We observed that acute thermal burn injury produced symptomatic hypocalcemia(↓ Ca), despite the enteral intake of Ca, 3g/m2/d immediately postburn. Therefore, we asked whether there was a defect in ↓ Ca-stimulated parathyroid hormone (PTH) levels, and in the renal & skeletal responses to administered PTH in 7 children (4-15 yo) following a burn to ≥30% total body surface area. Blood was obtained for simultaneous levels of ionized Ca (iCa), magnesium (Mg), and intact (i) PTH daily for 4-15d postburn. Between 7-20d. postburn, they received PTH i.v. to elicit changes in iCa, urinary cAMP and phosphate excretion. Results: ↓ Ca (iCa = 1.08± 0.04 [mean ± SD]; nl:1.12-1.2mM), reduced iPTH (8 ± 5; nl:15-50 pg/mL), and ↓ Mg (0.72 ± 0.08; nl: 0.8-1.2 mM) were found before PTH was given. 16 of 19 (84%) values in 5 pts. had iPTH levels below the 99% confidence limit for iCa; all were below the mean values. Renal resistance to i.v. PTH (rise in urinary cAMP = 7.3±2.4; nl: 541±319 nmol/L glomerular filtrate; fall in TmP/GFR=13.1±18.3%; nl: 28.1±4.6%) was seen. No calcemic response was observed after PTH administration. ↓ Ca was associated with ↓ Mg(X-square = 4.5, p < 0.05), suggesting a mechanism for PTH unresponsiveness to iCa levels and PTH infusion. In conclusion, children with severe burns develop symptomatic hypoparathyroidism acutely, with PTH resistance at the kidney and bone. ↓ Mg may be a 1° precipitant to these changes. A trial of magnesium supplementation may be warranted in acute thermal burn injury in children.