Got heartburn? Avoid these common acid-blocking drugs

That’s where PPIs come in. Sold under brand names like Prilosec (omeprazole) and Nexium (esomeprazole), PPIs work by curbing production of stomach acid. Doctors prescribe these drugs to treat GERD, a condition that develops when stomach acid backs up into the esophagus. PPIs also treat Helicobacter pylori, a bacteria that can cause ulcers in the stomach and small intestine.

If you have silent reflux, however, you do not get heartburn. Many people do not feel pain at all – or at least it’s only minor. That is why it is called “silent” reflux. Most doctors treat refluxers who have GERD (short for gastroesophageal reflux disease).

These include prescription-strength famotidine (Pepcid), nizatidine and ranitidine (Zantac). These medications are generally well-tolerated but long-term use may be associated with a slight increase in risk of vitamin B-12 deficiency and bone fractures. Medications to reduce acid production.

Although symptoms were similar in the two treatment groups at the start of the study, a big difference in symptoms was seen in the weeks after the active treatment group stopped taking the PPI. Reimer and colleagues recruited 120 healthy adults with no history of acid reflux disease for the study. “We have known for years that long-term treatment with PPIs induces a temporary increase in the secretion of acid, but the thinking has been that this probably wasn’t clinically relevant,” lead researcher Christina Reimer, MD, of Copenhagen University tells WebMD. PPIs like Aciphex, Prilosec, Prevacid, Nexium, and Protonix are among the most widely used prescription medications in the world. By one estimate, 5% of adults in developed countries take the acid-reducing drugs.

The American Gastroenterological Association reported in 2017 that PPI users should not be routinely screened for bone mineral density, magnesium, or vitamin B12, which is mind-boggling to me. (58) Not all studies have confirmed correlations between nutrient deficiencies and acid-suppressing drugs, but patients need to be informed about the real risks of PPI use, especially as more and more take them for extended periods of time. Gastroesophageal reflux disease (GERD) causes uncomfortable, painful symptoms-but the health risks of the drugs used to treat it can be even more distressing.

  • The consensus document went on to review health related quality of life data pertinent to the cardinal reflux symptoms, heartburn and regurgitation to define ‘troublesome’.
  • Furthermore, the growing number of reports about the different adverse events of long-term PPI treatment drive patients to seek alternative therapeutic options.
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However, none of these findings necessarily mean that the patient’s symptoms are caused by reflux. Even within the domain of typical esophageal symptoms (heartburn, regurgitation, chest pain), there are distinct phenotypes of incomplete PPI response to consider. There is the immediate problem that no symptom is 100% specific for GERD. Hence, persistent heartburn, regurgitation or chest pain may alternatively be related to esophagitis of another etiology (eosinophilic, infectious, pill), severe dysmotility such as achalasia, rumination, functional heartburn, or functional chest pain. And then, within the spectrum of GERD there are instances in which reflux continues to cause symptoms despite PPI therapy.

Conceptual model of the pathophysiological triggers of GERD symptoms. The fundamental abnormalities are of symptomatic reflux events and prolonged clearance. However, the effect of reflux in eliciting symptoms is linked to the toxicity of gastric juice even though this factor is usually normal in GERD patients.

If you use PPI for more than a few weeks, the stomach will produce more acid once you stop using the PPI. If the food stays longer in the stomach due to PPIs, then there is more time for reflux. It is even possible for PPIs to increase silent reflux symptoms. If a two-week treatment helps, GERD is the likely reason of the symptoms. If not, it’s probably something else.

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