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OBJECTIVE To mine and analyze the adverse drug events （ADE） signals of two camptothecin topoisomerase 1 inhibitors， i.e. irinotecan and topotecan， and to provide reference for clinical medication safety. METHODS Based on the U.S. Food and Drug Administration Adverse Event Reporting System （FAERS） database， ADE report data for the aforementioned two drugs were extracted from January 1， 2004 to March 31， 2023. After processing the data， signal mining was conducted by using the reporting odds ratio in conjunction with the Bayesian confidence propagation neural network， followed by analysis. RESULTS A total of 14 738 relevant ADE reports were screened， among which 11 483 were associated with irinotecan and 3 255 with topotecan. The ADE reports for irinotecan were predominantly male， whereas for topotecan， they were predominantly female； the age of patients using the two drugs mainly concentrated in 45-＜75 years old. A total of 847 signals were detected， involving 24 system organ classes （SOCs）. Among them， 565 signals of irinotecan were detected， involving 24 SOCs， primarily concentrating on gastrointestinal disorders， general disorders and administration site conditions， blood and lymphatic system disorders； the most frequently reported ADE was diarrhea， and the ADE with the strongest signal intensity was cholinergic syndrome. A total of 282 signals of topotecan were detected， involving 22 SOCs， primarily concentrating on general disorders and administration site conditions， investigations， blood and lymphatic system disorders， and gastrointestinal disorders； the most frequently reported ADEs were death and anemia， and the ADE with the strongest signal intensity was febrile bone marrow aplasia. ADE signals for irinotecan such as metastatic colorectal cancer， peripheral sensory neuropathy， steatohepatitis， and those for topotecan such as iris atrophy， retinal degeneration， vitreous hemorrhage， were not documented in their respective drug instruction. CONCLUSIONS ADEs of irinotecan and topotecan primarily involve the digestive and hematologic systems， warranting close clinical monitoring. Cholinergic syndrome caused by irinotecan should be concerned. In addition， patients receiving irinotecan should also be monitored for ADE such as metastatic colorectal cancer， peripheral sensory neuropathy， steatohepatitis， and proteinuria； for patients using topotecan， enhanced surveillance of ocular diseases is recommended to ensure medication safety.
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ObjectiveTo investigate the correlation between HBsAg, prothrombin time activity (PTA), and indocyanine green retention rate at 15 minutes (ICG R15) in patients with HBeAg-positive chronic HBV infection. MethodsA total of 92 patients with HBeAg-positive chronic HBV infection who were admitted to The First Hospital of Lanzhou University from December 2015 to April 2016 were enrolled and divided into chronic hepatitis B (CHB) group (24 patients), compensated liver cirrhosis group (38 patients), and decompensated liver cirrhosis group (30 patients). Serum HBsAg quantitation, PTA test, and liver reserve function test (ICG R15) were performed for all patients. The chi-square test was used for comparison of categorical data between groups, an analysis of variance was used for comparison of continuous data between multiple groups, and a Pearson correlation analysis was also performed. ResultsThere were significant differences between the three groups in serum HBsAg quantitation (3.82±0.43 log10IU/ml vs 2.88±0.36 log10IU/ml vs 2.60±0.27 log10IU/ml, F=25.19, P＜0.001), ICG R15 (7.51%±3.10% vs 9.57%±8.18% vs 24.13%±14.28%, F=24.00, P=0.001), and PTA (8100%±1762% vs 83.08%±9.64% vs 62.32%±16.90%, F=13.42, P=0.009). The correlation analysis showed that PTA was negatively correlated with ICG R15 in all three groups (r=-0.948, -0.602, and -0.735, all P＜0.01). In the compensated liver cirrhosis group and decompensated liver cirrhosis group, HBsAg was positively correlated with PTA (r=0.410 and 0.473, both P＜0.05) and negatively correlated with ICG R15 (r=-0.427 and -0.768, P＜0.01). ConclusionIn HBeAg positive patients, there are certain correlations between HBsAg, PTA, and ICG R15, which, to a certain degree, reflects the liver reserve function in patients with chronic HBV infection.
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Toll-like receptor 4 (TLR4) is an important pattern recognition receptor and plays an important role in the inhibition of hepatitis B virus (HBV) infection. It identifies the HBV-related proteins and produces inflammatory factors, such as tumor necrosis factor-α, interleukin-6, and interleukin-12, and type I interferon through the myeloid differentiation factor 88 (MyD88) and the non-MyD88 pathway, and thus TLR4 exerts its antiviral effect. Meanwhile, it has been found that TLR4 regulates the balance between T helper 1 and T helper 2 cells, promotes the adhesion of CD8+ T lymphocytes in the liver, induces the secretion of inducible nitric oxide synthase, and thus inhibits HBV. If overexpressed, TLR4 will aggravate liver inflammation by excessively activating the body's immune system, aggravating liver ischemia/reperfusion, and activating hepatic stellate cells. This article reviews related articles published at home and abroad in recent years, discusses the mechanisms of action of TLR4 in the pathogenesis of hepatitis B, and summarizes the association between TLR4 and hepatitis B, in order to find new therapies for hepatitis B and new protocols which delay the progression of hepatitis B to liver cirrhosis and liver cancer through the studies on the association between TLR4 and hepatitis B.