Histological Confounders of Liver Stiffness
Histological Confounders of Liver Stiffness
复制标题
肝硬化的组织学混杂因素
DOI：
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发表时间：
2020
期刊：
影响因子：
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通讯作者：
C. Lackner
中科院分区：
文献类型：
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作者：
S. Mueller;C. Lackner
在对肝脏硬度(LS)的组织学研究中，纤维化与相关系数在0.7到0.8之间显示出最密切的相关性。这些纤维化特征包括间隔的宽度和数目。LS升高的其他细胞外沉积包括淀粉样蛋白。纤维化特征之后是气球膨胀的迹象，在现在被称为Mallory-Denk小体的Mallory‘s玻璃体中积累，这些小体主要填充着CK18细胞角蛋白细丝。在气球膨胀的特征之后是炎症的迹象，如中性粒细胞或其他炎症细胞的渗入。在炎症的背景下，很有可能更多的细胞招募和增加的灌流(压力)都会导致LS升高。炎症之后是其他与LS显著相关的细胞死亡的组织学特征：微小肉芽肿、嗜酸性小体、巨线粒体、糖化核和大脂肪肉芽肿。值得注意的是，大小脂滴形式的脂肪变性与LS无关。一些争议可能源于这样一个事实，即在许多活组织检查的队列中，脂肪变性往往与肝脏损害并存。当排除这些混杂因素时，脂肪甚至会对僵硬产生负面影响。由于脂肪变性在正常、健康的肝脏和终末期肝硬变中都很低，因此脂肪的粘弹性是否对疾病进展具有生物力学上的有利作用仍有待研究。
In histological studies on liver stiffness (LS), fibrosis shows the closest association with correlation coefficients ranging from 0.7 to 0.8. These fibrosis features include width and number of septa. Other extracellular deposits of elevated LS include amyloid. Fibrosis features are followed by signs of ballooning, accumulation of Mallory’s hyaline in the now called Mallory–Denk bodies that are largely stuffed with CK18 cytokeratin filaments. Features of ballooning are followed by signs of inflammation such as infiltrates of neutrophils or other inflammatory cells. In the context of inflammation, it is highly conceivable that both recruitment of more cells and increased perfusion (pressure) will cause LS elevation. Inflammation is followed by other histological features of cell death that are significantly associated with LS: microgranulomas, acidophil bodies, megamitochondria, glycogenated nuclei, and large lipo-granulomas. Notably, steatosis in form of large and small lipid droplets is not associated with LS. Some controversies may result from the fact that in many biopsied cohorts, steatosis often coexists with liver damage. When ruling out these confounders, fat can even have a negative impact on stiffness. Since steatosis is low in normal, healthy livers but also end-stage cirrhotic livers, it remains to be studied whether viscoelastic properties of fat have a biomechanical beneficial effect on disease progression.
影响因子：
29.4
作者：
Altamirano J;Miquel R;Katoonizadeh A;Abraldes JG;Duarte-Rojo A;Louvet A;Augustin S;Mookerjee RP;Michelena J;Smyrk TC;Buob D;Leteurtre E;Rincón D;Ruiz P;García-Pagán JC;Guerrero-Marquez C;Jones PD;Barritt AS 4th;Arroyo V;Bruguera M;Bañares R;Ginès P;Caballería J;Roskams T;Nevens F;Jalan R;Mathurin P;Shah VH;Bataller R
通讯作者：
Bataller R
影响因子：
13.5
作者：
Dechene, Alexander;Sowa, Jan-Peter;Canbay, Ali
通讯作者：
Canbay, Ali