Bauer A G, Lamberts S W, Wilson J H
Horm Res. 1982;16(2):126-32. doi: 10.1159/000179493.
Chronic liver disease is associated with raised basal and TRH-stimulated PRL and GH levels. In a recent study we found the kidney to be the main site of prolactin elimination in patients with liver disease. In order to determine whether this is specific for PRL or a more general mechanism for polypeptide removal, we studied the elimination of GH, which resembles PRL in molecular weight and primary amino acid sequence, in 5 patients with portal hypertension and hepatic cirrhosis and 5 patients with noncirrhotic portal hypertension. Plasma GH levels were measured before and after TRH in peripheral, hepatic and renal vein samples, taken during diagnostic hepatic vein catheterization. An excessive paradoxical increase of GH after THR stimulation was found in 4 out of 5 cirrhotic patients but in none of the noncirrhotic individuals (p less than 0.025). After TRH the mean hepatic venous levels were significantly lower than the peripheral venous levels in 4 out of 5 noncirrhotic patients but in only 1 of the 5 cirrhotic patients (p less than 0.05). The mean renal vein GH levels were significantly lower than the peripheral levels in 3 out of 5 noncirrhotic patients and in none of the cirrhotic patients. In 2 patients in whom renal and hepatic plasma flow was measured, renal extraction of GH was found to be 0 to 6.4 micrograms, while liver extraction amounted to 22.1 and 34.7 micrograms of GH during the same 60-min period. Despite the similarity in molecular weight and primary amino acid sequence between PRL and GH, GH appears to be mainly taken up by the liver while PRL is mainly eliminated by the kidney in this group of patients with portal hypertension. This suggests that the renal elimination of prolactin is not solely dependent on glomerular filtration. The selective hepatic removal of growth hormone is probably related to a specific action of growth hormone on liver metabolism.
慢性肝病与基础及促甲状腺激素刺激的催乳素和生长激素水平升高有关。在最近的一项研究中，我们发现肾脏是肝病患者催乳素清除的主要部位。为了确定这是催乳素特有的现象还是多肽清除的更普遍机制，我们研究了5例门静脉高压和肝硬化患者以及5例非肝硬化门静脉高压患者中生长激素的清除情况，生长激素在分子量和一级氨基酸序列上与催乳素相似。在诊断性肝静脉插管期间，采集外周、肝和肾静脉样本，分别在促甲状腺激素刺激前后测量血浆生长激素水平。5例肝硬化患者中有4例在促甲状腺激素刺激后出现生长激素过度反常升高，而非肝硬化患者中无一例出现（p<0.025）。促甲状腺激素刺激后，5例非肝硬化患者中有4例肝静脉平均水平显著低于外周静脉水平，而5例肝硬化患者中只有1例如此（p<0.05）。5例非肝硬化患者中有3例肾静脉生长激素平均水平显著低于外周水平，而肝硬化患者中无一例如此。在2例测量了肾和肝血浆流量的患者中，发现肾对生长激素的摄取量为0至6.4微克，而在同一60分钟期间肝脏摄取量分别为22.1和34.7微克生长激素。尽管催乳素和生长激素在分子量和一级氨基酸序列上相似，但在这组门静脉高压患者中，生长激素似乎主要被肝脏摄取，而催乳素主要由肾脏清除。这表明催乳素的肾脏清除并非仅依赖于肾小球滤过。生长激素的选择性肝脏清除可能与生长激素对肝脏代谢的特定作用有关。
