; 38.9% low serum sodium vs 18.8% normal serum sodium, P = 0.010). There was a significant inverse association of serum 25(OH)D concentration with body mass index (r = −0.311, P = 0.002), serum total cholesterol (r = −0.168, P = 0.037) and creatinine concentrations (r = −0.162, P = 0.024) that were also significant predictors to serum 25(OH)D concentration.
The overall severe vitamin D deficiency in patients with spinal cord injury at admission to hospital is similar to the general population, however patients in some subgroups had worse vitamin D status. Strategies for systematic screening and efficacy of vitamin D supplementation in patients with spinal cord injury need to be implemented and further investigated in order to prevent the vitamin D deficiency-related chronic complications including osteoporosis, bone fractures and cardiovascular disease.
