Dabigatran-Induced Esophageal Injury: A Case Report
Atrial fibrillation (AF) is a significant risk factor for stroke, increasing the incidence of stroke by fivefold. For many years, warfarin has been the primary anticoagulant prescribed to reduce thrombotic risk in AF patients. However, due to its unpredictable pharmacokinetics, the need for frequent international normalized ratio (INR) testing, and complex food-drug interactions, warfarin has been increasingly replaced by direct oral anticoagulants (DOACs). Dabigatran, a potent, competitive, and reversible DOAC that directly targets thrombin, was approved by the US Food and Drug Administration (FDA) in 2010 as an alternative antithrombotic option for nonvalvular AF.
The Randomized Evaluation of Long-Term Anticoagulation Therapy (RE-LY) trial, which compared warfarin with dabigatran in AF patients, demonstrated that dabigatran is as effective as warfarin in preventing stroke or systemic embolism. However, the adverse effects of dabigatran also warrant attention. Among these, dabigatran-induced esophagitis (DIE) has emerged as a notable concern, with several case reports highlighting this issue. Recent studies suggest that elderly patients are more susceptible to DIE. However, this case report presents a younger male patient who developed DIE after taking dabigatran.
The patient was a 37-year-old male with a two-year history of symptomatic, drug-refractory paroxysmal AF. He was referred to the cardiology center for catheter ablation. The patient had no prior comorbidities, including gastrointestinal (GI) issues. Following a successful ablation procedure, he was prescribed 150 mg of dabigatran etexilate twice daily to prevent stroke and pantoprazole once daily to prevent esophageal injury. Approximately two months after starting these medications, the patient presented to the GI clinic with a four-day history of dysphagia and retrosternal discomfort. His vital signs were stable. An esophagogastroduodenoscopy (EGD) revealed erosive esophageal mucosal changes in the middle esophagus. The patient was advised to replace dabigatran with rivaroxaban while continuing pantoprazole. His symptoms improved within seven days.
Since its introduction to the Chinese market in March 2013, dabigatran has increasingly replaced warfarin as the preferred antithrombotic option for nonvalvular AF due to its safety and convenience. Unlike other DOACs, dabigatran contains a tartaric acid core as an excipient to reduce variability in its absorption. However, if the capsule adheres to the esophageal wall, the locally released tartaric acid can damage the esophageal lining, which may explain the mechanism of DIE. Therefore, it is crucial to take dabigatran with sufficient water (200–300 mL) or food and to maintain an upright position for at least 30 minutes after ingestion.
Previous studies have indicated that elderly patients are more prone to drug-induced esophagitis due to prolonged esophageal peristalsis, diminished esophageal contraction amplitude, and reduced saliva production. Recent studies on DIE also found that the majority of affected patients are elderly. However, the patient in this case was a younger male who developed esophagitis despite correctly ingesting dabigatran and using pantoprazole prophylactically. This raises questions about whether proton-pump inhibitors (PPIs) can effectively alleviate esophageal injury caused by the local dissolution of dabigatran. The underlying mechanism of DIE remains to be further explored.
The esophagus is located close to the posterior wall of the left atrium, and the reported incidence of esophageal injury in patients undergoing radiofrequency catheter ablation (RFCA) can be as high as 47%. Given the upper gastrointestinal non-bleeding adverse events associated with dabigatran, it is unclear whether dabigatran-induced esophageal injury could exacerbate esophageal changes and increase the incidence of left atrial-esophageal fistula (LAEF), a potentially lethal complication of catheter ablation for AF. Additionally, since the symptoms of DIE and LAEF overlap, clinicians should specifically inquire about GI symptoms in patients after RFCA and provide clear instructions on the correct administration of dabigatran. If DIE is suspected, dabigatran should be replaced with other anticoagulants such as rivaroxaban or apixaban, and potent PPIs should be prescribed, although this approach remains empirical.
In conclusion, while dabigatran offers a convenient and effective alternative to warfarin for stroke prevention in AF patients, its potential to cause esophageal injury, particularly in the form of DIE, cannot be overlooked. This case report highlights the occurrence of DIE in a younger patient, emphasizing the need for awareness and proper administration techniques to minimize the risk of esophageal injury. Further research is needed to elucidate the mechanisms of DIE and to determine the efficacy of PPIs in preventing or mitigating this adverse effect. Clinicians should remain vigilant for GI symptoms in patients taking dabigatran, especially those who have undergone RFCA, and consider alternative anticoagulants when DIE is suspected.
doi.org/10.1097/CM9.0000000000001173
Was this helpful?
0 / 0