-
Canadian Journal of Gastroenterology &... 2019Esophageal candidiasis (EC) is the most common type of infectious esophagitis. In the gastrointestinal tract, the esophagus is the second most susceptible to candida... (Review)
Review
Esophageal candidiasis (EC) is the most common type of infectious esophagitis. In the gastrointestinal tract, the esophagus is the second most susceptible to candida infection, only after the oropharynx. Immunocompromised patients are most at risk, including patients with HIV/AIDS, leukemia, diabetics, and those who are receiving corticosteroids, radiation, and chemotherapy. Another group includes those who used antibiotics frequently and those who have esophageal motility disorder (cardiac achalasia and scleroderma). Patients complained of pain on swallowing, difficulty swallowing, and pain behind the sternum. On physical examination, there is a plaque that often occurs together with oral thrush. Endoscopic examination is the best approach to diagnose this disease by directly observing the white mucosal plaque-like lesions and exudates adherent to the mucosa. These adherent lesions cannot be washed off with water from irrigation. This disease is confirmed histologically by taking the biopsy or brushings of yeast and pseudohyphae invading mucosal cells. The treatment is by systemic antifungal drugs given orally in a defined course. It is important to differentiate esophageal candidiasis from other forms of infectious esophagitis such as cytomegalovirus, herpes simplex virus, gastroesophageal reflux disease, medication-induced esophagitis, radiation-induced esophageal injury, and inflammatory conditions such as eosinophilic esophagitis. Except for a few complications such as necrotizing esophageal candidiasis, fistula, and sepsis, the prognosis of esophageal candidiasis has been good.
Topics: Antifungal Agents; Candidiasis; Esophagitis; Humans
PubMed: 31772927
DOI: 10.1155/2019/3585136 -
Gastroenterology Jan 2018Eosinophilic esophagitis is an emerging disease that is distinguished from gastroesophageal reflux disease by the expression of a unique esophageal transcriptome and... (Review)
Review
Eosinophilic esophagitis is an emerging disease that is distinguished from gastroesophageal reflux disease by the expression of a unique esophageal transcriptome and the interplay of early life environmental factors with distinct genetic susceptibility elements at 5q22 (TSLP) and 2p23 (CAPN14). Rare genetic syndromes have uncovered the contribution of barrier disruption, mediated in part by defective desmosomes and dysregulated transforming growth factor beta production and signaling, to eosinophilic esophagitis pathophysiology. Experimental modeling has defined a cooperative role of activated eosinophils, mast cells, and the cytokines IL-5 and IL-13, mediated by allergic sensitization to multiple foods. Understanding these processes is opening the way to better treatment based on disrupting allergic inflammatory and type 2 cytokine-mediated responses, including anti-cytokine therapeutics and dietary therapy.
Topics: Adult; Age Factors; Allergens; Biopsy; Child; Cytokines; Ehlers-Danlos Syndrome; Eosinophilic Esophagitis; Eosinophils; Epigenesis, Genetic; Esophageal Stenosis; Esophagus; Female; Fibrosis; Food Hypersensitivity; Gastroesophageal Reflux; Gastrointestinal Microbiome; Genetic Predisposition to Disease; Glucocorticoids; Humans; Loeys-Dietz Syndrome; Male; Mast Cells; Prevalence; Proton Pump Inhibitors; Sex Factors; Transcriptome
PubMed: 28757265
DOI: 10.1053/j.gastro.2017.06.065 -
Acta Bio-medica : Atenei Parmensis Dec 2018Gastroesophageal reflux disease (GERD) is due to the chronic exposure of the esophageal mucosa to acid secretion from the stomach. Helicobacter pylori (H.p.) infection,... (Review)
Review
Gastroesophageal reflux disease (GERD) is due to the chronic exposure of the esophageal mucosa to acid secretion from the stomach. Helicobacter pylori (H.p.) infection, is a risk factor for the development of peptic ulcer, atrophic gastritis and gastric cancer, and causes various effects on gastric function. The relationship between GERD and H.pylori infection is still subject of debate. Background and aim: In literature no clear causal relationship has been established between GERD and H. pylori infection, although some papers support the onset of esophagitis in patients in whom the infection has been cured. Aim of this work is to review the most recent literature data about the relationship between reflux disease and H. pylori infection. Methods: Articles reviewed were found through literature searches on PubMed, Google Scholar using keywords such as gastroesophageal reflux disease, Helicobacter pylori, acid-related disorders, GERD and esophagitis.
Topics: Anti-Bacterial Agents; Causality; Esophagitis, Peptic; Gastritis; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Humans; Peptic Ulcer; Smoking; Stomach Neoplasms
PubMed: 30561416
DOI: 10.23750/abm.v89i8-S.7918 -
Gastroenterology Jan 2018Eosinophilic esophagitis (EoE) has emerged over the past 2 decades as a major cause of upper gastrointestinal morbidity. Over this time, the epidemiology of EoE has... (Review)
Review
Eosinophilic esophagitis (EoE) has emerged over the past 2 decades as a major cause of upper gastrointestinal morbidity. Over this time, the epidemiology of EoE has also rapidly evolved. EoE has transformed from a rare case-reportable condition to disease that is commonly encountered in the gastroenterology clinic, hospital emergency room, and endoscopy suite. The incidence and prevalence are increasing at rates that outpace increased disease recognition. Current incidence estimates range from 5 to 10 cases per 100,000, and current prevalence estimates range from 0.5 to 1 case per 1000. We review the data and potential reasons behind this increase, examine risk factors, and identify important areas for research into disease etiology. The article also discusses the progression of EoE from an inflammatory to fibrostenotic phenotype. An accurate view of the natural history of EoE is central to discussions with patients regarding disease prognosis and decisions about long-term use of medical, endoscopic, and diet therapies. Progressive remodelling appears to be gradual, but not universal, and the duration of untreated disease is the best predictor of stricture risk. Ultimately, prospective, long-term outcome studies focusing on multiple aspects of disease activity are needed to fully understand the natural history of EoE.
Topics: Administration, Oral; Adult; Age Factors; Child; Diet Therapy; Disease Progression; Eosinophilic Esophagitis; Esophageal Stenosis; Esophagoscopy; Esophagus; Fibrosis; Helicobacter Infections; Helicobacter pylori; Humans; Immunotherapy; Incidence; Prevalence; Prognosis; Proton Pump Inhibitors; Remission, Spontaneous; Risk Assessment; Risk Factors
PubMed: 28774845
DOI: 10.1053/j.gastro.2017.06.067 -
World Journal of Gastroenterology Aug 2019Eosinophilic esophagitis is an immune-allergic pathology of multifactorial etiology (genetic and environmental) that affects both pediatric and adult patients. Its... (Review)
Review
Eosinophilic esophagitis is an immune-allergic pathology of multifactorial etiology (genetic and environmental) that affects both pediatric and adult patients. Its symptoms, which include heartburn, regurgitation, and esophageal stenosis (with dysphagia being more frequent in eosinophilic esophagitis in young adults and children), are similar to those of gastroesophageal reflux disease, causing delays in diagnosis and treatment. Although endoscopic findings such as furrows, esophageal mucosa trachealization, and whitish exudates may suggest its presence, this diagnosis should be confirmed histologically based on the presence of more than 15 eosinophils per high-power field and the exclusion of other causes of eosinophilia (parasitic infections, hypereosinophilic syndrome, inflammatory bowel disease, among others) for which treatment could be initiated. Currently, the 3 "D"s ("Drugs, Diet, and Dilation") are considered the fundamental components of treatment. The first 2 components, which involve the use of proton pump inhibitors, corticosteroids, immunosuppressants and empirical diets or guided food elimination based on allergy tests, are more useful in the initial phases, whereas endoscopic dilation is reserved for esophageal strictures. Herein, the most important aspects of eosinophilic esophagitis pathophysiology will be reviewed, in addition to evidence for the various treatments.
Topics: Diagnosis, Differential; Diet Therapy; Dilatation; Eosinophilic Esophagitis; Eosinophils; Esophageal Mucosa; Esophageal Stenosis; Esophagoscopy; Fibrosis; Gastroesophageal Reflux; Glucocorticoids; Humans; Hypereosinophilic Syndrome; Immunosuppressive Agents; Inflammatory Bowel Diseases; Parasitic Diseases; Proton Pump Inhibitors
PubMed: 31528089
DOI: 10.3748/wjg.v25.i32.4598 -
MASCC/ISOO clinical practice guidelines for the management of mucositis secondary to cancer therapy.Cancer May 2014Mucositis is a highly significant, and sometimes dose-limiting, toxicity of cancer therapy. The goal of this systematic review was to update the Multinational... (Review)
Review
BACKGROUND
Mucositis is a highly significant, and sometimes dose-limiting, toxicity of cancer therapy. The goal of this systematic review was to update the Multinational Association of Supportive Care in Cancer and International Society of Oral Oncology (MASCC/ISOO) Clinical Practice Guidelines for mucositis.
METHODS
A literature search was conducted to identify eligible published articles, based on predefined inclusion/exclusion criteria. Each article was independently reviewed by 2 reviewers. Studies were rated according to the presence of major and minor flaws as per previously published criteria. The body of evidence for each intervention, in each treatment setting, was assigned a level of evidence, based on previously published criteria. Guidelines were developed based on the level of evidence, with 3 possible guideline determinations: recommendation, suggestion, or no guideline possible.
RESULTS
The literature search identified 8279 papers, 1032 of which were retrieved for detailed evaluation based on titles and abstracts. Of these, 570 qualified for final inclusion in the systematic reviews. Sixteen new guidelines were developed for or against the use of various interventions in specific treatment settings. In total, the MASCC/ISOO Mucositis Guidelines now include 32 guidelines: 22 for oral mucositis and 10 for gastrointestinal mucositis. This article describes these updated guidelines.
CONCLUSIONS
The updated MASCC/ISOO Clinical Practice Guidelines for mucositis will help clinicians provide evidence-based management of mucositis secondary to cancer therapy.
Topics: Amifostine; Analgesics; Anti-Infective Agents; Anti-Inflammatory Agents; Anti-Ulcer Agents; Antineoplastic Agents; Cryotherapy; Cytokines; Esophagitis; Evidence-Based Medicine; Humans; Hyperbaric Oxygenation; Intercellular Signaling Peptides and Proteins; Low-Level Light Therapy; Mucositis; Neoplasms; Oral Hygiene; Phototherapy; Proctitis; Protective Agents; Radiation-Protective Agents; Radiotherapy; Stomatitis; Sucralfate
PubMed: 24615748
DOI: 10.1002/cncr.28592 -
Clinical Microbiology and Infection :... Jan 2020Mediastinitis is a rare but severe infection, defined as an inflammation of the connective tissues and structures within the mediastinum. Due to its proximity to vital... (Review)
Review
BACKGROUND
Mediastinitis is a rare but severe infection, defined as an inflammation of the connective tissues and structures within the mediastinum. Due to its proximity to vital structures, mediastinitis represents a highly morbid pathological process associated with a high risk of mortality. In most cases mediastinitis requires treatment in the intensive care unit.
OBJECTIVES
To highlight to the reader the clinical features of mediastinitis, to attempt to define each clinical scenario, to describe the responsible pathogens and finally to depict both the medical and surgical treatments.
SOURCES
We performed a literature search of the PubMed and Cochrane libraries, limited for articles published between January 2003 and December 2018, reporting on acute mediastinitis.
CONTENT
The term covers different entities of different aetiologies including deep sternal wound infection related to sternotomy; oesophageal perforation or anastomosis leakage; and finally descending necrotizing mediastinitis, often secondary to oropharyngeal abscess. The responsible pathogens and therefore subsequent management depends on the underlying aetiology. Empirical antimicrobial therapy should cover the suspected microorganisms while surgery and supportive measures should aim to reduce the inoculum of pathogens by providing adequate drainage and debridement.
IMPLICATIONS
Literature concerning mediastinitis in the intensive care unit is relatively scarce. We have collated the evidence and reviewed the different causes and treatment options of acute mediastinitis with a particular focus on microbiological epidemiology. Future research in larger cohorts is needed to better understand the treatment of this difficult disease.
Topics: Abscess; Anti-Bacterial Agents; Bacteria; Bacterial Infections; Debridement; Drainage; Humans; Intensive Care Units; Mediastinitis; Oropharynx; Sepsis
PubMed: 31306791
DOI: 10.1016/j.cmi.2019.07.005 -
The British Journal of Dermatology Sep 2019Dupilumab blocks the shared receptor component for interleukin (IL)-4 and IL-13. It is approved in the U.S.A. for patients aged ≥ 12 years with moderate-to-severe...
BACKGROUND
Dupilumab blocks the shared receptor component for interleukin (IL)-4 and IL-13. It is approved in the U.S.A. for patients aged ≥ 12 years with moderate-to-severe atopic dermatitis (AD) uncontrolled by topical prescription medicines or who cannot use topical medicines, for patients in Japan whose AD is uncontrolled with existing therapies, for patients with moderate-to-severe AD in Europe who are candidates for systemic therapy and for patients aged ≥ 12 years for maintenance treatment of moderate-to-severe asthma uncontrolled with their current medicines. AD trials have reported increased incidence of conjunctivitis for dupilumab vs. placebo.
OBJECTIVES
To characterize further the occurrence and risk factors of conjunctivitis in dupilumab clinical trials.
METHODS
We evaluated randomized placebo-controlled trials of dupilumab in AD (n = 2629), asthma (n = 2876), chronic rhinosinusitis with nasal polyps (CRSwNP) (n = 60) and eosinophilic oesophagitis (EoE) (n = 47).
RESULTS
In most AD trials, dupilumab-treated patients had higher conjunctivitis incidence than placebo controls. Higher baseline AD severity and previous history of conjunctivitis were associated with increased conjunctivitis incidence. Conjunctivitis was mostly mild to moderate. Most cases recovered or resolved during the treatment period; two patients permanently discontinued dupilumab due to conjunctivitis or keratitis. Common treatments included ophthalmic corticosteroids, antibiotics, and antihistamines or mast cell stabilizers. Most cases were diagnosed by the investigators. In asthma and CRSwNP trials, the incidence of conjunctivitis was lower for both dupilumab and placebo than in AD trials; dupilumab did not increase the incidence compared with placebo. In the EoE trial, no patients had conjunctivitis.
CONCLUSIONS
Conjunctivitis was more frequent with dupilumab treatment in most AD trials. In dupilumab trials in other type 2 diseases, incidence of conjunctivitis was overall very low, and was similar for dupilumab and placebo. In AD, the incidence of conjunctivitis was associated with AD severity and prior history of conjunctivitis. The aetiology and treatment of conjunctivitis in dupilumab-treated patients require further study. What's already known about this topic? Ocular disorders, including allergic conjunctivitis, are common in patients with atopic dermatitis (AD). In most dupilumab AD trials, dupilumab-treated patients had higher conjunctivitis incidence than those receiving placebo. Most cases were mild to moderate and recovered or were recovering during study treatment; study treatment discontinuation due to conjunctivitis was rare. Conjunctivitis incidence was very low and similar for dupilumab and placebo in clinical trials in asthma, chronic rhinosinusitis with nasal polyps and eosinophilic oesophagitis. What does this study add? This analysis confirms and extends the results of the individual clinical trials. Baseline disease-related factors, including AD severity, prior conjunctivitis history and certain biomarkers (thymus and activation-regulated chemokine, IgE, eosinophils), were associated with increased incidence of conjunctivitis. Patients who responded well to dupilumab had reduced incidence of conjunctivitis. Further study is needed to elucidate the aetiology and treatment of conjunctivitis in dupilumab-treated patients with AD.
Topics: Adult; Antibodies, Monoclonal, Humanized; Asthma; Conjunctivitis; Dermatitis, Atopic; Eosinophilic Esophagitis; Humans; Incidence; Interleukin-4 Receptor alpha Subunit; Nasal Polyps; Placebos; Randomized Controlled Trials as Topic; Rhinitis; Risk Factors; Severity of Illness Index; Sinusitis; Young Adult
PubMed: 30851191
DOI: 10.1111/bjd.17869 -
The Journal of Allergy and Clinical... Oct 2022Transient increases in blood eosinophil counts have been observed in dupilumab clinical trials.
BACKGROUND
Transient increases in blood eosinophil counts have been observed in dupilumab clinical trials.
OBJECTIVE
To assess eosinophil counts and eosinophilia-related treatment-emergent adverse events (TEAEs) across 11 dupilumab clinical trials, comparing adult and adolescent patients with asthma and adult patients with chronic rhinosinusitis with nasal polyps (CRSwNP), atopic dermatitis, and eosinophilic esophagitis.
METHODS
Eosinophil counts, rates of eosinophilia-related TEAEs or treatment-emergent eosinophilia (>1,500 cells/μL), discontinuations, clinical symptoms, and efficacy in patients with asthma or CRSwNP with treatment-emergent eosinophilia are presented.
RESULTS
Transient increases in mean eosinophil counts were observed in dupilumab-treated patients with asthma (mean range across studies at baseline: 349-370 cells/μL; week 4: 515-578 cells/μL), CRSwNP (baseline: 440-448 cells/μL; week 16: 595 cells/μL), and atopic dermatitis (baseline: 434-600 cells/μL; week 4: 410-710 cells/μL), followed by a decline starting by week 24 to baseline or lower. No increases were seen in patients with eosinophilic esophagitis (baseline: 310 cells/μL; week 4: 230 cells/μL). In dupilumab-treated patients across all studies, rates of eosinophilia TEAEs were 0% to 13.6%. Clinical symptoms associated with increased eosinophils were rare (seven of 4,666 dupilumab-treated patients, including six cases of eosinophilic granulomatosis with polyangiitis) and occurred only in patients with asthma or CRSwNP. Eosinophilia was not associated with reduced dupilumab efficacy.
CONCLUSIONS
Transient increases in eosinophil counts with dupilumab treatment did not affect efficacy and were rarely of clinical consequence. It remains important for physicians to base judgment on individual patient history and baseline eosinophil counts and to be alert to hypereosinophilic symptoms.
Topics: Adolescent; Adult; Antibodies, Monoclonal, Humanized; Asthma; Chronic Disease; Churg-Strauss Syndrome; Dermatitis, Atopic; Enteritis; Eosinophilia; Eosinophilic Esophagitis; Eosinophils; Gastritis; Granulomatosis with Polyangiitis; Humans; Nasal Polyps; Rhinitis; Sinusitis
PubMed: 35636689
DOI: 10.1016/j.jaip.2022.05.019 -
Frontiers in Cellular and Infection... 2023Eosinophilic esophagitis (EoE) is an antigen-mediated chronic inflammatory disease of the esophagus, the prevalence of which has steadily increased in recent years. The... (Review)
Review
Eosinophilic esophagitis (EoE) is an antigen-mediated chronic inflammatory disease of the esophagus, the prevalence of which has steadily increased in recent years. The pathogenesis of EoE is not yet well-defined; however, recent studies have demonstrated that the esophageal microbiota is an essential regulator of physiological and pathological processes of EoE. Currently, research on EoE and microbiota is an emerging field of study that is receiving increasing attention. Here, we review existing EoE-related esophageal microbiota studies to explore the potential mechanisms underlying esophageal microbiota-mediated EoE. The esophageal microbiome is altered in patients with EoE. Although α diversity is usually not significantly different, an increase in and a decrease in were observed in EoE patients. The role of microbiota in initiating and perpetuating inflammation is not fully understood. Current evidence suggests that the penetration of microbiota leads to the activation of epithelial cells as well as innate and adaptive immune cells, with the subsequent release of cytokines, leading to immune responses and inflammation. The involvement of toll-like receptors in EoE also supports the potential role of the microbiota in the progression of this disease. While EoE-induced inflammation can also lead to alterations in the local microbiome. Moreover, dietary modifications, proton pump inhibitors, and corticosteroids can modulate the esophageal microbiota; however, definitive conclusions about the alterations of microbes after treatment cannot be drawn. These findings provide promising avenues for future studies.
Topics: Humans; Eosinophilic Esophagitis; Inflammation; Cytokines; Microbiota
PubMed: 37600943
DOI: 10.3389/fcimb.2023.1206343