Objectives: Pancreatic cancer and prediabetes pose significant public health challenges. Given the lack of strong evidence we performed a meta-analysis to assess the risk of pancreatic cancer in prediabetes. Materials and Methods: We performed a thorough search of the major databases over the last 10 years to identify relevant articles. The pooled odds ratio (OR) and hazard ratio (HR) were combined to calculate the effect size (ES). Results: We analyzed 5 studies including 5,425,111 prediabetic individuals and 16,096,467 normoglycemic population across 5 countries with a median follow-up of 8.5 years. We identified a noteworthy association between prediabetes and pancreatic cancer, reporting an unadjusted ES of 1.36 (95% confidence interval [CI] 1.05-1.77, P = 0.02) and an adjusted ES of 1.40 (1.23-1.59, P < 0.01). Subgroup analyses by age revealed variations in risk, with studies involving participants aged 60 and above exhibiting a higher ES (ES 1.83, 95% CI 1.28-2.62, P < 0.01). Geographical differences were also observed, with Japanese studies reporting a higher risk (ES 1.89, 95% CI 1.15-3.10, P < 0.01) compared with those from the United States (ES 1.32, 95% CI 1.13-1.53, P < 0.01). Conclusions: We identified 40% higher risk of pancreatic cancer in patients with prediabetes than those with normal blood glucose necessitating urgent attention for further research and policy change.

BACKGROUND AND AIMS:Prediabetes is often underdiagnosed and underreported due to its asymptomatic state in over 80% of individuals. Considering its role in promoting cancer incidence and limited evidence linking prediabetes and colorectal cancer (CRC), we conducted a systematic review and meta-analysis to evaluate the incidence of colorectal cancer in people with prediabetes. METHODS:A comprehensive search through PubMed/Medline, Embase, Scopus, and Google Scholar was performed until June 1, 2022, to screen for studies reporting CRC incidence/risk in prediabetics. Binary random-effects models were used to perform meta-analysis and subgroup analyses. Sensitivity analysis was done using leave-one-out method. The quality of the studies was assessed by the Newcastle Ottawa Scale for observational studies. RESULTS:Seven prospective and one retrospective study comprising 15 cohorts and a pooled number of 854,876 cases and 219,0511 controls were included in the analysis (2 Japan, 2 Korea, 1 Sweden, 1 UK, 1 China, and 1 USA). After combining all the studies, the forest plots for adjusted analysis shows a statistically significant increase in odds of having CRC with prediabetes (OR=1.16; 1.08-1.25, p< 0.01; I2=56.06%) and unadjusted analysis also shows a statistically significant increase in odds of having CRC with prediabetes (OR=1.62; 1.35-1.95, p< 0.01; I2=85.72% ). Sensitivity analysis using the Leave-one-out method did confirm equivalent results. Subgroup analysis based on type of study, the odds of developing CRC was higher in prospective studies (OR=1.175; 1.065-1.298) (p=0.001) than retrospective studies (OR=1.162; 1.033- 1.306) (p=0.012). The odds of developing CRC were not significantly higher in ages >60 (OR=1.446; 0.887-2.356) (p=0.139) compared to less than 60 years. The strongest association b/w prediabetes and CRC was found on a median 5-10 years (aOR=1.257; 1.029-1.534) (p=0.025) follow-up compared to < 5 years and 10 years and higher. CONCLUSIONS:This study showed that the odds of developing CRC is 16% higher in patients with prediabetes than those with normal blood glucose. Lifestyle modifications such as weight loss, proper diet, and exercise are essential to control prediabetes. This study further warrants a specific prediabetes screening for patients already at high risk of colorectal cancer with other risk factors.

Introduction: Portal vein thrombosis (PVT) is a narrowing or blockage of the portal vein by a blood clot. Thrombosis can develop in the main body of the portal vein or its intrahepatic branches and may even extend to the splenic or superior mesenteric veins (SMV). PVT frequently occurs with cirrhosis of the liver. Dehydration is a known independent risk factor for the development of thrombosis; however there is insufficient evidence to form a strong association. In this case we present a case of 48 year old man who presented with portal vein superior mesentric vein and splenic vein thrombosis with dehydration as the only risk factor. Case Description/Methods: A 48-year-old healthy man, who presented complaining of abdominal pain for the past 6 days, described as dull epigastric pain, 10/10 that radiates to his back. He reports that he recently immigrated from Brazil to USA and underwent a strenuous journey which involved walking across Mexico for 40 days where he had limited access to water and food. On examination there was no tenderness on palpation, and abdominal sounds were normal. On laboratory workup amylase, lipase, LFTs, alkaline phosphatase, were normal. Since the exam and laboratory workup does not explain why he would have 10/10 pain, a CT angiogram of the abdomen was ordered, which showed: Hyperdense acute thrombotic occlusion of the portal vein, superior mesenteric vein and splenic vein. Hypercoagubality workup was done: PT, PTT, INR normal. Factor S and C activity normal. Flow cytometry for PNH was normal. Factor II gene mutation not detected. Antithrombin III normal. Factor 5 leiden not detected. ANA, anticardiolipin, beta 2 microglobulin, and lupus anticoagulant negative. CEA, CA19-9, and AFP normal. Since all his workup was negative, this massive thrombosis was attributed to dehydration in the extreme circumstances he went through, and he was started bridged to warfarin. Discussion: In adult and pediatric cerebral thrombosis due to dehydration has been reported. However, there is no published case report that the authors are aware of that presents the findings of a portal vein thrombosis provoked by dehydration in a young, healthy adult, in which dehydration was suggested as a possible cause.

Introduction: Kaposi sarcoma (KS) is a vascular tumor linked to human herpesvirus 8 (HHV-8). It has 4 commonly identified types associated with HHV-8. We present a case report of a patient with AIDS-related or epidemic KS, which can vary from an incidental finding to a rapidly progressing neoplasm. While it usually manifests as a skin disease, untreated KS can spread to other organs. In rare instances, lower gastrointestinal KS may be found without cutaneous involvement. Case Description/Methods: A 29-year-old man with HIV and inconsistent antiretroviral therapy presented to the ED with severe abdominal pain, nausea, vomiting, and bloody diarrhea. The patient had a prior diagnosis and treatment for a perirectal abscess, along with multiple hospital admissions for a few months preceding the current presentation. Physical examination revealed a large perianal mass. CT scan showed suspicious neoplasm and enlarged pelvic and inguinal lymph nodes (Figure 1). Surgical excision with biopsy confirmed Anaplastic histological variant of Kaposi sarcoma positive for HHV-8. Immunohistochemistry results were positive for HHV-8 LNA-1 antibody, as well as the lymphatic endothelial cell markers CD34, factor VIII, and PECAM-1 (Table 1). Treatment included initiating HAART and outpatient follow-up, but the patient was lost to follow-up. Upon readmission, CT revealed proctitis and metastatic disease with enlarged lymph nodes. Efforts were made to ensure HAART adherence and treatment with liposomal doxorubicin (6 cycles). Discussion: KS lesions that develop outside of the skin often exhibit histological differences compared to those on the skin. The anaplastic variant of KS is particularly aggressive locally, with a higher likelihood of deeper invasion and metastasis. Histologically, it displays variable morphological characteristics, including increased nuclear and cellular pleomorphism and a higher mitotic index. Failing to correctly identify such lesions as KS can result in delayed diagnosis or inappropriate management.Figure 1.: A : CT abdomen and pelvis at the time of presentation showing the evidence of 6.4x4.8cm perianal soft tissue mass. B: Follow-up CT abdomen and pelvis showing notable evidence of Proctitis with multiple enlarged pelvis and bilateral inguinal lymph nodes,likely secondary to metastatic disease. Table 1. - WBC count 8000 cells/cmm Hemoglobin 8.6 g/dl MCV 91.9 fL/cell Serum Albumin 1.7 g/dL % CD4 cells count 15.5 Absolute CD4 Cells Count 326 /uL % CD8 Cells Count 77.6 Absolute CD8 cells count 1630 /uL %CD3 cells Count 93.9 Absolute CD3 count 1972 /uL T-lymphocyte CD4/CD8 Ratio 0.20

Introduction: Sump syndrome is a rarely seen complication of choledochoduodenostomy (CDD) in the era of Endoscopic retrograde cholangiopancreatography (ERCP). We present a case of recurrent cholangitis post-CDD. Case Description/Methods: A 78 y/o. female with a PMH of CDD, cholangitis status post-ERCP with CBD stent placement presented to the ER with lethargy, decreased oral intake, and vague non-radiating epigastric pain for 1 week. The patient couldn’t provide past medical and surgical records. She was hypotensive on arrival, with blood pressure at 84/61 mm Hg and a temperature of 101.8F. CT scan of the abdomen and pelvis without contrast showed post-cholecystectomy changes, mild non-specific stranding, and edema in the periportal region. AST, ALT, and ALP are 56, 46, and 362, respectively. The patient was admitted to ICU for septic shock secondary to possible cholangitis and/or choledocholithiasis and started on empiric IV antibiotics. ERCP was performed due to concern for acute cholangitis. Evidence of prior cholecystectomy was seen in the lower third of the main bile duct. The biliary tree was swept with a 12 mm balloon starting at the bifurcation. Pus and debris were swept from the duct appeared to be secondary to sump syndrome. One Fr by 7 cm plastic stent was placed into the common bile duct. The flow of pus through the stent was noted. She was followed up after 6 weeks of outpatient for ERCP and stent removal (Figure 1A, 1B). Discussion: Sump syndrome is a rare long-term complication of CDD, a common surgical procedure before the advent of ERCP. It is caused by the buildup of lithogenic bile, debris, and duodenal contents in the distal common biliary duct (CBD), which causes biliary cholangitis and pancreatic complications. The bile no longer drains through the distal CBD in this setting. As a result, the CBD distal to the anastomosis transforms into a poorly drained reservoir, making this sump prone to debris accumulation. Indigestion, abdominal pain, nausea, vomiting, postprandial discomfort, and jaundice are presenting symptoms. Diagnostic findings on imaging include debris/stones in the CBD, with the possibility of pancreatitis, cholangitis, or a liver abscess. To confirm the diagnosis of sump syndrome, an ERCP or percutaneous transhepatic cholangiography (PTC) is required. Management includes the drainage of debris endoscopically. In refractory cases, surgical treatment includes CDD revision to a Roux-en-Y hepaticojejunostomy. Sump syndrome is less common as ERCP replaces CDD.Figure 1.: A) Endoscopic retrograde cholangiopancreatography and B) Computed tomography abdomen showing dilated biliary tree.

North Shore University Hospital, USA; Jacobi Medical Center, USA; Marshall University, USA; Rosalind Franklin University of Medicine and Science, USA; Khyber Girls Medical College, Pakistan; Dow University of Health Sciences, Pakistan; New York Medical college - Saint Michaels Medical Center, USA; Rutgers New Jersey Medical School, USA; Ziauddin University, Pakistan; University of Illinois System, USA; Hackensack Meridian Jersey Shore University Medical Center, USA; Khyber Medical University, Pakistan.

Introduction: Although a respiratory virus, COVID-19 can affect multiple organ systems, including hepatobiliary and gastrointestinal systems. Acute pancreatitis is commonly reported, with symptoms resolving in a few days. We report a case of acute necrotizing hemorrhagic pancreatitis caused by COVID-19 infection. Case Description/Methods: A 65-year-old male with no past medical history presented with abdominal pain, generalized weakness, and syncope. On arrival, the patient was tachycardic with a blood pressure of 67/48 mm Hg. SARS antigen was positive for COVID-19. Hemoglobin on admission was 11.6 and lipase of 80. CT abdomen and pelvis with contrast showed acute pancreatitis with necrosis and retroperitoneal hemorrhage was suspected. CT angiography of the abdomen and pelvis showed active bleeding around the head of the pancreas. He has no history of alcohol or medication use, and no evidence of gallstones or hypertriglyceridemia. He was admitted to ICU for vasopressor support and broad-spectrum antibiotics were started. Repeat labs showed hemoglobin drop by more than 4 grams/dl. A massive transfusion protocol was initiated, and the patient received 6 units of packed red blood cells and 3-units of fresh frozen plasma (FFP). While undergoing transfusion, the patient had a cardiac arrest. After resuscitation, he underwent mesenteric angiography with embolization of multiple bleeding vessels. His prognosis was very and eventually succumbed (Figure 1). Discussion: SARS CoV-2 affects vital organs in addition to the lung, including the heart, gastrointestinal tract, hepatobiliary tract, and kidney. Most common gastrointestinal presentations include nausea and vomiting, diarrhea, abdominal pain, liver enzyme abnormalities, and pancreatic injury. The common causes of acute pancreatitis include gallstones and alcohol but rarely viral etiology. COVID-19-induced pancreatic injury is caused by the virus's direct cytotoxic effect and a dysregulated immune response. Because pancreatic cells express more ACE2 receptors, they are prime targets for dysregulated immune responses and subsequent pancreatitis. COVID-19 infection complicated by acute necrotizing hemorrhagic pancreatitis is uncommon, with high morbidity and mortality, and there have been fewer than 5 cases reported. Treatment is mostly focused on surgical intervention, including debridement and necrosectomy in selected patients, besides fluids and empiric antibiotics. Surgery might not be feasible in hemodynamically unstable patients.Figure 1.: Panel 1: Computed tomography axial Angiogram of the abdomen at the pancreatic head reveals peri-pancreatic inflammatory changes (red arrow), consistent with underlying acute pancreatitis. There is evidence of acute contrast extravasation at the pancreas's head/uncinate process (blue arrow), which is consistent with hemorrhagic pancreatitis. Panel 2: Angiogram of the anterior-superior pancreatico-duodenal artery demonstrates area of active contrast extravasation (blue arrow) from the terminal branches. Note the tip pf micro-catheter is in the anterior-superior pancreaticoduodenal artery (red arrow), while the parent catheter tip is in the celiac artery (yellow arrow) Panel 3: Celiac artery angiogram with the microcatheter tip om the Gastro-duodenal artery (yellow arrow) post coil embolization (orange arrows) of the superior-anterior pancreatico-duodenal artery shows interval cessation of previously noted active contrast extravasation. Panel 4: Angiogram of the inferior-pancreatico-duodenal artery demonstrates evidence of active contrast extravasation from terminal branches (blue arrow). Note the tip of the parent catheter is in the superior mesenteric artery (yellow arrow) Panel 5: Superior Mesenteric Artery (SMA- yellow arrow) angiogram post embolization of the inferior-pancreatico-duodenal artery with multiple vascular coils (orange arrows) demonstrated interval cessation of previously noted active contrast extravasation. Panel 6: Pathophysiology of acute pancreatitis in COVID-19.

Introduction: Anemia in alcoholics is often multifactorial. Zieve’s syndrome (ZS) is a triad of jaundice, hemolytic anemia, and hyperlipidemia that develops secondary to alcohol use disorder (AUD). Anemia is very common in alcoholics, and it is often multifactorial. Here we are reporting a case of ZS causing persistent hemolytic anemia and hyperbilirubinemia in alcoholic patient. Case Description/Methods: 47-year-old F prior medical history hypertension, fibroids, AUD was sent to the ED for evaluation of low Hb 6.4 (MCV 90). Last menstrual period was normal one month ago. Denied any melena or hematochezia. Recent EGD showed grade D esophagitis and colonoscopy done 1 month ago showed internal hemorrhoids. She used to drink 3 to 4 beers daily since age of 18 and quit 2 weeks ago. She was admitted 3 times in last 8 months for anemia. Afebrile and hemodynamically stable with no evidence of overt bleeding. Anemia workup done during this and previous admission consistent with nonimmune hemolytic anemia. Labs showed haptoglobin < 31 mg/dl, LDH 440, negative coombs test, total bilirubin 8.6 mg/dl (direct bili 2.2), AST/ALT 43/11 with ALP/GGT WNL, PT/INR 22/1.92, ferritin 862, low TIBC, iron sat 43.1, folic acid/vit B12 WNL, platelets were 108, albumin 2.6. APRI and fib 4 score consistent with advanced fibrosis secondary to AUD. Lipid panel unremarkable except total cholesterol 251. Adam TS13 activity, G6PD (Quant), lupus anticoagulant, autoimmune panel, antimitochondrial antibody, hepatitis panel, HIV were negative. Peripheral blood smear showed anisocytosis with some burr cells. US abdomen showed echogenic liver with hepatofugal venous flow and no biliary dilatation. In view of non-immune hemolytic anemia, jaundice in a patient with alcoholic liver disease with negative above-mentioned workup, diagnosis of Zieve's syndrome was made. She was transfused with 2 units of PRBC during this admission and was counseled regarding importance of alcohol abstinence in treating the anemia due to Zieve's syndrome. She was discharged with outpatient follow-up. Discussion: Treatment of ZS includes supportive management with blood transfusion and abstinence from alcohol. Even though ZS is rarely reported, it should be suspected in patients with worsening hemolytic anemia with no apparent explanation, especially in alcoholics. Being aware of ZS can limit workup, cost and help avoid using unnecessary drugs that can worsen the condition.

Introduction: Liver abscess caused by Klebsiella pneumoniae (KLA) is a potentially life threatening infection characterised by the formation of pus-filled cavities in the liver. Risk factors include bacterial virulence factors, host susceptibility and anatomical factors. In recent years, the incidence has increased globally. We are presenting a case of a 56-year old South American Hispanic woman with a history of cholecystectomy admitted to the hospital for KLA without geographical risk factors. Case Description/Methods: A 56-year-old South American woman with no past medical history other than cholecystectomy 18 years prior presented to the emergency department with right upper quadrant pain and vomiting for 1 week duration. Her symptoms began after swimming and eating at a waterpark, however no other family members were affected. She denies recent travel outside of the state, exposure to animals or pets. Vital signs revealed tachycardia and borderline low blood pressure. Physical exam revealed tenderness in the epigastric and RUQ and negative Murphy’s sign. Labs were AST 44, ALT 62, Alk-phos 262, T-bili of 1.0, no leukocytosis. CT abdomen showed hypotenuse irregular 5.5 cm mass in the II and IV segment of the liver (Figure 1). On day 3 of admission, she developed a fever of 101 F. Septic workup was positive for gram negative rods (Klebsiella pneumoniae) in the blood, elevated procalcitonin and CRP. She was started on meropenem, later de-escalated to ceftriaxone. Fevers continued and a WBC scan was performed positive for liver abscess. Interventional radiology placed a percutaneous drain removing 50 cc of pus like fluid. Cultures of the fluid grew up Klebsiella pneumoniae. Drain was removed 4 days later after imaging revealed a decrease in the collection. She was discharged home on oral ciprofloxacin. Discussion: KLA has been widely reported in Asian populations and countries. We are presenting a rare occurrence in a patient with no comorbidities or travel history to Asia. KLA is caused by hyper mucoid strains of K1, K2 serotypes. Presenting factors include fever, chills and abdominal pain and 10%-16% of cases have metastatic spread of infection resulting in significant ICU morbidity and mortality. Clinical suspicion with prompt recognition and treatment are vital in preventing complications.Figure 1.: CT scan of the abdomen with IV contrast reveal a hypodense mass in the live.

Introduction: Metastatic colon cancer of the umbilicus is an uncommon phenomenon. An estimated 1%-3% of abdominopelvic malignancies have been shown to metastasize to the umbilicus. These metastatic umbilical nodules, also known as Sister Mary Joseph’s nodules, can vary in size, cause pain, and may discharge fluid. Although these nodules are rare, they are an important finding on physical exam as they are a sign of malignancy with metastasis. Herein, we are presenting a case of a 46-year-old man with metastatic colon cancer presenting with an ulcerated umbilical nodule, which was later diagnosed as Sister Mary Joseph’s nodule. Case Description/Methods: 46-year-old man with a past medical history of colon cancer with metastasis to the liver status post transverse colectomy and transverse colostomy, thrombosis of the right and left brachiocephalic arteries and thrombosis of the proximal superior vena cava presents to the clinic for evaluation complaining of a protruding umbilical mass of 2 months duration. The umbilical mass is ulcerated with some drainage at the site. He never had any preventative screening workup, including a colonoscopy. On physical exam, the patient was a healthy-appearing man. No signs of scleral icterus or jaundice. He had a soft, non-tender pendulous abdomen with a protuberant well defined, soft, non-tender, verrucous mass of 2 cm tethered to the umbilicus. Palpation did not elicit tenderness or bleeding. The patient was admitted to the hospital for further evaluation. The umbilicus was prepped with chloroprep and local anesthetic of 1% lidocaine was injected. The patient underwent a biopsy of the umbilicus. Histopathology showed adenocarcinoma likely metastasized from the colon. Discussion: Sister Mary Joseph nodule represents metastasis to Umbilical skin from visceral malignancy. The approach to the diagnosis demands thorough knowledge of underlying causes. The causes are not limited to GI, renal and GYN malignancies but also benign causes like endometriosis are possible. Thorough physical examination, basic blood tests, and imaging guide in diagnosis the primary tumor in case of metastasis. Biopsy and histochemical staining are invaluable tools in diagnosis majority of the cases. Endoscopy, colonoscopy, and PET scan are warranted for complete evaluation. Management depends on the nature of the underlying cause which includes resection, chemotherapy and radiation. Medical therapy alone may be sufficient in case of benign causes (Figure 1).Figure 1.: A. Sister Mary Joseph nodule. B, C. HPE showing adenocarcinoma.

Conclusion: Hospitalized patients with IBD had an increased rate of psychiatric comorbidities, which was associated with signi fi cantly increased LOS, but not total cost of hospitalization. Our results demonstrated a modest impactonLOS in patients withanxiety, depressionor bipolar disorder and a moresigni fi cant impactin patients withpsychosis, schizophrenia,delusion or personality disorder. Thelack of an e ff ect on overall cost of hospitalization is unexpected, though may suggest that patients with IBD and a comorbid psychiatric condition receive fewer costly treatment elements. This study emphasizes the importance of identifying and addressing psychiatric comorbidities in patients with IBD to decrease overall LOS, and highlights the need for further studies exploring inpatient procedures and treatments received within this population.

Introduction: Isolated myeloid sarcomas (MS) are proliferation of myeloblasts at extramedullary sites without any bone marrow involvement. These tumors are extremely rare and pose a diagnostic and therapeutic challenge. Case Description/Methods: A 68-year man with history of coronary artery disease and stent placement, diabetes mellitus, hypertension, gastroesophageal reflux disease and smoking presented with hematemesis and melena since 3 weeks. Patient was admitted for acute blood loss anemia due to upper gastrointestinal bleed. The hemoglobin dropped from 8.3 g/dl to 7.1 g/dl in 24 hours. Patient was transfused. He underwent endoscopy which revealed multiple large nodules in gastric body, fundus, and antrum with volcano-like with ulceration, which were biopsied (Figure 1). This endoscopic appearance was concerning for metastatic disease/ lymphoma. Patient’s biopsy of gastric nodules revealed poorly differentiated malignancy with immunotypic features suggestive of transitional cell carcinoma with neuroendocrine features. The oncologist requested a second surgical pathology consultation. Haematoxylin and eosin staining revealed diffuse infiltration and expansion of poorly differentiated atypical cells. Immunohistochemical staining was positive for lysozyme stain throughout lamina propria going in favor of granulocyte tumor of myeloid origin. The tumor cells were negative for CD20, CD79a, CD3, CK20, CD30 and myeloperoxidase (MPO). These findings were diagnostic for hematopoietic neoplasm, consistent with myeloid sarcoma of monocytic lineage. Discussion: Our patient presented with signs and symptoms of upper gastrointestinal bleed which necessitated further evaluation leading to the diagnosis of this rare neoplasm. In case report by Huang XL et al, the presentation was non-specific making the diagnosis difficult. In such cases immunohistochemical staining is helpful. Menasce et al described the immunotypic features of 26 cases of extramedullary MS that suggested that tumor markers like MPO and lysozyme indicate myeloid differentiation. Classically, MS expresses myeloid markers but they are not present in all cases. Our case was negative for MPO indicating poorly differentiated myeloid neoplasm which made the diagnosis challenging. The study also found that CD79a, CD20, CD3 and CD30 were negative in all cases, which is synonymous with our case.Figure 1.: Gastric endoscopy: Black arrows indicate multiple nodules in fundus and gastric body. The nodules seen were volcano-like with ulceration.

Introduction: According to the literature, Inflammatory Bowel Disease (IBD) patients with opioid dependency have a threefold higher mortality risk than non-users. Some studies suggest the role of cannabis usage in IBD due to its anti-inflammatory properties. However, no literature indicates the impact of cannabis usage on opioid-dependent IBD. Using a national propensity-matched sample, we assessed inpatient hospital outcomes of opioid-dependent IBD patients with Cannabis Use Disorder (CUD) vs non-CUD. Methods: The Nationwide Inpatient Sample database (2019) was queried to identify opioid-dependent IBD in CUD vs non-CUD cohorts. A Pearson Chi-square test and Mann-Whitney U tests were used to compare categorical and continuous variables between propensity-matched cohorts. In-hospital complications were the primary outcome; Length-Of-Stay and hospital expenses were secondary. Results: Of all opioid-dependent IBD hospitalizations, age and sex-matched CUD and non-CUD cohorts were studied. Both groups had 995 patients and a median age of 37 and shared similar sociodemographic characteristics. Comorbidities such as alcohol use disorder (18.1% vs. 6.0%; P< 0.001), complicated hypertension (8.5% vs. 4.5%; P< 0.001), tobacco use disorder (59.8% vs. 44.2%; P< 0.001), and chronic pulmonary disease (25.6% vs. 20.6%; P=0.008) were more common in the CUD cohort. The CUD cohort had higher odds of AKI (OR:1.94; 95CI:1.02-3.68; P=0.043), which was statistically significant, unlike MACCE (OR:1.28; 95CI:0.26-6.21; P=0.761) and sepsis (OR:3.35; 95CI:0.56-20.23; P=0.186). Although not statistically significant, the CUD cohort had lower odds of intestinal obstruction and non-routine discharge compared to routine discharge. The CUD cohort also had a more extended hospital stay (5 vs. 4 days) and higher hospital charges ($31847 vs. $31190; P=0.066) (Figure 1). Conclusion: Our study shows that the CUD cohort had higher odds of AKI vs the non-CUD cohort in opioid-dependent IBD. Given the increased frequency of polysubstance use in the United States, additional prospective studies on the dosage, mode, and duration of recreational or medicinal cannabis use in opioid-dependent IBD patients are necessary.Figure 1.: A. Odds Ratio of outcomes in patients with and without CUD B. Distribution of population before and after matching.

Introduction: Clostridioides difficile infection (CDI) is notorious for its substantial healthcare burden and possible association with an increased risk of colorectal cancer (CRC) due to alterations in the gut microbiome. Our study aims to compare CDI outcomes in patients with and without CRC in the United States. Methods: This retrospective longitudinal study collected data from the National Inpatient Sample (NIS) from 2016-2020. Adult patients with a primary diagnosis of CDI were identified and cohorted based on the presence or absence of CRC using the ICD-10-CM codes. The 2 cohorts of patients were compared using a t-test and chi-square tests. Multivariate regression analysis was performed to assess outcomes while adjusting for confounders. All P-values < 0.05 were statistically significant. Results: A total of 875,775 adults with a CDI were identified; among them, 1.1% (n=10,145) had CRC. The CDI CRC cohort had a higher mean age (67 vs 64 years; P=0.001) and length of stay (9 vs 7 days; P=0.001) than the non-CRC cohort. The CDI CRC cohort had a higher proportion of Whites (74%; P=0.01) and males (47%; P=0.001). No statistical difference was noted in socioeconomic status (P=0.12) and geographic location (P=0.15) between the 2 groups (Table 1). The CDI CRC cohort had higher odds of intestinal perforation 2% (aOR=4.6, 95% CI 3.3-6.3, P=0.001), bright red bleeding per rectum 1.3% (aOR=2.1, 95% CI 1.4-3.2, P=0.001), colectomy 4.6% (aOR=3.4, 95% CI 2.7-4.2, P=0.001), intestinal obstruction 5.3% (aOR=4.9, 95% CI 4.0-5.9, P=0.001), and requirement for blood transfusion (aOR=1.4, 95% CI 1.2-1.5, P=0.001). However, there was no significant difference in the rates of peritonitis (P=0.06), melena (P=0.05), hematemesis (P=0.5), and inpatient mortality (P=0.10) between the 2 groups. Conclusion: Our analysis demonstrates that CDI hospitalizations with CRC had higher healthcare utilization and odds of severe complications and interventions compared to CDI hospitalizations without CRC. This may, in part, be attributed to the immunosuppressive effects of CRC treatment on the gut microbiome and immune system, predisposing to severe CDI and its complications. However, we did not find a statistical difference in the inpatient mortality rates between the 2 cohorts. Additional large prospective studies are needed to further validate our findings. Table 1. - Baseline characteristics and outcomes in patients with clostridium difficile infection (CDI) with and without colorectal cancer (CRC) Variables CDI With CRC, % (N) CDI Without CRC, % (N) OR, 95% CI P-Value Total cases (n=875,775) 1.1% (10,145) 98.9 (865,630) - 0.001 Baseline characteristics Mean Age (Years) 67.6 64.7 - 0.001 Gender 0.001 Male 46.8 (4,750) 43 (372,605) - Female 53.1 (5,395) 56.9 (492,990) Race 0.01 White 74.1 (7,345) 73 (617,855) - Black 11 (1,085) 13 (111,460) - Hispanic 8.9 (885) 8.7 (73,550) - Asian or Pacific Islander 2.6 (255) 1.9 (15,795) - Native American 0.5 (50) 0.7 (6,355) - Others 2.8 (280) 2.4 (20,270) - Insurance 0.001 Medicare 64.3 (4,645) 65.7 (415,720) - Medicaid 9.8 (710) 13.1(83,195) - Private insurance 23.8 (1,720) 18.8 (119,095) - Self-pay 2 (145) 2.3 (14,740) - Alcohol use 1.9 (200) 6.5 (56,565) - 0.001 Smoking 10 (1,020) 13.1 (114,130) - 0.0001 Length of stay 9.26 7.76 - 0.001 Outcomes Mortality 6.9 (705) 6.0 (52,570) 1.1 (0.9-1.3) 0.10 Intestinal perforation 2 (205) 0.4 (3,785) 4.6 (3.3-6.3) 0.001 BRBPR 1.3 (135) 0.6 (5,245) 2.1 (1.4-3.2) 0.001 Transfusion 13.2 (1,345) 9.8 (84,530) 1.4 (1.2-1.5) 0.001 Colectomy 4.6 (465) 1.3 (11,520) 3.4 (2.7-4.2) 0.001 Obstruction 5.3 (540) 1.1 (9,970) 4.9 (4.0-5.9) 0.001 Peritonitis 1 (105) 0.6 (5,985) 1.5 (0.9-2.3) 0.06

Introduction: A Clostridioides difficile infection (CDI) can be self-limiting or develop into fulminant colitis, ileus, or toxic megacolon, which are serious and potentially fatal conditions. Patients taking cancer chemotherapy without previous antibiotic medication have been observed to develop colitis and infections caused by C. difficile. Chemotherapeutic drugs can modify the natural bowel flora and lead to significant intestinal inflammation, which promotes C. difficile growth and toxin generation. Our case identified C. difficile colitis in ovarian cancer patients following each infusion of cisplatin-based combination chemotherapy. Case Description/Methods: 71-year-old woman, prior medical history of hypertension, hypothyroidism, ovarian cancer. Patient presented to ED with Grade 1 diarrhea for 4 days following 2 weeks of chemotherapy, associated lethargy and abdominal cramps. Diarrheal episodes are watery, 3-4 bowel movements per day, no melena or hematochezia. Review of systems positive for dizziness, anxiety, subjective shortness of breath. Patient denied any fever, chills, hematemesis, hemoptysis, cough, chest pain. Vitals stable, abdominal examination is soft and non-tender. Labs: Bicarb 8, Hemoglobin 5.8 gm/dl, Positive for C. difficile GDH Antigen and Toxin A along with B, Negative for other GI infectious organisms. CT abdomen: minimal ascites, diffuse colitis. Treated with 2 Units of PRBC’s transfusion. For C. difficile after first 2 chemotherapy cycles, treated with vancomycin for the initial 2 episodes. Treated with fidaxomicin following the 3 consecutive chemotherapy cycles. Discussion: Adults with cancer had a 7%-14% higher incidence of C. difficile infection (CDI) than the overall hospitalized population (1%-2%). Although there is a dearth of data, it appears that the varied symptoms, treatment, and outcome are identical to those for instances associated with antibiotics. Chemotherapy related diarrhea due to inflammation unlike C. difficile infection is known to us in literature. It's possible that C. difficile infections linked to chemotherapy go unreported because they are not suspected or because their true prevalence is hidden by frequent concurrent antibiotic use. Every time a patient receiving antineoplastic treatment experiences diarrhea, C. difficile infection should be considered. Early therapy and prompt, appropriate diagnostic testing may prevent morbidity and death.