Antacid Therapy May Lead to Lung Infections in Esbriet-Treated IPF Patients, Study Reports

Antacid Therapy May Lead to Lung Infections in Esbriet-Treated IPF Patients, Study Reports

Antacid therapy (AAT) may lead to major digestive problems and severe lung infections in idiopathic pulmonary fibrosis (IPF) patients who take Esbriet (pirfenidone), a study reports.

The research, “Antacid Therapy and Disease Progression in Patients with Idiopathic Pulmonary Fibrosis Who Received Pirfenidone” was published in the journal Respiration.

Gastroesophageal reflux disease (GERD) may contribute to IPF progression, some studies have reported. In fact, the incidence of GERD is considerably higher in IPF patients than the general population.

AAT is one of the treatment options for GERD. AAT’s impact on IPF disease progression has been a subject of debate, particularly when administered with Esbriet, a widely used IPF therapy.

Researchers decided to investigate AAT’s effect on IPF progression in patients receiving Esbriet.

They analyzed data from IPF patients enrolled in three clinical trials: CAPACITY 2 (NCT00287716), CAPACITY 1 (NCT00287729) and ASCEND (NCT01366209).

The 623 patients, who received 2,403 mg of Esbriet a day, were divided into two groups – the 44% receiving AAT and the 56% who weren’t.

Researchers compared several parameters in the groups over 52 weeks, including pulmonary function, tolerance to exercise, hospitalizations, adverse events, and survival.

They used a number of measurements to determine whether the patients’ IPF had progressed. One was a decrease in forced vital capacity (FVC), a measure of lung function, of 10% or more. Another was a decrease in six-minute walking distance, a test of exercise capacity, of 50 meters or more. The third measurement of disease progression was a patient’s death.

Researchers found no statistically significant differences between the AAT and non-AAT groups in most parameters. They included disease progression — 24.9 versus 30.6%; mortality rate from all causes — 2.9 versus 4.0%; IPF-related mortality rate — 1.1 versus 2.0%; hospitalization rate from all causes — 16.1 versus 18.3%. In addition, AAT patients had a mean percentage change in FVC of –2.7%, versus –3.1% in the non-ATT group.

AAT patients did show a relative decline in FVC of 10% or more, however, and they were more prone to developing severe gastrointestinal problems and pulmonary infections.

Overall, this study “does not suggest that AAT might be beneficial as a treatment for IPF in combination with pirfenidone,” researchers wrote, since patients may be at higher risk of developing severe digestive problems and lung infections.

“We believe that the role of AAT in IPF, either alone or in combination with antifibrotic drugs, should be prospectively assessed in a randomized, double-blind, placebo-controlled trial before being considered a specific treatment for IPF,” researchers concluded.


  1. Anton Michel says:

    I am worried that the way this is reported may cause some people to stop taking their antacid therapy with negative consequences.
    I do not have full access to the paper but I wonder if you or the authors have considered the possibility that the effects seen are due to Esbriet exacerbating pre-existing GERD and causing GI/pulmonary lung problems rather than suggesting that antacid therapy is not a beneficial treatment in combination with Pirfenidone?. The distinction between the 2 possibilities is very important.
    I have GERD that was almost silent (despite an Hiatus Hernia) until I started Pirfenidone. My own experience is that once I reached the full dose of Pirfenidone my GERD increased and was almost out of control for a period and this caused a dramatic decline in lung function (subsequent LFTs showed a 10% decline in both FVC and DLCO). This decline was rapid, as measured using an exercise-induced desaturation test, and occurred over a 2 week period of intense GERD (belching, regurgitation, acid taste etc) and the decline only stopped once I increased my GERD medication (night-time ranitidine, more care with PPI dosing, twice daily PPI, Gaviscon/Alginate) and took various other steps to address my GERD (smaller meals, eliminating certain foods, raised bed). Since I have introduced these treatments my GERD has become more tolerable and I have not suffered any further declines in Lung function. As a result, I feel that antacid therapy (and treating GERD) was beneficial in helping me cope with the GI side effects of Pirfenidone (and possible associated pulmonary effects) rather than the antacid therapy being responsible for any detrimental effects as described in the paper. I would be worried that if anyone with GERD stopped taking their antacid therapy while on Pirfenidone they might make their condition worse.

  2. Anton Michel says:

    With respect to above comment – I have just noticed in the abstract of the paper that the study was conducted on the placebo group and not the Pirfenidone group. However you say that the study looked at those on Pirfenidone. This has a major impact on how you interpret the paper and should be corrected.

    I also found a podcast where the authors says that the bottom line of paper is that antacids (GERD meds) should not be used alone as an IPF treatment, particularly in patients with no sign of the disease (ie Silent GERD). The issue about antacids and Pirfenidone is not discussed to best of my knowledge. I still feel it is best to remove any reference to pirfenidone and antacids from article in case it causes people on both to stop taking their antacids

  3. Anton Michel says:

    Please ignore 2nd comment – that relates to the Lancet paper by the same authors that was published in March 2016 and which was conducted on Placebo group. I mistook this older paper for the current paper when I went back to check on the publication you refer to here. The abstracts for the 2016 and 2017 papers are almost identical and easy to mix up. The original concerns expressed in first comment above remain.

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