Annals of medicine and surgery (2012) · 2025
Chronic liver disease and radiation-induced second primary liver malignancy: a retrospective cohort based on SEER database 2010-2021.
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Ellaithy Asmaa, Serageldeen Aya, Alhusban Alhareth, Seif Mariam Emad, Abdelhamid Mahmoud Essam, Al-Shaikh Bushra, Ibrahim Asmaa Sayed, Elshennawy Eslam Mohamed, Ellaithy Ibrahim
Аннотация
INTRODUCTION: Cirrhotic patients are at a high risk of developing radiation-induced liver toxicities despite the modern safe radiation delivery techniques due to the low liver tolerance. Recent studies demonstrated a potential risk of second primary malignancies (SPMs) following radiotherapy (RT) with further investigations for strategies to decrease RT-induced SPMs. However, it is insufficiently addressed if developing liver SPMs is a serious adverse event following RT for cirrhotic patients. Thus, we aimed to quantitatively assess the risk of gastrointestinal (GI) and liver SPMs following RT in patients with liver fibrosis.
METHODS: The SEER*Stat beta software version 9.0.32 was used to obtain and analyze the data of patients with chronic liver disease diagnosed from 2010 to 2021. We sub-grouped patients according to the history of receiving RT for prior cancer treatment into two groups and excluded patients with unknown RT administration history.
RESULTS: We observed 215 cirrhotic patients developed GI SPMs (O/E = 2.76, P < 0.05, ER = 45.51), 106 of them developed liver SPMs (O/E = 8.80, P < 0.05). Patients with liver cirrhosis who received RT had an increased risk for GI SPMs (Observed = 24, O/E = 3.34, P < 0.05) compared to who received no RT (O/E = 2.71, P < 0.05, ER = 43.72). Liver SPMs after RT in cirrhotic patients had an O/E of 12.31 (Observed = 13, P < 0.05) while the group who received no RT had an O/E of 8.46 (Observed = 93, P < 0.05, ER = 29.77).
CONCLUSION: Cirrhotic patients who received RT before had an increased risk for GI SPMs by three folds and a 12-fold increased risk for liver SPMs. However, who received no RT had an 8-fold increased risk for liver SPM. Thus, screening for HCC in cirrhotic patients exposed to RT is a must for early detection and better management outcome.
METHODS: The SEER*Stat beta software version 9.0.32 was used to obtain and analyze the data of patients with chronic liver disease diagnosed from 2010 to 2021. We sub-grouped patients according to the history of receiving RT for prior cancer treatment into two groups and excluded patients with unknown RT administration history.
RESULTS: We observed 215 cirrhotic patients developed GI SPMs (O/E = 2.76, P < 0.05, ER = 45.51), 106 of them developed liver SPMs (O/E = 8.80, P < 0.05). Patients with liver cirrhosis who received RT had an increased risk for GI SPMs (Observed = 24, O/E = 3.34, P < 0.05) compared to who received no RT (O/E = 2.71, P < 0.05, ER = 43.72). Liver SPMs after RT in cirrhotic patients had an O/E of 12.31 (Observed = 13, P < 0.05) while the group who received no RT had an O/E of 8.46 (Observed = 93, P < 0.05, ER = 29.77).
CONCLUSION: Cirrhotic patients who received RT before had an increased risk for GI SPMs by three folds and a 12-fold increased risk for liver SPMs. However, who received no RT had an 8-fold increased risk for liver SPM. Thus, screening for HCC in cirrhotic patients exposed to RT is a must for early detection and better management outcome.