4.6 Article

The effect of liver transplantation on circulating levels of estradiol and progesterone in male patients:: Parallelism with hepatopulmonary syndrome and systemic hyperdynamic circulation improvement

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JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION
卷 24, 期 7, 页码 503-509

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SPRINGER
DOI: 10.1007/BF03343883

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hepatopulmonary syndrome; liver transplantation; sex hormones

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The correction of hepatopulmonary syndrome (HPS) after liver transplantation (LT) remains controversial. The aims of our study were to: 1)analyze whether LT reverses HPS; 2) note any relationship between HPS and the systemic hemodynamic disturbance; and 3) note changes in circulating sex hormones and the possible association with pulmonary and systemic hemodynamic changes. Systemic hemodynamic parameters, cardiac output and systemic vascular resistance (SVR), sex hormones, and intrapulmonary vasodilatation assessed by contrast transesophageal echocardiography, and gas exchange abnormalities were investigated in 19 patients with advanced cirrhosis prior to and 6 months (176.8 +/- 30 days) after LT. LT was followed by a marked reduction in cardiac output (6.6 +/-1.7 vs 3.5 +/-0.5 l/min; p<0.001) and SVR (1039460 vs 1978 +/- 294 dyn.sec.cm(-5); p<0.005). Before LT, circulating estradiol and progesterone levels were invariably elevated (6622 pg/ml and 1.8 +/-1.1 ng/ml, respectively, normal values <31 pg/ml and 0.35 ng/ml, respectively), and dropped after LT (2812 pg/ml p<0.001 and 0.380.2 ng/ml; p<0.001, respectively). Seventeen of 19 patients had intrapulmonary vasodilatation and increased alveolar-arterial oxygen difference, thereby fulfilling diagnostic criteria for HPS. Patients with HPS presented higher cardiac output (p<0.05), lower SVR (p<0.01), and higher progesterone and estradiol levels than patients without HPS (p<0.05). LT produced normalization of intrapulmonary vasodilatation in all patients. LT normalized hyperdynamic circulation and is a useful therapeutic option in patients with HPS. Normalization of sex hormone levels after LT suggests that they could play a pathogenic role in the development of HPS, (J. Endocrinol. Invest. 24: 503-509, 2001) (C) 2001, Editrice Kurtis.

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