Kirch W, Höfig M, Ledendecker T, Schmidt-Gayk H
I. Medizinische Klinik, Christian-Albrechts-Universität, Kiel, Germany.
J Clin Endocrinol Metab. 1990 Dec;71(6):1561-6. doi: 10.1210/jcem-71-6-1561.
Fifty patients with liver cirrhosis (36 alcoholic, 1 drug-induced, 7 posthepatitic, and 6 cryptogenic) and normal renal function were investigated to determine whether PTH levels in serum, measured using the common midregion human PTH-(44-68) RIA, are elevated in such patients and whether this is related to impaired liver function rather than to the effect of secondary hyperparathyroidism. Their data were compared with those from 25 control subjects. The median PTH level of 462 +/- 18 ng/L (+/- SEM) was significantly increased (P less than 0.01) in cirrhotics compared with that of 236 +/- 13 ng/L in the control group. Significant correlations were found between PTH levels and parameters of liver function such as prothrombin time (r = -0.40; P less than 0.01), albumin as a percentage of total protein (r = -0.48; P less than 0.01), bilirubin (r = 0.35; P less than 0.05), albumin (r = -0.34; p less than 0.05), and cholesterol (r = -0.32; P less than 0.05), but not for antipyrine clearance, suggesting increasing PTH with decreasing liver function. The median calcium level (2.26 +/- 0.03 mmol/L), corrected for changes in albumin, was near the lower limit of the normal range (2.25-2.60), but corrected calcium and PTH were positively correlated (r = 0.33; P less than 0.05), indicating that the elevation is not reactive to calcium depletion. A negative correlation existed between PTH and 25-hydroxy-cholecalciferol (r = -0.49; P less than 0.05), the main circulating metabolite of vitamin D. Normal values in an immunoradiometric assay that detects the whole sequence of human PTH-(1-84) suggest that fragments rather than the intact hormone are responsible for PTH elevations in cirrhosis. The positive correlation between midregion PTH and corrected calcium is probably an artifact of the correction formula. In conclusion, midregion PTH fragments are increased in patients with liver cirrhosis. The reason for this elevation may well be the impaired liver function rather than secondary hyperparathyroidism.
对50例肝硬化患者(36例酒精性肝硬化、1例药物性肝硬化、7例肝炎后肝硬化和6例隐源性肝硬化)且肾功能正常者进行研究,以确定使用常用的人甲状旁腺激素中段(44 - 68)放射免疫分析法测定的血清甲状旁腺激素(PTH)水平在这类患者中是否升高,以及这是否与肝功能受损有关而非继发性甲状旁腺功能亢进的影响。将他们的数据与25名对照者的数据进行比较。肝硬化患者的PTH中位数水平为462±18 ng/L(±标准误),与对照组的236±13 ng/L相比显著升高(P<0.01)。发现PTH水平与肝功能参数之间存在显著相关性,如凝血酶原时间(r = - 0.40;P<0.01)、白蛋白占总蛋白的百分比(r = - 0.48;P<0.01)、胆红素(r = 0.35;P<0.05)、白蛋白(r = - 0.34;P<0.05)和胆固醇(r = - 0.32;P<0.05),但与安替比林清除率无关,提示随着肝功能下降PTH升高。校正白蛋白变化后的钙中位数水平(2.26±0.03 mmol/L)接近正常范围下限(2.25 - 2.60),但校正钙和PTH呈正相关(r = 0.33;P<0.05),表明这种升高并非对钙缺乏的反应。PTH与维生素D的主要循环代谢产物25 - 羟基胆钙化醇之间存在负相关(r = - 0.49;P<0.05)。检测人甲状旁腺激素(1 - 84)全序列的免疫放射分析中的正常值表明,片段而非完整激素是肝硬化中PTH升高的原因。中段PTH与校正钙之间的正相关可能是校正公式的假象。总之,肝硬化患者中段PTH片段升高。这种升高的原因很可能是肝功能受损而非继发性甲状旁腺功能亢进。