Fleischer Jessica, McMahon Donald J, Hembree Wylie, Addesso Vicki, Longcope Christopher, Shane Elizabeth
Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Transplantation. 2008 Mar 27;85(6):834-9. doi: 10.1097/TP.0b013e318166ac10.
Men undergoing heart transplantation during the early 1990s had declines in testosterone associated with rapid bone loss. It is unclear whether low testosterone still occurs in an era of lower prednisone doses, whether cyclosporine A (CsA) contributes, whether hypothalamic-pituitary-gonadal (HPG) suppression or direct testicular effects are responsible, and whether low testosterone influences bone loss in men receiving therapy to prevent osteoporosis.
Serum testosterone, estradiol, sex hormone binding globulin, gonadotropins, and bone density were measured and prednisone and CsA doses and levels for the first 2 years after transplantation were recorded in a more recently transplanted cohort of 108 participants in a trial comparing alendronate and calcitriol for prevention of posttransplant osteoporosis.
Total and free testosterone levels were lowest during the first month (257+/-131 and 6.2+/-3 ng/dL, respectively) and normalized by 2 months. Gonadotropins were low in the majority, suggesting HPG suppression. Low total testosterone persisted in 14% at 1 year and 18% at 2 years. Prednisone was the major predictor of serum testosterone. No adverse effect of CsA and no relationship between serum testosterone and bone density change were detected.
Low serum testosterone levels still occur in the early posttransplant period, probably related to HPG suppression by prednisone rather than direct testicular effects of CsA. They are not associated with bone loss in men receiving therapies to prevent osteoporosis. At later time points, low testosterone levels are common and apparently related to primary gonadal dysfunction, suggesting that long-term male heart transplant recipients should be evaluated for hypogonadism.
20世纪90年代初接受心脏移植的男性出现睾酮水平下降，并伴有快速的骨质流失。目前尚不清楚在泼尼松剂量较低的时代，低睾酮现象是否仍然存在，环孢素A（CsA）是否起作用，下丘脑-垂体-性腺（HPG）轴抑制或直接的睾丸效应是否是其原因，以及低睾酮是否会影响接受预防骨质疏松治疗的男性的骨质流失。
在一项比较阿仑膦酸钠和骨化三醇预防移植后骨质疏松的试验中，对108名近期移植的参与者进行了血清睾酮、雌二醇、性激素结合球蛋白、促性腺激素和骨密度的测量，并记录了移植后头两年的泼尼松和CsA剂量及水平。
总睾酮和游离睾酮水平在第一个月最低（分别为257±131和6.2±3 ng/dL），并在2个月时恢复正常。大多数人的促性腺激素水平较低，提示HPG轴受到抑制。14%的人在1年时总睾酮水平仍低，18%的人在2年时仍低。泼尼松是血清睾酮的主要预测因素。未检测到CsA的不良影响，也未发现血清睾酮与骨密度变化之间的关系。
移植后早期仍会出现低血清睾酮水平，这可能与泼尼松对HPG轴的抑制有关，而非CsA对睾丸的直接作用。在接受预防骨质疏松治疗的男性中，低血清睾酮水平与骨质流失无关。在后期时间点，低睾酮水平很常见，且显然与原发性性腺功能障碍有关，这表明长期男性心脏移植受者应接受性腺功能减退的评估。
