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Clinical studies of hepatocellular carcinoma with liver cirrhosis and ascites
Insights
Hepatocellular carcinoma (HCC) patients with liver cirrhosis (LC) present with ascites more frequently than LC patients without HCC. These ascites in HCC patients may be caused by factors unrelated to serum albumin or blood flow, leading to poorer outcomes.
Area of Science:
- Hepatology
- Oncology
Background:
- Liver cirrhosis (LC) is a major cause of morbidity and mortality.
- Hepatocellular carcinoma (HCC) frequently complicates LC, altering clinical presentation.
- Ascites is a common complication in both LC and HCC, but its characteristics and prognosis differ.
Purpose of the Study:
- To compare the clinical findings of patients with LC and HCC versus those with LC alone.
- To investigate the clinical characteristics and potential causes of ascites in HCC patients with LC.
Main Methods:
- Retrospective comparison of clinical data from 59 LC patients with HCC and 164 LC patients without HCC.
- Analysis of patient demographics, clinical signs (e.g., hepatomegaly, ascites, edema), and ascitic fluid characteristics.
Main Results:
- HCC patients were older and exhibited more hepatomegaly, vascular spider, and pleural effusion than LC patients.
- Ascites was more prevalent in HCC patients, even with preserved serum albumin and hepatic function, and in the absence of peripheral edema.
- Ascitic fluid protein levels were similar between groups; malignant cells were found in only 14% of HCC ascites.
- Prognosis was significantly worse for HCC patients with ascites (96% mortality) compared to LC patients with ascites (54% recovery).
Conclusions:
- Ascites in HCC patients with LC may be driven by factors independent of serum colloid osmotic pressure and hepatic blood flow.
- The presence of ascites in HCC patients indicates a poor prognosis and warrants further investigation into underlying mechanisms.
Abstract:
A comparison was made of the clinical findings of 59 patients with liver cirrhosis (LC) accompanied with hepatocellular carcinoma (HCC) (of which 35 had ascites and 24 did not at the time of admission) and 164 patients with LC, but without HCC (of which 39 had ascites and 125 did not). HCC patients were older and more often had hepatomegaly, vascular spider and pleural effusion than LC patients. Ascites was more frequently observed in HCC than in LC patients when the serum albumin level and the indocyanine green disappearance rate were relatively well maintained and when peripheral edema was absent. There was no difference in the ascitic protein concentration between LC and HCC patients. Malignant cells were detected in ascites only in 14% of the HCC patients. These facts indicate the presence of ascites-inducing factors in HCC patients which have no direct relation to serum colloid osmotic pressure and effective hepatic blood flow. Almost all of the HCC patients with ascites (96%) died with ascites, whereas 54% of the LC patients with ascites recovered from the ascitic condition.