Wg. Goodman et al., Altered diurnal regulation of blood ionized calcium and serum parathyroid hormone concentrations during parenteral nutrition, AM J CLIN N, 71(2), 2000, pp. 560-568
Background: Little is known about parathyroid gland function in patients re
ceiving total parenteral nutrition (TPN).
Objective: Our objective was to determine whether parathyroid gland functio
n is abnormal in TPN recipients.
Design: Six patients with a mean (+/- 1 SD) age of 45.5 +/- 8.0 y who had b
een receiving TPN for 18.7 +/- 2.8 y underwent bone TPN for 18.7 +/- 2.8 y
underwent bone biopsy, bone mass measurements with dual-energy X-ray absorp
tiometry, and dynamic tests of parathyroid gland function. Diurnal variatio
ns in blood ionized calcium (iCa(2+)) and serum parathyroid hormone (PTH) c
oncentrations were also assessed. Results were compared with those of healt
hy volunteers.
Results: Bone mass and bone formation were subnormal in all patients. Basal
serum PTH concentrations were moderately higher in the TPN recipients than
in healthy volunteers, and values obtained every 30 min over 24 h were sig
nificantly higher (P < 0.001) in TPN recipients (5.0 +/- 0.9 pmol/L) than i
n healthy volunteers (2.6 +/- 0.6 pmol/L). The percentage increase in serum
PTH during citrate-induced hypocalcemia was lower in the TPN recipients, c
onsistent with secondary hyperparathyroidism. Evening infusions of calcium-
containing TPN eliminated the nocturnal rise in serum PTH, increased the am
plitude of change for iCa(2+) and PTH over 24 h, increased the orderliness
of change for iCa(2+) and PTH as measured by approximate entropy (ApEn), an
d enhanced the synchrony of change between iCa(2+) and PTH. Treatment for 1
0 d with calcium-free TPN restored the nocturnal rise in serum PTH and incr
eased ApEn for PTH. ApEn for iCa (2+) remained low, suggesting that a compo
nent of nutrient solutions, bur not calcium per se, enhances the regularity
of PTH release in TPN recipients.
Conclusion: Parathyroid gland function is abnormal in long term TPN recipie
nts, which may contribute to disturbances in bone metabolism.