Phantosmia, the perception of an odor when no external odorant is present, sits within a broader family of qualitative olfactory disorders that also includes parosmia, in which a real odor is perceived in a distorted form. Clinicians generally group smell disturbances into quantitative problems, such as reduced sensitivity or complete loss of smell, and qualitative problems, in which perception is altered or invented. Quantitative losses are far more commonly reported and studied, which is partly why a case of phantom cigarette smoke tied to digestive disease stands out. The olfactory system’s wiring also helps explain why smell symptoms can be so unsettling: olfactory signals travel to structures involved in memory and emotion, and irritation anywhere along the nasal mucosa, olfactory epithelium, or central olfactory pathways can potentially distort perception. Because phantom odors can occasionally signal serious underlying conditions, including tumors, epileptic foci, or neurodegenerative disease, the authors of the report were careful to weigh alternative explanations before suggesting a reflux connection.

The temporal pattern in this case is what gives the observation its interest. The patient’s heartburn and bloating worsened for a week before the smoke sensations began, the olfactory episodes fluctuated alongside her digestive symptoms, and both briefly returned together during a flare before subsiding for good. This kind of symptom concordance, in which two seemingly unrelated complaints rise and fall in parallel, is often more persuasive than simple improvement after treatment, because it reduces the chance that the association is coincidental. The authors noted that the patient herself perceived the connection and adjusted her diet accordingly, an observation that, while subjective, illustrates how patients sometimes detect symptom relationships before formal testing can confirm them.

Several mechanisms could plausibly link reflux to smell disturbances. Refluxate containing acid and bile can reach the pharynx and larynx, and experimental and clinical work has suggested that this material may inflame the nasal and upper airway mucosa. Chronic inflammation of the olfactory epithelium can damage olfactory receptor neurons or alter their signaling, potentially producing both quantitative losses and qualitative distortions. Microaspiration of refluxate into the airway during sleep is another proposed pathway, and it is notable that this patient’s episodes clustered around sleep and waking. Additionally, vagal reflexes connecting the esophagus and airway could theoretically modulate nasal sensation, although this remains speculative. The authors of the case report did not identify which mechanism applied to their patient, and no objective olfactory testing was performed, so the pathway remains an open question.

The prior literature on reflux and smell provides useful context. Studies have documented impaired odor threshold, discrimination, and identification in patients with GERD, and some work has correlated the severity of reflux with subjective taste and smell complaints. A scoping review concluded that while the evidence base is limited and heterogeneous, several studies support an association between laryngopharyngeal reflux and olfactory dysfunction. More persuasively, a prospective study found that measured olfactory function improved after twelve weeks of proton pump inhibitor therapy in patients with laryngopharyngeal reflux, suggesting that the relationship may be at least partly reversible with acid suppression. What none of these studies established was a link specifically to phantosmia, which is the gap this case report begins to fill. The distinction matters because quantitative and qualitative olfactory disorders may involve different mechanisms; a phantom odor suggests aberrant firing or disinhibition within the olfactory system rather than simple receptor damage.

The diagnostic workup in this case also illustrates the practical challenges of evaluating phantosmia. Formal olfactory testing, such as standardized smell identification batteries, was not performed, nor was ambulatory reflux monitoring, which would have objectively correlated reflux episodes with olfactory symptoms. The patient declined recommended upper endoscopy, leaving the hiatal hernia and reflux documented only on barium esophagram. After a fall, a head CT showed no acute intracranial abnormality, but that scan was obtained for trauma evaluation rather than as a targeted assessment of the olfactory complaints, and no EEG, dedicated brain MRI, or neurologic consultation was completed. These gaps mean that focal epilepsy, in particular, was considered but not definitively excluded. The déjà vu that accompanied the episodes is a feature that neurologists typically associate with temporal lobe seizures, and the authors acknowledged this possibility while noting that the episodes occurred during routine waking activities without loss of consciousness and that the tight coupling with heartburn argued against a purely epileptic process.

The alternative diagnoses considered reflect the standard differential for phantom odors. Migraine with aura can produce olfactory hallucinations, and this patient carried that diagnosis. Allergic rhinitis, which she also had, is a well-recognized cause of smell disturbance through mucosal inflammation. Psychiatric conditions, medications, and prior head trauma round out the usual considerations. The authors’ approach of treating the most likely contributor while keeping alternatives in view is consistent with general guidance that unexplained phantosmia warrants evaluation for neurologic, sinonasal, and psychiatric causes before attributing symptoms to a gastrointestinal source.

The treatment response adds another layer of interest. The patient took omeprazole each morning before breakfast, a timing chosen to maximize acid suppression when proton pumps are most active after eating. She also adopted lifestyle measures including trigger avoidance, earlier meals, head-of-bed elevation, and weight management. Because she was already using intranasal corticosteroids and an oral antihistamine for allergic rhinitis without a change in that regimen when the olfactory symptoms began, the authors argued that the improvement was more plausibly attributable to the reflux-directed therapy than to any new rhinitis treatment. Still, the outcomes were entirely patient-reported, and placebo effects or natural symptom fluctuation cannot be excluded in a single unblinded case.

The authors were appropriately measured in their conclusions, emphasizing that a single case cannot establish causation. Case reports serve primarily to generate hypotheses and alert clinicians to possibilities they might otherwise overlook. If the association between GERD and phantosmia is real, confirming it would require systematic studies with objective olfactory testing, validated reflux monitoring such as pH impedance, and comparison groups. Until such evidence exists, the practical takeaway for clinicians is less about treatment and more about attention: patients presenting with phantom odors may merit questions about digestive symptoms, and patients with reflux flares who report new smell disturbances may deserve a fuller evaluation rather than immediate reassurance. The case also underscores the value of careful timelines in clinical documentation, since the parallel course of heartburn and olfactory symptoms was only visible because both were tracked over months.

For patients, the report offers a reminder that symptoms in one organ system can sometimes manifest in another, and that describing symptom relationships to clinicians, as this patient did, can shape diagnosis. The complete resolution of her phantom smoke sensations by three months, alongside controlled reflux, provided reassurance during a stressful period of her life that included an international move. Whether future research will confirm reflux as a genuine cause of phantosmia, or reveal that this case reflected an unusual coincidence of two common conditions, the observation expands the recognized clinical footprint of gastroesophageal reflux disease and highlights how much remains to be learned about the interactions between the digestive tract and the senses.

Subject of Research: Phantosmia associated with gastroesophageal reflux disease in a single case report

Article Title: Case Report: When reflux smells like smoke: a case of phantosmia associated with gastroesophageal reflux

Article References: Visak, C., Ketteler, S., Husami, S., & Shafqat, I. (2026). Case Report: When reflux smells like smoke: a case of phantosmia associated with gastroesophageal reflux. Frontiers in Gastroenterology, 5, Article 1867837. https://doi.org/10.3389/fgstr.2026.1867837

Image Credits: AI Generated

DOI: 10.3389/fgstr.2026.1867837

Keywords: phantosmia, gastroesophageal reflux disease, olfactory dysfunction, proton pump inhibitor, case report, hiatal hernia, laryngopharyngeal reflux, omeprazole, olfactory hallucinations, migraine with aura, focal seizures, allergic rhinitis