Think of acidity, and bang, a phrase most medical students are familiar with comes to mind – hurry, worry, curry. These are the three established causes of acidity. A number of other causes had been proposed throughout history, and then came the revolutionary theory that argued acidity was an infection caused by an organism called H Pylori. When the original paper was published in 1982 by Barry James Marshall, then Registrar of Medicine at the Royal Perth Hospital, and Robin Warren, a pathologist, the world laughed at the suggestion that a microorganism could survive in the acidic environment of the stomach.
Marshall insisted that he was right in spite of strong opposition he received at that point. To that effect, the adventurous Marshall drank a dish of H Pylori and developed a massive stomach inflammation, proving his point. In 2005, the pair was awarded the Nobel Prize in Physiology or Medicine. Whatever the cause of acidity, the mainstay of therapy was antacids, which every layman is known to take from time to time. At one point, every emergency in a public hospital saw one or two patients with a perforated intestine, caused due to a duodenal ulcer (upper part of the intestine).
These patients required emergency surgery before they could develop inflammation of the abdominal cavity. As young physicians we used to joke that the duodenal ulcer and appendicitis were the bread and butter of the surgeon. Then came the era of simple pop-ready antiacidity drugs. These were mostly H2 blockers like Cimetidine and Ranitidine, which blocked the secretion of acid. With the widespread use of these drugs, the stomach ulcer, which was so common, came rapidly under control and surgical instances of perforated ulcers disappeared.
By the end of the 70s, a more effective molecule to block the final step of acid secretion appeared in the market – the Proton-Pump Inhibitor (PPI). Molecules like Omeprazole and Pantaprole are effective in blocking acid secretion and a drug composed of these is now widely used. In fact, every patient admitted in an Intensive Care Unit (ICU) is administered this drug because it helps prevent stress ulcers that can form during hospitalisation. It also prevents various concomitant medication from irritating the stomach. Even today, it is rare to see an ICU patient who is not prescribed these drugs.
In August 2009 Medsafe Journalpublished a study stating that these drugs reduced the effect of a common blood thinner used in the ICU. This had the physicians concerned. Several papers suggested that some of these drugs did not affect the thinner; at the present moment there is no clear answer. The PPI is a common acidity drug sold over the counter. I have known patients advising other patients to take them because they are effective and safe.
I have seen people using it before cocktail parties and large Mughlai meals to reduce chances of acidity. Such usage may be innocuous but long-term suppression of stomach acidity has its own concern. There have been fears of stomach cancer, although not proven. One must remember the acid of the stomach has as its purpose the destruction of bacteria which may find their way to the lower intestine and cause gastroenteritis, resulting in diarrhoea. A new study by Dr Nigam Shah, assistant director of the Stanford Center for Biomedical Informatics Research, and his colleagues claims that long-term use of these drugs increases the risk of heart attack by 16 per cent. They suggest the general usage of this molecule causes more harm than good.
This study involves 2.9 million individuals and they suggest the drug interferes with the chemical (nitric oxide) in the inner lining of the heart arteries. This chemical is necessary for maintaining the heart’s health. What we did yesterday is wrong today and what we do today might be wrong tomorrow. This is evidenced in the evolution of medical theories. As of now, it is safe to say that the easy popping of so-called “can’t-do-no-harm” drugs is not as innocuous as it seems.