One cannot help but admire the amazing developments in medicine. I recall when I started out as a pharmacist in the early nineties the medicines available for the management of ulcer. These were the Antacids, Mit, Magnesium Trisilicate (MMT), Tabs, Magnesium Trisilicate Compound, and Aluminium Hydroxide.
There were the anticholinergics (antispasmodics), (Probanthin), Hyoscine Butyl Bromide ((Buscopan) and Belladonatincture. The antacids were meant to physically neutralise the acid in the stomach. One had to drink lot of MMT.
A patient could be given 2 litres of MMT. Some facilities used to incorporate 5ml of Belladona tincture in each 100ml of MMT. At the time, that was the knowledge available about acid secretion. The anticholinergics as mentioned earlier were meant to block secretion of acetyl choline, a mediator in the secretion of gastric acid.
Around that time there was what I will call in medicine, a revolution! A new molecule emerged on the block called Tagamet (Cimetide)).
This was the first histamine 2 ( H-2) receptor antagonist. We knew about histamine being blocked by some molecules (Chlorpheniramine, Diphenhydramine, Promethazine, etc). I will come to these molecules referred to as histamine 1 (H-1)) receptor antagonist in another piece.Acid secretion was therefore found to be mediated by histamine through a new receptor H-2.
It was a big deal in those days. In pharmaceutical circles a molecule like that is called a blockbuster because it generates more than $1 billion sales per annum. Tagamet had a major drawback. It interfered with some enzymes in the liver responsible for the elimination of several drugs from the body.
This therefore led to the accumulation of these drugs when used together with Cimetidine, e.g. Warfarin, Phenytoin, Metronidazole, Nifedipine, Carbamazepine. It was an enzyme inhibitor and required a lot of caution when used in persons taking other medications.
This was the main reason for the success of another H-2 receptor after Cimetidine, that is Ranitidine (Zantac). Zantac was devoid of many of the drug interactions associated with Tagamet and also became a blockbuster molecule. I must say that H-2 receptor antagonists greatly reduced sufferings of persons with ulcer. Their advent saw the relegation of anticholinergics such as Belladonna tincture , Propantheline to the background.
As anticholinergics, they dried secretions almost everywhere in the body. One could not even properly shed tears when bereaved. One could not also properly sweat in response to physical activity. Persons with glaucoma could not also use anticholinergics because of increases in intra-ocular pressure.
Notwithstanding these developments in ulcer treatment, it was observed that not all persons were properly responding to treatment by these H-2 receptor antagonist.Thus the discovery of a new molecule- Omeprazole (Losec) referred to as Proton pump inhibitors (PPIs). This molecule blocks acid secretion in the stomach by inhibiting the parietal cell H+/K+ ATP pump.
Other molecules have since been introduced in this line with examples being Esomeprazole, Rabeprazole, Lansoprazole, etc.. This step is regarded as the final step in production of acid in the stomach.
It therefore accounts for their higher effectiveness as compared to other agents used to manage peptic ulcer disease. It is useful to mention other agents used to manage peptic ulcer disease. In the stomach is a mucosal lining that serves as a barrier against acid erosion of the lining of the stomach.
Even though acid is necessary for digestion in the stomach there is a physiological mucosal barrier in the lining of the stomach to protect it from the effects of the acid. Some aggressors such as NSAIDs (Ibuprofen, Diclofenac, Naproxen, Indomethacin, Aspirin, etc) erode this barrier and lead to peptic ulcer disease. Agents such as Misoprostol is used to restore the integrity of this mucosal barrier.
Something interesting happened in the course of ulcer research . A germ Helicobacter pylori (H. Pylori) was found to be closely associated with duodenal ulcer (DU) and gastric ulcer (GU). Indeed at least 90% of duodenal ulcers (DU) are caused by H. pylori..
At least 70% of gastric ulcers are caused by H. pylori. This germ thrives in acidic medium, an enabling environment as found in the stomach. This explains the triple therapy regime for the management of peptic ulcer disease (PUD).
This consists of a PPI (Omeprazole, Esomeprazole, Rabeprazole, Lansoprazole, etc) plus two antibiotics from a pool of Amoxycillin, Clarithromycin, and Metronidazole. So you could end up with Omeprazole plus Amoxycillin plus Metronidazolefor a 7 or 14 days depending on some peculiarities identified your physician.
Notwithstanding the close association of H.pylori with both DU and GU, its presence will usually be confirmed before triple or eradication therapy.
I began by a humble observation of what I saw as a young pharmacist, the usual treatment for peptic ulcer disease. It is amazing to observe the evolution of molecules to treat DU and GU.
It is important to adhere to therapy if you have been put on any of these medications by your physician. If in doubt about the appropriate use of the medication ,kindly talk to your pharmacist.