Severe Upper Gastrointestinal Hemorrhage Caused by Reflux Esophagitis.

BACKGROUND: There are few reports about reflux esophagitis (RE) as a cause of severe upper gastrointestinal bleeding (UGIB). AIMS: This study aims to evaluate (1) changes in its prevalence over the last three decades and (2) clinical and endoscopic characteristics and 30-day outcomes among RE patients with and without focal esophageal ulcers (EUs) and stigmata of recent hemorrhage (SRH). METHODS: A retrospective study of prospectively collected data of esophagitis patients hospitalized with severe UGIB between 1992 and 2020. Descriptive analysis and statistical comparisons were performed. RESULTS: Of 114 RE patients, the mean age was 61.1 years and 76.3% were males. 38.6% had prior gastroesophageal reflux disease (GERD) symptoms; overall 36% were on acid suppressants. Over three consecutive decades, the prevalence of RE as a cause of severe UGIB increased significantly from 3.8 to 16.7%. 30-day rebleeding and all-cause mortality rates were 11.4% and 6.1%. RE patients with focal EUs and SRH (n = 23) had worse esophagitis than those with diffuse RE (n = 91) (p = 0.012). There were no differences in 30-day outcomes between RE patients with and without EUs and SRH. CONCLUSIONS: For patients with severe UGIB caused by RE, (1) the prevalence has increased significantly over the past three decades, (2) the reasons for this increase and preventive strategies warrant further study, (3) most patients lacked GERD symptoms and did not take acid suppressants, and (4) those with focal ulcers and SRH had more severe esophagitis and were treated endoscopically.

Drug-Induced Esophageal Ulcer in Adolescent Population: Experience at a Single Medical Center in Central Taiwan.

Background and Objectives: Drug-induced esophageal ulcer is caused by focal drug stimulation. It may occur in adults and children. Limited research is available in pediatric patients with drug-induced esophageal ulcer; therefore, we designed this study to determine the characteristics of this disease in this population. Materials and Methods: Thirty-two pediatric patients diagnosed with drug-induced esophageal ulcers from a hospital database of upper gastrointestinal tract endoscopies were included. After treatment, patients were followed for 2 months after upper gastrointestinal endoscopy. Results: Female patients were predominant (56.2%/43.8%). The mean age of patients was 15.6 years (median, 16 years; interquartile range, 2 years). Doxycycline was administered in most cases (56.3%); other drugs were dicloxacillin, amoxicillin, clindamycin, L-arginine, and nonsteroidal anti-inflammatory drugs. Doxycycline was associated with kissing ulcers. Esophageal ulcers induced by nonsteroidal anti-inflammatory drugs were more often associated with gastric or duodenal ulcers. The most common location was the middle-third of the esophagus (78.1%). Patients were treated with proton pump inhibitors, sucralfate, or H2-blockers. The mean duration for which symptoms lasted was 9.2 days. No esophageal stricture was found in 24 patients who were followed for 2 months after upper gastrointestinal endoscopy. Conclusions: The authors suggest informing patients to take medicine with enough water (approximately 100 mL) and enough time (15-30 min) before recumbency, especially high-risk drugs, such as doxycycline or nonsteroidal anti-inflammatory drugs.

[Evaluation and management of infectious esophagitis in immunocompromised patients and immunocompetent individuals].

Among the many causes of the inflammatory process in the esophagus, infectious diseases are becoming increasingly important due to their steady growth. Previously esophageal infections have traditionally been associated with immunodeficiency syndromes, but now in clinical practice, these disorders are becoming increasingly recognized in immunocompetent individuals. Early diagnosis of infectious esophagitis is necessary to develop effective treatment tactics, and, as a result, reduce the risk of complications and adverse outcomes of the disease. This study reviewed the most clinical relevant pathogens of infectious esophagitis, both among patients with immunodeficiency and among healthy individuals. Specific diagnostic, risk factors, clinical presentation and therapeutic features were considered depending on the immune status of patients.

Comparison of Clinical Characteristics of Patients with Acute Esophageal Mucosal Lesion and those with Severe Reflux Esophagitis.

BACKGROUND: The term "acute esophageal mucosal lesion (AEML)" includes black esophagitis, and non-black esophagitis characterized by diffuse circumferential erosions without black-appearing mucosa. Black esophagitis is easily diagnosed, whereas non-black esophagitis is often misdiagnosed as severe reflux esophagitis (sRE). The aim of this study was to determine differences in clinical characteristics of patients with AEML and those with sRE. METHODS: Thirty-nine patients with sRE and 32 patients with AEML were diagnosed on the basis of endoscopic findings from 2009 to 2016. Characteristics assessed included age, sex, medication use, coexisting endoscopic finding, comorbidities, laboratory tests results, and chief complaints. RESULTS: In contrast with sRE, male sex, need for emergency endoscopy, presence of duodenal lesions, hypertension, and renal dysfunction were positively associated with AEML. Analysis of associations between laboratory data and AEML showed that high white blood cell count, blood urea nitrogen, and blood glucose were significantly associated with an increase OR for AEML. CONCLUSIONS: We showed that AEML differed from sRE regarding both endoscopic findings and clinicopathological features. AEML has not been widely recognized, but it should be defined as a distinct inflammatory disease of the esophagus consisting of both black and non-black esophagitis.

Hepatocyte Growth Factor Facilitates Esophageal Mucosal Repair and Inhibits the Submucosal Fibrosis in a Rat Model of Esophageal Ulcer.

BACKGROUND/AIMS: Esophageal mucosal damage often causes scar tissue, leading to refractory stricture. The aim of this study was to clarify the effect of hepatocyte growth factor (HGF) on esophageal mucosal repair and fibrosis leading to stricture in a rat model of esophageal ulcer. METHODS: Esophageal ulcers were induced in rats by topical exposure of the lower esophageal serosa to acetic acid, followed by intraperitoneal administration of HGF (200 µg/day) using an osmotic pump for 7 days. The effect of HGF on esophageal mucosal injury was investigated macroscopically and microscopically. The effect of HGF on epithelial cell proliferation and the expression of genes closely associated with the development of fibrosis were also examined. RESULTS: The administration of HGF for 7 days led to a significant reduction in the ulcerative area and enhanced the proliferation of esophageal epithelial cells. HGF treatment significantly decreased the fibrosis, and subsequently attenuated not only the foreshortening but also the narrowing of the esophagus. The expression levels of tissue inhibitor of metalloproteinase (TIMP)-1, -2, and matrix metalloproteinase (MMP)-2, -9 were significantly decreased among rats treated with HGF. CONCLUSION: HGF facilitates the repair of esophageal mucosal injury and may also ameliorate the esophageal fibrosis, possibly through enhanced re-epithelization.

Side Effects of Stem Cell Transplant Mimicking Symptoms of Known Amyloidosis.

Introduction: AL amyloidosis can involve the gastrointestinal (GI) tract in a sporadic manner, affecting certain anatomical areas while sparing others. Case Presentation: Our patient with AL amyloidosis and confirmed colonic involvement was found to have new odynophagia, GI bleeding, and imaging findings that might suggest AL amyloidosis. However, negative pathology results from esophageal biopsies suggested the patient's new ulcerations were more likely a side effect of her autologous stem cell transplant (SCT) and chemotherapy meant to target amyloidosis, as opposed to an effect of amyloid infiltration itself. Conclusion: GI involvement of amyloidosis requires a high degree of clinical suspicion and should be considered in patients with systemic diseases affecting the kidney, heart, and GI tract; however, when satisfactory biopsies obtained from endoscopy results are negative, other causes should be considered.

Esophageal Ulceration Following the Ingestion of a Single Dose of Doxycycline: A Case Report.

Doxycycline is one of the medications that cause drug-induced esophagitis. This condition occurs due to prolonged contact of the medications with the esophageal mucosa, leading to erosion, ulcers, and, in some cases, stricture of the esophagus. Chest pain, dysphagia, and odynophagia are the most common symptoms. Endoscopy is the gold standard for confirming the diagnosis. The treatment consists of stopping the offending medication and starting proton pump inhibitors (PPIs) and sucralfate. Herein, we describe a middle-aged man who presented with severe chest pain, odynophagia, and dysphagia that started two hours after ingesting the first doxycycline pill. An endoscopy showed multiple longitudinal ulcers in the distal esophagus. Symptoms significantly improved after starting a PPI and sucralfate, and feeding was resumed two days later. A follow-up with endoscopy after two months reported completely healed esophageal ulcers. In conclusion, doxycycline-induced esophageal injury is often an underdiagnosed and underreported condition. Physicians and patients should be more aware of doxycycline's detrimental effect on the esophagus, as it can induce esophageal ulceration even after a single dose if not administered properly. Therefore, all patients prescribed oral doxycycline should receive appropriate instructions to minimize this side effect.

Pemphigus vulgaris presenting with epigastric pain.

Pemphigus vulgaris is an autoimmune mucocutaneous disease with an involvement in gastrointestinal tract especially in oral cavity and esophagus. Ulcers can be the initial presentation even before visible mucosal or cutaneous lesions. The presenting symptoms will be in accordance with the affected organ such as throat pain, hoarseness, dysphagia, odynophagia, or even bleeding. Here, we report a case of undiagnosed pemphigus vulgaris presenting with epigastric pain whose endoscopy showed oropharyngeal involvement and isolate esophageal ulcer, which failed proton pump inhibitor treatment.

Esophageal Ulcer After Intravitreal Ranibizumab Injection in a Patient With Age-Related Macular Degeneration.

Ranibizumab is a monoclonal antibody fragment targeted against vascular endothelial growth factor (VEGF) A isoform (VEGF-A). This study aimed to report a case of esophageal ulcer that developed soon after intravitreal ranibizumab injection in a patient with age-related macular degeneration (AMD). A 53-year-old male patient diagnosed with AMD received ranibizumab through intravitreal injection in the left eye. Mild dysphagia occurred 3 days after receiving intravitreal ranibizumab injection for the second time. The dysphagia exacerbated remarkably and was accompanied by hemoptysis 1 day after receiving ranibizumab for the third time. Severe dysphagia accompanied by intense retrosternal pain and pant emerged after injecting ranibizumab for the fourth time. An esophageal ulcer was observed through ultrasound gastroscopy, covered with fibrinous tissue, and surrounded by flushing and congestive mucosae. The patient received proton pump inhibitor (PPI) therapy combined with traditional Chinese medicine (TCM) after discontinuation of ranibizumab. The dysphagia and retrosternal pain were gradually relieved after treatment. Afterwards, the esophageal ulcer has not relapsed since permanent discontinuation of ranibizumab. To our best knowledge, this was the first case of esophageal ulcer related to intravitreal ranibizumab injection. Our study indicated that VEGF-A played a potential role in the development of esophageal ulceration.

Heterotopic Gastric Mucosa in Middle Esophagus Complicated with Esophageal Ulcers.

Heterotopic gastric mucosa (HGM) of esophagus, primarily occurring in cervical esophagus, is usually asymptomatic. A healthy woman (mid-40s) with postprandial heartburn was diagnosed with middle esophageal HGM and esophageal ulcers by esophagogastroduodenoscopy. Using 8-channel pH monitoring, a sensor near the HGM area detected postprandial acid phase (pH 3-4), while areas adjacent to the proximal and distal sensors were neutral, suggesting acid secretion from the HGM. A biopsy showed fundic gland tissue expressing H+/K+-ATPase and pepsinogen-I. Oral vonoprazan improved the clinical symptoms and endoscopic findings. This is the first report using 8-channel pH monitoring to diagnose extremely rare middle esophageal HGM.

Metachronous Esophageal Ulcers after Immune-mediated Colitis Due to Immune Checkpoint Inhibitor Therapy: A Case Report and Literature Review.

Although cases of gastrointestinal toxicity of pembrolizumab have been reported, cases of acute immune-mediated colitis accompanied with metachronous esophageal disorders (esophagitis and ulcer) are rare. We herein report a case of acute colitis and metachronous esophageal ulcers due to an immune-related adverse event following concomitant pembrolizumab chemotherapy for lung adenocarcinoma. To our knowledge, there have so far been no reports of cases in which both acute immune-mediated colitis and metachronous esophageal ulcers developed. We therefore report the details of this case along with a review of the pertinent literature.

Esophageal achalasia with mucosal damage due to enteric-coated aspirin.

A 76-year-old man was referred to our hospital for examination and treatment of dysphagia. He has been taking enteric-coated aspirin for myocardial infarction. Esophagogastroduodenoscopy (EGD) revealed the presence of esophageal ulcers in the distal esophagus and five to six tablets of enteric-coated aspirin. The esophageal ulcers were believed to have been caused by the retention of aspirin within the esophagus due to achalasia. We substituted enteric-coated aspirin with powdered aspirin. A follow-up EGD performed 1 month later showed improvement of esophageal mucosa. The patient was diagnosed with type I achalasia. Per-oral endoscopic myotomy was performed, and his symptoms improved after the procedure. Although a few studies have investigated the direct effect of aspirin, none of them has reported on the direct effect of aspirin on the esophagus. It might be effective to administer powdered aspirin for patients with achalasia to prevent esophageal ulcers caused by the direct effect of aspirin.

A Case of Refractory Esophageal Ulcer Caused by Radiotherapy for Hepatocellular Carcinoma.

A 77-year-old man who underwent radiotherapy for hepatocellular carcinoma 6 months prior consulted for esophageal obstruction. Esophagogastroduodenoscopy revealed an esophageal ulcer caused by radiotherapy for hepatocellular carcinoma. He was treated with dietary counseling and vonoprazan. After 9 months, the ulcer improved but a moderate stenosis remained. Several factors such as high fraction size, history of chemotherapy, and stress associated with food intake might involve in the development of a radiation-associated ulcer. Opportunities to choose radiotherapy for hepatocellular carcinoma may increase, so we hypothesize that esophageal ulcers might be a complication that should be noted associated with this therapy.

Esophageal Ulcers Associated with Ulcerative Colitis: A Case Series and Literature Review.

Ulcerative colitis, a chronic and recurrent inflammatory disease, is localized to the colonic mucosa but can affect other organs and lead to various complications. Gastroduodenitis associated with ulcerative colitis has been reported. However, little is known about esophageal ulcers. We herein report two rare cases of esophageal ulcers associated with ulcerative colitis. Furthermore, the clinical and histological characteristics of 18 previously reported cases are summarized. This case series and literature review will encourage the accurate diagnosis and treatment of esophageal ulcers associated with ulcerative colitis.

Possible involvement of autophagy in esophageal ulcers in anorexia nervosa.

Although patients with anorexia nervosa (AN) present with various gastrointestinal disorders, little has been understood regarding the incidence and pathophysiology of gastrointestinal ulcers related to AN. A 20-year-old woman with a past history of AN was hospitalized for further examination of dysphagia and chest pain. Her nutritional status was very poor as evidenced by very low body mass index. Esophagogastroduodenoscopy detected longitudinal and geographical ulcers in the entire circumference of the cervical and upper esophagus. Enhanced expression of autophagy-related proteins, LC3B and p62, was seen in the esophageal epithelium surrounding the active ulcers. Expression of these autophagy markers disappeared from the esophageal epithelium soon after the nutritional rehabilitation. Given the fact that starvation and malnutrition are potent inducers for autophagy, these findings suggest that autophagy might be involved in the development of gastrointestinal ulcers in patients with AN.

Esophageal Ulcer Due to Ectopic Pancreatic Tissue: A Case Report.

Heterotopic pancreatic tissue, known as pancreatic rest, is a pancreatic tissue that lacks anatomic and vascular continuity with the main body of the pancreas. Common locations for this tissue include the stomach, duodenum, jejunum, Meckel diverticulum, and ileum. In this report, we present a case of a patient whose pancreatic rest was diagnosed primarily during the investigation of dysphagia with solid foods and it was located in the mid esophagus as an unusual location.

Two cases of esophageal ulcer after surgical treatment for ulcerative colitis.

The incidence of postoperative esophageal ulcers has been rarely reported associated with severe ulcerative colitis (UC). We report two cases of esophageal ulcers accompanied by acute necrotizing esophagitis after undergoing surgery for severe UC. Both patients, 47- and 53-year-old, were diagnosed with severe UC and underwent subtotal colectomy with sigmoid mucous fistula and ileostomy. In both cases, they had epigastralgia or digestive track bleeding and upper gastrointestinal endoscopy revealed an esophageal ulcer with acute necrotizing esophagitis accompanied by a black degeneration of mucosa after surgery. Conservative treatments improved the lesions. Esophageal stricture requiring endoscopic dilatation occurred in both cases. An acute UC requiring surgery seems to warrant caution in the merger of esophageal ulcer and acute necrotizing esophagitis.