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    2020-08-05


    Lawlor et al. [18] used EGG to evaluate gastric function in eso-phageal cancer patients after neoadjuvant chemoradiotherapy and fol-lowing surgery. Chemoradiotherapy contributed to a significant in-crease in the abnormal gastric myoelectric activity, involving changes in tachygastria and a decrease in motility as measured by power ratio. In turn, a significant increase in bradygastria, which persisted at 6 months but not at 12 months post-surgery, was documented [18]. Our series included 75% of patients subjected to chemotherapy, and prob-ably it was the systemic treatment which also contributed to the pro-found myoelectric abnormalities observed in this group. However, the performance status of all of them was good (0 or 1). Our patients were not treated with chemotherapy during the investigation. Hence, the results of our study are not direct effect of chemotherapy but indirect. The systemic treatment might contribute to the sympathetic over-activity and cardiovascular hemodynamic consequences thereof ob-served in our series. Both, cancer itself and anticancer surgery, may result in acute or chronic Tadalafil of the colon or rectum. The impairment of autonomic control or direct damage to autonomic fibers may be additional pathophysiological mechanisms involved in carci-nogenesis [25,26,39]. However, our knowledge regarding the influence of chemotherapy on GI function is still limited.
    In our present study, colorectal and gastric cancer patients pre-sented with lower values of HRV indices: LF and HF parameters, and higher Tadalafil LF/HF ratio at rest than the controls. These findings point to disturbances of sympathetic-parasympathetic balance of the autonomic nervous system. The results of previous studies imply that cancer pa-tients show less fluctuations in vagal activity (as demonstrated by lower values of HRV indices), which can be attributed either to an increase in sympathetic activity or to a decrease in parasympathetic drive [23,40,41].
    The principal limitation of this study stems from the fact that the
    EGG recordings were not obtained at the same time as the measure-ments of gastric emptying. Moreover, GI motility was evaluated in-directly, on the basis of contractility index values determined during EGG. Finally, the pathomechanism of abnormal gastric myoelectric activity in colorectal cancer patients still remains unclear and needs further investigation. Both our findings and the results of previous studies imply that carcinogenesis may contribute to disturbances in gastric myoelectric activity due to inflammatory damage of the ENS. Dysfunction of the autonomic nervous system in cancer patients, especially disturbances of the sympathy-vagal balance, can cause effect in cardiovascular system regulation, due to hemodynamic disturbances. Lesser responsiveness to sympathetic and parasympathetic modulation points to autonomic dysfunction as a potential common pathophysiological mechanism of gastric dysmotility in cancer patients.
    5. Conclusions
    Colorectal and gastric cancers affect gastric myoelectric activity, decreasing normogastria and slow wave coupling. Moreover, GI cancer patients do not show adequate gastric motility response to food. Cancer
    - induced autonomic disturbances may contribute to impaired gastric electric motility.
    Conflict of interest
    The authors declare no conflict of interest.
    Financial disclosure
    The study was supported from the grant no. K/ZDS/004569 (spe-cific subsidy from the Polish Ministry of Science and Higher Education for holding the research capacity).
    Acknowledgement
    We express our gratitude to patients who participated in this trial.
    The author contribution
    Study Design: Aneta Zygulska, Agata Furgała, Krzysztof Krzemieniecki, Piotr Thor
    Data Collection: Aneta Zygulska, Beata Włodarczyk
    Statistical Analysis: Agata Furgała
    Data Interpretation: Agata Furgała, Aneta Zygulska
    Manuscript Preparation: Aneta Zygulska, Agata Furgała Literature Search:Aneta Zygulska, Agata Furgała Funds Collection: Krzysztof Krzemieniecki
    Appendix A. Supplementary data
    References
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