Vitamin D metabolites were measured on admission in eight patients intoxicated with ergocalciferol (serum calcium 3.01-4.05 mmol/l) and also during the subsequent 2 months in six of the eight. Serum concentrations of 25-hydroxyergocalciferol, on admission, were grossly elevated in all patients (range 583-1843 nmol/l). Serum calcium concentration was related significantly only to the concentration of 25-hydroxyergocalciferol (P = 0.003). Concentrations of 25-hydroxyergocalciferol in serum were significantly related to those of calciferol (P = 0.004). Elevated initial concentrations of 1,25-dihydroxycalciferol, mainly as 1,25-dihydroxyergocalciferol, were found in seven of the eight patients (range 179-313 pmol/l). It is suggested that the hypercalcaemia in these patients may be explained by the action of 25-hydroxyergocalciferol at high concentration in competing for 1,25-dihydroxycalciferol receptors, thus exerting a biological effect per se, and also by increasing the synthesis of 1,25-dihydroxycalciferol through a mass-action effect on the renal 1 alpha-hydroxylase.

The serum concentrations of 25-hydroxycholecalciferol (25 OH D3), 24,25-dihydroxycholecalciferol [24,25(OH)-2D3] and 1,25-dihydroxycholecalciferol [1,25(OH)2D3] were measured in twenty-one patients with untreated hyperthyroidism. Compared with control subjects, 25 OH D3 concentrations were not altered, 24,25(OH)2D3 concentrations were increased, although not significantly and 1,25(OH)2D3 concentrations were decreased (P = 0.01). Following oral carbimazole therapy, 24,25(OH)2D3 concentrations fell (P less than 0.01), 1,25(OH)2D3 concentrations increased (P less than 0.01) and 25 OH D3 concentrations were unchanged. The altered 1,25(OH)2D3 and 24,25(OH)2D3 concentrations found in hyperthyroidism are probably due to the effects of thyroid hormone on bone and mineral metabolism. Increased serum calcium and phosphate concentrations with secondary hypoparathyroidism result in stimulation of the renal 24-hydroxylase and suppression of the 1-hydroxylase enzymes. In addition, serum 24,25(OH)2D3 concentrations were significantly correlated with serum triiodothyronine levels (T3) (r = 0.66, P less than 0.002) before treatment. This may indicate a direct stimulatory effect of T3 on 24-hydroxylase activity. No relationship was found between serum 1,25(OH)2D3 concentrations before therapy and serum T3.

The seasonal changes in the biochemical indices of vitamin D nutrition have been measured in elderly people with differing requirements for institutionalized care. Residents of local authority homes (LAH) showed an increase in serum 25-hydroxyvitamin D3 [25(OH)D3] between spring and autumn (means 14-17 nmol/l, P less than 0.002). No significant seasonal changes were seen in patients on long-stay wards [(GW) serum 25(OH)D3 9.5 and 9.5 nmol/l] and in day-hospital attenders [(GDH) 25 and 26.8 nmol/l]. Significant differences (P less than 0.02 to P less than 0.0001) were found between the mean serum 25(OH)D3 amongst the three groups. A significant linear relationship (r = 0.84, P = 0.036) was found between mean serum 25-hydroxyvitamin D2[25(OH)D2] and dietary vitamin D2. The intake of vitamin D was suboptimal in all groups. The incidence of 25-hydroxyvitamin D deficiency [25(OH)D less than 12.5 nmol/l] varied from 11.7% of residents in LAH in autumn to 47% of GW patients in spring; but hypocalcaemia occurred less often (LAH 1.3% in autumn, GW 4.7% in spring). The diet assumes a greater role in protecting against vitamin D deficiency when the total 25(OH)D is low. Because most diets contain insufficient amounts of vitamin D, elderly institutionalized people will remain at high risk of developing vitamin D deficiency unless specific preventative measures are adopted.

A comparison of two regimens of vitamin D prophylaxis in elderly institutionalized subjects has been made. Sixty-six subjects received 2.5mg vitamin D2 by mouth in December 1982; a further group of 62 received the same dose in December 1982 and again in June 1983. Blood samples have been analysed for 25-hydroxyvitamin D2 [25(OH)D2] in 10 subjects from each group over a 12-month period. The serum 25(OH)D2 was maintained at normal concentrations for most of the year in the once-a-year dosage group but at the end of 12 months only 60% were fully protected. The twice-per-year regimen offered complete protection maintaining the serum 25(OH)D2 above the threshold associated with osteomalacia. It is concluded that a twice-yearly regimen of vitamin D supplementation is a practical method for prophylaxis in institutionalized elderly people.

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