Influence of a single oral dose of vitamin D(2) on serum 25-hydroxyvitamin D concentrations in tuberculosis patients.

SETTING: Newham Chest Clinic, London, UK. OBJECTIVE: To determine the safety and efficacy of the administration of bolus-dose vitamin D(2) in elevating serum 25-hydroxyvitamin D (25[OH]D) concentrations in tuberculosis (TB) patients. DESIGN: A multi-ethnic cohort of TB patients was randomised to receive a single oral dose of 2.5 mg vitamin D(2) (n = 11) or placebo (n = 14). Serum 25(OH)D and corrected calcium concentrations were determined at baseline and 1 week and 8 weeks post-dose, and compared to those of a multi-ethnic cohort of 56 healthy adults receiving an identical dose of vitamin D(2). RESULTS: Hypovitaminosis D (serum 25[OH]D < 75 nmol/l) was present in all patients at baseline. A single oral dose of 2.5 mg vitamin D2 corrected hypovitaminosis D in all patients in the intervention arm of the study at 1 week post-dose, and induced a 109.5 nmol/l mean increase in their serum 25(OH)D concentration. Hypovitaminosis D recurred in 10/11 patients at 8 weeks post-dose. No patient receiving vitamin D(2) experienced hypercalcaemia. Patients receiving 2.5 mg vitamin D(2) experienced a greater mean increase in serum 25(OH)D at 1 week post-dose than healthy adults receiving 2.5 mg vitamin D(2). CONCLUSION: A single oral dose of 2.5 mg vitamin D(2) corrects hypovitaminosis D at 1 week but not at 8 weeks post-dose in TB patients.

Serum glycated albumin and fructosamine in renal dialysis patients.

The effect of uraemia on protein glycation was studied by measuring glycated albumin and fructosamine in 50 non-diabetic dialysis patients (31 continuous ambulatory peritoneal dialysis, CAPD, 19 haemodialysis). After correction for serum albumin concentration, glycated albumin (g/100 g) was increased in the haemodialysis group (1.94 +/- 0.40) compared with both CAPD patients (1.46 +/- 0.37; p < 0.001) and controls (1.52 +/- 0.29; p < 0.001), but did not differ between CAPD patients and controls (p > 0.05). Serum fructosamine, corrected for either serum albumin or total protein concentration (mumol/100 g), was raised in CAPD (828 +/- 90, 386 +/- 41, respectively) and haemodialysis patients (802 +/- 123, 391 +/- 42, respectively) compared with controls (609 +/- 69, 332 +/- 27, respectively; p < 0.0001 in all cases), but did not differ between the two dialysis groups (p > 0.05). A single haemodialysis cycle had no effect on the measurement of glycated albumin or fructosamine (p > 0.05). The results confirm that glycated protein levels are generally raised in dialysis patients. In CAPD patients, altered albumin metabolism resulting from large peritoneal losses is likely to have caused a decrease in the amount of albumin glycated, an effect less apparent on the concentration of fructosamine because of the additional contribution of glycated globulins.

Effects of parathyroid hormone and 1,25(OH2)D3 on protein glycation in moderate uraemia.

Glucose intolerance in uraemia may be a consequence of secondary hyperparathyroidism. In this study fructosamine and glycated albumin have been used as markers of long-term glycaemic control in a group of pre-end-stage, non-diabetic uraemic patients with secondary hyperparathyroidism. The serum fructosamine level (mumol/100 g total protein) was significantly higher (p = 0.005) in uraemic patients (364 +/- 42) than in a group of 25 non-uraemic controls (332 +/- 27), but the content of glycated albumin did not differ (p > 0.05; 1.6 +/- 0.5 vs. 1.5 +/- 0.3%). In the uraemic patients, there was a significant relationship between serum 1,25-dihydroxycholecalciferol [1,25(OH2)D] (median 4.2, range 1.0-38 ng/l) and fructosamine (r = -0.66, p < 0.01; fructosamine = -2.76 1,25(OH2)D + 389), but not glycated albumin (r = -0.22, p > 0.1). No relationship existed between serum parathyroid hormone (median 15.4, range 7.0-55 pmol/l) and either glycated albumin or fructosamine (p > 0.1). In patients treated with oral calcitriol (0.25 microgram/day), significant reductions in serum parathyroid hormone after both 4 (p = 0.03) and 8 weeks (p = 0.02) and concomitant increases in serum 1,25(OH2)D (p < 0.02) after 8 weeks of treatment were not accompanied by any change in fructosamine, glycated albumin, total calcium, or ionized calcium (p > 0.05). Elevation of serum fructosamine in these patients is consistent with the impaired glucose tolerance of uraemia. The evidence presented supports a relationship between long-term glycaemic control and 1,25(OH2)D3, but not parathyroid hormone, in moderately uraemic patients with secondary hyperparathyroidism; however, serum fructosamine was not altered by treatment with calcitriol over an 8-week period.