To review the current literature about the epidemiology, clinical presentation, diagnosis, and treatment of laryngopharyngeal reflux (LPR).
PubMed, Cochrane Library, and Scopus.
A comprehensive ...review of the literature on LPR epidemiology, clinical presentation, diagnosis, and treatment was conducted. Using the PRISMA statement, 3 authors selected relevant publications to provide a critical analysis of the literature.
The important heterogeneity across studies in LPR diagnosis continues to make it difficult to summarize a single body of thought. Controversies persist concerning epidemiology, clinical presentation, diagnosis, and treatment. No recent epidemiologic study exists regarding prevalence and incidence with the use of objective diagnostic tools. There is no survey that evaluates the prevalence of symptoms and signs on a large number of patients with confirmed LPR. Regarding diagnosis, an increasing number of authors used multichannel intraluminal impedance-pH monitoring, although there is no consensus regarding standardization of the diagnostic criteria. The efficiency of proton pump inhibitor (PPI) therapy remains poorly demonstrated and misevaluated by incomplete clinical tools that do not take into consideration many symptoms and extralaryngeal findings. Despite the recent advances in knowledge about nonacid LPR, treatment protocols based on PPIs do not seem to have evolved.
The development of multichannel intraluminal impedance-pH monitoring and pepsin and bile salt detection should be considered for the establishment of a multiparameter diagnostic approach. LPR treatment should evolve to a more personalized regimen, including diet, PPIs, alginate, and magaldrate according to individual patient characteristics. Multicenter international studies with a standardized protocol could improve scientific knowledge about LPR.
Summary Objective The aim of this paper is to shed light on the pathogenesis and pathophysiological mechanisms underlying the development of hoarseness related to laryngopharyngeal reflux disease ...(LPRD). Material and methods PubMed, Embase, and The Cochrane Library were searched for the terms reflux, laryngopharyngeal, laryngitis, voice, and hoarseness. Experimental and clinical studies providing substantial information about the occurrence of voice disorders, laryngeal histologic changes, or any pathophysiological processes related to LPRD were included by two independent investigators. Results Of the 104 studies reviewed, 47 studies that met our inclusion criteria were analyzed. LPRD leads to significant macroscopic and microscopic histopathologic changes in the mucosa of the vibratory margin of the vocal folds. More and more studies suspect that epithelial cell dehiscence, microtraumas, inflammatory infiltrates, Reinke space dryness, mucosal drying, and epithelial thickening are probably responsible for the hoarseness related to reflux and the impairment of the subjective and objective voice quality evaluations. Conclusion Future clinical studies examining the pathophysiology of hoarseness related to LPRD should take into consideration all potential mechanisms involved in the development of hoarseness.
Objectives
To investigate the role of laryngopharyngeal reflux (LPR) in the development of benign lesions of the vocal folds (BLVF).
Methods
PubMed, Cochrane Library, and Scopus were searched by ...three independent investigators for articles published between January 1990 and November 2018 providing substantial information about the role of LPR in the development of nodules, polyps, cysts, Reinke's edema, and sulcus vocalis. Inclusion, exclusion, diagnostic criteria and clinical outcome evaluation of included studies were analyzed using Preferred Reporting Items for Systematic Reviews and Meta‐Analyses criteria.
Results
Of the 155 relevant publications, 42 studies were included. Thirty‐five were clinical studies and seven were experimental research studying the impact of reflux on vocal fold tissue. Only seven clinical studies utilized objective LPR diagnoses (pH monitoring), suggesting an association between LPR and the development of nodules, polyps, and Reinke's edema. These studies were characterized by a substantial heterogeneity due to discrepancies in inclusion/exclusion criteria, diagnostic methods, and clinical outcome evaluation. The few basic science studies on this topic support that LPR creates an environment that may predispose to BLVF through changes in defense mechanisms of the vocal folds, cell‐to‐cell dehiscence, inflammatory reaction of the vocal folds, and reaction to phonotrauma.
Conclusions
Caustic mucosal injury from LPR could cause increased susceptibility of the vocal fold mucosa to injury and subsequent formation of nodules, polyps, or Reinke's edema. However, the heterogeneity and the low number of high‐quality studies limit the ability to draw definitive conclusions. Future clinical and experimental studies are needed to better identify the role of reflux in development of BLVF.
Laryngoscope, 129:E329–E341, 2019
Validity and Reliability of the Reflux Sign Assessment Lechien, Jérôme R.; Rodriguez Ruiz, Alexandra; Dequanter, Didier ...
Annals of otology, rhinology & laryngology,
04/2020, Letnik:
129, Številka:
4
Journal Article, Web Resource
Recenzirano
Odprti dostop
Objective:
To develop and validate the Reflux Sign Assessment (RSA), a clinical instrument evaluating the physical findings of laryngopharyngeal reflux (LPR).
Methods:
A total of 106 patients ...completed a 3-month treatment based on the association of diet, pantoprazole, alginate, or magaldrate with the LPR characteristics (acid, nonacid, mixed). Forty-two asymptomatic individuals completed the study (control group). The RSA results and reflux finding score (RFS) were documented for the LPR patients at baseline and after treatment. Intrarater reliability was assessed through a test-retest blinded evaluation of signs (7-day intervals). Interrater reliability was assessed by comparing the RSA evaluations of three blinded otolaryngologists through Kendall’s W. Responsiveness to change was evaluated through a comparison of the baseline and 3-month posttreatment findings. The RSA cutoffs for determining the presence and absence of LPR were examined by receiver operating characteristic (ROC) analysis.
Results:
A total of 102 LPR patients completed the study (68 females). The mean age was 53 years. The mean RSA at baseline was 25.95 ± 9.58; it significantly improved to 18.96 ± 7.58 after 3 months of therapy (P < .001). RSA exhibited good intra- (r = 0.813) and interrater (Kendall’s W = 0.663) reliabilities (N = 56). There was no significant association between the RSA, gastrointestinal endoscopy findings, and the types of reflux (acid, nonacid, or mixed) according to impedance-pH monitoring. An RSA >14 may be suggestive of LPR.
Conclusion:
The RSA is a complete clinical instrument evaluating both laryngeal and extralaryngeal findings associated with LPR. The RSA demonstrated high intra- and interrater reliabilities and responsiveness to change.
To review the recent literature on presentation, diagnosis and treatment of laryngopharyngeal reflux.
Patients with laryngopharyngeal reflux have a higher risk for gastroesophageal reflux and ...respiratory-related diseases. Many symptoms and findings are underestimated, contributing to the inconclusive results of many therapeutic trials. Additionally, little significance is given to nonacid and mixed refluxates, although a significant prevalence. The association between symptoms, signs, impedance-pH studies and pepsin detection could be the most accurate way for a clear diagnosis. 'Reflux profiling' is also important for the administration of a personalized treatment based on diet, proton pump inhibitors, alginate, magaldrate and other second-line drugs. There are only a handful of studies focusing on the addition of alginate or magaldrate to the treatment of laryngopharyngeal reflux, although their contribution has extensively been demonstrated.
Diagnosis remains controversial despite improvement in impedance and availability of pepsin detection in daily practice. With recent studies exhibiting a significant prevalence of nonacid or mixed refluxes, the addition of alginate or magaldrate to proton pump inhibitors should be considered. Future studies are needed to assess these new therapeutic schemes in moderate and severe laryngopharyngeal reflux.
Objectives/Hypothesis
Empiric proton pump inhibitor (PPI) trials for laryngopharyngeal reflux (LPR) are common. A majority of the patients respond to acid suppression. This work intends to evaluate ...once‐daily, 40 mg omeprazole and once‐nightly, 300 mg ranitidine (QD/QHS) dosing as an alternative regimen, and use this study's cohort to evaluate empiric regimens prescribed for LPR as compared to up‐front testing with pH impedance multichannel intraluminal impedance (MII) with dual pH probes and high‐resolution manometry (HRM) for potential cost minimization.
Study Design
Retrospective cohort review and cost minimization study.
Methods
A chart review identified patients diagnosed with LPR. All subjects were treated sequentially and outcomes recorded. Initial QD/QHS dosing increased after 3 months to BID if no improvement and ultimately prescribed MII and HRM if they failed BID dosing. Decision tree diagrams were constructed to determine costs of two empiric regimens and up‐front MII and HRM.
Results
Ninety‐seven subjects met the criteria. Responders and nonresponders to empiric therapy were identified. Seventy‐two subjects (74%) responded. Forty‐eight (67% of responders and 49% of all) improved with QD/QHS dosing. Forty‐nine (51%) subjects escalated to BID dosing. Twenty‐four subjects (33% of responders and 25% of all) improved on BID therapy. Twenty‐five subjects (26%) did not respond to acid suppression. Average weighted cost was $1,897.00 per patient for up‐front testing, $3,033.00 for initial BID, and $3,366.00 for initial QD/QHS.
Conclusions
An alternate QD/QHS regimen improved the majority who presented with presumed LPR. Cost estimates demonstrate that the QD/QHS regimen was more expensive than the initial BID high‐dose PPI for 6 months. Overall per‐patient cost appears less with up‐front MII and HRM.
Level of Evidence
4. Laryngoscope, 127:S1–S13, 2017
Objectives/Hypothesis
To evaluate the presence of laryngopharyngeal reflux (LPR) and the potential association between presence of LPR symptoms and obstructive sleep apnea (OSA) in a representative ...sample from a population‐based study.
Study Design
Cross‐sectional study.
Methods
Participants of the follow‐up of the Epidemiological Sleep Study were evaluated. Sleep was assessed through questionnaires and polysomnography. The presence of LPR was based on the questionnaire Reflux Score Index (RSI), and scores higher than 13 were suggestive of LPR. A general linear model test was used for comparison of continuous data and Pearson's chi‐square test was used to compare categorical variables. Predictors of LPR were obtained by regression analysis.
Results
701 were enrolled (54.8% female, 45.2% male; mean age, 50.2 ± 13.3 years). The mean apnea‐hypopnea index score was 17 ± 18.3 events/hr, and the mean RSI score was 7.0 ± 8.1. LPR was found in 17% of the volunteers, whereas OSA was present in 38.5% of the sample. Specifically, in those patients with OSA, the prevalence of LPR was 45.4%; however, there was no statistically significant association between LPR and the presence of OSA. The severity of OSA was not associated with RSI score. The presence of LPR was associated with older age, smoking, excessive daytime sleepiness and worse quality of life and sleep scores questionnaires.
Conclusions
Age, smoking, but not body mass index, were associated with LPR. There was not statistically significant association of LPR with OSA. Individuals with symptoms of LPR had greater drowsiness and worse quality of life and sleep.
Level of Evidence
3 Laryngoscope, 132:1877–1882, 2022
To psychophysically evaluate olfaction in patients with laryngopharyngeal reflux (LPR).
Prospective controlled study.
Tertiary medical center.
From January 2021 to January 2022, patients with LPR ...diagnosed with hypopharyngeal-esophageal multichannel intraluminal impedance-pH monitoring underwent psychophysical evaluation of the sense of smell. Reflux symptoms and findings were assessed with the Reflux Symptom Score (RSS) and Reflux Sign Assessment (RSA). Nasal symptoms were assessed through the Sino-Nasal Outcome Test 22 (SNOT-22). From pre- to posttreatment, patients underwent identification Sniffin' Sticks test and olfactory cleft examination. Clinical outcomes were compared between LPR patients and healthy individuals.
In total, 107 patients and 76 healthy individuals completed the evaluations. LPR patients reported significant higher RSS, RSA, and SNOT-22 scores. Psychophysical olfactory evaluations were significantly lower in reflux patients compared with controls, while there were no significant differences in olfactory cleft score. RSS and RSA significantly improved from baseline to 3 months posttreatment. SNOT-22, olfactory cleft endoscopy scale, and psychophysical olfactory evaluations did not change throughout treatment. Patients with higher number of acid pharyngeal reflux events reported lower psychophysical olfactory scores (P = .025).
LPR disease was associated with low odor identification results in patients without olfactory cleft abnormalities. The sense of smell did not improve after 3-month therapy. Future controlled studies using threshold, discrimination, and identification testing are needed.
Laryngopharyngeal reflux disease (LPRD) is an inflammatory condition in the laryngopharynx and upper aerodigestive tract mucosa caused by reflux of stomach contents beyond the esophagus. LPRD ...commonly presents with sym-ptoms such as hoarseness, cough, sore throat, a feeling of throat obstruction, excessive throat mucus. This complex condition is thought to involve both reflux and reflex mechanisms, but a clear understanding of its molecular mechanisms is still lacking. Currently, there is no standardized diagnosis or treatment protocol. Therapeutic strategies for LPRD mainly include lifestyle modifications, proton pump inhibitors and endoscopic surgery. This paper seeks to provide a comprehensive overview of the existing literature regarding the mechanisms, patho-physiology and treatment of LPRD. We also provide an in-depth exploration of the association between LPRD and gastroesophageal reflux disease.
Objectives/Hypothesis
To assess the impact of diet on the saliva pepsin concentration of patients with laryngopharyngeal reflux (LPR).
Study Design
Non‐controlled Prospective Study.
Methods
Patients ...with positive LPR regarding hypopharyngeal–esophageal impedance‐pH monitoring (HEMII‐pH) were enrolled from three European Hospitals. Patients collected three saliva samples, respectively, in the morning (fasting), and 1 to 2 hour after lunch and dinner. Patients carefully detailed foods and beverages consumed during meals and before the pepsin samples. The 3‐month treatment was based on the association of diet, proton pump inhibitors, alginate, or magaldrate regarding the HEMII‐pH characteristics. Reflux Symptom Score (RSS) and Reflux Sign Assessment (RSA) were used for assessing the pre‐ to posttreatment clinical evolution. The Refluxogenic Diet Score and the Refluxogenic Score of a Dish (RESDI) were used to assess the refluxogenic potential of foods and beverages. The relationship between saliva pepsin concentration, HEMII‐pH, RESDI, RSS, and RSA was investigated through multiple linear regression.
Results
Forty‐two patients were included. The saliva pepsin concentration of the 24‐hour period of testing was significantly associated with foods and beverages consumed during the testing period and the evening dinner (rs = 0.973, P < .001). RSS and RSA significantly improved throughout treatment. The level of saliva pepsin in the morning was a negative predictive factor of the therapeutic response regarding RSA and RSS (P < .036).
Conclusions
Foods and beverages may significantly impact the saliva pepsin concentration of patients with LPR. Patients with high‐level saliva pepsin in the morning had lower therapeutic response compared with those with low‐level saliva pepsin.
Level of Evidence
4 Laryngoscope, 131:350–359, 2021
