We thank Dioscoridi et al1 for their interest in our letter.2 In our letter, we presented a conservative approach to the management of GI bleeding in 6 patients with coronavirus disease 2019 (COVID-19) early in the pandemic. Dioscoridi et al2 discuss that GI bleeding in COVID-19 is self-limited because of a 2-hit mechanism.
To understand whether this mechanism is plausible, it is important to identify the causes of GI bleeding. Unfortunately, as the authors state, the majority of COVID-19 patients with GI bleeding do not undergo endoscopy and have self-limited bleeding.2, 3, 4 We recently expanded on our initial case series and described the risk factors and outcomes in 314 COVID-19 patients with GI bleeding during the pandemic.5 Of the 314 patients (point prevalence of 3%), only 6% underwent endoscopy. Of the patients who underwent endoscopy, 55% had gastroduodenal ulcers, and the rest had lesions such as esophagitis, gastritis, colitis. We found that anticoagulation was not a risk factor for GI bleeding, similarly as in the study by Martin et al.3
It is likely that COVID-19–induced coagulopathy does play a role in GI bleeding. This would explain the endoscopy findings of bleeding esophagitis, gastritis, duodenitis, and colitis seen in these patients.3, 4, 5, 6 It would also explain why the dosing of anticoagulants does not appear to increase the risk of GI bleeding in these patients3 , 5 and showed a mortality benefit in retrospective studies.7 , 8
In conclusion, the mechanism for GI bleeding in COVID-19 does appear complex. We agree with Dioscordi et al1 that a 2-hit mechanism is possible. However, the lack of complete endoscopic data from COVID-19 GI bleeders, and the retrospective nature of the data, limit our knowledge of the mechanism of bleeding and the potential therapeutic effect of anticoagulation therapy.
Disclosure
Dr Trindade is a consultant for Pentax Medical and the recipient of research support from Ninepoint Medical. The other author disclosed no financial relationships.
References
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