MadSci Network: Biochemistry
Query:

Re: Are gastric complaints caused by too much HCl or too little HCl?

Date: Mon Aug 2 22:31:51 2010
Posted By: Billy Carver, Grad student, Biomedical Sciences, Vanderbilt University
Area of science: Biochemistry
ID: 1280614146.Bc
Message:

GERD/Low Stomach pH

Hello Claire –

Thank you very much for your question regarding gastroesophageal reflux disease (GERD). As I’m sure you know, GERD is a condition that affects many people and can lead to more serious diseases of the upper digestive systems. As you explained in your question, conventional wisdom suggests that GERD is primarily caused by too much acid, and thus a low pH, in the stomach. Hydrochloric acid (HCl) is pumped into the stomach by cells embedded within the lining of the stomach called parietal cells. These cells can be inhibited by several different kinds of drugs. Two of the most widely prescribed classes of drugs used in treating GERD are called Proton Pump Inhibitors (PPIs) and H2 antagonists. PPIs prevent proton pumps on parietal cells from pumping acid into the stomach, while H2 antagonists prevent parietal cells from responding to histamine – histamine activates parietal cell acid production.

 

Both of these drugs work by decreasing the amount of acid in the stomach, and this is important because pH influences how a patient perceives GERD. While two people could have stomach contents refluxing into their esophagus, it is entirely possible that only one would sense this and feel the classic heartburn symptoms of GERD. Researchers have determined that there are two primary factors that determine whether reflux will be symptomatic: pH and location. Researchers found that if the stomach liquid reaching the esophagus is less than pH 4 (more acidic), patients are more likely to feel heartburn. Similarly, if the stomach contents reached further into the esophagus it was more likely to cause perceived GERD. The point I am trying to make here is that while lowering stomach acid secretion is a treatment for the symptoms of GERD, it is not necessarily the cause of GERD – but I digress.

 

The truth is, naturally occurring low stomach acid (hypochlorhydria or achlorhydria) has not been extensively studied in patients with GERD. I was only able to find a single article that mentioned any link at all between hypochlorhydria and GERD, and it only mentioned briefly that another older article mentioned a potential correlation:

 

“There is little information in the literature on reflux symptoms in patients with achlorhydria. Palmer described 22 cases of oesophagitis in patients with achlorhydria, also suggesting that non-acid reflux can induce [esophageal] inflammation. However, in Palmer’s report, no mention was made of the symptoms experienced by his patients.”

 

Palmer, for his part, had only this to say:

 

“Twenty-two patients with achlorhydria were found to have subacute erosive esophagitis. This association, with the support of previously described histopathological evidence, indicates that refluxing acid pepsis is not the cause of this form of esophagitis.”

 

Unfortunately – and even Dr. Palmer admits this – checking the pH of the stomach or esoaphagus reliably was simply not possible in the late 1950’s, and so the reliability of this statement can be called into question. So, though he says that the patients suffered from achlorhydria, he has no way of knowing the pH of any reflux reaching the esophagus over a longer period of time. Sadly, this is really the only scientifically-reviewed journal article I could find that links low stomach acid secretion and GERD.

 

I hope this sheds a little light on your question!

Billy.

 

A. Bredenoord, A. Baron, and A. Smout. “Symptomatic gastro- oesophageal reflux in a patient with achlorhydria.” Gut. 2006;55:1054- 1055.

 

A. Bredenoord, B. Weusten, W. Curvers, R. Timmer, and A. Smout. “Determinants of perception of heartburn and regurgitation.” Gut. 2006;55:313- 318.

 

E. Palmer. Subacute erosive (‘peptic’) esophagitis associated with achlorhydria.” New England Journal of Medicine. 1960;262:927–929.

 

 


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