Curtò Lorenzo, Giovinazzo Salvatore, Alibrandi Angela, Campennì Alfredo, Trimarchi Francesco, Cannavò Salvatore, Ruggeri Rosaria Maddalena
Unit of EndocrinologyDepartment of Clinical and Experimental Medicine, University of Messina, AOU Policlinico 'G. Martino' (Pad H, Floor 4), Via Consolare Valeria, 1, Messina 98125, ItalyDepartment of Statistical Sciences (SEFISAST)Unit of Nuclear MedicineDepartment of Biomedical Sciences and of Morphological and Functional Images, University of Messina, Messina, Italy
Unit of EndocrinologyDepartment of Clinical and Experimental Medicine, University of Messina, AOU Policlinico 'G. Martino' (Pad H, Floor 4), Via Consolare Valeria, 1, Messina 98125, ItalyDepartment of Statistical Sciences (SEFISAST)Unit of Nuclear MedicineDepartment of Biomedical Sciences and of Morphological and Functional Images, University of Messina, Messina, Italy.
Eur J Endocrinol. 2015 May;172(5):543-52. doi: 10.1530/EJE-14-0966. Epub 2015 Feb 2.
Despite the well-known effects of GH/IGF1 signaling on the thyroid, few data are available on the risk of developing nodular goiter in hypopituitary subjects during GH replacement therapy (GHRT). We aimed to define the effects of GH therapy on thyroid volume (TV) and nodular growth.
The records of 96 subjects (47 males and 49 females, median age 48 years) with GH deficit (GHD) were investigated. Seventy also had central hypothyroidism (CH). At the time of our retrospective evaluation, median treatment duration was 5 years.
Pre-treatment TV was smaller in GHD patients than in healthy subjects (P=0.030). During GH treatment, TV significantly increased (P=0.016 for the entire group and P=0.014 in euthyroid GHD patients). Before starting GH therapy, 17 patients harbored thyroid nodules. During GH therapy, nodule size increased slightly in seven patients, and new thyroid nodules occurred in nine patients. Among the 79 patients without pre-existing thyroid nodules, 17 developed one or more nodules. There was no difference in the prevalence of CH in GHD patients with or without thyroid nodules (P=0.915; P=0.841, when patients with pre-therapy nodular goiter were excluded), the main predictor for nodule development being serum IGF1 (P=0.038).
GHRT is associated with TV's increase in GHD patients. Thyroid nodules developed in 27% of patients, mainly in relation to pre-therapy IGF1 levels, independently of normal or impaired TSH stimulation.
尽管生长激素/胰岛素样生长因子-1（GH/IGF1）信号通路对甲状腺的影响已为人熟知，但关于垂体功能减退患者在接受生长激素替代治疗（GHRT）期间发生结节性甲状腺肿风险的数据却很少。我们旨在确定生长激素治疗对甲状腺体积（TV）和结节生长的影响。
对96例生长激素缺乏（GHD）患者（47例男性和49例女性，中位年龄48岁）的记录进行了研究。其中70例还患有中枢性甲状腺功能减退（CH）。在我们进行回顾性评估时，中位治疗时间为5年。
GHD患者治疗前的TV小于健康受试者（P = 0.030）。在生长激素治疗期间，TV显著增加（整个组P = 0.016，甲状腺功能正常的GHD患者P = 0.014）。在开始生长激素治疗前，17例患者有甲状腺结节。在生长激素治疗期间，7例患者的结节大小略有增加，9例患者出现了新的甲状腺结节。在79例无既往甲状腺结节的患者中，17例出现了一个或多个结节。有或无甲状腺结节的GHD患者中CH的患病率无差异（P = 0.915；排除治疗前结节性甲状腺肿患者后P = 0.841），结节发生的主要预测因素是血清IGF1（P = 0.038）。
GHRT与GHD患者的TV增加有关。27%的患者出现了甲状腺结节，主要与治疗前IGF1水平有关，与促甲状腺激素（TSH）刺激正常或受损无关。
