Laryngopharyngeal Reflux (LPR) 2022 Research

Laryngopharyngeal Reflux Research Findings (2022)

Brief takeaways from LPR research in 2022 are compiled below in list format.

We be burnin’ – Sean Paul

Age associated with LPR: Older age is associated with increased risk of LPR.

Alginate suspension vs. PPI (omeprazole): Thrice daily administration of alginate suspension (magnesium alginate) might be as effective as omeprazole (20 mg) – when combined with diet/lifestyle changes for the treatment of LPR.

Allergic rhinitis as a predictive characteristic (?): One study found that, after adjusting for various confounds, allergic rhinitis (AR) has the highest predictive value of any characteristic for LPR. AR positively correlates with LPR and LPR rates are higher among patients with AR.

Allergies & LPR: Patients with allergies may have increased incidence of LPR-related symptoms.

Anatomic & manometric abnormalities: Standalone LPR presents with anatomic and manometric abnormalities that are distinct from comorbid LPR+GERD – and both standalone LPR and comorbid LPR+GERD have distinct abnormalities relative to healthy controls.

Anxiety & depression: Are strongly associated with the occurrence, development and treatment efficacy of refractory (i.e. treatment-resistant) laryngopharyngeal reflux (LPR). Even among individuals who don’t think they have anxiety/depression may benefit from pharmacological treatment.

Cancer: LPR was suggested as a possible link to laryngeal cancer in young adult patients.

Carbonated beverages linked to LPR: There’s a significant dose-response between intake of carbonated beverages and laryngopharyngeal reflux disease (LPRD). Patients with this condition should be advised to avoid carbonated beverages.

Chocolate consumption & LPR: A study found that individuals with LPRD have a higher rate of chocolate consumption. (Chocolate contains theobromine which can cause LES relaxation.)

COVID-19 infection: There’s a plausible mechanism by which COVID-19 infection could cause and/or exacerbate preexisting LPR. Additionally, some researchers think that COVID-19 may provoke a variety of laryngeal symptoms as a result of binding to ACE-2 receptors in the nasopharynx (wherein it has the highest viral load) and causing subsequent inflammation.

Dental disorders in LPR: Patients with LPR have higher rates of dental disorders regardless of the presence of pepsin. More sensitivity, erosion/wear, decay, missing teeth, filled teeth, demineralization, etc. LPR patients also have altered salivary pH (impaired buffering capacity) and lower salivary flow relative to those without LPR.

Dysphonia from LPR: A subset of individuals seem to experience dysphonia as a symptom of LPR. Treating LPR with a combination of dietary changes, PPIs, magaldrate, and alginate – for 3 to 6 months reverses the dysphonia.

Eustachian tube dysfunction: One study found that laryngopharyngeal reflux disease (LPRD) independently correlates with abnormal eustachian tube function (evidenced by ETS-7 scores). PPI treatment reverses eustachian tube dysfunction resulting from LPRD.

Eye problems from LPR: Higher RSI scores for LPR are more common among individuals with dry eye disease (DED) and are associated with more severe ocular symptoms in patients with dry eye disease and other ocular conditions. Some believe that LPR may cause eye problems or damage over time.

Gaviscon advance: Both Gaviscon Advance (GA) and Gaviscon Double Action (GDA) seem to protect/preserve epithelial barrier function from pepsin-acid mediated insult.

Hard voice onset: Patients with LPR may be more susceptible to hard voice onset than those without LPR.

Higher anxiety = more successful surgery (?): One study found that individuals with high anxiety/hypervigilance scores were more likely to respond significantly to anti-reflux surgery for LPR and GERD.

Laryngeal diseases influenced by LPR (?): LPR may play different roles in specific laryngeal diseases such as vocal cord polyps, vocal cord leukoplakia, and laryngeal carcinoma.

Low BMI linked to LPR: A study found that high BMI was negatively correlated with LPRD – and that those with a low BMI are more likely to have LPRD.

Microbiota dysbiosis in LPR: Dominant microflora in the laryngopharynx of LPRD patients was significantly different from that of healthy people, suggesting that the change of laryngopharynx microbiota may play an important role in the pathogenesis of LPRD.

No link between OSA & LPR (?): One study found no definitive link between OSA & LPR. Theoretically: (1) LPR could cause apnea by inflaming the airways, throat, and/or sinuses – and (2) OSA could trigger/exacerbate LPR during apnea events (drawing gastric contents into the nasopharynx).

Obstructive sleep apnea (OSA) & LPR link (?): One study involving 68 LPR patients found a link between RSI/RFS values + pepsin in tears (associated with LPRD) and AHI/ODI scores (associated with OSA).

Persistent throat symptoms vs. LPR: Some physicians/patients may use the term laryngopharyngeal reflux to encompass persistent throat symptoms. That said, the term “persistent throat symptoms” is more appropriate because LPR is a specific clinical entity wherein reflux needs to be validated as the cause.

Poor sleep quality + shorter sleep duration linked to LPR: Poor subjective sleep quality and shorter night sleeping time – are both correlated with laryngopharyngeal reflux disease (LPRD). Improving sleep quality and extending night sleeping time may help treat LPRD.

Predicting LPR treatment responses (?): One study found that hiatal hernia (or lack thereof), baseline RSS (reflux symptom score), and 6-week RSS (after PPI + alginate use for 6 weeks) – seemed to predict whether someone would respond to LPR treatment.

Psycho-emotional health correlates with reflux severity: One study found that psycho-emotional health correlated with symptom intensity of both GERD and LPR.

Recurrent respiratory papillomatosis: LPR is common in patients with recurrent respiratory papillomatosis (RRP) – significantly more common in RRP patients than healthy controls.

Sleep abnormalities: One study reported zero association between LPR and OSA (despite ~45% of patients with OSA having symptoms of LPR) – but significant associations between LPR and sleep score questionnaire data and excessive daytime sleepiness – were found.

Sleep disorders cause/sustain LPRD (?): Evidence suggests that sleep disorder is an independent risk factor for development of laryngopharyngeal reflux disease (LPRD). Sleep disorder also worsens anxiety and depression in patients with LPRD. Treating sleep disorders may help simultaneously counteract LPRD.

Sleep-related laryngospasm (SLR) in LPR: A small study found that LPR may cause sleep-related laryngospasm (SLR). Effective treatment for LPR seems to completely stop the sleep-related laryngospasm in most patients.

Smoking associated with LPR: Multiple studies have found associations between smoking and LPR.

Unilateral Vocal Fold Hypomobility (UVFHM): May be associated with LPR.

Vocal signals & symptoms of LPR: Individuals with LPR tend to have a “rough” vocal quality type with “slight degree of deviation.” A subset of individuals with LPR will have clear “deviation” evidenced by scores on VoiSS.

Note: I’ll update this page at various intervals throughout 2022 as more LPR-focused research is published.

Table of Contents

LPR Research 2022

Included below are summaries of papers (published in 2022) in which laryngopharyngeal reflux (LPR) is a primary focus.

April 2022

Correlation between refractory LPRD & Symptoms of Anxiety and Depression (R)

Huang et al.: “Anxiety and depressive symptoms influence the occurrence, development, and treatment efficacy of refractory LPRD. Attention to and targeted treatment of anxiety and depressive symptoms can help improve the treatment outcomes of patients with LPRD.”

  • 28 patients with LPRD were evaluated for anxiety and depression and treated with both omeprazole (20 mg, b.i.d.); flupentixol (antipsychotic); and melitracen (tricyclic antidepressant).
  • When LPRD remains unresponsive to PPI therapy after 2+ months, psychological disorders commonly occur – particularly anxiety and depression.
  • Patients with LPRD may present with chest distress, dizziness, and/or other physical discomfort symptoms without organic pathological changes on cardiovascular/cerebrovascular examinations.
  • This study found that reflux symptoms and objective signs (i.e. visual presentation) are more severe in patients with anxiety and depression.
  • The result of this study is consistent with evidence correlating LPRD with mental/psychological factors.

Critical thinking…

It’s possible that individuals with “refractory” LPRD developed anxiety and/or depression due to the disease itself rather than had anxiety and/or depression prior to LPRD onset. We also don’t know whether all patients legitimately had LPRD – diagnoses may have been inaccurate.

This is a small study with just 28 patients so may be subject to underpowering – such that results may have been the same regardless of intervention(s).

There was no randomization, blinding, or control group (e.g. placebo recipients) in this study – making it difficult to know whether the benefit observed following flupentixol/melitracen was due to a placebo effect.

Additionally, it is unknown as to whether flupentixol/melitracen are legitimately improving LPRD or merely improving tolerability and/or altering perception of LPRD symptoms (such that they’re perceived as less intense by patients).

We also don’t know whether the benefit from flupentixol/melitracen was actually due to treating anxiety/depression – as its therapeutic effects could’ve been primarily due to normalization of: (1) CNS activity; (2) vagal nerve function; and/or (3) the gut-brain axis – from a pathogenic (LPR-sustaining) state.

Why might this be possible? Because patients who failed to reach thresholds for “anxiety” and “depression” on tests still derived benefit from flupentixol/melitracen for LPRD.

Authors theorized the following: “After treatment, the mental state of the patient improves, gastrointestinal autonomic nerve dysfunction is regulated, and visceral hypersensitivity is reduced.”

They also believe that: “Mental factors can change hormone secretion and the kinetic response in the GI tract through cerebral intestine reflexes and stress while regulating esophageal sensations – causing patients to perceive low-tone esophageal stimuli and feel pain and discomfort.”

Studies have shown that depression is associated with autonomic function control disorders which may be related to the nervous system and pathological basis of functional impairment.

Association between LPR & OSA in adults (R)

Tamin et al.: “There was no significant difference in RSI (reflux symptom index) and RFS (reflux finding score) between OSAS and non-OSAS groups.”

  • Study attempted to correlate LPR (as measured by RSI & RFS) with OSAS (obstructive sleep apnea syndrome).
  • 64 subjects underwent anamnesis to complete the RSI and ESS (Epworth Sleeping Scale) and were then divided into: OSAS & non-OSAS groups based on the AHI (apnea-hypopnea index) obtained via polysomnography.
  • Both groups also underwent flexible fiberoptic nasopharyngeal/laryngoscopy exam to evaluate RFS.
  • LPR was determined based on a combination of RSI & RFS.
  • Average BMI of the OSAS group was significantly higher than the non-OSAS group. Most subjects with OSAS exhibited mild-to-moderate symptoms (AHI 10-29) and severe OSAS occurred in 7 subjects.
  • Average RSI/RSF values did NOT differ significantly between non-OSA, mild-to-moderate OSA, and severe OSA subjects.
  • RSI/RFS did NOT correlate with AHI and proportion of LPR between ESS(+) vs. ESS(-) groups was almost equal.
  • This study supports the idea that LPR does NOT correlate with sleep apnea.

Glottic Insufficiency in the Vertical Plane in Patients with Unknown-Source Unilateral Vocal Fold Hypomobility (R)

Xu et al.: “Unexplained UVFHM patients have higher RSI and RFS compared to control subjects, warranting further research about the relationship between UVFHM and LPR.”

  • Aim: Evaluate the laryngeal CT and strobe laryngoscopy signs of unilateral vocal fold hypomobility (UVFHM) in patients with well-closed glottises in the horizontal plane.
  • 18 subjects with well-closed glottises were examined via laryngoscopy: 9 with unilateral vocal fold hypomobility with unknown etiology vs. 9 healthy matched subjects with symmetrical bilateral vocal fold movement.
  • Results: Patients with unexplained UVFHM have higher RSI and RFS scores relative to controls – suggesting a possible association between UVFHM and LPR.

GERD & Salivary Pepsin in Patients with Heterotopic Gastric Mucosa in the Upper Esophagus (R)

Xiong et al.: “GERD, especially GERD with proximal acid reflux and related symptoms was common in HGMUE patients. The salivary pepsin test could be an additional useful test for testing reflux in HGMUE patients, but it will not replace MII-pH.”

  • Researchers evaluated whether pepsin could be used to diagnose GERD – especially in proximal reflux – in HGMUE patients.
  • 153 HGMUE patients and 50 healthy volunteers participated.
  • Measures: RSI; endoscopy; barium ESG; HRM; 24-hour pH-metry; salivary pepsin test.
  • Results: Salivary pepsin test showed a sensitivity of 85.9% and specificity of 56.9% for diagnosing GERD. Male sex, RSI, AET, proximal acid reflux episodes – positively predicted the occurrence of pepsin (+) in HGMUE patients.

Critical thinking…

This study involved patients with HGMUE and 95 (62.1%) were diagnosed with GERD – but it remains unclear as to how many actually had LPR.

Additionally, it remains unknown as to whether salivary pepsin tests are more or less useful in HGMUE patients relative to patients without HGMUE but LPR or GERD.

Note: Heterotopic gastric mucosa (HGM) refers to gastric mucosal tissue outside the stomach.

Distinct microbiota dysbiosis in patients with LPR compared to healthy controls (R)

Chen et al.: “Dominant microflora in the laryngopharynx of LPRD patients was significantly different from healthy people, suggesting that the change of laryngopharynx microflora may play an important role in the pathogenesis of LPRD. Smoking, drinking, eating habits, and age correlated with different genus levels of the laryngopharynx microbiota.”

  • 23 patients with LPR underwent 8 weeks of PPI therapy vs. 23 healthy controls – had laryngopharynx secretions collected and the microbiota composition was analyzed with sequencing.
  • Results: No significant difference in microbial alpha and beta-diversity between the groups. Some advantageous bacteria were significantly different:
    • Prevotella was significantly higher in the LPR group than controls.
    • Fusobacterium and Porphyromonas were significantly lower in the LPR group than controls.
    • Smoking status positively correlated with Pectin, Lactobacillus, and Clostridium.
    • Alcohol was negatively correlated with Streptococcus.

Critical thinking…

This study tells me almost nothing and included just 23 LPR patients and 23 controls.

Do changes in the microbiota actually cause LPR? Unlikely, but possibly. No evidence of causality.

What came first the LPR or the microbiota dysbiosis in the laryngopharynx? Unclear. Possibly co-emerged as a result of reflux events altering the microbial composition of the laryngopharynx.

Are changes in the microbiota a result of specific diet/lifestyle choices associated with LPR development/persistence (e.g. carbonated beverages, high-fat foods, acidic foods, smoking/nicotine, alcohol intake, eating late at night, binge eating, etc.).

Are changes in the microbiota a result of refluxate and reflux events? This would be my guess. Stomach contents regularly back-flowing up the esophagus/laryngopharynx likely alters microbial composition.

Could the changes in microbial composition actually be protective? Although this report implies that the microbiota changes are unfavorable (“dysbiosis”) – it’s possible that recomposition of microbiota could somehow be protective or a defense mechanism in LPR.

Could the changes be explained by PPI therapy? The patients with LPR underwent 8 weeks of PPI therapy which is known to alter microbial composition due to stomach acid changes – perhaps this is the most logical explanation. (Might’ve been more interesting to evaluate microbial composition pre-PPI therapy.)

Long-term upper aerodigestive sequelae as a result of COVID-19 (R)

Allisan-Arrighi et al.: “In patients with persistent dyspnea, dysphonia, or dysphagia after recovering from SARS-CoV-2, early otolaryngology consultation should be considered. Accurate diagnosis and prompt management of these common underlying etiologies may improve long-term patient outcomes.”

  • Researchers conducted a retrospective analysis of patients who presented with laryngeal complaints post-COVID infection.
  • Voice, airways, and/or swallowing symptoms were examined and reviewed to determine whether these may have resulted from COVID-19 infection.
  • 81 patients met inclusion criteria for the study.
  • Common symptoms included: dysphonia (71.6%); dysphagia/odynophagia (19.75%); and sore throat (11.11%).
  • Intubated patients were more likely to be diagnosed with granulomas – whereas non-intubated patiens were significantly more likely to be diagnosed with: muscle tension dysphonia and LPR.
  • 19/81 patients (23.45%) were diagnosed with laryngopharyngeal reflux (LPR) – and this diagnosis was significantly more common among non-intubated patients (18/50) than intubated patients (1/31).

Critical thinking…

Researchers state that a large volume of patients presented to outpatient medical facilities with laryngeal dysfunction after recovery from COVID-19.

The etiology of laryngeal manifestations may be the inflammatory nature of COVID-19 infections – and the upper digestive tract is the primary target of SARS-CoV-2.

SARS-CoV-2 enters the upper digestive tract by attaching to ACE-2 receptors – and has a high viral load in the oropharynx and nasopharynx.

Theoretically, SARS-CoV-2 might cause LPR or exacerbate preexisting LPR for some individuals.

That said, LPRD is a very common condition – estimated to affect 18.8% of those in the Greek general population – with a higher prevalence rate between ages 50-64. (R) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4687326/

The mean age of patients with LPR in this study was ~45.84 years old (+/- 12.13 years).

This study has numerous limitations including: retrospective analysis, small sample size, and unknown laryngeal status prior to COVID-19.

Furthermore, it is unclear as to whether COVID-19 infection was the true cause of LPR in any of the patients diagnosed – as it may have merely exacerbated preexisting LPR symptoms OR been nothing more than a correlational factor.

March 2022

Persistent throat symptoms vs. LPR (R)

O’Hara et al.: “This study demonstrates that individual symptoms cannot be used to group patients. This analysis supports the use of a broad umbrella term such as “persistent throat symptoms.”

  • Aim: Explore a clinical trial’s baseline dataset for patterns of presenting symptoms which might provide a more rational basis for treatment.
  • 344 participants in the “Trial of Proton-Pump Inhibitors in Throat Symptoms” were analyzed: age; BMI; RSI; C-RSS; LPR-health-related QoL; and RFS (endoscopic examination).
  • Measures: Questionnaires & objective examinations.
  • Results: Throat clearing and globus were the highest ranked scores for the participants. Increasing age was inversely associated with symptom severity. There was no relationship between RFS and any of the 3 questionnaires. EFA (exploratory factor analysis) produced a 7-factor model with clinically meaningful labels: voice, cough, GI symptoms, airway symptoms & dysphagia, throat clearing, lump in throat, and life events.
  • Conclusion: Individual throat/voice symptoms should not be used to categorize groups of patients – as this is unreliable. A term such as “persistent throat symptoms” is more appropriate than “laryngopharyngeal reflux.” Why? Because many individuals with persistent throat symptoms do NOT have LPR.

Reflux Symptom Index & Singing Voice Handicap Index in Singing Students (R)

Nacci et al.: In case of significant RSI for LPR, it is possible to observe a significant association with some symptoms described in SVHI. RSI and SVHI administered to singers in the form of SVHI10-LPRD can represent a simple screening to reveal possible alterations in signing voice that correlate to LPR.

  • Aim: Analyze the correlation between RSI and SVHI in a group of singing students with a specific anamnestic questionnaire which analyzes physical, social, emotional and economic impacts of voice problems.
  • 42 singing students (ages 16-46) participated in the study.
  • Measures: Singing Voice Handicap Index (SVHI) & Reflux Symptom Index (RSI)
  • Results: 31% of participants were suspected of having LPR due to RSI scores above 13. SVHI scores revealed disordered voices in 71.4% of participants. There was no relationship between RSI and SVHI score. Specific items on SVHI (#1, #5, #20, etc.) correlated with RSI.
  • Researchers proposed using a combined SVHI-10-LPRD questionnaire to effectively diagnose LPR in singers.
  • Limitations: Small sample size. No objective confirmation of LPR (e.g. 24-hour pH monitoring). Unclear as to how well SVHI-10-LPRD actually works.

Impact of LPR on Occurrence & Clinical Course of Recurrent Respiratory Papillomatosis (R)

Gluvajic et al.: “LPR is common in RRP patients and significantly more prevalent compared to healthy controls. Our results show that saliva analyses are a better office-based tool than RSI questionnaires and RFS scores for diagnosing LPR in RRP patients.”

  • Aim: Determine whether LPR is a trigger for RRP and how it might alter the clinical presentation of RRP.
  • 106 subjects in this study: RRP (N=36); LPR (N=28); healthy controls (N=46).
  • Measures: RSI; RFS; saliva analysis (pH, pepsin, bile acid, pepsin enzyme activity)
  • Results: RRP group showed significant differences in RSI and RFS scores relative to LPR patients in RSI and RFS. RRP group showed significantly higher values in all measures (RSI, RFS, saliva markers) than the healthy controls.
  • Critical thinking: Sample size is small – such that results may be due to random chance. Unclear as to how LPR patients were diagnosed (some may have been misdiagnosed). If LPR is common in RRP – then why were there significant differences in RSI/RFS scores between LPR and RRP groups? It could also be possible that RRP causes elevations in RSI/RFS scores relative to healthy controls – without LPR being the cause.

Effects of Hard Voice Onset on Objective Function in Patients with LPR (R)

Xu et al.: “Changes in vocal production may occur in LPR patients, causing them to be more susceptible to hard voice onset.”

  • Aim: Examine the rates of hard voice onset in patients with LPR and effects of hard voice onset on objective voice function in patients with LPR.
  • Sample: 40 patients with confirmed LPR vs. 40 healthy subjects (non-LPR)
  • Measures: Laryngeal high-speed video-endoscopy by experienced laryngologists. Laryngologists determined presence or absence of hard voice onset in each subject. LPR patients were divided into hard voice onset vs. non-hard voice onset groups. Voice onset time (VOT) was measured and compared between the groups of LPR patients. Laryngeal aerodynamic exams were performed.
  • Results: Inter-rater consistency was substantial between the laryngologists for hard voice onset and non-hard voice onset. 17/40 (42.5%) of patients with LPR had hard voice onset – significantly more than controls (8/40 – 20%). LPR patients had significantly greater VOT, PTP, and shimmer than in non-hard voice onset groups.

Alginates for Protection Against Pepsin-Acid Induced Aerodigestive Epithelial Barrier Disruption (R)

Samuels et al.: “GA and GDA preserved epithelial barrier function during pepsin-acid insult better than placebo suggesting that protection was due to alginate. These data support topical protection as a therapeutic approach to GERD and LPR.”

  • Aim: Assess the topical protective capacity of alginate-based Gaviscon Advance (GA) and Double Action (GDA) against pepsin-acid mediated aerodigestive epithelial barrier dysfunction in vitro.
  • Immortalized human esophageal and vocal cord epithelial cells cultured in transwells were treated with liquid formula GA, GDA, matched-viscous placebo, or saline (control) – then treated with: saline, acid (pH 3-6), or pepsin (0.1-1 mg/mL) at pH 3-6 – for 1 hour.
  • Endpoint measure was taken of horseradish peroxidase (HRP) allowed to diffuse across monolayers for 2 hours.
  • Results: Pepsin at pH 3-6 increased HRP flux through cultures pretreated with saline or placebo; acid alone did not. GA and GDA prevented barrier dysfunction.
  • Limitations: In vitro – not necessarily generalizable to in vivo (patients with actual reflux diseases). No comparison products (non-Gaviscon) with alginates – or generic alginate suspensions were evaluated.

February 2022

Vocal deviation in individuals with suggestive signs and symptoms of LPR (R)

Sartori et al.: “Individuals with deviated voice reported higher occurrence of LPR related vocal signals and symptoms measured by VoiSS and RSI.”

  • Aim: Verify and compare vocal deviation in quality, vocal symptoms, and reflux symptom index in patients with clinical diagnosis of LPR.
  • 100 patients with LPR had their voices analyzed: 34 were “adapted” and 66 were “deviated.”
  • Average vocal quality type was “rough” and a “slight degree of deviation.”
  • Average scores on VoiSS (Voice Reflux Symptom Scale) and RSI of individuals with deviated voices were significantly higher than those with adapted voices.
  • Researchers noted that the theories about LPR disease make it impossible to draw any firm conclusions.

Analysis of effects of LPRD & PPI treatment on Eustachian Tube function in Patients with OSA (R)

Yan et al.: “LPRD may be a considerable factor for the high incidence of abnormality rate of ETS-7 in OSA patients. PPI therapy is of significant value in improving eustachian tube function in OSA patients with LPRD.”

  • Examine the effect of LPRD and PPI treatment on eustachian tube function in patients with obstructive sleep apnea (OSA).
  • Measures: ETS-7 (eustachian tube score-7)
  • Groups: OSA-only; OSA + LPRD; control.
  • Results: No difference in age, sex, smoking, drinking between 3 groups. BMI in control group was lower than other groups. Pre-PPI therapy ETS-7 in OSA + LPRD group was significantly different from the OSA-only group and controls. PPI therapy normalized ETS-7 scores in the OSA + LPRD group. Multivariate analyses revealed that only LPRD had an independent correlation of abnormal ETS-7 score.

Acoustic measurements are useful therapeutic indicators of patients with dysphonia-related to reflux (R)

Lechien et al.: “Acoustic measurements may be an interesting indicator of treatment in LPR patients who reported dysphonia.”

  • Aim: Determine utility of acoustic measurements as therapeutic outcomes for patients with dysphonia related to LPR.
  • 109 patients with LPR based on HEMII-pH divided into 2 groups based on presence of dysphonia (49 dysphonic vs. 60 non-dysphonic).
  • Treatment consisted of dietary changes, PPIs, magaldrate, and alginate for 3-6 months.
  • Measures: RSS; RSA; percent jitter; percent shimmer; noise-to-harmonic ratio (NHR).
  • Results: Baseline clinical and acoustic features were similar between groups at baseline. RSS & RSA significantly improved from pre-treatment to 3-month post-treatment in both groups. Jitter, Shimmer, and NHR significantly improved from pre-treatment to 3-month post-treatment in dysphonic patients. Acoustic parameters were unchanged in patients without dysphonia.

LPR: Evolution & Predictive Value of Symptoms and pH-impedance Features on Clinical Evolution (R)

Lechien et al.: “Hiatal hernia, baseline RSS, and 6-week RSS were the most predictive indicators of therapeutic effectiveness in patients with LPR.”

  • Aim: Investigate features of patients with LPR who don’t respond to medical treatment.
  • 148 patients with LPR at 24-hour pH-impedance monitoring were recruited from 3 university centers and treated with PPI + alginate for 3-6 months and categorized as: mild-to-moderate responders; high responders; or non-responders based on RSS (reflux symptom score) at 6 months.
  • Variables such as: epidemiology, HEMII-pH, GI endoscopy findings, baseline RSS & reflux sign assessment, and early therapeutic response (6-week RSS) – were documented.
  • Results: 40 mild-to-moderate responders (20-60% RSS change); 76 high responders (>60% RSS change); and 32 non-responders. Non-responders presented more often with hiatal hernia and lower esophageal sphincter (LES) insufficiency compared to responders. Baseline RSS and number of pharyngeal reflux events were predictive of 6-month therapeutic response. Early therapeutic response (6 weeks) was predictive of the 6-month response.

Prevalence of LPR-Related Symptoms in Patients with Allergy (R)

Hamdan et al.: “The results of this study provide evidence that patients with allergy have increased incidence of LPR related symptoms using the RSS.”

  • 84 allergy patients enrolled in this study: 52 filled RSI & 32 filled RSS.
  • Demographic data included: age, gender, history of smoking, eczema history, atopy, asthma, food & drug allergy.
  • 36 of 52 patients received RSI = allergic to at least one allergen.
  • 21 of 32 patients received RSS = allergic to at least one allergen.
  • Results: No significant difference in number of positive RSI scores between patients with at least one allergy relative to patients with no allergy. Individuals with positive RSS scores were more likely to have allergy relative to those with negative RSS scores.

Critical thinking…

This study examined the prevalence of LPR-related symptoms in allergy patients – which is NOT the same as primary laryngopharyngeal reflux (LPR)… just means symptoms are related.

Many conditions present with LPR-related symptoms – but this does NOT mean that patients actually have laryngopharyngeal reflux (LPR) or laryngopharyngeal reflux disease (LPRD).

For example, an undetected longstanding allergy may cause: globus sensation, postnasal drip, frequent throat clearing, chronic cough, etc. – all of which are “LPR-related symptoms.”

In other words, there’s such significant overlap in symptoms, that even if someone has LPR-related symptoms – it doesn’t mean that they even have any LPR.

Nonetheless, it is definitely possible that there’s causal interplay between allergy and LPR such that: (A) allergy causes and/or exacerbates LPR; and/or (B) LPR causes and/or exacerbates allergy.

Certain types of allergies (e.g. food allergies) may cause gastroesophageal reflux and/or laryngopharyngeal reflux – as an ongoing reaction until exposure to the allergenic substance ceases.

It’s also possible that certain physiological changes associated with LPR cause or exacerbate allergy (and vice-versa) – without the LPR condition itself causing or exacerbating allergy AND without allergy causing or exacerbating LPR.

We should also consider that some patients with chronic and/or untreated allergies end up misdiagnosed with laryngopharyngeal reflux disease (LPRD) due to significant symptom overlap between the conditions.

Although this study used both RSI (reflux symptom index) and RSS (reflux symptom score) – it’s problematic in that we don’t actually know if reflux is occurring! Someone with untreated allergy will likely have a high RSI and RSS – regardless of whether there’s any reflux.

For this reason, it would’ve been much smarter for authors to employ 24-hour pH monitoring to determine the number of reflux events that occur. It would’ve also been useful to evaluate the effect of treating allergy on “LPR-related symptoms.”

Moreover, it probably would’ve been ideal to start with a sample of patients with confirmed laryngopharyngeal reflux as evidenced by 24-hour pH monitoring, transnasal endoscopy, plus RSI – rather than just RSI and RSS.

It also needs to be said that a significant number of people will likely have at least one allergy on allergy testing – such that allergy prevalence may not be much differ between those with LPR-like symptoms and those without. Additionally, there was no significant correlation between positive RSI and allergy (despite there being a correlation between RSS and allergy).

Overall there’s not much that can be concluded from this study – as there are way too many limitations.

Association of Dry Eye with LPR in Clinical Practice (R)

Bonini et al.: “Patients with DED are at eight times higher risk for having pathological RSI than NEG patients. Pathological RSI was associated with more severe ocular symptoms both in DED and non-DED patients.”

  • Aim: Evaluate the prevalence and relevance of LPR in DED (dry-eye disease) patients and those with refractive problems (RP) without DED (non-dry eye group a.k.a. NEG).
  • 245 subjects analyzed: 152 DED vs. 93 NEG (age/sex-matched).
  • Results: Pathological RSI (13+) was detected in 80 subjects: 68 (85%) with DED & 12 (15%) in control group. In NEG, pathological RSI score was associated with worsening of symptoms based on various tests (SANDE, OSDI, Shirmer scores). In DED patients, pathological RSI was associated with higher OSDI values.
  • This study indicates that DED is ~8-fold more likely in patients with pathological RSI scores (LPR) than those with non-dry eye conditions. Pathological RSI scores (LPR) were associated with worsening of ocular symptoms in DED and non-dry eye patients.
  • Overall, there seems to be a correlation between LPR and ocular symptoms/problems.

A characterization study of patients visiting the hospital due to LPR suspicion (R)

Chang et al.: “The SFAR and incidence of AR are high in patients with positive LPR, and AR may be a risk factor for LPR.”

  • This study sought to explore the characteristics of LPR and the association between LPR and allergic rhinitis (AR).
  • 102 patients with suspected LPR (from 2019-2021) were included in this prospective case-control study. Patients were divided into groups: (A) LPR-positive and (B) LPR-negative – based on 24-hour pH monitoring.
  • LPR characteristics, scores of allergic rhinitis (SFAR), and AR prevalence – were compared between groups.
  • Results: Total SFAR was significantly higher in LPR-positive patients than LPR-negative controls. Prevalence of AR was 60% in LPR-positive patients – significantly higher than LPR-negative controls (36.54%). AR positively correlated with LPR after adjusting for confounds. Prevalence of LPR with AR was 2.372-fold higher than non-AR. AR has the highest predictive value for LPR of analyzed characteristics.

Critical thinking…

AR may cause LPR – and LPR may cause AR.

Individuals with LPR may be more susceptible to developing AR as a result of LPR – and individuals with AR may be more susceptible to developing LPR as a result of AR.

It’s possible that specific genetic and/or physiological presentations are associated with predisposition to AR and LPR – despite the condition AR not causing LPR and the condition LPR not causing AR.

It’s also possible that individuals with LPR may end up misdiagnosed with AR due to symptom overlap (e.g. LPR-induced nasopharyngeal inflammation and mucus production).

Researchers did NOT evaluate whether treating the LPR improved AR symptoms – or whether treating the AR improved LPR symptoms.

Obstructive sleep apnea patients vs. LPRD (R)

Pace et al.: There seems to be a strong linear correlation between RFS & RSI scores (associated with LPRD) – and obstructive sleep apnea (AHI & ODI scores).

  • Aim: Evaluate whether LPR is more frequent in OSA patients than controls.
  • Methods: Use a non-invasive protocol with RSI, RFS test (with light vs. NBI techniques), followed by pepsin detection in tears.
  • 68 LPR patients evaluated: 45 with OSA vs. 23 without OSA.
  • Results: A strong linear relationship between AHI (apnea/hypopnea index) and ODI (oxygen desaturation index) was found – and patients who presented pepsin in tears had higher values of AHI and ODI relative to those without it. Pathological RFS, NBI, and RSI were associated with higher AHI and ODI values relative to controls.
  • Critical thinking: Since 24-hour pH monitoring was not utilized – it’s unclear as to whether patients actually had legitimate LPR (24-hour pH monitoring is gold standard). This study was also relatively small – meaning the results could’ve been due to chance.

Correlation and influencing factors between LPRD and sleep status in patients (R)

Liu et al.: “Sleep disorder may lead to the occurrence or aggravation of anxiety and depression in patients with LPRD and is an independent risk factor for the development of LPRD. Clinical attention to the treatment of sleep disorders in patients with LPRD may be conductive to improving the efficacy of LPRD.”

  • Researchers analyzed the correlation between LPRD and sleep status – as well as related factors in LPRD.
  • 416 subjects were divided into groups: (1) LPRD (RSI above 13) vs. (2) controls (RSI below 13).
  • Measures: General health information, diet/lifestyle/substance use, sleep state (PSQI), emotional state (HADS), influencing factors for LPRD, correlation between sleep state and depression in LPRD.

Results…

  • Most common symptoms in LPRD group included: foreign body sensation in throat; keep voice clear; excessive phlegm/nasal discharge reflux.
  • PSQI and HADS scores in LPRD patients were higher than those in the control group.
  • High-fat diet and high PSQI score were risk factors for LPRD. PSQI score in LPRD patients correlated with HADS score.

Researchers highlighted possible interactions between sleep disorders and LPRD via numerous mechanisms:

  1. Sleep disorders: reduce melatonin secretion, promote gastric acid/pepsin secretion, increase LES relaxation, and cause corresponding GI motility disorders and reflux diseases by disrupting the circadian rhythm.
  2. Sleep disorders: cause GI motility disorders, increasing the incidence of reflux.
  3. Sleep disorders: stimulate the formation of excessive free radicals, inhibit antioxidant capacity of cells, causing or aggravating pathological damage of multiple systems – inducing various inflammation-related diseases.
  4. Sleep disorders: might affect the reproduction of intestinal flora – which can alter brain development by itself or via metabolites, thus affecting physiological activities.
  5. Sleep disorders: associated with mental and psychological disorders – and negative emotions such as anxiety and depression may cause or exacerbate LPRD.

Critical thinking…

This study was limited by its reliance on subjective examinations (RSI, PSQI, HADS).

RSI should not be used as a standalone evaluation to determine whether someone has LPRD – and PSQI doesn’t necessarily indicate that someone has a sleep disorder.

Results would’ve been higher-quality if researchers utilized transnasal endoscopy, 24-hour pH-monitoring, and polysomnography (sleep studies) to evaluate both LPR and sleep in an objective manner.

In any regard, it’s possible that sleep disorders and subsequent physiological/psychological effects – could cause and/or exacerbate LPRD.

It’s also possible that LPRD is the underlying reason for sleep disorders OR that there’s a bidirectional relationship between sleep disorders and LPRD wherein each condition has potential to worsen or reinforce the other.

Finding relief for the self-conscious esophagus: Laparoscopic anti-reflux surgery and the esophageal hypersensitivity & anxiety scale (R)

Hill et al.: “Measures of psycho-emotional health correlate better with symptom intensity than objective pathology. We found that patients with a higher EHAS score have greater symptom severity and lower quality of life at baseline. Patients with a higher preoperative EHAS benefitted more from surgery and not less.”

Aim: Determine whether anxiety/hypervigilance as measured preoperatively with the esophageal hypervigilance scale (EHAS) is associated with improvement in GERD-specific PROMs and EHAS scores 6 months after LARS.

102 adult patients (31% male, ~64 years old) – underwent LARS (laparoscopic anti-reflux surgery) and were analyzed at baseline. 70 patients repeated surveys 6-months postoperatively.

Measures: GERD-HRQL; LPR-RSI; EHAS; standard reflux workup (endoscopy, manometry, barium swallow, pH study). For all 3 surveys, a higher score = worse symptom severity. Measures were collected at baseline (preoperatively and after 6 months post-surgery).

Results: Significant reductions in GERD-HRQL; LPR-RSI; and EHAS were noted 6 months after LARS. Higher baseline EHAS scores were independently associated with greater improvement in GERD-HRQL and LPR-RSI 6-month post-surgery. Degree of improvement in all measures was not influenced by the type of LARS performed or disease severity.

What can we learn here? Psycho-emotional health correlated better with intensity of reflux symptoms than objective pathology analysis. Individuals with higher baseline anxiety/hypervigilance benefitted more from surgery (on average) relative to those with less.

Critical thinking…

It’s possible that anxiety/hypervigilance is triggered or exacerbated by reflux conditions (LPR or GERD) in some patients – such that once the reflux was treated with LARS, the anxiety/hypervigilance diminished.

It’s possible that anxiety/hypervigilance amplified the perceived severity of reflux symptoms in some patients – such that GERD-HRQL and LPR-RSI are subjectively more severe pre-surgery in anxious/hypervigilant patients than post-surgery (when the reflux is better managed).

There may also be some sort of a placebo-like effect at play here wherein patients believe LARS will produce significant benefit for reflux conditions – such that physiological changes corresponding with this belief occur post-surgery which reduce anxiety/hypervigilance.

Because full-text of this paper was inaccessible for me, I’m unsure about the number of patients that had LPR vs. GERD vs. both LPR and GERD.

This study is limited by the fact that it did NOT objectively measure reflux severity with 24-hour pH monitoring after the study to determine degree of change in the reflux condition. For this reason, stating that psycho-emotional health correlates with reflux severity may be misleading.

Assessment of LPR & Obstructive Sleep Apnea (R)

Campanholo et al.: “Age and smoking – but not BMI – were associated with LPR. There was not statistically significant association of LPR with OSA.”

  • Researchers analyzed associations between LPR symptoms and OSA in a representative sample from a population-based study.
  • 701 subjects were enrolled in the study as a follow-up from an Epidemiological Sleep Study.
  • Measures: Sleep (polysomnography & questionnaires); LPR (RSI scores); lifestyle/habits.
  • Results: LPR was found in 17% of subjects (RSI above 13) – and OSA was present in 38.5% of subjects. In patients with OSA, the presence of LPR was 45.4% – but there was no significant association between LPR and presence of OSA. LPR was associated with older age; smoking; excessive daytime sleepiness; worse quality of life; and worse sleep score questionnaires.
  • Limitations: No objective LPR diagnosis. Inability to assess causation.
  • Critical thinking: LPR was found in over 45% of OSA patients – which seems like a lot. Generally poor sleep quality/duration may correlate with LPR given that excessive daytime sleepiness and worse sleep scores correlated with LPR.

Risk Factor-Related Lifestyle Habits of Patients with LPR (R)

Wang et al.: Patients with LPRD may have certain lifestyle habits. It is recommended to avoid carbonated beverages and enhance sleep for the treatment of LPRD.

  • Aim: Evaluate the role of lifestyle/habits in patients with LPRD.
  • 1658 subjects received questionnaires to evaluate lifestyle habits that may be risk factors for LPRD.
  • Meaures: RSI (LPRD diagnosis was based on an RSI score above 13); PSQI (sleep quality); smoking status; drinking status; physical exercise; BMI; diet/beverage intake; lifestyle.

Results…

  • Significant dose-response between carbonated beverage intake and LPRD.
  • Significant associations found between poor subjective sleep quality and shorter night sleeping time – and LPRD.
  • Reflux was significantly higher among those who sleep 3-5 hours a night vs. those who sleep 8+ hours a night.
  • High BMI may have a negative correlation with LPRD (as subjects with lower BMI were more likely to have LPRD).
  • Higher daily smoking was associated with LPRD.
  • Higher chocolate consumption rate was associated with LPRD.

Critical thinking…

RSI cannot be used to objectively diagnose LPRD. Therefore, assuming patients had LPRD based on RSI scores above 13 is problematic.

PSQI scores do not confirm reported sleep abnormalities by patients. Polysomnography would be necessary to confirm patient-reported poor sleep quality/shorter sleep time.

It’s also possible that LPRD is the reason individuals have: (1) poorer sleep quality; (2) shortened sleeping time; and (3) lower BMI – in some cases.

The Association Between Laryngopharyngeal Reflux & Insomnia (R)

Kang et al. (2022): “Patients with LPR are more likely to experience insomnia than healthy controls and the severity of reflux symptoms was related to the severity of insomnia.”

  • Aim: Determine the relationship between insomnia severity and LPR symptoms.
  • 69 patients with LPR vs. 61 healthy controls were analyzed by researchers.
  • LPR diagnosis was confirmed via 24-hour multichannel pH monitoring.
  • Measures: Reflux symptoms (Reflux Symptom Index)) & sleep disturbances (Insomnia Severity Index).
  • Results: (A) Insomnia was significantly more common in patients with LPR (46.3%) than healthy controls (29.5%); (B) Severity of reflux-related symptoms was correlated with insomnia severity; (C) Patients with LPR & nighttime reflux events are more likely to have sleep disturbances than those with LPR but no nighttime reflux.

Critical thinking…

It’s possible that insomnia plays a role in the pathogenesis and maintenance of LPR via a variety of mechanisms: (1) inflammation; (2) oxidative stress; (3) compromised physiological repair (of the esophagus) during sleep; (4) psychological stress (possible psychogenic underpinnings); (5) ANS & vagal dysfunction; (6) hormonal changes – all of which might induce esophageal dysfunction and LPR secondary to altered circadian rhythms and/or suboptimal sleep duration/quality.

The fact that the severity of LPR symptoms correlated well with insomnia severity suggests a possible causal or bidirectional relationship. That said, it is unclear as to objective insomnia symptom severity correlated with objective LPR severity vs. correlation of subjective severities vs. both (objective & subjective symptom correlation).

Similarly, it’s also possible that LPR plays a role in the pathogenesis of insomnia.  It could be that underlying physiological changes associated with LPR (e.g. inflammation of the laryngopharynx) cause symptoms such as burning, pain, discomfort, and difficulty breathing – such that this causes insomnia and interrupted sleep.

However, just because: (1) insomnia could cause LPR and/or (2) LPR could cause insomnia – doesn’t mean that any causality actually exists.

Perhaps individuals with LPR are more likely to: have medical comorbidities; use prescription medications (some might interfere with sleep); have unhealthy lifestyles/habits; use nicotine, alcohol, caffeine, etc.; and/or have undiagnosed sleep disorders (e.g. UARS & sleep apnea) – all of which could simultaneously cause and/or aggravate both LPR and insomnia.

Limitations associated with this study include: small sample size; lack of objective measurement for insomnia (sleep monitoring & polysomnography); lack of definitive LPR diagnosis (24-hour pH gives a general idea but isn’t always diagnostically accurate); failure to rule out UARS & sleep apnea; etc.

It’s also unclear as to whether researchers controlled for: substance use (e.g. psychostimulants, caffeine/coffee, nicotine, alcohol, etc.); body size/BMI (high BMI = increased apnea); and/or lifestyle/habits – as these variables may have better explained the correlation.

On May 3 (2022) – there was a reply to the letter to the editor regarding this study from Kang et al. (R)

Note: I’m unable to access the full-text of the original study and reply – and am curious about the discussion.

January 2022

Laryngopharyngeal reflux induced sleep-related laryngospasm (R)

O’Shea et al.: “SRL is a largely unknown and under-diagnosed condition. We believe this study provides supportive evidence for the causal relationship between LPR and SRL.”

  • Aim: Determine if LPR causes SLR symptoms observed in 19 patients.
  • A retrospective chart assessment of patients with SRL was performed.
  • Patients with risk factors for LPR were identified based on: smoking status, alcohol intake, dyspepsia, history of GERD, history of late-night eating, and history of eating spicy/fatty foods before bed.
  • A clinical diagnosis based on the history and response to management was made for LPR patients. All patients were advised to avoid late-night eating and those with signs of nasopharyngitis used PPIs.
  • Results: 19 patients had at least 1 risk factor for LPR and 10 had signs of nasopharyngitis on endoscopic exam. Following treatment, 17 (89.5%) reported no further SRL symptoms at 1-year follow-up.

Critical thinking…

This study suggests that LPR may cause sleep-related laryngospasm – evidenced by the fact that treating LPR with PPIs seems to stop the SLR.

That said, this was a “retrospective” study involving just 19 patients – so it’s possible that (with this small sample) results may have been attributable to random chance.

Also possible is that many individuals spontaneously recovered from SLR within 1-year of onset – irrespective of LPR improving from PPI therapy.

Reflux-related Extraesophageal Symptoms Until Proven Otherwise (R)

Suzuki et al.: “A conventional diagnostic approach using endoscopy and MII-pH may not be sufficient to evaluate patients with EES suggestive of LPR. HMII is essential to evaluate patients with EES, and APE could be a reliable indicator for successful treatment outcomes.”

  • Retrospective study involving patients with extraesophageal symptoms (EES) for 12+ weeks despite PPI therapy – without endoscopic evidence of GERD and negative MII-pH.
  • 21 patients were referred for evaluation of EES of unknown etiology and underwent laryngoscopy and HMII (hypopharyngeal MII) – which directly measures LPR events.
  • Abnormal proximal exposure (APE) was defined as LPR > 1/day and/or full column reflux (reflux 2 cm distal to UES) > 4/day.
  • 17/21 patients (81%) had APE. 8 patients who had undergone ARS (anti-reflux surgery) had significant symptom improvement in RSI.

Critical thinking…

This was a very small study with just 21 patients – such that results may have been subject to random chance rather than a true effect.

AET (acid exposure time) values may not have been accurate due to the fact that distal pH probe may not have been exactly 5 cm to the gastroesophageal junction (as a result of laroscopic placement).

AET value could’ve also been influenced by patient habitus (height, length of esophagus, etc.) – such that it’s higher/lower than what was recorded.

Recordings were for 24 hours and results of MII-pH and HMII may vary depending on specific patient conditions.

Various parameters such as gastroesophageal junction morphology, motility value of HRM test, mean nocturnal baseline impedance, and post-reflux swallow-induced peristaltic wave index in MII-pH were not utilized.

Magnesium Alginate vs. PPIs for the Treatment of LPR (R)

Pizzorni et al.: “After 2 months of treatment, LPR symptoms and signs are significantly reduced irrespective of treatment. Alginate was non-inferior to PPIs and may represent an alternative treatment to PPIs for the treatment of LPR.”

  • Aim: Evaluate the efficacy of an alginate suspension (Gastrotuss) vs. PPIs (omeprazole) in the treatment of LPR in a non-inferiority RCT.
  • 50 patients with LPR (RSI = 13+ & RFS = 7+) were randomly assigned to 2 treatment groups: (A) alginate suspension (20 mL, 3x daily) vs. (B) Omeprazole (20 mg daily).
  • Measures: RSI: Reflux Symptom Index (subjective) and RFS: Reflux Finding Score (objective).
  • It was noted that RSI & RFS scores were similar between groups at baseline.
  • Results: From baseline to 2 months post-treatment, RSI & RSF scores significantly decreased in both the alginate suspension and PPI groups. Differences between groups were not significant for RSI & RSF change.

Critical thinking…

This study suggests that both alginate suspension (20 mL, 3x daily) and omeprazole (20 mg daily) – are equally efficacious for the treatment of LPR over a 2-month period.

This was a relatively small study (50 patients – 25 patients per group) AND had zero controlling – which means the outcome could’ve been explained by: random chance, placebo-like effects, diet & lifestyle recommendations (given to all patients at baseline) and/or as a function of time (e.g. spontaneous resolution of LPR over 2 months) in one or both groups.

Additionally, non-inferiority to PPIs may not be a useful standard given that current data are inconclusive regarding the efficacy of PPIs for LPR.

We must also consider the possibility that a subset of participants diagnosed with LPR did not actually have LPR – as this is relatively difficult to properly diagnose.

Video laryngoscopy (objective signs) coupled with subjective symptoms might be effective for diagnosis in some cases – but endoscopy and/or 24-hour pH monitoring should’ve been employed to rule out other conditions.

Furthermore, perhaps it would’ve been better to include 24-hour pH monitoring to objectively record reflux events “before” and “after” treatment (2 months) for greater clarity on degree of improvement.

Limitations: Small sample size (non-inferiority margin adjusted to achieve adequate power); diagnosis of LPR was empirical (no 24-hour pH monitoring); no control group receiving lifestyle & diet recommendations; no placebo controlling; etc.

Overall I like what the researchers did in this study given the fact that their sample size was downgraded from SARS-CoV-2 spreading and 24-hour pH monitoring is time-intensive, difficult-to-tolerate for some, and costly (perhaps unfeasible for most studies).

My guess is that PPIs and alginate suspension helped some patients with legitimate LPR – particularly when combined with diet/lifestyle modifications over a 2-month span.

Anatomic & Manometric Abnormalities of the Upper & Lower Esophageal Sphincters in Patients with Reflux Disease (R)

Balouch et al.: “Anatomic and Manometric abnormalities are present in subjects with LPR with or without GERD and may contribute to the pathogenesis of reflux disease.”

  • The goal of this study was to evaluate the anatomical and manometric variations of the esophagus among those with LPR.
  • 169 patients who underwent diagnostic workup for reflux complaints with 24-hour multichannel intraluminal pH-impedance testing and esophageal manometry were included in this retrospective study.
  • There were 3 groups: (A) LPR diagnosis = 10+ proximal reflux events; (B) LPR plus GERD diagnosis = 10+ proximal reflux events & 73+ distal reflux events; (C) failing to meet diagnostic criteria for LPR and GERD.

What were the findings?

LPR group: Significantly higher UES relaxation pressures and greater UES length vs. controls. Intrabolus pressure significantly lower than control group. Significantly fewer swallows with incomplete clearance than control group.

LPR plus GERD group: Significantly shorter intra-abdominal portion of the LES vs. LPR-only group and control group. Intrabolus pressure significantly lower than control group. Distal wave amplitude significantly lower than LPR group and control group. Percentage of swallows with incomplete clearance significantly greater in LPR + GERD gropu than control group and LPR group.

Control group: LES relaxation pressure was significantly higher than LPR group and LPR/GERD group.

Dental Disorders and Salivary Changes in Patients with LPR (R)

Casciaro et al.: “The finding of demineralization and dental carries on intraoral evaluation must raise the suspicion of LPR. Reflux treatments should be aimed at correcting salivary alterations, in order to preserve the buffering capacity and salivary pH, thus preventing mucosal and dental damage.”

  • Aim: Evaluate possible association between dental disorders and LPR – focusing on the role of salivary changes.
  • 30 patients who complained of signs/symptoms associated with GERD/LPR (ages 19-69) and were referred to an otolaryngology clinic for evaluation via transnasal laryngoscopy.
  • Measures: Schiff Index Sensitivity Scale (SISS); Basic Erosive Wear Examination (BEWE); Decayed, Missing, Filled Teeth (DMFT) scores; Reflux Symptom Index (RSI); saliva analysis (qualitative & quantitative).
  • Results: LPR patients had higher rates of dental disorders – regardless of the presence of salivary pepsin and thus statistically significant higher scores on: RSI; SISS; BEWE; and VAS. These individuals also had lower salivary flow compared to healthy controls.

Critical thinking…

Sample size of the study was extremely small – meaning results could’ve been due to random chance (such that the outcomes are not an accurate depiction of dental status in LPR).

Modality of LPR diagnosis used in this study (transnasal laryngoscopy) may be inadequate for proper LPR diagnosis (such that a subset of those considered to have LPR may not have had it).

Subjective measures used to assess dental disorders might be another limitation (this was acknowledged by authors) – but this is unlikely much of a problem here.

It is important to emphasize that this is a correlation study and, even if findings are accurate, it does not prove that LPR causes dental problems (though one might hypothesize it could via refluxate entering the oral mucosa).

It’s also possible that various diet/lifestyle habits (e.g. acidic food/drink intake, smoking, alcohol/nicotine use, caffeine/coffee intake, etc.) contributing to the pathogenesis and/or persistence of LPR – better explain dental abnormalities than the actual “LPR” condition.

Additionally, it’s possible that individuals with LPR are less health conscious and thus neglect oral hygiene more significantly than those without LPR – accounting for why they developed both conditions.

Other papers…

Association between thyroid gland disorders and LPR requires esophageal functional examinations (R)

Laryngopharyngeal reflux, chronic rhinosinusitis and nasopharyngeal pH monitoring (R)

Laryngeal cancers in pediatric & young adult patients (R): The development of laryngeal cancer in young adults is multifactorial and may be linked to laryngopharyngeal reflux (LPR) – among other things such as: carcinogens, occupational factors, immunosuppression, HPV infection, and genetic polymorphisms.

Laryngopharyngeal reflux and insomnia (R)

Different characteristics of oropharyngeal pH changes in different laryngeal diseases (R): 123 patients with suspected LPRD; 45 patients with vocal cord polyps; 40 patients with vocal cord leukoplakia; 54 patients with laryngeal carcinoma – were included in this study. There were different oropharyngeal pH characteristics in patients with different laryngeal diseases – indicating that LPR may play different roles in different diseases.

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