Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a viral respiratory illness initially described in Wuhan, China, and was declared a pandemic by World Health Organization (WHO) in 2020, and the disease is named coronavirus disease (COVID-19). SARS-CoV2 is known to cause fever, cough, fatigue, and acute respiratory distress syndrome. As more patients become infected, extrapulmonary manifestations came to rise and hypercoagulability is one among those. COVID-19 could predispose patients to both venous and arterial thromboembolic events which are commonly treated with unfractionated heparin or low molecular weight heparin (LMWH). The treatment of patients who develop heparin-induced thrombocytopenia (HIT) while being treated with heparin or LMWH for COVID-induced thromboembolic complications is challenging. We describe a patient admitted to the hospital with COVID-19 pneumonia, found to have a cerebrovascular event treated with unfractionated heparin. She also received therapeutic LMWH for anticoagulation on day 1 of presentation due to atrial fibrillation. She was diagnosed with HIT and was found to have a pulmonary embolism, aortic arch mural thrombus, and arterial thrombi in the lower extremities. As more recent studies showed HIT antibodies in COVID-19 patients who are naive for heparin-based products, COVID-19 may be an independent risk factor for the development of HIT. The role of COVID-19 in the development of HIT is uncertain. High vigilance is required to diagnose and initiate treatment for HIT early in the disease course as it can be life-threatening.

Background Patients with liver cirrhosis have altered hepatic synthetic functions which theoretically result in reduced levels of pro-and anti-coagulant factors as well as thrombocytopenia. Initially, cirrhotic patients were thought to be at an increased risk of bleeding and a reduced risk of thrombosis. Several studies have recently reported an increased occurrence of venous thromboembolism (VTE) in cirrhotic patients. In this study, we aimed to assess the current practice of deep venous thrombosis (DVT) prophylaxis, the incidence and predictors of VTE, and the associated bleeding sequelae in patients with liver cirrhosis. Methods A retrospective cohort study was performed. We included all adult patients with a diagnosis of liver cirrhosis from January 2010 to June 2019 admitted to the hospital. Our cohort patients were divided into two groups, cirrhotic patients with pharmacological VTE prophylaxis and those with mechanical or no VTE prophylaxis. Results We included 601 cirrhotic patients in our study. The incidence of VTE occurring within the first 6 months of their admission was 1.5%. Seven patients (1.49%) developed VTE with the majority being DVTs while not on pharmacologic prophylaxis, and two patients developed VTE despite being on pharmacologic prophylaxis; however, there was no statistical difference. Alcohol use was the most common underlying cause of liver cirrhosis (40.4%), followed by chronic hepatitis C (21.1%), and nonalcoholic steatohepatitis (11.3%). Out of the 601 patients included, 69 patients received neither pharmacologic nor mechanical VTE prophylactic agent (11.48%), while the remaining majority received either pharmacological or mechanical prophylaxis (88.52%). Conclusions Our study did not show a statistically significant association between the use of pharmacological VTE prophylactic agents and a reduction in the risk of VTE in cirrhotic patients. The rates of usage of DVT prophylactic agents among our Northwell hospitals during the study period appeared to be no longer suboptimal when compared to prior studies. Low albumin appears to be a predictor factor to develop VTE. There was a statistically significant increase in bleeding risk and transfusion requirement in cirrhotic patients receiving no pharmacological VTE prophylactic agents. Further prospective trials are needed to shed more light on this subject and identify the group of cirrhotic patients who could safely benefit from pharmacologic VTE prophylaxis.

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Emerging data have suggested that circulating tumor DNA (ctDNA) can be a reliable biomarker for minimal residual disease (MRD) in CRC patients. Recent studies have shown that the ability to detect MRD using ctDNA assay after curative-intent surgery will change how to assess the recurrence risk and patient selection for adjuvant chemotherapy. We performed a meta-analysis of post-operative ctDNA in stage I–IV (oligometastatic) CRC patients after curative-intent resection. We included 23 studies representing 3568 patients with evaluable ctDNA in CRC patient post-curative-intent surgery. Data were extracted from each study to perform a meta-analysis using RevMan 5.4. software. Subsequent subgroup analysis was performed for stages I–III and oligometastatic stage IV CRC patients. Results showed that the pooled hazard ratio (HR) for recurrence-free survival (RFS) in post-surgical ctDNA-positive versus -negative patients in all stages was 7.27 (95% CI 5.49–9.62), p < 0.00001. Subgroup analysis revealed pooled HRs of 8.14 (95% CI 5.60–11.82) and 4.83 (95% CI 3.64–6.39) for stages I–III and IV CRC, respectively. The pooled HR for RFS in post-adjuvant chemotherapy ctDNA-positive versus -negative patients in all stages was 10.59 (95% CI 5.59–20.06), p < 0.00001. Circulating tumor DNA (ctDNA) analysis has revolutionized non-invasive cancer diagnostics and monitoring, with two primary forms of analysis emerging: tumor-informed techniques and tumor-agnostic or tumor-naive techniques. Tumor-informed methods involve the initial identification of somatic mutations in tumor tissue, followed by the targeted sequencing of plasma DNA using a personalized assay. In contrast, the tumor-agnostic approach performs ctDNA analysis without prior knowledge of the patient’s tumor tissue molecular profile. This review highlights the distinctive features and implications of each approach. Tumor-informed techniques enable the precise monitoring of known tumor-specific mutations, leveraging the sensitivity and specificity of ctDNA detection. Conversely, the tumor-agnostic approach allows for a broader genetic and epigenetic analysis, potentially revealing novel alterations and enhancing our understanding of tumor heterogeneity. Both approaches have significant implications for personalized medicine and improved patient outcomes in the field of oncology. The subgroup analysis based on the ctDNA method showed pooled HRs of 8.66 (95% CI 6.38–11.75) and 3.76 (95% CI 2.58–5.48) for tumor-informed and tumor-agnostic, respectively. Our analysis emphasizes that post-operative ctDNA is a strong prognostic marker of RFS. Based on our results, ctDNA can be a significant and independent predictor of RFS. This real-time assessment of treatment benefits using ctDNA can be used as a surrogate endpoint for the development of novel drugs in the adjuvant setting.

4091 Background: The relationship between Helicobacter pylori (H.pylori) and hepatocellular carcinoma (HCC) was first proposed in 1994. Since then, several studies have been performed to explore the association. The role of Hepatitis C (HCV) viruses coexisting with H.pylori in causing HCC was also studied. With the emergence of data in this regard, a causal relationship has been postulated, but not confirmed, and hence the relationship remains controversial. Our meta-analysis aims to summarize the research on this topic and investigate if there exists a relationship between H. pylori infection and the development of HCC and if the presence of HCV along with H.pylori plays a role in liver carcinogenesis. Methods: Following PRISMA guidelines, we performed a systematic review of all relevant studies published in the literature using keywords “Helicobacter pylori” and “Hepatocellular carcinoma” on major literature databases, including PubMed, EMBASE, Web of Science, and Cochrane controlled trials register. A total of 656 studies were identified between 1994 to March 2020, out of which 26 studies qualified under our selection criteria. Patients positive for HCC are included as cases and patients that did not have HCC under control group. In both groups, H.pylori positive patients and their HCV status, was identified. Results: Out of the 26 studies included in the final analysis, the prevalence of H. pylori infection was 64.78% (561 of 866) amongst HCC cases and 47.92% (1718 of 3585) in the non-HCC control group. The summary odds ratio for the association of H. pylori infection with the risk for HCC using the random-effects model was determined to be 4.75 (95% CI, 3.06-7.37), I²=63%. Subgroup analysis to determine the odds of developing HCC in the presence of H.pylori and HCV coinfection, was 13.97 (95% CI, 3.94-49.61), I²=81%. Whereas, the odds of developing HCC in the presence of only HCV without H.pylori was found to be 2.21 (0.70-6.94), I²=79. Subgroup analysis by study design showed no significant difference between the study groups (P= 0.5705). Conclusions: Our meta-analysis showed a positive association between H. pylori infection and the development of HCC. It showed a significantly higher risk of developing HCC in the presence of HCV infection along with H.pylori. Further prospective cohort studies are needed to prove the causal relationship, especially in cases of Hepatitis B, C coinfection, and cirrhotic patients.[Table: see text]

Acute respiratory distress syndrome is a sudden in onset, diffuse inflammatory form of lung injury which may be associated with a variety of etiologies such as pneumonia, sepsis, aspiration, and severe trauma. Prompt recognition and treatment of acute respiratory distress syndrome is critical to reduce the associated high mortality. Severe lung injury presenting as acute respiratory distress syndrome secondary to gadolinium contrast media (gadobutrol) is rarely reported. We describe an interesting case of a 47-year-old woman who presented to the emergency department with acute respiratory failure after gadolinium administration. She was diagnosed with acute respiratory distress syndrome, was admitted to the intensive care unit due to requiring mechanical ventilation. Her condition improved with epinephrine and steroids and she was successfully extubated and discharged from the hospital in one week.

We commonly see patients presenting with either portal hypertensive gastropathy (PHG) or radiation gastritis. Radiation-induced hemorrhagic gastritis is an unusual lethal complication postradiation. Patients with preexisting PHG have very friable mucosa that can easily bleed after radiation for cancer treatment. There is an increased risk of bleeding with both entities present together. Our aim is to focus on treatment and possible prevention of gastrointestinal bleeding in patients with preexisting PHG undergoing radiation therapy for newly diagnosed cancer. Several therapies like prednisolone, argon plasma coagulation, laser coagulation have been proposed. There are no set guidelines for treatment. In these patients, if radiation therapy is indicated either for hepatic or gastrointestinal malignancy, it is suggested to premedicate with proton pump inhibitors or sucralfate. We describe a case of 73-year-old female who presented with upper gastrointestinal bleeding. She had liver cirrhosis secondary to nonalcoholic fatty liver disease and diagnosed with pancreatic cancer, for which she received chemoradiation. She was found to have both radiation gastritis and PHG with diffuse erythematous, edematous, congested mucosa with diffuse oozing blood in the antrum making it very challenging to treat.

Paraneoplastic neurological syndromes (PNS) are a group of rare immune-mediated disorders with neurological sequela in cancer patients. It usually occurs when an immune response against a systemic tumor is incorrectly directed to the nervous system. Compared to other reported manifestations of PNS in breast cancer, Guillain Barre syndrome (GBS) is exceedingly rare. There is only one other reported case in the literature of GBS that was diagnosed in a breast cancer patient. We report the second recorded case of a 61-year-old female with a history of early-stage breast cancer, who presented with symptoms of lower extremity weakness initially suspected to be GBS but later found to have been recurrent breast cancer. No specific guidelines are available for the treatment of PNS. Treatment of underlying malignancy with chemotherapy and immunotherapies are usually recommended.