Müller B, de Marco D, Bürgi U, Mullis P E
Abteilung für Endokrinologie und Diabetologie, Universität Bern, Inselspital.
Schweiz Med Wochenschr. 1999 Aug 21;129(33):1152-61.
Acromegaly is usually due to autonomous, excessive secretion of growth hormone from a pituitary adenoma. One would expect growth hormone-releasing factor (GHRH) in these patients to be suppressed. In the available literature referring to acromegaly, immunoreactive GHRH levels were determined in 259 acromegalic patients. When growth hormone was measured simultaneously, no correlation was found between serum growth hormone and plasma GHRH concentrations, irrespective of whether the acromegalic patients were treated or not. A possible explanation for this finding might be the lack of a feedback regulation between plasma growth hormone and GHRH. Also, since growth hormone is secreted in a pulsatile fashion the interpretation of single growth hormone values can be difficult. IGF I, which correlates well with mean growth hormone production, may therefore represent a more valuable criterion for the assessment of activity and GHRH plasma levels in acromegalics. However, no study has yet been performed to elucidate the relationship between GHRH and IGF I in acromegaly. To examine this relationship we measured the concentration of plasma GHRH and IGF I in 18 treated patients with acromegaly (age range 32-64 years median 50.5 years; median follow-up 6.5 years, range 3 months to 33 years). All immunoreactive GHRH levels were within the limits described as normal in the literature (mean +/- SD 22.89 +/- 2.72 pg/ml, range 19-28 pg/ml). The IGFI level was 396.78 +/- 224.26 ng/ml (mean +/- SD, range 71-876 ng/ml; reference ranges, age group 25-39 years: 114-492 ng/ml; 40-54 years: 90-360 ng/ml; > 55 years: 71-290 ng/ml). We found no correlation between IGF I and GHRH concentrations (r = 0.17). We therefore conclude that measuring plasma GHRH is not useful in the evaluation of the activity or therapy of acromegaly but may be helpful in its differential diagnosis since a massive elevation of GHRH is typically associated with the ectopic GHRH syndrome, a rare cause of acromegaly.
肢端肥大症通常是由于垂体腺瘤自主分泌过量生长激素所致。人们预期这些患者的生长激素释放因子（GHRH）会受到抑制。在现有的关于肢端肥大症的文献中，对259例肢端肥大症患者测定了免疫反应性GHRH水平。当同时测量生长激素时，无论肢端肥大症患者是否接受治疗，血清生长激素与血浆GHRH浓度之间均未发现相关性。这一发现的一个可能解释可能是血浆生长激素与GHRH之间缺乏反馈调节。此外，由于生长激素是以脉冲方式分泌的，单次生长激素值的解释可能会很困难。因此，与平均生长激素分泌密切相关的IGF I可能是评估肢端肥大症患者活动度和GHRH血浆水平更有价值的指标。然而，尚未有研究阐明肢端肥大症中GHRH与IGF I之间的关系。为了研究这种关系，我们测量了18例接受治疗的肢端肥大症患者（年龄范围32 - 64岁，中位数50.5岁；中位随访6.5年，范围3个月至33年）的血浆GHRH和IGF I浓度。所有免疫反应性GHRH水平均在文献中描述的正常范围内（均值±标准差22.89±2.72 pg/ml，范围19 - 28 pg/ml）。IGF I水平为396.78±224.26 ng/ml（均值±标准差，范围71 - 876 ng/ml；参考范围，年龄组25 - 39岁：114 - 492 ng/ml；40 - 54岁：90 - 360 ng/ml；>55岁：71 - 290 ng/ml）。我们发现IGF I与GHRH浓度之间无相关性（r = 0.17）。因此，我们得出结论，测量血浆GHRH对肢端肥大症的活动度评估或治疗无用，但可能有助于其鉴别诊断，因为GHRH的大量升高通常与异位GHRH综合征相关，而异位GHRH综合征是肢端肥大症的一种罕见病因。
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