Riikonen R, Simell O, Jääskeläinen J, Rapola J, Perheentupa J
Arch Dis Child. 1986 Jul;61(7):671-6. doi: 10.1136/adc.61.7.671.
Kidney histology of five infants who died during or immediately after treatment with adrenocorticotrophic hormone (ACTH) showed severe tubular and interstitial calcinosis. We therefore studied serum concentrations of calcium, inorganic phosphate, and parathormone, serum activities of alkaline phosphatase, and urinary excretion of calcium, inorganic phosphate, and cyclic adenosine monophosphate (cAMP) in 16 other children with infantile spasms before, during, and after 6 weeks of treatment with ACTH. During the treatment the following observations were made: hypocalcaemia developed in three infants; the mean daily urinary excretion of calcium in the group increased threefold and seven infants had hypercalciuria; the excretion of phosphate increased but its tubular reabsorption remained stable; and in most infants serum parathormone and urinary cAMP excretion increased, and in four infants they increased to supranormal concentrations. These biochemical changes were reversible in most infants. Radiographs suggested loss of bone mass by 3-4 weeks of treatment, with rapid recovery after treatment. We conclude that infants treated with ACTH for infantile spasms are at risk of suffering disturbance in calcium and phosphate homeostasis, which leads to nephrocalcinosis.
五名在接受促肾上腺皮质激素（ACTH）治疗期间或治疗后不久死亡的婴儿的肾脏组织学检查显示出严重的肾小管和间质钙化。因此，我们研究了另外16名患有婴儿痉挛症的儿童在接受ACTH治疗6周之前、期间和之后的血清钙、无机磷和甲状旁腺激素浓度、血清碱性磷酸酶活性以及钙、无机磷和环磷酸腺苷（cAMP）的尿排泄情况。在治疗期间有以下观察结果：三名婴儿出现低钙血症；该组中钙的平均每日尿排泄量增加了三倍，七名婴儿有高钙尿症；磷酸盐排泄增加但其肾小管重吸收保持稳定；并且在大多数婴儿中血清甲状旁腺激素和尿cAMP排泄增加，四名婴儿增加到超正常浓度。这些生化变化在大多数婴儿中是可逆的。X线片显示治疗3 - 4周时骨量减少，治疗后迅速恢复。我们得出结论，接受ACTH治疗婴儿痉挛症的婴儿有发生钙和磷稳态紊乱的风险，这会导致肾钙化。
