临床放射学杂志
臨床放射學雜誌
림상방사학잡지
JOURNAL OF CLINICAL RADIOLOGY
2001年
5期
361-364
,共4页
小肝癌%螺旋CT%增强%诊断
小肝癌%螺鏇CT%增彊%診斷
소간암%라선CT%증강%진단
目的回顾性分析螺旋CT增强动脉期扫描对小肝癌(HCCs)诊断的作用，探讨部分小HCCs不强化的病理基础。材料与方法搜集158例共186个病灶。临床记录初诊主诉、肝炎、肝硬化史和AFP。手术病理记录肝脏有无肝硬化、病灶的包膜和边缘、出血坏死囊变及透明细胞变等。CT扫描记录病灶平扫的密度和均匀性及动脉期和门脉期有无强化、均匀性和轮廓等改变。结果 80.4%的病例有肝炎、肝硬化病史。66.5%的患者AFP阳性。术中见肝硬化者占83.9%。28%的病灶有完整包膜，29%的病灶包膜不完整。20.4%的病灶内见出血坏死，16.7%的病灶内出现透明细胞变或全灶为透明细胞癌。CT平扫发现不到71.7%的病灶。动脉期强化呈高密度者占78.3%，等密度8.5%，低密度13.2%。低密度主要由坏死造成，透明细胞变可能是原因之一。结论动脉期大部分小HCCs病灶出现强化，不强化者占13.2%。其动脉期不强化的常见原因是坏死，透明细胞变可能为另一原因。
目的迴顧性分析螺鏇CT增彊動脈期掃描對小肝癌(HCCs)診斷的作用，探討部分小HCCs不彊化的病理基礎。材料與方法搜集158例共186箇病竈。臨床記錄初診主訴、肝炎、肝硬化史和AFP。手術病理記錄肝髒有無肝硬化、病竈的包膜和邊緣、齣血壞死囊變及透明細胞變等。CT掃描記錄病竈平掃的密度和均勻性及動脈期和門脈期有無彊化、均勻性和輪廓等改變。結果 80.4%的病例有肝炎、肝硬化病史。66.5%的患者AFP暘性。術中見肝硬化者佔83.9%。28%的病竈有完整包膜，29%的病竈包膜不完整。20.4%的病竈內見齣血壞死，16.7%的病竈內齣現透明細胞變或全竈為透明細胞癌。CT平掃髮現不到71.7%的病竈。動脈期彊化呈高密度者佔78.3%，等密度8.5%，低密度13.2%。低密度主要由壞死造成，透明細胞變可能是原因之一。結論動脈期大部分小HCCs病竈齣現彊化，不彊化者佔13.2%。其動脈期不彊化的常見原因是壞死，透明細胞變可能為另一原因。
목적회고성분석라선CT증강동맥기소묘대소간암(HCCs)진단적작용，탐토부분소HCCs불강화적병리기출。재료여방법수집158례공186개병조。림상기록초진주소、간염、간경화사화AFP。수술병리기록간장유무간경화、병조적포막화변연、출혈배사낭변급투명세포변등。CT소묘기록병조평소적밀도화균균성급동맥기화문맥기유무강화、균균성화륜곽등개변。결과 80.4%적병례유간염、간경화병사。66.5%적환자AFP양성。술중견간경화자점83.9%。28%적병조유완정포막，29%적병조포막불완정。20.4%적병조내견출혈배사，16.7%적병조내출현투명세포변혹전조위투명세포암。CT평소발현불도71.7%적병조。동맥기강화정고밀도자점78.3%，등밀도8.5%，저밀도13.2%。저밀도주요유배사조성，투명세포변가능시원인지일。결론동맥기대부분소HCCs병조출현강화，불강화자점13.2%。기동맥기불강화적상견원인시배사，투명세포변가능위령일원인。
Objective To evaluate enhanced spiral CT scan in the diagnosis of small HCCs, and to study the pathology of non-enhanced small HCCs. Materials and Methods 186 lesions found in 158 patients were collected. Clinical complains, history of cirrhosis due to hepatitis and AFP were recorded. Present or absent of cirrhosis, capsule and margin of the lesion, necrosis and cellular hyaline degeneration founded on surgery and pathologic examination were also documented. The attenuation, homogeneity and edge of the non-enhanced lesions on CT in arterial and portal phase were observed and analyzed. Results Up to 80.4% of patients had a history of hepatitis and cirrhosis. AFP was elevated in 66.5% of patients. Cirrhosis in 83.9% cases was found in surgery. On CT, the lesions were well-defined (72.6%) with complete (28%) or incomplete (29%) capsule. On pathological examination, necrosis (20.4%) and hyaline degeneration (16.7%) within the lesions were seen. Less than 71.7% of the lesions could be demonstrated with plain CT scans. During arterial phase, the lesions displayed hyper- (78.3%), iso- (8.5%) or hypo-density (13.2%). Low density area was mainly due to the necrosis, and, perhaps, hyaline degeneration was another cause. Conclusion During arterial phase most small HCCs show enhancement, only 13.2% of lesions are not enhanced. The reasons for non-enhancement are mainly due to necrosis and, probably, hyaline degeneration.
