I'm not a Doctor, Pharmacist, or Healthcare Practitioner, but, in reading the following Abstract, it would seem that Pepsin might be contributing to your issue:Reflux Revisited: Advancing the Role of Pepsin/www.ncbi.nlm.nih.gov/pmc/articles/PMC3216344
Gastroesophageal reflux disease is mediated principally by acid. Today, we recognise reflux reaches beyond the esophagus, where pepsin, not acid, causes damage. Extraesophageal reflux occurs both as liquid and probably aerosol, the latter with a further reach. Pepsin is stable up to pH 7 and regains activity after reacidification. The enzyme adheres to laryngeal cells, depletes its defences, and causes further damage internally after its endocytosis. Extraesophageal reflux can today be detected by recognising pharyngeal acidification using a miniaturised pH probe and by the identification of pepsin in saliva and in exhaled breath condensate by a rapid, sensitive, and specific immunoassay. Proton pump inhibitors do not help the majority with extraesophageal reflux but specifically formulated alginates, which sieve pepsin, give benefit. These new insights may lead to the development of novel drugs that dramatically reduce pepsinogen secretion, block the effects of adherent pepsin, and give corresponding clinical benefit.
Also, one of the above authors, Peter Dettmar, is referenced in the following articles:What Is Silent Reflux? The Mechanism Revealed!/www.refluxgate.com/what-is-silent-refluxInterview: Prof. Peter Dettmar – the Role of Pepsin in LPR/www.refluxgate.com/peter-dettmar-pepsin
I hope this helps. Or, at least, leads you to something that helps.