A bottle of antacid tablets
An antacid is any substance, generally a base or basic salt, which counteracts stomach acidity. In other words, antacids are stomach acid neutralizers.
Action mechanism
Antacids perform a neutralization reaction, i.e. they buffer gastric acid, raising the pH to reduce acidity in the stomach. When gastric hydrochloric acid reaches the nerves in the gastrointestinal mucosa, they signal pain to the central nervous system. This happens when these nerves are exposed, as in peptic ulcers. The gastric acid may also reach ulcers in the esophagus or the duodenum.
Other mechanisms may contribute, such as the effect of aluminum ions inhibiting smooth muscle cell contraction and delaying gastric emptying.
Indications
Wyeth amphojel tablets of aluminum hydroxide.
Antacids are taken by mouth to relieve heartburn, the major symptom of gastroesophageal reflux disease, or acid indigestion. Treatment with antacids alone is symptomatic and only justified for minor symptoms. Peptic ulcers may require H2-receptor antagonists or proton pump inhibitors.
The utility of many combinations of antacids is not clear, although the combination of magnesium and aluminium salts may prevent alteration of bowel habits.
Side effects
Excess calcium from supplements, fortified food and high-calcium diets, can cause the milk-alkali syndrome, which has serious toxicity and can be fatal. In 1915, Bertram Sippy introduced the "Sippy regimen" of hourly ingestion of milk and cream, the gradual addition of eggs and cooked cereal, for 10 days, combined with alkaline powders, which provided symptomatic relief for peptic ulcer disease. Over the next several decades, the Sippy regimen resulted in renal failure, alkalosis, and hypercalemia, mostly in men with peptic ulcer disease. These adverse effects were reversed when the regimen stopped, but it was fatal in some patients with protracted vomiting. Milk alkali syndrome declined in men after effective treatments for peptic ulcer disease. But during the past 15 years, it has been reported in women taking calcium supplements above the recommended range of 1200 to 1500 mg daily, for prevention and treatment of osteoporosis, and is exacerbated by dehydration. Calcium has been added to over-the-counter products, which contributes to inadvertent excessive intake.
The New England Journal of Medicine reported a typical case of a woman who arrived in the emergency department vomiting and altered mental status, writhing in pain. She had consumed large quantities of chewable antacid tablets containing calcium carbonate (Tums). She gradually recovered.[1]
Compounds containing calcium may also increase calcium output in the urine, which might be associated with kidney stones.[2] Calcium salts may cause constipation.
Other adverse effects from antacids include:
Interactions
Altered pH or complex formation may alter the bioavailability of other drugs, such as tetracycline. Urinary excretion of certain drugs may also be affected.
Problems with reduced stomach acidity
Reduced stomach acidity may result in an impaired ability to digest and absorb certain nutrients, such as iron and the B vitamins. Since the low pH of the stomach normally kills ingested bacteria, antacids increase the vulnerability to infection. It could also result in reduced bioavailability of some drugs. For example, the bioavailability of ketoconazole (antifungal) is reduced at high intragastric pH (low acid content).
Drug names
Examples of antacids (brand names may vary in different countries).
See also
References
- ^ Gabriely, I.; Leu, J. P.; Barzel, U. S. (May 1, 2008). "Clinical problem-solving, back to basics". New England Journal of Medicine 358 (18): 1952–6. doi:10.1056/NEJMcps0706188. PMID 18450607, http://www.ncbi.nlm.nih.gov/pubmed/18450607?dopt=Abstract. Retrieved on 29 May 2008.
- ^ Cooke, N.; Teitelbaum, Ss; Avioli, L. V. (1978). "Antacid-induced osteomalacia and nephrolithiasis". Archives of Internal Medicine 138 (6): 1007–9. doi:10.1001/archinte.138.6.1007. PMID 646554, http://www.ncbi.nlm.nih.gov/pubmed/646554. Retrieved on 29 May 2008.
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