Pirlich M, Selberg O, Böker K, Schwarze M, Müller M J
Abteilung für Gastroenterologie und Hepatologie, Medizinische Hochschule Hannover, Germany.
Hepatology. 1996 Dec;24(6):1422-7. doi: 10.1002/hep.510240620.
The creatinine-method to estimate muscle mass is frequently used in clinical studies, although the validity of this approach is uncertain in patients with cirrhosis. In this study 102 patients with cirrhosis differing in cause, clinical state, liver, and renal function were investigated to determine whether reduced liver or renal function may explain in part the low levels of urinary creatinine excretion frequently observed in these patients. Muscle mass assessed by 24-hour urinary creatinine excretion was compared with anthropometrically obtained muscle mass calculated from arm muscle area (AMA), and with body cell mass (BCM) estimated by bioelectrical impedance analysis and total body potassium counting. In cirrhosis, the 24-hour urinary creatinine excretion was 10.4% and AMA was 19% lower than predicted values. The differences between the results obtained by different methods did not show any relation to parameters of liver function (ICG-t1/2, caffeine-t1/2, MEGX-test, cholinesterase) or the severity of liver disease (i.e., Child-Pugh score). In contrast, renal function was strongly correlated with the differences between creatinine- and anthropometric-muscle mass (r = .64, P < .001). At the same time, patients with normal renal function (62% of the whole population) had significantly higher creatinine (29.1 +/- 8.5 vs. 15.8 +/- 6 kg, P < .001) and anthropometric-muscle mass (22.4 +/- 6 vs. 17.9 +/- 5.3 kg; P < .01) than patients with reduced renal function (38% of the patients). In addition, significantly higher differences between measured and predicted values of urinary creatinine excretion (-0.389 +/- 0.33 vs. 0.06 +/- 0.31 g/24 h; P < .001) and of AMA (13.2 +/- 12 vs. 7.2 +/- 12 cm2; P < .03) were found in the subgroup with impaired renal function. In conclusion, renal dysfunction but not reduced liver function systematically affects the urinary creatinine method for the estimation of skeletal muscle mass in cirrhosis.
尽管在肝硬化患者中这种方法的有效性尚不确定,但肌酐法估算肌肉量在临床研究中仍被频繁使用。在本研究中,对102例病因、临床状态、肝脏和肾功能各异的肝硬化患者进行了调查,以确定肝功能或肾功能降低是否可部分解释这些患者中经常观察到的尿肌酐排泄水平低的现象。将通过24小时尿肌酐排泄评估的肌肉量与根据臂肌面积(AMA)计算得出的人体测量肌肉量以及通过生物电阻抗分析和全身钾计数估算的身体细胞量(BCM)进行比较。在肝硬化患者中,24小时尿肌酐排泄比预测值低10.4%,AMA比预测值低19%。不同方法所得结果之间的差异与肝功能参数(吲哚菁绿t1/2、咖啡因t1/2、MEGX试验、胆碱酯酶)或肝病严重程度(即Child-Pugh评分)无关。相反,肾功能与肌酐法和人体测量肌肉量之间的差异密切相关(r = 0.64,P < 0.001)。同时,肾功能正常的患者(占总人数的62%)的肌酐(29.1±8.5 vs. 15.8±6 kg,P < 0.001)和人体测量肌肉量(22.4±6 vs. 17.9±5.3 kg;P < 0.01)显著高于肾功能降低的患者(占患者总数的38%)。此外,在肾功能受损的亚组中,尿肌酐排泄实测值与预测值之间(-0.389±0.33 vs. 0.06±0.31 g/24 h;P < 0.001)以及AMA实测值与预测值之间(13.2±12 vs. 7.2±12 cm2;P < 0.03)的差异显著更高。总之,是肾功能不全而非肝功能降低系统性地影响了肝硬化患者中用于估算骨骼肌量的尿肌酐法。