George L D, Nicolau N, Scanlon M F, Davies J S
Department of Endocrinology, Metabolism and Diabetes, University Hospital of Wales, Cardiff, UK.
Clin Endocrinol (Oxf). 2000 Nov;53(5):595-9. doi: 10.1046/j.1365-2265.2000.01137.x.
Cabergoline therapy normalizes prolactin levels and reduces the size of macroprolactinomas. However there are no data indicating whether cabergoline can normalize growth hormone secretion in patients who were growth hormone deficient at the time of diagnosis of a macroprolactinoma.
We studied nine patients with biochemical and radiological evidence of a macroprolactinoma who were also growth hormone deficient (peak growth hormone response to insulin-induced hypoglycaemia < 10 mU/l). Patients were assessed before and after cabergoline therapy to assess their growth hormone secretory status, IGF-I levels, cortisol response and change in tumour size.
Treatment with cabergoline was associated with a significant reduction in prolactin concentration (74341 +/- 31939 mU/l vs. 265.9 +/- 86.3, P = 0.009). The mean change in peak growth hormone response to insulin-induced hypoglycaemia was significantly greater following cabergoline therapy compared with pretreatment levels (33.5 +/- 11.8 mU/l vs. 4. 34 +/- 1.21 mU/l, P = 0.022). However IGF-I levels were not different after treatment when compared with baseline although a nonsignificant trend towards improvement was noted (24.2 +/- 3.97 nmol/l vs. 18.4 +/- 4.94 nmol/l, P = 0.058). The mean peak cortisol concentration was 407.7 +/- 64.1 nmol/l before treatment with a nonsignificant rise to 477.4 +/- 84.8 nmol/l, P = 0.813 after treatment. These changes were associated with a significant reduction in mean maximal tumour diameter (21.2 +/- 2.9 mm vs. 29.1 +/- 2.8 mm, P = 0.009). There was no significant difference in either prolactin concentration or tumour size pre- or post-treatment between those who recovered growth hormone secretion and those that did not. Six of the nine (67%) patients recovered a normal growth hormone response (> 10 mU/l) after cabergoline therapy. Those that remained growth hormone deficient after treatment were all panhypopituitary at baseline while those that recovered showed only partial anterior hypopituitarism.
These data indicate that growth hormone secretion may recover following successful reduction of prolactin levels after cabergoline therapy for a mean of 22 months (range 6-28 months) in most but not all subjects with a macroprolactinoma. It is therefore advisable that individuals with a macroprolactinoma in whom growth hormone replacement therapy is being considered undergo repeat assessment of growth hormone secretion following medical treatment.
卡麦角林疗法可使催乳素水平正常化并缩小大泌乳素瘤的大小。然而，尚无数据表明卡麦角林能否使在诊断大泌乳素瘤时生长激素缺乏的患者的生长激素分泌正常化。
我们研究了9例有大泌乳素瘤的生化及影像学证据且生长激素缺乏的患者（胰岛素诱发低血糖后生长激素峰值反应<10 mU/l）。在卡麦角林治疗前后对患者进行评估，以评估其生长激素分泌状态、胰岛素样生长因子-I（IGF-I）水平、皮质醇反应及肿瘤大小变化。
卡麦角林治疗使催乳素浓度显著降低（74341±31939 mU/l 对 265.9±86.3，P = 0.009）。与治疗前水平相比，卡麦角林治疗后胰岛素诱发低血糖后生长激素峰值反应的平均变化显著更大（33.5±11.8 mU/l 对 4.34±1.21 mU/l，P = 0.022）。然而，与基线相比，治疗后IGF-I水平无差异，尽管有不显著的改善趋势（24.2±3.97 nmol/l 对 18.4±4.94 nmol/l，P = 0.058）。治疗前平均皮质醇峰值浓度为407.7±64.1 nmol/l，治疗后无显著升高至477.4±84.8 nmol/l，P = 0.813。这些变化与平均最大肿瘤直径显著减小相关（21.2±2.9 mm 对 29.1±2.8 mm，P = 0.009）。生长激素分泌恢复者与未恢复者在治疗前后的催乳素浓度或肿瘤大小均无显著差异。9例患者中有6例（67%）在卡麦角林治疗后恢复了正常的生长激素反应（>10 mU/l）。治疗后仍生长激素缺乏的患者在基线时均为全垂体功能减退，而恢复者仅表现为部分垂体前叶功能减退。
这些数据表明，在大多数（但并非所有）大泌乳素瘤患者中，卡麦角林治疗成功降低催乳素水平平均22个月（范围6 - 28个月）后，生长激素分泌可能恢复。因此，对于正在考虑生长激素替代治疗的大泌乳素瘤患者，建议在药物治疗后对生长激素分泌进行重复评估。
