To investigate the serum vitamin D level and its determinant factors in stroke patients.
Fifty-one stroke patients who had documented serum level of 25-hydroxyvitamin D(25(OH)D) were included. Patients were divided into subacute (n=23) and chronic groups (n=28). The mean levels of 25(OH)D of the two groups were compared. Correlations between each 25(OH)D level and post-stroke duration were also analyzed. To assess other possible influencing factors, patients were subdivided by ambulation ability and feeding methods for comparison of 25(OH)D level.
The mean level of 25(OH)D was significantly lower in the chronic group than in the subacute group (12.3 vs. 16.3 ng/mL; p<0.05). The serum 25(OH)D level decreased according to the duration after stroke (r=−0.52, p=0.01). Patients with a history of total parenteral nutrition had lower 25(OH)D levels than subjects who had enteral nutrition in the subacute group (7.3 vs. 18.8 ng/mL; p<0.01). However, the levels of 25(OH)D were not different between the oral feeding and tube feeding groups. Among the chronic group subjects, patients who could walk without assistance had higher 25(OH)D levels than non-ambulatory patients (ambulatory vs. non-ambulatory group; 18.3 vs. 11.3 ng/mL; p<0.05).
After stroke onset, serum vitamin D level decreases with time regardless of feeding methods, and total parenteral nutrition may aggravate its deficiency. In terms of long-term care, non-ambulatory patients might be at a higher risk of vitamin D deficiency. Supplementation of vitamin D should be considered especially for stroke patients who are non-ambulatory and on total parenteral nutrition.
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To investigate the correlation between depressive symptoms and serum vitamin D levels in stroke patients.
In total, 126 stroke patients were analyzed. The 25-hydroxyvitamin D (25-OHD) concentration of each patient was used to determine their vitamin D status. Depressive symptoms were assessed using the Beck Depression Inventory II (BDI-II) and the Patient Health Questionnaire 9 (PHQ-9). Functional status was evaluated with the Korean version of the Modified Barthel Index (K-MBI). We compared the clinical questionnaires of a vitamin D-deficient group and a normal group, and evaluated the correlations between BDI-II, PHQ-9, K-MBI, and serum 25-OHD levels.
In the vitamin D-deficient group, BDI-II (16.0±12.1) and PHQ-9 (7.4±4.2) scores were significantly higher than those of the normal group (BDI-II, 9.1±7.2; PHQ-9, 4.2±2.9; p<0.01). In a Spearman correlation analysis, a significant negative correlation was found between serum 25-OHD levels and BDI-II (Spearman r=0.177, p=0.048), but there were no significant correlations between serum 25-OHD levels and PHQ-9 or K-MBI.
Vitamin D deficiency was correlated with the symptoms of depression in stroke patients.
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Objective: To assess change of bone metabolism in hemiplegic patients after stroke.
Method: Sera were collected from 19 hemiplegic patients after stroke. Sera were assayed for 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2D), parathyroid hormone (PTH), calcium and osteocalcin.
Results: Serum 25-OHD and 1,25-(OH)2D concentration were 15.13 mg/mL and 20.88 pg/mL, respectively. Serum PTH was 47.23 pg/mL. In 5 (26%) of the patients, the serum 25-OHD concentration were ＜10 ng/mL (deficient level). Ten (52%) of the patients had vitamin D concentrations between 10 and 20 ng/mL (insufficient level). The mean PTH concentration was not significantly higher in patients with deficient levels of 25-OHD (61.80 pg/mL) than those with insufficient (43.63 pg/mL) or sufficient (38.05 pg/mL) levels of 25-OHD. Serum 25-OHD concentration were lower in the late group (11.11 mg/mL) than in the early group (18.05 mg/mL), whereas serum PTH concentration were higher in the late group (58.96 pg/mL) than in the early group (38.70 pg/mL).
Conclusion: Compensatory hyperparathyroidism with hypovitaminosis D occurred in the hemiplgic patients after stroke, especially more than one year from onset.
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