key: cord-0730709-0fxcm536 authors: Cavaliere, Kimberly; Trindade, Arvind J. title: Response date: 2021-04-17 journal: Gastrointest Endosc DOI: 10.1016/j.gie.2021.01.015 sha: c379c71cb6aecd0f6808f49c4bdf290267e74458 doc_id: 730709 cord_uid: 0fxcm536 nan esophagitis, gastritis, gastroduodenitis, or Forrest's type III ulcers were mostly found. [1] [2] [3] Usually, these kinds of lesions do not require endoscopic hemostasis. 4 With regard to the interaction between SARS-CoV-2 and the digestive system, it is known that this virus can bind and affect the cells of the GI system through angiotensin converting enzyme 2 and transmembrane serine protease 2, which are expressed on the enterocyte membrane and can therefore generate organ damage through the establishment of a prothrombotic state. 5 Thus, the cause of GI bleeding can be related to both primary and secondary mechanisms. On one hand, direct injury of the GI mucosa due to viral infection generates active mucosal inflammation sustained by an associated systemic cytokine storm. On the other hand, indirect damage from tissue hypoxia, coagulopathy, and acute illness-related stress worsens the pathologic changes in the mucous membrane of the whole digestive system. 5, 6 This can explain the clinical finding of self-limited bleeding that does not need hemostasis during endoscopy. GI bleeding seems to be part of the COVID-19 presentation as it responds to systemic therapy (as other signs and symptoms), including anticoagulation therapy with low-molecular-weight heparin. In this report, multivariate analysis to determine potential predictors of upper and lower GI bleeding in COVID-19 patients confirmed that anticoagulants did not statistically increase this risk. 7 This "double-hit" damage explains the decreased need for urgent endoscopy in COVID-19 patients with GI bleeding; however, it remains a challenging topic because of the complexity of this multiorgan systemic disease and its related therapy. Many other risk factors (associated antiplatelet therapy, administration of steroids, history of GI bleeding) must be taken into consideration to tailor the endoscopic approach. All authors disclosed no financial relationships. Digestive We thank Dioscoridi et al 1 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 al 2 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 patients 3, 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 al 1 that a 2-hit mechanism is possible. However, the lack of complete endoscopic data from COVID-19 GI bleeders, Use of the ACES (Appearance, Classification, Enhanced endoscopy, and Safe resection) algorithm for the recognition and management of malignant polypsda letter in response to the Multi-Society Task Force on Colorectal Cancer recommendations To the Editor: We sincerely appreciate the efforts of the Multi-Society Task Force (MSTF) on Colorectal Cancer to provide rec-ommendations on the recognition and management of malignant colorectal polyps. [1] [2] [3] Upon reviewing the recommendations we came across certain inconsistencies that may have far-reaching clinical implications for patients, endoscopists, pathologists, journal readers, funding agencies, and the general public. 4 The inconsistencies are in the presented methods, terminology, algorithms, and pathologic results. Contrary to their described grading methods, the MSTF recommendsdin statements 2b, 3, and 5dafter having classified the strength of such recommendations as "weak." These imprecisions may cause confusion. The MSTF suggests that "endoscopists discuss appropriate terminology with their pathologists and pathologists to avoid using the terms "carcinoma" or "cancer:" in describing tumor in situ. In contrast to the American Cancer Society description, 5 the World Health Organization description, 6 and the Vienna classification, 7 the MSTF describes high-grade dysplasia as "dysplastic changes confined to the epithelium, lamina propria, or muscularis mucosa." Tumor in situ describes cancer invasion into the lamina propria through the muscularis mucosa with no extension into the submucosa. We would like a clarification of how carcinoma in the lamina propria should be described, given that adenoma or high-grade dysplasia cannot be in the lamina propria. We are concerned that such nonstandard terms will lead to confusion and hamper a universal exchange of data. MSTF's Figure 8 depicts malignant polyps rather than adenomas. We also wonder whether the nonstandard design of the algorithm describing the evaluation of polyps might lead to confusion (MSTF Fig. 9 ). This algorithm suggests that the Narrow-Band Imaging (NBI) International Classification Endoscopy (NICE) is useful in differentiating granular from nongranular lesions, but it is not. 8, 9 Furthermore, the MSTF recommendations begin with a statement regarding image enhancement; we wonder whether it gives an incorrect impression that malignant polyp evaluation begins with image-enhanced endoscopy. To provide clarification, we offer the following description (see Fig. 1 ): Endoscopists' evaluation of the likelihood of malignancy is based on the general appearance, size, morphology, and close-up evaluation of the surface of the lesion. 10 Its general appearance, such as fold convergence, Management of upper GI bleeding in patients with COVID-19 pneumonia Upper gastrointestinal bleeding in COVID-19 inpatients: incidence and management in a multicenter experience from northern Italy Peptic ulcer disease as a common cause of bleeding in patients with coronavirus disease 2019 The role of endoscopy in the management of patients with peptic ulcer disease Severe colon ischemia in patients with severe coronavirus-19 (COVID-19) Covid-19, coronavirus, SARS-CoV-2 and the small bowel Gastrointestinal bleeding in patients with coronavirus disease 2019: a matched case-control study A "double-hit" damage mechanism can explain self-limited GI bleeding in COVID-19 pneumonia Management of upper GI bleeding in patients with COVID-19 pneumonia Gastrointestinal bleeding in patients with coronavirus disease 2019: a matched case-control study Upper gastrointestinal bleeding in COVID-19 inpatients: incidence and management in a multicenter experience from Northern Italy Gastrointestinal bleeding in hospitalized COVID-19 patients: a propensity score matched cohort study SARS-CoV-2 gastrointestinal infection causing hemorrhagic colitis Association of treatment dose anticoagulation with in-hospital survival among hospitalized patients with COVID-19 Anticoagulation, bleeding, mortality, and pathology in hospitalized patients with COVID-19