摘要目的 探讨药物性肝损伤的MSCT表现.方法 回顾性分析2008年5月至2010年1月间经临床及病理证实的40例药物性肝损伤患者的MSCT影像及临床资料,总结其影像表现特征.结果 药物性肝损伤的MSCT影像表现主要有3种类型.(1)弥漫性肝脏损害2例:平扫肝脏密度均匀性减低,增强扫描肝实质轻度均匀强化.病理表现为肝细胞脂肪变性;混合炎性细胞浸润,点状坏死,毛细胆管淤胆.(2)灶性肝脏损害6例:肝内大片或多发小片状坏死灶5例.平扫肝脏密度不均匀,病变区为低密度改变;增强后病变区强化,特别是静脉期与平扫图像比较呈反转表现.另1例病程20 d的移植肝显示肝内弥漫的结节样再生.CT平扫可见肝内弥漫分布的稍高密度结节灶,增强后动脉期病灶强化,静脉期及延迟期近似于肝实质密度.5例患者病理表现为肝细胞片状及桥接坏死,大量混合炎性细胞浸润;1例重度淤胆,假小叶形成,肝细胞羽毛变性.(3)肝硬化表现2例:平扫肝脏表面呈结节状,肝叶比例失调,肝裂增宽.增强后肝脏强化一致,同时伴有脾大、腹水、侧支循环.病理为纤维组织增生,点状坏死和毛细胆管淤胆.结论 药物性肝损伤的MSCT影像表现具有一定的特征性,对临床诊断具有重要的参考价值.

abstractsObjective To demonstrate the spectrum of multi-detector spiral CT (MSCT) findings of drug-induced liver injury (DILI). Methods From May 2008 to January 2010, DILI was identified in 10 cases based on their clinical and pathological results. The spectrum of CT findings was analyzed retrospectively. Results According to the CT features, DILI were divided into three types. ( 1 ) Two cases presented diffuse hepatic injury, which appeared as homogeneous hypo-attenuation in precontrast CT scan and mild enhancement after contrast injection. The histopathological findings of the involved 1ivers include hepatocellular steatosis, neutrophil and eosinophil infiltration, punctiform necrosis and canalicular cholestasis. (2) Six cases presented focal hepatic injury, including massive wedge-shaped necrosis in 4,multiple small necroses in 1 and multiple regenerated nodules in 1. In precontrast CT scan, hepatic necroses were seen as inhomogeneous hypo-attenuation areas, which turned to hyper-attenuation after contrast injection and presented "flip-flop" sign between precontrast CT scan and portal venous phase scan. In the case with regenerated nodules, slight hyper-attenuation lesions were detected with diffuse distribution in liver in precontrast CT scan, which showed enhancement in hepatic arterial phase and turned to iso-attenuation in portal venous phase and equilibrium phase. The histopathological changes included massive necrosis or bridging necrosis with abundant neutrophil and eosinophil infiltration in 5 cases, nodular regeneration with cholestasis and feathery degeneratin in 1 case. (3) Two cases presented liver cirrhosis. CT displayed obvious nodularity of liver, which complicated with splenomegaly, ascites and collateral veins. The histopathological changes of these two cases included punctiform necrosis, canalicular cholestasis and pseudolobular formation. Conclusion CT signs of DILl have certain characteristics, which may help in detecting and determining the severity of liver damage.