Use of antacids found to promote liver disease
pharmafile | October 10, 2017 | News story | Manufacturing and Production, Research and Development | biotech, drugs, liver disease, pharma, pharmaceutical
A study emerging from the University of California, San Diego, has revealed a correlation between the use of common acid reflux medications and chronic liver disease. At the heart of the study was the revelation that a particular type of medicine, proton pump inhibitors (PPI), significantly altered gut bacteria.
The research is particularly significant because of the amount of individuals who take acid reflux medicines, with as much as 10% of the population of the US taking PPIs. The number can increase seven-fold when individuals are experiencing chronic liver disease, potentially this may be caused, to a certain degree, by the use of the drugs.
It was found that stomach acid suppression altered the gut bacteria in such a way as to increase likelihood of damage to the liver and to promote three types of chronic liver disease.
“Our stomachs produce gastric acid to kill ingested microbes, and taking a medication to suppress gastric acid secretion can change the composition of the gut microbiome,” said senior author Bernd Schnabl, Associate Professor of Gastroenterology at UC San Diego School of Medicine. “Since we found previously that the gut microbiome — the communities of bacteria and other microbes living there — can influence liver disease risk, we wondered what effect gastric acid suppression might have on the progression of chronic liver disease. We found that the absence of gastric acid promotes growth of Enterococcus bacteria in the intestines and translocation to the liver, where they exacerbate inflammation and worsen chronic liver disease.”
When found in increased levels, the Enterococcus bacterium was associated with mild steatosis and increased alcohol-induced liver disease in mouse models. In long-term studying of data, the researchers found that use of PPIs was associated with an increased 10-year risk of diagnosis of alcoholic liver disease of an 8.3% higher risk of liver disease against those who never used PPIs.
The study concluded that there is a strong association between PPI use among people who abuse alcohol and risk of liver disease. Researchers also suggested that there may an increased risk in healthy individuals of liver disease as a result of use of PPIs.
However, a caveat was laid that a further large-scale and controlled clinical trial would have to be established to ascertain firm links, beyond causal association, of this relationship.
The study noted that there are inexpensive alternatives to PPIs, though these may also exhibit a relationship between the reduction of gastric acids and the rise of Enterococcus bacteria. It further advised that some individuals using PPIs could benefit from non-pharmacological options for reducing heartburn, such as losing weight, reducing intake of alcohol and caffeine.
Ben Hargreaves
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