Use of Proton-Pump Inhibitor


The topic of this paper is the use of proton pump inhibitors in patients with chronic peptic ulcer. It is considered as a rather significant topic because the peptic ulcer is a serious disease and many doctors have experienced difficulties when choosing the most appropriate treatment for it. Currently, there are three main groups of drugs used to treat acid-related conditions. They include antacids, blockers of histamine H2-receptor, and proton pump inhibitors. The latter group of drugs is considered the most efficient in the treatment of chronic peptic ulcers. It is associated with the fact that drugs of this group have a small number of side effects. Thus, many doctors choose this form of treatment. The paper studies different drugs of this group and their wide application.

Keywords: peptic ulcer, Helicobacter pylori, disease, acid, proton pump inhibitors

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In most cases, chronic diseases of the upper digestive tract are closely linked with the production of hydrochloric acid in the stomach and with the violation of the acid formation mechanisms. At the same time, a change of production of hydrochloric acid in the stomach may serve as a starting point for the development of various pathologies of the gastrointestinal tract. There is even a postulate – “no acid – no ulcer”. The violation of the mechanism of acid formation leads not only to the emergence of ulcers but also to inflammatory processes in the esophagus and stomach.

The process of acid formation is complex and diverse. It involves the central and autonomic nervous system, endocrine glands, and receptors of the mucous membrane of the gastrointestinal tract that are responsive to mechanical and chemical irritation. Doctors have been struggling with increased acid production for a long time. They used to prescribe various medications that neutralize acid such as salts and alkali to patients with severe pain in the epigastric region. However, the effect of the use of these medications was usually short-lived.

In addition, the condition of patients became worse after they stopped taking medicine. Currently, there are three main groups of drugs aimed at regulating acid. They include antacids, blockers of histamine H2-receptors, and proton pump inhibitors. Inhibitors stop the mechanisms of active transportation of hydrogen ions from the intracellular space into the excretory ducts of the gastric glands. The use of proton pump inhibitors in the treatment of chronic peptic ulcer has started a new era in gastroenterology. The purpose of the paper is to study the use of proton pump inhibitors in the management of patients with chronic peptic ulcer and to discuss its nursing implications.

Several years ago peptic ulcer was considered to be an extremely severe disease. In the book Proton Pump Inhibitors, it is written that “peptic ulcers such as gastric and duodenal ulcers, had long been a significant and intractable condition in humans until the discovery of the histamine H2- receptor antagonist cimetidine in the late 1970s, which led to the dramatic improvement in treatment” (Chiba, Malfertheiner, & Satoh, 2013, pp. 1-2). The application of blockers of histamine H2-receptors is limited to the exposure to only one type of receptors, whereas acid hypersecretion may again arise in the stimulation of other receptors with gastrin.

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Besides, the therapeutic efficacy of blockers of histamine H2-receptors is provided by a high level of drug in the blood. Therefore, multiple doses are required. However, prolonged use of this group of drugs may lead to the development of tolerance, while the abrupt withdrawal can cause the appearance of the “rebound” effect. Tolerance may appear within two days after the beginning of treatment. Due to the above-mentioned facts, blockers of histamine H2-receptors are not used as the main treatment of chronic peptic ulcer. Antacids do not control the production of acid and, thus, they cannot be used as the primary means of treatment of chronic peptic ulcer. In addition, prolonged use of antacids can lead to disruption of stool, a change in the mineral balance, and the development of alkalosis.

As a result of studying the molecular mechanisms of the formation of hydrochloric acid of gastric juice, there was found a key element, which is the active secretion of protons, realized with a special membrane complex, known as the proton pump. While the formation of protons during intracellular reactions is monitored by various regulatory factors, the work of the proton pump is practically not related to the physiological regulatory mechanisms.

Drugs that block the formation of hydrochloric acid on the level of the sodium-potassium pump in the membrane of the parietal cells are called proton pump inhibitors. The prototype of this group of drugs was first synthesized in 1974 (Chiba, Malfertheiner, & Satoh, 2013). A year later, the first industrial sample, pantoprazole, appeared, and in 1979, omeprazole was synthesized (Chiba, Malfertheiner, & Satoh, 2013). Since that time, proton pump inhibitors are highly widespread.

Proton pump inhibitors belong to the chemical class of substituted benzimidazole derivatives and exert antisecretory action by inhibiting H +, K + -ATPase of the parietal cells of the gastric mucosa (Chiba, Malfertheiner, & Satoh, 2013). In gastric glands tubules, proton pump inhibitors have weak bases, so they react with the hydrogen ions. They are transformed into sulfonamide derivatives, which form covalent bonds with cysteine SH-groups of H +, K + -ATPase on the surface of the apical membrane, facing the lumen of gastric glands, and block the final stage of the formation of hydrochloric acid (Chiba, Malfertheiner, & Satoh, 2013). Such a connection is irreversible and, thus, the duration of actions of proton pump inhibitors depends on the rate of synthesis of new molecules of the proton pump, as well as on the duration of circulation of the drug in the blood.

Currently, a family of proton pump inhibitors includes several drugs: pantoprazole, rabeprazole, lansoprazole, and omeprazole (Chiba, Malfertheiner, & Satoh, 2013). In addition, this group allocates additional composes, for example, esomeprazole, which is the levorotatory isomer of omeprazole. All compounds in this group are quickly activated in a strongly acidic medium. Proton pump inhibitors reduce basal and stimulated gastric acid secretion irrespective of the nature of the stimulus and have the highest clinical efficacy among other means that suppress acid. In this group of drugs, there are some differences in metabolism, pharmacokinetics, and indicators of the antisecretory activity (Chiba, Malfertheiner, & Satoh, 2013).

Nevertheless, tolerance is not developed, and the “rebound” effect is not observed after the withdrawal of medication. Moreover, there are no significant side effects. It should be noted that omeprazole, lansoprazole, and pantoprazole are slowly converted into the active form. In this connection, rabeprazole, a new proton pump inhibitor, is of great interest, as its mechanisms of action, as well as those of other drugs in this group, are associated with the blocking activity of the enzyme - H +, K + -ATPase, which is a proton pump or a pump of the membrane of the gastric parietal cell (Chiba, Malfertheiner, & Satoh, 2013).

The high level of selectivity of the drug is provided by the fact that only in the presence of H + ions at a high concentration is accumulated and converted into an active form. 0 sulfa drug form of rabeprazole binds with sulfhydryl groups of H +, K + - ATPase membrane of the lining cell and blocks the activity of this enzyme by inhibiting K + -dependent dephosphorylation, which incapacitates the proton pump and leads to the inhibition of yield of free H + ions into the lumen of the gastric during the first day of treatment (Chiba, Malfertheiner, & Satoh, 2013). Thus, many doctors choose this drug from the family of proton pump inhibitors.

At the World Congress of Gastroenterology in Rome, proton pump inhibitors were recognized as the main group of drugs that control acid (Moini, 2015). However, the use of proton pump inhibitors did not cure patients of peptic ulcer disease. In a while after the reparation of ulcer defect and the drug withdrawal, the disease was manifested with renewed vigor. The recurrence of the disease usually aggravated the general condition of the patient, Surgical treatment was frequently applied as a radical solution to the problem. It was especially used in cases of a complicated course of the disease.

According to numerous studies, the infectious factor plays a key position in the development of the inflammatory process of the mucous membrane of the digestive system in addition to the excessive production of hydrochloric acid. In 1983, a new microorganism was detected. It lives on the surface of the gastric mucosa in the aggressive acidic environment. It was named Helicobacter pylori. Further researches allowed recognizing this microorganism as the underlying cause of inflammatory processes of the mucous membrane, including peptic ulcer disease. Basing on these data, there has been added a postulate: “no acid – no ulcer, no Helicobacter pylori – ulcer”.

The author Jahangir Moini (2015) affirms that “peptic ulcer disease is believed to be caused by high gastric secretion. H. pylori are found in 75% of duodenal ulcers” (p. 311). The main objective in the treatment of diseases, associated with Helicobacter pylori, is the eradication of microorganisms from the mucosal surface. When Helicobacter pylori disappear, there is the reparation of the ulcer defect and the restoration of the structure of the mucous membrane (Moini, 2015). Currently, doctors use a combined therapy in order to achieve the eradication of the disease (Moini, 2015). It comprises several groups of drugs that are directed at both the reduction of gastric acid-forming functions and the destruction of Helicobacter pylori on the mucosal surface.

A peptic ulcer is polietiologic, genetic, and pathogenetic inhomogeneous disease. Among the adverse premorbid factors that increase the risk of ulcers, heredity occupies an important place. Probably, it is the tendency to a disease that is inherited rather than the disease itself (Lubin, Dodson, & Winawer, 2013). Without a certain hereditary predisposition, it is hard to imagine the emergence of a peptic ulcer. Moreover, it should be noted that children with burdened heredity have a so-called ‘advance syndrome’. It means that they usually start to be sick with peptic ulcer earlier than their parents and close relatives. The hereditary tendency is usually triggered by such factors as emotional stress, gross errors in diet, and harmful habits.

An important role in the realization of the hereditary tendency to the peptic ulcer is assigned to nonsteroidal anti-inflammatory drugs. There is a number of risk factors, as one can be orally infected with Helicobacter pylori through food, during endoscopic manipulation, and probing (Lubin, Dodson, & Winawer, 2013). When penetrating through the protective layers of slime, a bacterium is attached to the epithelial cells, it penetrates in the crypts and the gastric glands destroys the protective layer of mucus, and provides the access of gastric juice to the tissues.

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The urease enzyme is one of the most important virulence factors of Helicobacter pylori, as it splits urea present in secretions of the stomach and the interstitial fluid. In the hydrolysis of urea, ammonia and carbon dioxide are produced. Ammonia damages the epithelium and alkalizes the environment around Helicobacter pylori, thus creating optimum conditions for it. Alkalization of epithelium leads to the increased secretion of gastrin, increased aggressive properties of gastric juice, and the damage of gastric mucosa.

In order to reduce acid production in the schemes of eradication therapy, proton pump inhibitors are widely used. They do not have H. pylori activity. Their action is aimed at changing the pH of the stomach. Under the influence of proton pump inhibitors, the production of hydrochloric acid decreases. It leads to alkalization of the medium in the antral stomach. Thus, vegetative forms of Helicobacter pylori, which protect themselves from exposure to acid with the help of the ammonium shell, die under the action of ammonia, formed in alkaline conditions. Bacteria that have preserved in the fundal department in the form of cocci with increasing pH in the stomach, pass into the vegetative form and become subjective to the effect of antibiotics or other drugs.

In such a way, proton pump inhibitors have no direct effect on Helicobacter pylori. Nevertheless, they create favorable conditions for the effects of antibiotics on them. For example, the usage of a combination of omeprazole with macrolides creates an increase in the bioavailability of both groups of drugs. In turn, it increases the degree of impact of macrolide on Helicobacter pylori. In the book Medical Management of the Surgical Patient, it is noted that “the medical treatment of peptic ulcer disease (proton pump inhibitors and Helicobacter pylori treatment) has resulted in a significant reduction in the amount of surgery done for complications of peptic ulcer disease” (Lubin, Dodson, & Winawer, 2013, p. 513). Therefore, the most effective treatment regimen that includes a combination of proton pump inhibitors and clarithromycin.

An aggressive impact of the excessive amount of acid that is produced in a stomach is sometimes not limited to the gastric mucosa. If there are certain predisposing factors such as the congenital short esophagus, hernia, violation of motor activity of the stomach (the appearance of the anesthetic wave), or an increased intra-abdominal pressure (flatulence, pregnancy), acidic contents of the stomach can enter the esophagus (Lubin, Dodson, & Winawer, 2013).

This fact causes irritation and leads to the inflammatory process. In order to deal with the short-term impact of these factors or minor mucosal changes, it is enough to use antacids. However, when the aggressive factors influence a patient for a long period of time, the gastroesophageal reflux disease can develop. It is often accompanied by the occurrence of erosions and ulcers.


The gastroesophageal reflux disease may develop even after a successful therapy against H. pylori. According to the research, Helicobacter pylori, situated on the mucosal surface, stimulates the peristaltic activity of the stomach treatment (Chiba, Malfertheiner, & Satoh, 2013). During the first period after the eradication therapy, peristalsis decreases. Nevertheless, after the withdrawal of the drug, the treatment, which suppresses the acid, remains the same (Chiba, Malfertheiner, & Satoh, 2013). The relative increase of the amount of acid in the lumen of the stomach can cause its penetration into the esophagus with the subsequent development of reflux esophagitis.

Proton pump inhibitors are successfully used for the treatment of gastroesophageal reflux disease in adults. Omeprazole has high lipophilicity. It can easily penetrate in the parietal cells of the gastric mucosa, where it is accumulated and activated in an acidic environment. It is also fast and almost completely sucked from the gastrointestinal tract. At the same time, bioavailability is no more than 50-55% due to the effect of the first pass through the liver treatment (Chiba, Malfertheiner, & Satoh, 2013). The maximum plasma concentration is achieved in about three hours. Plasma protein binding reaches 95% (Olbe, 2012).

A period of half-life is one hour with normal liver functioning and three hours with chronic liver disorders. Omeprazole is exposed to biotransformation in the liver. It is excreted by the kidneys as metabolites and through the intestines. After a single dose of 20 mg, inhibition of gastric secretion occurs within one hour (Olbe, 2012). It reaches its peak after two hours and lasts for about 24 hours. The intensity of the effect depends on the dose. The ability of the parietal cells to produce hydrochloric acid is recovered in 3-5 days after the end of the therapy (Olbe, 2012). After repeated use, the absorption of the drug increases, and its antisecretory effect enhances. It should be noted that omeprazole is not accompanied by the development of tolerance. In addition, after its cancellation, the “rebound” syndrome is absent.

The use of omeprazole with prokinetic agents helps to cure the inflammation of the mucous membrane. Besides, this combination restores the normal peristaltic activity of the upper gastrointestinal tract. A dual mechanism of action is particularly important for the treatment of functional pathology. Functional dyspepsia, motor disturbances in chronic gastritis, and supporting therapy after the main treatment of gastroesophageal reflux disease are only several conditions, in which the combined use of proton pump inhibitors and prokinetic agents are effective.

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To date, there is a combined drug Omez D. In its composition it contains proton pump inhibitors (omeprazole) and prokinetics (domperidone) (Olbe, 2012). There is 10 mg of each component. This drug is used to treat the dispersion, and its efficiency in dyspeptic complaints is confirmed by clinical studies. A low-dose therapy with Omez D minimizes the possibility of side effects occurrence (Olbe, 2012). Combination therapy can reduce the number of consumed drugs and has a positive effect on adherence to the therapy. It is rather important due to the high value of the psycho-emotional factors in the etiology of functional disorders of the upper gastrointestinal tract.

There can be both oral and intravenous methods of introducing proton pump inhibitors. The intravenous route of administration is more commonly used by nurses in emergency surgery in cases of gastrointestinal bleeding. It can quickly suppress acid production and reduce the probability of recurrent bleeding. However, there are no significant differences between the various routes of administration and proton pump inhibitors drugs within the first 72 hours after successful hemostasis (Olbe, 2012). pH was significantly higher with the treatment of proton pump inhibitors than without such treatment.

In recent years, hypotheses about the adverse effects of the long-term use of proton pump inhibitors are actively discussed. For seven years omeprazole therapy has not been accompanied by any neoplastic or dysplastic processes in the endocrine cells of the stomach. Proton pump inhibitors' security issues are particularly noteworthy. It is associated with their powerful antisecretory effect. Results of the study that indicate the existence of the connection of the use of proton pump inhibitors with osteoporosis and bone fractures are contradictory in the risk assessment (Olbe, 2012).

These phenomena are not connected with the preparation, but they are related to the low acidity of the stomach. All proton pump inhibitors are destroyed in an acid environment. Thus, their effectiveness may be reduced during passage through the stomach. In order to protect the active ingredient, the shell of proton pump inhibitors is made of acid-resistant capsules (Lubin, Dodson, & Winawer, 2013). Considering a fact that omeprazole has a low incidence of side effects, compared to other proton pump inhibitors, this drug can be used successfully for the treatment of chronic peptic ulcer, gastroesophageal reflux disease, and gastropathy, caused by the intake of nonsteroidal anti-inflammatory drugs.


In addition to drug treatment, a rational therapy of peptic ulcers should include mode, healthy food, psychotherapy, physiotherapy, and spa treatment. Current approaches to dietary therapy in peptic ulcer disease are characterized by the rejection of strict diets. Diet restrictions are sensible only if there are complications. Thus, nurses should carefully monitor not only the drug treatment of patients but also other elements that are mentioned above.

In recent decades, there has been a fundamental change in terms of the etiology and pathogenesis of peptic ulcer. The belief “no Helicobacter pylori – no ulcer” substituted the paradigm “no acid – no ulcer”. Therefore, in order to treat peptic ulcers, it is necessary to control the level of acid and to eliminate Helicobacter pylori. Since it was determined that the major component of gastric acid is hydrochloric acid, the various methods were proposed to neutralize or inhibit its formation in the treatment of peptic ulcers.

There are clear quantitative clinical and physiological performance criteria of antisecretory drugs in the treatment of peptic ulcers. An antisecretory class of proton pump inhibitors drugs has the highest efficiency. They are able to keep an optimal level of pH within the stomach and have the fewest number of adverse side effects. In addition, combination therapy is considered the most effective in the treatment of peptic ulcers.

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