Heartburn treatments, such as antacid therapy (AAT), may not be effective or safe as an add-on treatment for idiopathic pulmonary fibrosis (IPF) patients receiving Esbriet (pirfenidone), according to a study.
The research, “Antacid Therapy And Disease Progression In Patients With Idiopathic Pulmonary Fibrosis Who Received Pirfenidone,” was published in the journal Respiration.
Patients with IPF have a high risk of developing other health conditions, including gastroesophageal reflux disease (GERD). This condition is characterized by heartburn, indigestion, regurgitation, and chest pain. It affects considerably more IPF patients than the general population.
GERD is associated with age and smoking, which are risk factors for IPF as well. It also may be triggered by lung fibrosis, although little is known about this possible link.
Current guidelines recommend AAT as an add-on IPF therapy. It relieves symptoms of excess stomach acid, also known as heartburn. But many doctors have little confidence in its ability to help IPF patients.
“Although some studies have demonstrated that AAT is associated with longer survival time and slower disease progression,” recent analyses fail to support the notion that AAT can help prevent the progression of IPF, the researchers wrote. That has “led to some discussion on the role of AAT in IPF.”
To evaluate AAT’s effect on IPF progression in patients taking Esbriet, researchers checked the records of IPF patients who received Esbriet in three trials: the CAPACITY trials (NCT00287716 and NCT00287729) and the ASCEND (NCT01366209) trial.
The data included patients’ pulmonary function, exercise tolerance, survival, hospitalizations, and adverse side effects during 52 weeks of treatment with Esbriet and AAT.
Disease progression was defined as a decrease in respiratory capacity of 10 percent or more in a patient’s forced vital capacity (FVC) score; a decrease in exercise capacity, with the measurement being a decline of 50 meters or more in patients’ six-minute walking distance; or the death of the patient within a year.
Forty-four percent of the 623 patients received AAT. Between AAT users and non-users, no significant 52-week changes were detected in disease progression — 24.9 versus 30.6 percent; death from all causes — 2.9 versus 4 percent; IPF-related mortality rate — 1.1 versus 2 percent; hospitalization rate from all causes — 16.1 versus 18.3 percent; or mean change in percent of FVC scores. The change in FVC scores was –2.7 percent in ATT users versus –3.1 percent in non-users.
AAT use was associated with higher frequency of severe gastrointestinal side effects — 3.7 of users versus 0.9 percent of non-users — and severe lung infections — 3.7 versus 1.1.
Together, the results showed that a combination of AAT and Esbriet produced similar outcomes on most measures of IPF as Esbriet alone.
“This study does not suggest that AAT might be beneficial as a treatment for IPF in combination with [Esbriet],” researchers wrote. “The data suggest that patients with IPF receiving [Esbriet] treatment who are receiving AAT might be at a higher risk of severe pulmonary infection than those not receiving AAT, and may have more [gastrointestinal] side effects.”
The team called for more studies to assess the role of AAT in IPF, alone or combined with antifibrotic drugs. Until then, “neither the effectiveness nor the safety of AAT as a treatment of IPF can be supposed,” the team wrote.
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