Ellis J S, Seymour R A, Monkman S C, Idle J R
Department of Operative Dentistry, Dental School, University of Newcastle upon Tyne, UK.
Lancet. 1992 Jun 6;339(8806):1382-3. doi: 10.1016/0140-6736(92)91199-i.
The mechanism of gingival overgrowth associated with long-term use of nifedipine and of other drugs that affect calcium homoeostasis, such as cyclosporin and phenytoin, is unknown. With an ultrasensitive assay, we measured the pharmacokinetics of nifedipine in plasma and gingival crevicular fluid (GCF) of nine patients receiving this drug for angina and hypertension. In seven patients, the maximum nifedipine concentration was in the range 15-316 (mean 84 [SD 105]) times greater in GCF than in plasma. The two patients with low (undetectable) GCF nifedipine did not have overgrowth. We propose that gingival tissues sequester nifedipine and that the very high nifedipine concentrations predispose the tissues to overgrowth.
长期使用硝苯地平以及其他影响钙稳态的药物（如环孢素和苯妥英）导致牙龈增生的机制尚不清楚。我们采用超灵敏检测法，测定了9例因心绞痛和高血压而服用该药的患者血浆和龈沟液（GCF）中硝苯地平的药代动力学。7例患者龈沟液中硝苯地平的最大浓度比血浆中高15 - 316倍（平均84倍[标准差105]）。龈沟液中硝苯地平浓度低（检测不到）的2例患者未出现牙龈增生。我们认为牙龈组织会螯合硝苯地平，而极高的硝苯地平浓度会使组织易于增生。
