Re: Do antacids really produce an acid rebound?

Hi Sara,

Antacid relief of heartburn symptoms with subsequent increase in gastric pH is something thought to occur as a potential side effect of using these medications. But to look at this more carefully lets do a quick overview of gastric acid secretion stimulation and how acid production is affected by various "antacid" medications.

First, the production of acid is stimulated by 3 phases:

1. The cephalic phase, which is mediated by sight/smell and taste of food. This is due mainly to the vagus nerve stimulating parietal cells of the stomach.

2. The gastric phase, which is from the actual chemical and mechanical presence of food within the stomach. Gastrin is a chemical mediator of this phase, which is made in the gastrin-expressing cells located in the antrum of the stomach.

3. The intestinal phase, which is a very small part of this, and no one is comepletely sure how this works.

4. Other stimulating agents include Acetylcholine and Histamine, while Somatostatin acts to reduce acid secretion.

As I said above, acid secretion is stimulated by histamine. This is the same molecule stored in some white blood cells that is resonsible for the allergic reaction of iching and redness in the skin. Located on parietal cells are type 2 histamine receptors (H2s) that when activated in turn cause the cell to pump out H+ ions via a hydrogen ion protein pump.

Acid is stimulated to be released from the parietal cell by the above mentioned factors. The lining of the stomach is protected from this acid by mucus that is made by goblet cells.

So your basic "antacids" are CaCO3 (aka TUMS) and Al(OH)3/Mg(OH)2 (aka Mylanta). These essentially are very brief acting bases that neutralize acid within the esophagus and stomach. What does not occur with this is the effect of stopping acid production, rather than briefly treating the symptoms. So is it a "rebound" or just the continued production of acid finally overcoming the limited amount of bicarbonate base available? One test (1) showed that the effect of relief was greatest in cases of increased esophageal acid levels with CaCO3, but little effect on gastric [H+]. Aluminum/Magnesium preparations lasted longer in the stomach compared to Calcium however, but still the mean duration was 26 min.

Still other types of medications are available for relief of reflux/heartburn. These are the H2 blockers (H2B's) such as ranitidine (aka Zantac), famotidine (aka Pepcid), and proton pump inhibitors (PPI's) such as omeprazole (aka Prilosec) and esomeprazole (aka Nexium). Each acts on a different mechanism to slow/decrease acid production and secretion into the gatric lumen.

So, H2 blockers do exactly that; they sit on the H2 receptor and prevent histamine from activating the system. PPI's block the H+ pump, thereby preventing H+ secretion in a stimulated cell.

Studies are now starting to come out stating that an increase in [H+] has been noted in patients treated short or long term with either H2B's or PPI's (2). Theory regarding these is that PPI's do not prevent stimulation and that withdrawal of these medications cause a rebound hypersecretion of H+ in hypertrophic, or overly stimulated cells.

So what are the pro's and con's? Untreated reflux over a long duration places people at an increased risk of sqamous cell cancer of the lower esophagus. Also, in people who have an ulcer from either overuse of other types of medications (aspirin, or prednisone) or from H. pylori can have further erosion of these until either a perforation of a vessel or mucosa occurs placing them at risk of death from bleeding.

With the various antiacid medictions there are also risks in taking them. Drug interactions are the most common. Of these, the PPI's are the most notorious because they can alter the level of metabolism of other drugs and increase or decrease their potency. The H2B's can have the side effect of allergic reaction, causing delerium in the elderly and also decreasing platelet levels. Plain old TUMS can cause a rare condition in people with renal failure by causing something called Milk Alkali syndrome that can be life threatening.

So, there is some evidence out there that the various antacid medications can cause some rebound of acid production. But honestly, this is not something commonly seen. In cases where addition of these medications leads to extreme acid production there could be some other underlying problem rather than the drug itself.

Hope this helps some. Check out the references below for more details in your science library or on-line at PubMed (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed).

Good luck,

Mark Sullivan, MD

References:

1. Decktor DL, Robinson M, Maton PN, Lanza FL, Gottlieb S. Effects of Aluminum/Magnesium Hydroxide and Calcium Carbonate on Esophageal and Gastric pH in Subjects with Heartburn. Am J Ther. 1995 Aug;2(8):546-552.

2. Farup PG, Juul-Hansen PH, Rydning A. Does short-term treatment with proton pump inhibitors cause rebound aggravation of symptoms? J Clin Gastroenterol. 2001 Sep;33(3):206-9.