Abstract
Silent gastroesophageal reflux disease (GERD) is an atypical form of reflux disease in which patients present predominantly with extra-esophageal manifestations rather than classic symptoms such as heartburn or acid regurgitation. In this form, gastric refluxate may reach the upper aerodigestive tract, leading to laryngeal or respiratory symptoms that are frequently misattributed to infectious or allergic conditions. The absence of typical gastrointestinal complaints often results in delayed diagnosis and repeated ineffective treatments. We report the case of a 27-year-old male who presented with acute dry cough and progressive hoarseness without gastrointestinal symptoms. After excluding infectious and allergic etiologies, and noting a poor response to antitussive and bronchodilator therapies, a presumptive clinical diagnosis was established. Recognition of dietary triggers and rapid symptom resolution following a 4-week empirical trial of proton pump inhibitor therapy—along with symptom recurrence upon temporary discontinuation—supported the diagnosis of silent GERD. This case highlights the importance of considering reflux-related etiologies in patients with unexplained cough and laryngeal symptoms to avoid diagnostic delays and unnecessary empirical treatments.
Keywords
Introduction
Gastroesophageal reflux disease (GERD) classically presents with heartburn and regurgitation; however, a subset of patients develop so-called silent GERD, in which extra-esophageal symptoms predominate. 1 Laryngopharyngeal reflux (LPR), a related clinical entity, may manifest with cough, hoarseness, throat clearing, or voice changes in the absence of typical gastrointestinal complaints.2-4 Diagnosing LPR remains challenging and heavily debated in the literature due to the high variability of symptom presentation, the limited specificity of laryngeal findings, and the lack of a universally accepted diagnostic gold standard. These atypical presentations are frequently misdiagnosed as viral upper respiratory tract infections, allergic conditions, or primary laryngeal disorders.
Acute and subacute cough are common reasons for outpatient medical visits and often lead to repeated empirical use of antitussives, antibiotics, or antihistamines. 5 When respiratory and infectious causes are excluded, GERD—particularly its silent form—should be considered as an underlying etiology. This case report emphasizes the diagnostic value of recognizing reflux-related triggers and therapeutic response to proton pump inhibitor (PPI) therapy in patients presenting with acute cough and hoarseness.
Case Presentation
A 27-year-old male Yemeni medical student, weighing 80 kg, presented to the outpatient clinic with a 1-week history of acute dry cough that was more pronounced at night and after meals. Three days after symptom onset, he developed progressive hoarseness of voice. He also reported mild rhinorrhea suggestive of a concurrent viral upper respiratory tract infection. The patient was a non-smoker, consumed no alcohol, had no occupational exposure to respiratory irritants, and had no history of chronic medical conditions such as bronchial asthma or allergic rhinitis. He noted a recent episode of sinusitis, which had been fully treated prior to presentation.
The patient denied heartburn, acid regurgitation, dysphagia, nausea, vomiting, abdominal pain, or any previous history of gastroesophageal reflux disease. Notably, he observed consistent worsening of cough following chocolate consumption, particularly during nighttime hours.
Prior to presentation, the patient self-administered an antitussive syrup and a salbutamol inhaler (suspecting bronchospasm) without any clinical improvement. Physical examination revealed normal vital signs, hoarseness of voice, and mild pharyngeal erythema on otolaryngologic examination. Lung auscultation was clear with no added sounds. Laboratory investigations showed mild lymphocytosis with a normal C-reactive protein level. A posteroanterior chest radiograph demonstrated clear lung fields (Figure 1).

Posteroanterior chest radiograph showing clear lung fields with normal lung parenchyma and cardiac silhouette.
Based on the nocturnal and postprandial nature of symptoms, dietary trigger association, lack of response to antitussive therapy, and the exclusion of infectious or allergic etiologies, a clinical diagnosis of silent GERD was considered. The patient was initiated on empirical PPI therapy (Lansoprazole 30 mg once daily, taken 30 minutes before breakfast) along with dietary modifications. Notably, when the patient attempted to temporarily discontinue the medication during that 1-month period, his symptoms rapidly recurred, further supporting the clinical diagnosis of reflux-related cough. After resuming and completing a full 4-week treatment course, his cough and hoarseness resolved completely.
Discussion
Silent GERD is a well-recognized but frequently underdiagnosed condition in which reflux manifests primarily through extra-esophageal symptoms rather than classic gastrointestinal complaints. Exposure of the laryngeal and pharyngeal mucosa to gastric acid and pepsin may result in inflammation, leading to hoarseness, throat irritation, and cough. 6 Additionally, reflux may activate esophagobronchial reflexes that contribute to cough even in the absence of visible esophageal injury.
In evaluating this patient, alternative causes of acute cough and hoarseness were systematically considered. Post-viral cough and acute laryngitis were deemed less likely given the progression of symptoms and lack of improvement over time. Upper airway cough syndrome (post-nasal drip) was ruled out as his recent sinusitis had been fully and effectively treated. Furthermore, cough-variant asthma was clinically excluded due to the absence of a personal or family history of atopy and the complete failure of a self-administered salbutamol inhaler. Consequently, the distinct symptom pattern strongly pointed toward an extra-esophageal reflux etiology.
In this case, several clinical features supported the diagnosis of silent GERD, including nocturnal symptom exacerbation, postprandial worsening, symptom provocation by chocolate intake, lack of response to antitussive therapy, and rapid improvement following PPI initiation. Chocolate is known to reduce lower esophageal sphincter tone, thereby facilitating reflux episodes. 4
Empirical PPI therapy is recommended in patients with suspected extra-esophageal GERD after the exclusion of alternative etiologies and may serve both diagnostic and therapeutic purposes. 7 This empirical approach is highly practical and cost-effective, particularly in resource-limited settings where objective testing may be unfeasible due to financial constraints. Ultimately, early recognition of silent GERD can prevent misdiagnosis, reduce unnecessary medication use, and shorten symptom duration, thereby improving patient outcomes.
Conclusions
Silent GERD should be considered in patients presenting with acute or subacute dry cough and hoarseness, particularly when symptoms worsen at night or after meals and fail to respond to standard antitussive or bronchodilator therapy. This case emphasizes the educational value of recognizing extra-esophageal reflux to avoid diagnostic delays and inappropriate empirical treatments. Identification of dietary triggers and assessing the response to PPI therapy provide highly valuable diagnostic insights, reducing unnecessary investigations and improving patient quality of life.
Limitations
We acknowledge that the diagnosis in this case remains presumptive, as it was established clinically and confirmed via a therapeutic trial of a PPI. No objective diagnostic evaluations—such as 24-hour esophageal pH monitoring, impedance testing, or direct laryngoscopy—were performed. While symptom improvement following PPI initiation strongly supports a reflux-related etiology, it does not definitively establish a causal relationship. However, in our resource-constrained clinical setting, pursuing expensive or invasive diagnostic procedures for an initial presentation is often unfeasible, making empirical therapy a necessary and standard approach.
Footnotes
Ethical Considerations
Ethical approval was obtained from the Institutional Review Board (IRB) of 21 September University for Medical and Applied Sciences.
Consent for Publication
Written informed consent for treatment and open-access publication was obtained from the patient.
Author Contributions
Concept and design: Hussein Mussa Muafa; Acquisition, analysis, or interpretation of data: Hussein Mussa Muafa; Drafting of the manuscript: Hussein Mussa Muafa; Critical revision of the manuscript for important intellectual content: Hussein Mussa Muafa; Supervision: Hussein Mussa Muafa.
Funding
The author received no financial support for the research, authorship, and/or publication of this article.
Declaration of Conflicting Interests
The author declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
