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Immortal time bias or sorafenib effect in elderly patients with HCC?
Author(s) -
Sanoff Hanna K.,
Chang YunKyung,
Lund Jennifer L.,
O'Neil Bert H.,
Dusetzina Stacie B.
Publication year - 2017
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.29250
Subject(s) - sorafenib , medicine , hazard ratio , propensity score matching , hepatocellular carcinoma , confidence interval , hepatology , oncology , observational study , population , environmental health
carcinoma in patients carrying the Z allele. While intriguing, the hypothesis raised by Ponzetto et al. remains highly speculative. Although Shimoda et al. found that CagA is present in serum-derived exosomes of patients infected with H. pylori, it is unknown whether these exosomes are released in sufficient amount to be taken up by hepatocytes and efficiently activate the c-Jun N-terminal kinase and c-Jun pathway. Moreover, activation of c-Jun by CagA has been observed in gastric epithelial cells exposed to H. pylori, and whether CagA can activate the c-Jun N-terminal kinase and c-Jun also in hepatocytes has to be shown. Co-occurrence of peptic ulcer by H. pylori has been observed in patients with alpha1-antitrypsin deficiency. However, whether infection with H. pylori is associated with a higher rate of liver disease in patients with alpha1-antitrypsin deficiency has not been investigated so far. In summary, extensive studies both in preclinical models and in the clinic are needed to show whether H. pylori is indeed a modifier of the expressivity of liver disease in alpha1-antitrypsin deficiency.