Case Of Esophageal Adenocarcinoma Research Articles

A Rare Case of Esophageal Adenocarcinoma with Signet Ring Cell Features

A Rare Case of Esophageal Adenocarcinoma with Signet Ring Cell Features

A case of Barrett's esophageal adenocarcinoma that could not be detected early with a small-caliber endoscope

A case of Barrett's esophageal adenocarcinoma that could not be detected early with a small-caliber endoscope

S2677 An Uncommon Case of Young Onset Esophageal Adenocarcinoma in a Female Patient Without Risk Factors

S2677 An Uncommon Case of Young Onset Esophageal Adenocarcinoma in a Female Patient Without Risk Factors

Abstract P059: A case of stage I esophageal adenocarcinoma diagnosed using a multi-cancer early detection test

Abstract Introduction: There is no guideline-recommended screening test for esophageal cancer, a cancer that occurs in approximately 1 in 125 men and 1 in 417 women in the US. Risk factors for esophageal adenocarcinoma include gastroesophageal reflux disease, Barrett’s esophagus, obesity, and smoking. A multi-cancer early detection (MCED) test that analyzes methylation patterns of cell-free DNA in the blood using sequencing assays and machine-learning classifiers is available as a complement to existing single-cancer screening tests. The MCED test reports either (1) ‘cancer signal detected’ with 1 or 2 cancer signal origin (CSO) prediction(s) or (2) ‘cancer signal not detected’. A case of esophageal adenocarcinoma is presented here to demonstrate early detection using the MCED test and to review the diagnostic journey following a cancer signal detected (positive) test result. Case Description/Methods: An asymptomatic 63-year-old White male (BMI: 27 kg/m2) with history of peptic ulcer disease was screened using the MCED test. He reported moderate alcohol use (6/week) and no tobacco use. His last colonoscopy was 5 years prior to using the test. Nine days after a blood sample was collected for analysis by the MCED test, a positive test result (CSO prediction=Stomach/Esophagus) was reported and communicated to the patient (Day 1). Computed tomography (CT) of the chest, abdomen, and pelvis with contrast showed no significant findings (Day 13). A submucosal bulge just below the gastroesophageal junction (GEJ) was noted on upper endoscopy. The lesion, and area above the GEJ were extensively biopsied (Day 15). Pathologic evaluation confirmed diagnosis of Clinical Stage I esophageal adenocarcinoma with superficial focally invasive adenocarcinoma arising in a background of intestinal metaplasia with high grade dysplasia (Day 29). The patient underwent total gastrectomy without complications (Day 104). He will undergo appropriate follow-up 6 months post-op. Discussion: The MCED test detected a cancer signal and predicted a gastrointestinal CSO for an asymptomatic individual with Clinical Stage I esophageal cancer. Diagnostic resolution was achieved within 1 month and treatment was provided with curative intent. Given that there is no guideline-recommended screening test available for esophageal cancer, the use of this MCED test detected cancer early, directed diagnostic workup, and potentially improved outcomes for this asymptomatic patient. Citation Format: David DeAtkine Jr. A case of stage I esophageal adenocarcinoma diagnosed using a multi-cancer early detection test. [abstract]. In: Proceedings of the AACR Special Conference: Precision Prevention, Early Detection, and Interception of Cancer; 2022 Nov 17-19; Austin, TX. Philadelphia (PA): AACR; Can Prev Res 2023;16(1 Suppl): Abstract nr P059.

S2406 A Case of Cervical Esophageal Adenocarcinoma Arising From Gastric Inlet Patch: A Benign Lesion With Malignant Potential

Introduction: Esophageal adenocarcinoma is typically localized to the distal third of the esophagus. It is associated with long-standing acid reflux and resultant Barrett’s esophagus. In contrast, adenocarcinoma in the proximal esophagus without Barrett’s metaplasia is extremely rare. A gastric inlet patch (GIP) is a lesion of ectopic gastric mucosa usually found in the cervical esophagus and is considered a benign lesion. However, albeit rare, malignant transformation of GIP can occur. Here, we present a case of cervical esophageal adenocarcinoma arising from gastric inlet patch. Case Description/Methods: A 50-year-old male with GERD presented with a 6-month history of progressive dysphagia to solids and liquids and 20-pound weight loss. He reported a 1 pack-year smoking history but quit 30 years prior and consumed alcohol socially. Family history was negative for esophageal cancer. Upper endoscopy (HQ190F) showed a malignant stricture (2 cm long, 6mm diameter) at 18 cm from the incisors and a gastric inlet patch adjacent to the stricture. The endoscope was downsized (XP190N), and the stricture was dilated (24F) and traversed. The Z-line was at 40 cm with Barrett’s esophagus extending from 36 cm to 40 cm. Pathology of biopsies from the stricture showed acute and chronic inflammation with increased intraepithelial eosinophils suggestive of acid reflux. CT scan of the neck with contrast showed a heterogeneously enhancing ill-defined mass involving the cervical esophagus below the cricoid cartilage indenting the posterior margin of the trachea. Bronchoscopy was negative for bronchogenic cancer. Endoscopic ultrasound showed a non-circumferential hypoechoic mass in the cervical esophagus 18 cm from the incisors extending to 20 cm. The mass was predominantly extrinsic but was also noted to have a luminal component and poorly defined endosonographic borders. Pathology of FNAB showed moderately differentiated adenocarcinoma (Figure). Discussion: Proximal esophageal adenocarcinoma is extremely rare, making up less than 1% of esophageal cancers. Case studies have been published associating GIP and esophageal adenocarcinoma, but the pathogenesis of malignant transformation remains unclear. There are no established screening guidelines for ectopic gastric mucosa and routine biopsies are not recommended as dysplasia within GIP is rare. GIP may be overlooked during EGD and NBI exam may improve detection rates. Our case re-emphasizes careful examination of GIP and to strongly consider biopsy if abnormal.Figure 1.: A) Endoscopic view of malignant stricture 18 cm from incisors. Gastric inlet patch (arrow) adjacent to stricture. B) Endoscopic ultrasound image at the level of esophageal stricture showing irregular hypodensity suggestive of malignancy. C) Pathology of biopsy performed through fine needle aspiration (EUS) of upper esophageal mass demonstrating moderately differentiated adenocarcinoma, cribriform pattern, with mild nuclear pleomorphism, abundant mitoses, and apoptosis (H&E, 10x).

Surveillance After Treatment of Barrett's Esophagus Benefits Those With High-Grade Dysplasia or Intramucosal Cancer Most.

Endoscopic eradication therapy with radiofrequency ablation (RFA) and endoscopic mucosal resection is a safe and effective treatment for Barrett's esophagus. Although the outcomes of surveillance endoscopy after successful endoscopic eradication therapy have been described, no previous studies have modeled the natural history or the effect of surveillance endoscopy after successful ablation to prevent progression to invasive esophageal adenocarcinoma. The US RFA Registry is a multicenter registry consisting of patients treated with RFA for Barrett's esophagus at 148 institutions (113 community-based and 35 academic-affiliated). The authors fit models to impute the natural history of recurrence and neoplastic progression after any recurrence or retreatment. Natural history estimates of invasive adenocarcinoma after ablation therapy were compared with as-treated estimates at 5 years to derive the preventive risk difference for surveillance. Natural history estimates for the postablation progression of high-grade dysplasia (HGD) or intramucosal adenocarcinoma to invasive adenocarcinoma after treatment were 6.3% at 5 years compared with 1.3% for low-grade dysplasia (LGD). The natural history model found a much higher preventative risk difference for surveillance for HGD/intramucosal adenocarcinoma (-4.8%), compared with LGD (-1.1%). The numbers needed to surveil at 5 years were 21 and 90 for these groups, respectively, to prevent one case of invasive esophageal adenocarcinoma, making surveillance after successful ablation of baseline HGD more than 4 times as effective at preventing invasive cancer than after successful ablation of baseline LGD. Endoscopic surveillance after successful ablation of baseline HGD or intramucosal cancer is much more effective than surveillance after successful treatment of baseline LGD in averting invasive adenocarcinoma. Although the modest benefits of surveillance for treated LGD may be greater than the risks for patients at average risk for adverse effects of endoscopy, clinicians should concentrate on retaining patients with baseline HGD or cancer in endoscopic surveillance programs.

A case of cervical esophageal adenocarcinoma originating from the ectopic gastric mucosa treated with endoscopic submucosal dissection

A case of cervical esophageal adenocarcinoma originating from the ectopic gastric mucosa treated with endoscopic submucosal dissection

S2008 A Case of Esophageal Adenocarcinoma in a Young Male With Longstanding Untreated Eosinophilic Esophagitis

INTRODUCTION: Eosinophilic Esophagitis (EoE) has been increasing in incidence over the last decade due to the increasing number of EGD with biopsies preformed. Up to 6.5% patients undergoing EGD for any indication are diagnosed with EoE and 22% in patients for dysphagia. EoE is present in all age groups but peak incidence is bimodal, in first and third decades of life. Here we describe a case of esophageal adenocarcinoma in a patient with history of EoE. CASE DESCRIPTION/METHODS: A 42 year-old male (BMI 27 kg/m2) with PMHx of untreated EoE for 10 years presented to the ED for food bolus impaction a few hours after eating pork. No history of alcohol or tobacco use. Emergent EGD was performed with successful removal of solid food bolus in middle third of the esophagus. There were endoscopic mucosal changes consistent with EoE (EoE-EREFS: Edema 1, Rings 2, Exudates 1, Furrows 1 and Stricture 0) within the entire esophagus and a nodularity appreciated at the GEJ. Biopsies obtained from proximal and distal esophagus showed more than 50 and 100 eosinophils/per HPF respectively. The GEJ lesion showed high grade dysplasia in the settings of goblet cell metaplasia. Repeat EGD 3 weeks later revealed a medium sized fungating and ulcerated mass at the GEJ which was circumferential and partially obstructing. The biopsies showed esophageal adenocarcinoma with indeterminate HER2 oncogene expression, staged as T3N1 based on mini-probe EUS. Oncology classified the patient as cT3N1Mx. The patient received chemo-radiation (5-fluorouracil/oxaliplatin) over 37 days followed by robotic assisted laparoscopic Ivor Lewis esophagogastrectomy with left gastric hepatic artery and celiac lymphadenectomy with successful remission, T0N0. Patient remained in clinical remission at 6 months follow up. DISCUSSION: An estimated 17,500 new cases of esophageal cancer were reported in 2016. Incidence was 4 in 100,000 and increases with age starting from 0.2 in 100,000 at age 30 increasing to 26 in 100,000 at age 80. Mortality was 3.9 in 100,000 deaths and has a 5 year survival of 18.9%. Current risk factors for development of esophageal cancer are alcohol, smoking, and obesity. No clear genetic factors have been associated with development and it is unknown if EoE is a risk factor. However, chronic inflammation and structural changes may be a contributor to malignancy and further research should focus on this area given diseases mortality rates.Figure 1.: A. Food Bolus at Middle Third of the Esophagus B. Abnormal Mucosa at the Gastro-Esophageal Junction C. Gastric Cardia, retroflex view: Mass.Figure 2.: Proximal esophagus shows increased intraepithelial eosinophils, consistent with eosinophilic esophagitis.Figure 3.: GE Junction biopsy shows adenocarcinoma arising in the background of barrett’s esophagus.

A rare case of esophageal adenocarcinoma with urinary bladder metastasis.

A 75-year-old man was admitted to our hospital for treatment of esophageal cancer (EC) in March 2017. Esophagogastroduodenoscopy revealed Barrett's esophagus and superficial, distal EC (type 0-IIc). Tumor biopsy showed esophageal adenocarcinoma. Computed tomography revealed no lymph node metastasis but did reveal a 19-mm tumor on the right side of the urinary bladder. Bladder cancer (BC) was also suspected, and the patient underwent endoscopic submucosal dissection for EC and transurethral resection of the bladder tumor. The pathological diagnosis of EC was moderately to poorly differentiated adenocarcinoma (tub2), pT1b (SM), ly0, v0. The pathological horizontal margin was negative and the vertical margin was positive. Additional esophagectomy and lymph node dissection were indicated for curability. Esophagectomy was difficult because the patient had severe cardiovascular disease, so follow-up observation was adopted. BC was classified as urothelial carcinoma Ta, ly0, v0. After 32months, multiple tumors were found in the bladder, and BC recurrence was suspected. Transurethral resection of the bladder was performed again for seven tumors, and pathological diagnosis was poorly differentiated adenocarcinoma (tub2). The immunohistochemical features matched those of EC. We diagnosed EC metastasis in the urinary bladder. Bladder adenocarcinoma is difficult to distinguish from metastasis from other organs, especially the upper gastrointestinal tract, and cytomorphological features and appropriate clinical history are required.

1794 Esophageal Adenocarcinoma in a Patient With Inclusion Body Myositis

INTRODUCTION: Inflammatory myopathies are rare autoimmune diseases characterized by chronic muscle inflammation and weakness. Dysphagia is often an early onset symptom in inflammatory myopathies. Here we present a case of esophageal adenocarcinoma diagnosed in a patient with inclusion body myositis (IBM) and chronic progressive dysphagia. CASE DESCRIPTION/METHODS: A 59 year old woman with an 8 year history of gradually progressive IBM presented to the ER with worsening dysphagia; she has had progressive dysphagia over the preceding 10 days to the point she is unable to tolerate solids. Despite longstanding, progressive symptoms, referral to a gastroenterologist was never made as it was assumed her symptoms were from her underlying IBM. On exam, she is a functional quadriplegic from her underlying IBM and is largely bedbound as a result. Her labs were notable for a macrocytic anemia with negative inflammatory myopathy antibody panel. Barium esophagram revealed a large filling defect in the mid to distal esophagus measuring approximately 3.6 × 2.4 cm and subsequent upper endoscopy revealed an 8cm nearly obstructive distal esophageal mass which appeared to arise in the setting of suspected Barrett’s esophagus. Biopsies demonstrated esophageal adenocarcinoma with signet cell features. Subsequent staging was consistent with cT3N0 disease though she was deemed not to be a surgical candidate due to her quadriplegia and severe deconditioning. An endoscopic esophageal bare metal stent was placed for symptom palliation and she was referred to hospice. DISCUSSION: The inflammatory myopathies are a group of autoimmune diseases characterized by chronic muscle inflammation accompanied by weakness. IBM, in contrast to polymyositis and dermatomyositis, has normal or minimally elevated creatine kinase, insidious progression, and is poorly responsive to immunosuppressive therapy. While IBM is generally not thought to be a paraneoplastic syndrome, there are case reports of them being paraneoplastic with a negative antibody panel (as seen in this case). Bulbar symptoms are common in IBM, and >50% of patients will develop oropharyngeal dysphagia usually due to cricoarytenoid weakness. In this case, the patient’s dysphagia was prematurely attributed to IBM, precluding a timely diagnosis of esophageal adenocarcinoma. In patients with inflammatory myopathy and dysphagia, endoscopy is still of utmost importance and symptoms should not be solely attributed to underlying IBM.

Esophageal adenocarcinoma with leukemoid reaction: a case report

BackgroundLeukemoid reaction (LR) is defined as a reactive leucocytosis with WBC counts exceeding 50,000/mm3, and a significant increase in early neutrophil precursors. LR may be a paraneoplastic manifestation of various malignant tumors. Tumor-related LR is a kind of neoplastic syndrome, unrelated to an infection or other diseases.Case presentationA 74-year-old male visited a local doctor with a 20-day history of progressive dysphagia. The complete blood count revealed leucocytosis. Bone marrow aspirates and a biopsy confirmed LR and excluded chronic myelogenous leukemia. Following radical esophagectomy for an adenocarcinoma the WBC counts successively decreased to 10,450/mm3 and 8670/mm3 within 1 week and 1 month, respectively.ConclusionWe report a rare case of esophageal adenocarcinoma complicated with excessive leucocytosis caused by paraneoplastic LR; we also present a review of literature and an investigation of the clinical features. To our knowledge, this is the first report of LR associated with esophageal adenocarcinoma.

An unusual case of esophageal adenocarcinoma presenting with disseminated intravascular coagulation (DIC) as a result of carcinomatosis of the bone marrow

We describe a rare case of esophageal adenocarcinoma presenting with carcinomatosis of the bone marrow resulting in disseminated intravascular coagulation (DIC). A 73-year-old male presented with fatigue, night sweats, and easy bruising. Laboratory evaluation showed severe anemia, thrombocytopenia, and a coagulopathy consistent with DIC. Bone marrow biopsy demonstrated markedly hypocellular marrow with involvement of metastatic adenocarcinoma. Upper endoscopy revealed a stenotic lesion at the gastroesophageal junction, and biopsies confirmed esophageal adenocarcinoma. Imaging studies showed no evidence of visceral metastases. DIC was attributed to diffuse bone marrow involvement of the primary esophageal cancer. The patient received intensive supportive care for his DIC followed by first-line chemotherapy with 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX). Treatment of the underlying malignancy resulted in stabilization of his DIC. This is the first reported case of esophageal adenocarcinoma with disseminated carcinomatosis of the bone marrow leading to DIC. We also discuss the prevalence and significance of bone marrow micrometastases in esophageal cancers as well as the association and clinical implications of DIC in solid tumor malignancies.

Esophageal adenocarcinoma and Barrett esophagus in a neurologically impaired teenager

Esophageal adenocarcinoma (EAC) accompanied by Barrett esophagus (BE) is rare in patients younger than 20years old. EAC in the upper esophagus is also rare. We report a rare case of EAC with BE that developed in the upper esophagus after chronic, untreated gastroesophageal reflux disease in a neurologically impaired teenager. A 19-year-old neurologically impaired man underwent endoscopy for evaluation of dysphagia and vomiting, and was diagnosed with EAC with BE. He underwent transthoracic esophagectomy, extensive lymph node dissection, and cervical esophagogastric anastomosis, but the prognosis was poor. Pathology indicated poorly differentiated adenocarcinoma with BE.

An Unusual Presentation of Metastatic Esophageal Cancer

Esophageal cancer is the 6th leading cause of death from cancer and the 5-year survival rate is dismal around 15%-25%. Metastatic spread to the intestinal tract is extremely rare and thus there are no guidelines suggesting preoperative colonoscopy. Here we present a case of esophageal adenocarcinoma which metastasized to the colon, an event that has so far been unreported in the literature. A 70 year old male with a past medical history of poorly differentiated pT3N1 esophageal adenocarcinoma diagnosed in June 2013 presented to the hospital in December 2015 with shortness of breath and weakness for the preceding two weeks. Patient's initial staging workup included CT of his chest, abdomen and pelvis and PET-CT which demonstrated a PET-avid lesion in his left upper lung. He received neoadjuvant chemotherapy with EOF (Epirubicin, Oxaliplatin and Fluorouracil) for five cycles and subsequently underwent both esophagectomy and left upper lobe wedge resection for his malignancies. He declined further adjuvant chemotherapy after his surgery. On admission, CT of the chest revealed a new pulmonary embolus. He was started on a heparin drip and subsequently had two episodes of hematochezia. Given his history of malignancy and new pulmonary embolus upper and lower endoscopy were pursued. EGD revealed a healthy anastomosis at 21 cm from the incisors. Colonoscopy revealed innumerable friable polypoid lesions, some with overlying exudate, measuring 5-30 mm in size found diffusely throughout the colon. Pathology from the biopsies revealed poorly differentiated adenocarcinoma with positive staining for cytokeratin AE1/AE3, CK7 and CDX2 and negative for HER2, CK20, P40, LCA (CD45), neuroendocrine and melanoma markers. Review of his prior pathology from his esophageal tumor demonstrated a matching immunologic profile consistent with the diagnosis of poorly differentiated metastatic esophageal adenocarcinoma. The patient was referred for systemic chemotherapy; however, he unfortunately expired one week after the diagnosis.Figure 1Esophageal adenocarcinoma is becoming more prevalent in the United States and yet remains a very deadly cancer. Despite strict staging protocols preoperatively, we present a case of esophageal adenocarcinoma metastasizing diffusely to the colon. Although rare and a previously unreported condition, it does raise the question of whether colonoscopic surveillance should be included in the staging guidelines for esophageal adenocarcinoma preoperatively.Figure 2

Multidisciplinary Management of a Rare Case of Esophageal Adenocarcinoma with Cardiac, Pulmonary, Liver, Adrenal Gland and Brain Metastasis

Multidisciplinary Management of a Rare Case of Esophageal Adenocarcinoma with Cardiac, Pulmonary, Liver, Adrenal Gland and Brain Metastasis

Multidisciplinary Management of a Rare Case of Esophageal Adenocarcinoma with Cardiac, Pulmonary, Liver, Adrenal Gland and Brain Metastasis

We report the case of a 48-year-old gentleman affected by diffuse metastatic gastroesophageal junction (GEJ). Positron emission tomography (PET) scan demonstrated diffuse metastatic disease involving brain, heart, lungs, liver and adrenal glands. Transthoracic echocardiogram showed a mass in the left ventricular apex measuring 2.46 cm × 1.32 cm. Cardiac Magnetic resonance imaging (MRI) showed 2.3 cm mass in the apex of the left ventricle. Peripheral blood circulating tumor DNA (ctDNA) analysis confirmed dissemination of cancer and showed mutations in TP53, AR, PIK3CA, and Erbb2 amplification. Combination chemotherapy consisting of trastuzumab, capecitabine and oxaliplatin was initiated with a significant reduction of tumor markers: CEA from 60.7 to 19.7 ng/mL (67.5%) and CA19-9 from 2104 to 139 Units/mL (93.4%). A repeated PET scan demonstrated resolution of FDG avidity of left ventricle/pericardium, decreased avidity and size of adrenal gland masses, lung nodules and primary esophageal mass. We reviewed and summarized the recent literatures regarding the clinical presentations, diagnostic tools, tumor histology, treatment modalities and clinical prognosis of cardiac metastases from esophageal cancer. This report also highlights the potential role of ctDNA as a cost effective marker in the management of metastatic esophageal cancer.

A Unique Case of Alpha-Fetoprotein-Producing Esophageal Adenocarcinoma

Alpha-fetoprotein (AFP)-producing esophageal adenocarcinoma (EAC) is a rare occurrence. Elevation of serum AFP is commonly associated with hepatocellular carcinoma and yolk sac tumors, but has also been reported in patients with other malignancies, most notably of gastrointestinal origin. However, the organs of origin typically include gastric, pancreatic, and biliary, but rarely esophageal. Here, we report a case of an AFP-producing EAC. A 51 year-old previously healthy man presented with new onset severe acid reflux and a weight loss of 35 pounds over a 2 week duration. He also endorsed 2 days of non-bloody emesis, but denied dysphagia or regurgitation of undigested food. Physical exam was only remarkable for right upper quadrant tenderness. The patient was slightly anemic with a hemoglobin of 12.8 g/dL. Elevated labs included: AST 66 U/L, ALT 81 U/L, CEA 6.4 ug/L, CA 19-9 317443 U/mL, and AFP 2524 ng/mL. Hepatitis B surface antigen and hepatitis C antibody were non-reactive. Computed tomography (CT) scan of the abdomen revealed abnormal thickening of the esophagus and multiple masses throughout the liver consistent with metastatic disease. CT-guided biopsy of one of the masses revealed CDX-2 positive adenocarcinoma, suggesting gastrointestinal origin. Subsequent upper endoscopy revealed a large, partially-obstructing mass in the lower third of the esophagus, the assumed primary source. Biopsy of the mass revealed ulcerated glandular mucosa with high grade dysplasia, with likely underlying malignancy. One month later, the patient underwent palliative esophageal stent placement. He was scheduled to begin FOLFOX/Herceptin therapy, but expired a week later. EAC is typically found in the lower third of the esophagus, and is associated with Barrett's esophagus, smoking, obesity, and epidermal growth factor polymorphisms. A previous study attempting to determine possible tumor markers in patients with esophagus cancer reported serum AFP levels >5 ng/mL in up to 18% of EACs, with the highest reported AFP level being 320ng/mL. However, to the best of our knowledge, our case is only the 14th AFP-producing EAC to be thoroughly described in the English literature. Patients with EAC and cirrhosis often share common risk factors that make the differential diagnosis of liver masses and elevated AFP challenging. Some AFP-producing EACs contain cells resembling hepatic cells and are termed hepatoid EAC. Although not possible in our case, serial measurement of serum AFP level may be useful for monitoring clinical status and response to treatment. Most cases are treated with surgery and adjuvant chemotherapy but with disappointing results given the advanced presenting stage, high liver metastatic potential, and poor prognosis of AFP-producing EAC.Figure 1Figure 2Figure 3

Long segmentバレット食道に発生した胸部中部食道腺癌および横行結腸癌の重複癌一切除例

Long segmentバレット食道に発生した胸部中部食道腺癌および横行結腸癌の重複癌一切除例

A Single-Center Experience Comparing Surveillance of Barrett’s Esophagus in Subjects With Liver Cirrhosis and Those Without Cirrhosis

Introduction: The epithelium of Barrett’s Esophagus (BE) could sequentially progress from metaplasia to low grade dysplasia (LGD) to high grade dysplasia (HGD) and finally Esophageal Adenocarcinoma (EAC). Our aim was to evaluate endoscopic surveillance for BE in patients with and without liver cirrhosis. Methods: We conducted a retrospective review of 1960 medical records of cirrhotic patients between 1997 and 2011 at a major urban hospital. Inclusion criteria for the case group consisted of cirrhotic patients with biopsy-proven BE. Matched controls with biopsy proved BE were identified using ICD-9, and were matched for the length of BE and the year of diagnosis. Risk factors analyzed included age, sex, body mass index, aspirin use, history of Gastroesophageal reflux disease (GERD), length of BE and proton pump inhibitor (PPI) use. Adequacy of surveillance was assessed based on the 2008 guidelines of the American College of Gastroenterology for the Diagnosis, Surveillance and Therapy of Barrett’s Esophagus. Results: In total, 23 cirrhotic patients with BE were compared with 23 matched controls. Mean age was significantly different (54.8±7.7 in cirrhotic vs. 65±11.6 in non-cirrhotic group) (p<0.001). The majority of patients were Caucasian (82.6% vs. 87%) and males (87% vs. 73.9%) in cirrhosis and non-cirrhosis groups, respectively. There was a significant difference in factors which may produce symptomatic disease with hiatal hernia was diagnosed in 8 patients (35%) in the cirrhotic group versus 16 (70%) in the non-cirrhotic group (p < 0.03). Rate of GERD was lower in the cirrhosis group with 11 patients (47.8%) versus 16 (69.6%) in the non-cirrhosis group (p=0.05). There was an equal number of patients with long and short segment BE, 13 (23%) (p >0.05). The rate of surveillance of BE in both groups was low with 15% in cirrhosis group versus 20% in the non-cirrhosis group having adequate surveillance (p< 0.56). There was no statistically significant difference in identified advanced disease between the two groups. In the cirrhosis group, there was one case of EAC that was treated with Endoscopic Mucosal Resection. Follow-up repeat endoscopy showed residual HGD. In the non-cirrhosis group, there were two patients with LGD and one patient with HGD. One case of LGD regressed to no dysplasia after treatment with PPI alone. The other two cases regressed to no dysplasia after treatment with EMR and radiofrequency ablation. Conclusion: Our study demonstrates poor surveillance of diagnosed BE in both cirrhotic and noncirrhotic patients. Those with cirrhosis were less likely to have GERD or hiatal hernia at the time of diagnosis. When surveillance resulted in diagnosis of dysplasia, early management was able to result in regression of disease.

Acid-suppressive medications and risk of esophageal adenocarcinoma in patients with Barrett’s esophagus: A systematic review and meta-analysis.

11 Background: Acid-suppressive medications, particularly proton pump inhibitors (PPI), may modify risk of esophageal adenocarcinoma (EAC) in patients with Barrett’s esophagus (BE). We performed a systematic review and meta-analysis of studies evaluating the association between PPIs and histamine receptor antagonists (H2RA) and risk of EAC or high-grade dysplasia (BE-HGD) in patients with BE. Methods: Through a systematic search up to June 2013, we identified 7 observational studies (5 cohort studies and 2 case-control studies; 2,813 patients with BE, 317 cases of EAC and/or BE-HGD, 84.4% PPI users) reporting the association between PPIs or H2RA and EAC in patients with BE. Summary odds ratio (OR) with 95% confidence intervals (CI) was estimated using random effects model, and heterogeneity was measured using the inconsistency index (I2). Results: On meta-analysis, PPI use was associated with 71% reduction in EAC risk in patients with BE (adjusted OR, 0.29; 95% CI, 0.12-0.71). There was a trend toward a dose-response relationship with PPI use for &gt;2 years protective against EAC [3 studies; PPI use &gt;2 years vs. &lt;2 years (as compared to no use): OR, 0.45 (0.19-1.06) vs. 1.09 (0.47-2.56)]. Considerable heterogeneity was observed in the overall analysis (I2=81%). On restricting analysis to 5 cohort studies, use of PPIs was consistently associated with a lower risk of EAC and/or BE-HGD (adjusted OR, 0.33; 95% CI, 0.19-0.58; I2=9%). H2RA use was not associated with decreased risk of EAC in patients with BE based on 2 studies (adjusted OR, 1.15; 95% CI, 0.77-1.72). Using a 67% summary risk reduction (derived from cohort studies) of EAC and/or BE-HGD with PPI use in patients with BE, and observed cumulative incidence rates of EAC and/or BE-HGD in patients with BE overall as 10.2 per 1,000 patient years, we estimate the number needed to treat with PPIs to prevent 1 case of EAC or BE-HGD in BE patients at 147. Conclusions: Based on meta-analysis of observational studies, the use of PPI, but not H2RA appears to be associated with a decreased risk of EAC and/or BE-HGD in patients with BE. PPI use should be considered in BE, and chemopreventive trials of PPIs in patients with BE are warranted.