Idiopathic hypoalbuminemia explained by reduced synthesis rate and an increased catabolic rate.
Idiopathic hypoalbuminemia explained by reduced synthesis rate and an increased catabolic rate.
复制标题
特发性低白蛋白血症的解释是合成率降低和分解代谢率增加。
DOI：
10.1016/s0009-9120(02)00357-0
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发表时间：
2002
影响因子：
2.8
通讯作者：
deSain-vanderVelden,MoniqueGM
中科院分区：
文献类型：
--
作者：
Prinsen,BerthilHCMT;Kaysen,GeorgeA;Klomp,LeoWJ;deBoer,Jose;Barrett,PHughR;Thornalley,PaulJ;Battah,Sinan;Berger,Ruud;Rabelink,TonJ;deSain-vanderVelden,MoniqueGM
ObjectiveTo determine the contribution of albumin synthetic and catabolic rates to steady state levels in a patient with idiopathic hypoalbuminemia.MethodsUsing L-[1-13C] valine, both FSR (fractional synthesis rate) as well as FCR (fractional catabolic rate) were studied. Human albumin cDNA analysis and determination of the exact albumin mass by electrospray mass spectrometry were performed.ResultsCompared with controls, plasma albumin concentration in the patient was reduced (6.7 vs. 37.0 ± 2.6 g/L). Albumin FSR (= FCR in steady state) was increased compared to controls. The ASR (absolute synthesis rate) of albumin was decreased based on the enrichment in plasma valine and KIV, but estimated to be normal based on VLDL apoB100 at plateau compared to controls. Direct estimation of albumin FCR rejected the latter. No mutation was found in the transcribed region of albumin gene. The exact mass of albumin (66.493 Da) was not different from controls.ConclusionThe hypoalbuminemia was a result of accelerated clearance of albumin from plasma in addition to defective albumin synthesis. This study also shows that the chosen method of the precursor pool could lead to misinterpretation of data in hepatic protein synthesis.
