Mukherjee A, Ryder W D J, Jöstel A, Shalet S M
Department of Endocrinology, Christie Hospital, Wilmslow Road, Manchester M20 4BX, United Kingdom.
J Clin Endocrinol Metab. 2006 Jul;91(7):2520-5. doi: 10.1210/jc.2005-2491. Epub 2006 Apr 18.
In adult life, considerable overlap in IGF-I status exists between normal and severely GH-deficient (GHD) subjects defined by conventional dynamic testing of GH secretion. IGF-I is not therefore widely viewed as a reliable diagnostic marker for GHD. Recognized factors influencing serum IGF-I level in GHD include age, gender, timing of onset of GHD, and exogenous estrogen therapy, but these do not fully explain GH/IGF-I discordance in severe GHD. The primary structures of prolactin and GH are closely related. Effects of hypoprolactinemia are not well described in humans, but laboratory studies suggest a role for prolactin in hepatic IGF-I release, possibly through a signal transducer and activator of transcription 5 (STAT5) pathway. The purpose of this study was to evaluate a potential contribution of prolactin to IGF-I status in severely GHD adults.
Using multiple regression analysis techniques, contributions of the following variables to age-adjusted IGF-I sd scores were evaluated in 162 (85 female) GHD adults: gender, timing of onset of GHD, presence or absence of prolactin deficiency, body mass index, number of additional pituitary deficits, and underlying pathology.
Childhood onset GHD (P < 0.0001) and presence of prolactin deficiency (P < 0.0001) were independently associated with reduced IGF-I status. The contributions of these parameters to IGF-I sd scores were -2.55 and -2.67, respectively. Gender (P = 0.06), body mass index (P = 0.99), number of additional pituitary deficits (P = 0.64), and underlying pathology (P = 0.06) did not significantly influence IGF-I status.
Prolactin deficiency is independently associated with reduced IGF-I status in hypopituitary adults. It is possible that prolactin deficiency is a surrogate for the degree of severity of GHD, implying a GHD paradigm undetected by conventional GH provocative tests; alternatively, it remains plausible that circulating prolactin contributes to IGF-I release in the absence of GH, possibly through a signal transducer and activator of transcription 5 (STAT5) pathway.
在成年期，通过传统的生长激素（GH）分泌动态测试定义的正常和严重生长激素缺乏（GHD）受试者之间，胰岛素样生长因子-I（IGF-I）状态存在相当大的重叠。因此，IGF-I未被广泛视为GHD的可靠诊断标志物。在GHD中，公认的影响血清IGF-I水平的因素包括年龄、性别、GHD发病时间和外源性雌激素治疗，但这些并不能完全解释严重GHD中GH/IGF-I的不一致。催乳素和GH的一级结构密切相关。人类中低催乳素血症的影响尚未得到充分描述，但实验室研究表明催乳素可能通过信号转导和转录激活因子5（STAT5）途径在肝脏IGF-I释放中发挥作用。本研究的目的是评估催乳素对严重GHD成年患者IGF-I状态的潜在影响。
使用多元回归分析技术，在162名（85名女性）GHD成年患者中评估以下变量对年龄校正后的IGF-I标准差分数的影响：性别、GHD发病时间、是否存在催乳素缺乏、体重指数、额外垂体缺陷的数量以及潜在病理。
儿童期发病的GHD（P < 0.0001）和催乳素缺乏的存在（P < 0.0001）与IGF-I状态降低独立相关。这些参数对IGF-I标准差分数的贡献分别为-2.55和-2.67。性别（P = 0.06）、体重指数（P = 0.99）、额外垂体缺陷的数量（P = 0.64）和潜在病理（P = 0.06）对IGF-I状态没有显著影响。
催乳素缺乏与垂体功能减退成年患者的IGF-I状态降低独立相关。催乳素缺乏可能是GHD严重程度的替代指标，这意味着传统GH激发试验未检测到的GHD模式；或者，在没有GH的情况下，循环催乳素可能通过信号转导和转录激活因子5（STAT5）途径促进IGF-I释放，这仍然是合理的。
