Effect of Laryngopharyngeal Reflux and Potassium-Competitive Acid Blocker (P-CAB) on the Microbiological Comprise of the Laryngopharynx.

OBJECTIVE: To probe the microbiota composition progressing from healthy individuals to those with laryngopharyngeal reflux disease (LPRD) and subsequently undergoing potassium-competitive acid inhibitor (P-CAB) therapy. STUDY DESIGN: Prospective case-control study. SETTING: Academic Medical Center. METHODS: Forty patients with LPRD and 51 patients without LPRD were recruited. An 8-week P-CAB therapy was initiated (post-T-LPRD), and 39 had return visits. In total, 130 laryngopharyngeal saliva samples were collected and sequenced by targeting the V3-V4 region of the 16S ribosomal RNA (rRNA) gene using an Illumina MiSeq. Amplicon sequence variants (ASVs) and clinical indices were analyzed. RESULTS: Alpha and beta diversities were compared among the non-LPRD, LPRD, and post-T-LPRD groups, and the Observed_ASVs were not significantly different. At the same time, the Shannon and Simpson indices, unweighted Unifrac, weighted Unifrac, and binary Jaccard distance were significantly different between non-LPRD and LPRD groups. In addition, significant differences were found in the abundance of Streptococcus, Prevotella, and Prevotellaceae in the LPRD versus non-LPRD groups, and Neisseria, Leptotrichia, and Allprevotella in the LPRD versus post-T-LPRD groups. The genera model was used to distinguish patients with LPRD from those without, and a better receiver operating characteristic curve was formed after combining the clinical indices of reflux symptom index, reflux finding score, and pepsin, with an area under the curve of 0.960. CONCLUSION: Laryngopharyngeal microbial communities changed after laryngopharyngeal reflux and were modified further after P-CAB treatment, which provides a potential diagnostic value for LPRD, especially when combined with clinical indices.

Helicobacter pylori in the tonsillar tissue: a possible association with chronic tonsillitis and laryngopharyngeal reflux.

OBJECTIVE: To identify Helicobacter pylori infection in tonsillar tissue samples from patients undergoing tonsillectomy for chronic tonsillitis versus tonsillar hypertrophy, and to assess the possible relationships between H pylori and patients' sociodemographic data and laryngopharyngeal reflux. METHODS: In this prospective study, 97 patients who underwent tonsillectomy were divided into the following 2 groups: patients with chronic tonsillitis (n = 62) and patients with tonsillar hypertrophy (control group; n = 35). H pylori infection in the tonsillar biopsy samples was identified using histochemical and rapid urease tests. RESULTS: The incidence of H pylori infection was significantly higher in the chronic tonsillitis group (56.5 per cent) compared to the control group (31.4 per cent). Similar findings were obtained for both subgroups of adults (68.6 vs 42.3 per cent) and children (40.7 vs 0.0 per cent). Significant relationships between a positive H pylori finding and laryngopharyngeal reflux related signs of vocal fold oedema, diffuse laryngeal oedema and hypertrophy of the posterior commissure were revealed. CONCLUSION: H pylori infection may be related to chronic tonsillitis and laryngopharyngeal reflux.

Laryngopharyngeal reflux and Helicobacter pylori.

Laryngopharyngeal reflux (LPR) occurs when gastric contents pass the upper esophageal sphincter, causing symptoms such as hoarseness, sore throat, coughing, excess throat mucus, and globus. The pattern of reflux is different in LPR and gastroesophageal reflux. LPR usually occurs during the daytime in the upright position whereas gastroesophageal reflux disease more often occurs in the supine position at night-time or during sleep. Ambulatory 24-h double pH-probe monitoring is the gold standard diagnostic tool for LPR. Acid suppression with proton pump inhibitor on a long-term basis is the mainstay of treatment. Helicobacter pylori (H. pylori) is found in many sites including laryngeal mucosa and interarytenoid region. In this paper, we aim to present the relationship between LPR and H. pylori and review the current literature.

Relationship between clinical factors and severity of esophageal candidiasis according to Kodsi's classification.

Severe Candida esophagitis (CE) may lead to development of strictures, hemorrhage, esophagotracheal fistula, and a consequent decrease in quality of life. Although the severity of CE has been classified based on macroscopic findings on endoscopy, the clinical significance remains unknown. The aim of the study was to elucidate the predictive clinical factors for endoscopic severity of CE. Patients who underwent upper endoscopy and answered questionnaires were prospectively enrolled. Smoking, alcohol, human immunodeficiency virus (HIV) infection, diabetes mellitus, chronic renal failure, liver cirrhosis, systemic steroids use, proton pump inhibitor use, H2 blocker use, and gastrointestinal (GI) symptoms were assessed on the same day of endoscopy. GI symptoms including epigastric pain, heartburn, reflux, hunger cramps, nausea, dysphagia, and odynophagia were assessed on a 7-point Likert scale. Endoscopic severity was classified as mild (Kodsi's grade I/II) or severe (grade III/IV). Of 1855 patients, 71 (3.8%) were diagnosed with CE (mild, n = 48; severe, n = 23). In the CE patients, 50.0% (24/48) in the mild group and 23.1% (6/23) in the severe group did not have any GI symptoms. In HIV-infected patients (n = 17), a significant correlation was found between endoscopic severity and declining CD4 cell count (Spearman's rho = -0.90; P < 0.01). Multivariate analysis revealed that GI symptoms (odds ratio [OR], 3.32) and HIV infection (OR, 3.81) were independently associated with severe CE. Patients in the severe group experienced more epigastric pain (P = 0.02), reflux symptoms (P = 0.04), dysphagia (P = 0.05), and odynophagia (P < 0.01) than those in the mild group. Of the GI symptoms, odynophagia was independently associated with severe CE (OR 9.62, P = 0.02). In conclusion, the prevalence of CE in adults who underwent endoscopy was 3.8%. Silent CE was found in both mild and severe cases. Endoscopic severity was associated with characteristic GI symptoms and comorbidity of HIV infection. A decline in immune function correlated with CE disease progression.

Helicobacter pylori infection in laryngeal diseases.

Clinical studies have shown that Helicobacter pylori can be found not only in the mucosa of the stomach, but in the pharyngeal and laryngeal regions as well. The aim of this prospective case-control study was to identify H. pylori infection in the biopsy material from the larynx of the patients suffering from benign laryngeal diseases (vocal fold polyps, laryngitis) and laryngeal cancer and to investigate the possible relationships between the laryngeal H. pylori and patients' socio-demographic data and laryngopharyngeal reflux. The results of the biopsy material from 67 adult patients treated for benign laryngeal diseases and laryngeal cancer and 11 individuals of the control group revealed that H. pylori infection could be identified in more than one-third of the patients. In the majority of cases H. pylori was found in the patients with chronic laryngitis (45.5%) and laryngeal cancer (46.2%). The findings of these sub-groups significantly differed from those of the control group (9.1%) (p < 0.05). No significant relationships between H. pylori infection found in the laryngeal region and patients' demographic data, their unhealthy habits and reflux-related symptoms or signs were obtained. It could be concluded that H. pylori can colonize in the larynx of patients with benign laryngeal diseases and laryngeal cancer. To clarify the role of H. pylori as a risk factor for laryngeal diseases further research is needed.

Does Helicobacter pylori exist in vocal fold pathologies and in the interarytenoid region?

The aim of this study was to investigate the existence of Helicobacter pylori (HP) in patients with benign and malignant vocal fold pathologies. This was a prospective clinical study conducted at a tertiary-care academic medical center. Fifty consecutive patients who had undergone microlaryngoscopy between August 2007 and July 2009 were included in the study. The patients with a reflux symptom index (RSI) above 12 and a reflux finding score (RFS) above 6 were accepted as having laryngopharyngeal reflux. Patients with urea breath test (UBT), HP-IgG, and HP cytotoxin-associated gene A (CagA)-IgG positivity were diagnosed as HP positive. During laryngoscopy, two surgical specimens were obtained, one from the primary vocal fold pathology and one from the interarytenoid region. The interarytenoid biopsy specimen was used for HP culture and PCR. The specimen from the vocal fold pathology was used to investigate the presence of HP. RSI was positive in 23 (46%) patients. The RFS positivity was 56%. The presence of HP was confirmed by UBT in 35 (70%), HP-IgG in 37 (74%), and HP CagA-IgG in 38 (76%) patients. There was no difference between RFS-positive and RFS-negative patients in terms of HP-IgG and UBT. None of the interarytenoid or vocal fold specimens showed the presence of HP. HP was not found in the histological specimens of vocal fold pathologies and the interarytenoid region. The presence of HP in the gastric mucosa does not have an effect on the RFS and RSI.

Treatment of clinically diagnosed laryngopharyngeal reflux disease.

OBJECTIVES: To determine the incidence of Helicobacter pylori (HP) stool antigen (HPSA) in patients with laryngopharyngeal reflux disease (LPRD), and to make a comparison of 2 treatment regimens that have been used based on the presence or absence of HPSA positivity in patients with LPRD. DESIGN: Randomized controlled study. SETTING: Suez Canal University Hospital, Ismalia, Egypt. PATIENTS: A total of 212 patients with symptoms of LPRD. INTERVENTION: Patients were evaluated by laryngoscopy, ambulatory pH monitoring for 24 hours, and HPSA testing. Esomeprazole magnesium as a monotherapy was evaluated vs triple therapy in patients with HP infection. MAIN OUTCOME MEASURES: To determine the incidence of HPSA in patients with LPRD, and to make a comparison of 2 treatment regimens that have been used based on the presence or absence of HPSA positivity in patients with LPRD. RESULTS: Persistent dry cough and a feeling of a lump in the throat (globus sensation) were the most frequent symptoms of LPRD, while posterior laryngeal inflammation was the main laryngoscopic finding. Results from the HPSA test were positive in 57% of the studied group. Patients with negative HPSA were treated with esomeprazole as single modality with a reported improvement score of 96.6%. Patients with positive HPSA test results were divided into 2 groups: 1 received only esomeprazole, with reported improvement in 40%, whereas the second group was treated with esomeprazole, plus amoxicillin sodium and clarithromycin (triple therapy) and reported a 90% incidence of symptom improvement. CONCLUSION: The incidence of HP infection in patients with LPRD in our study was 57%. Triple therapy showed a higher cure rate in patients with HPSA-positive test results.