Abstract
Omeprazole (OME) is commonly used to treat gastrointestinal disorders. However, long-term use of OME can increase the risk of gastric cancer. We aimed to characterize the pharmacological effects of OME and to correlate its adverse effects and toxicogenetic risks to the genomic instability mechanisms and cancer-based on database reports. Thus, a search (till Aug 2019) was made in the PubMed, Scopus, and ScienceDirect with relevant keywords. Based on the study objective, we included 80 clinical reports, forty-six in vitro, and 76 in vivo studies. While controversial, the findings suggest that long-term use of OME (5 to 40 mg/kg) can induce genomic instability. On the other hand, OME-mediated protective effects are well reported and related to proton pump blockade and anti-inflammatory activity through an increase in gastric flow, anti-inflammatory markers (COX-2 and interleukins) and antiapoptotic markers (caspases and BCL-2), glycoprotein expression, and neutrophil infiltration reduction. The reported adverse and toxic effects, especially in clinical studies, were atrophic gastritis, cobalamin deficiencies, homeostasis disorders, polyp development, hepatotoxicity, cytotoxicity, and genotoxicity. This study highlights that OME may induce genomic instability and increase the risk of certain types of cancer. Therefore, adequate precautions should be taken, especially in its long-term therapeutic strategies and self-medication practices.
Highlights
Cumulative reports suggest that a high prevalence of gastroesophageal diseases and drug-induced side effects may result in genomic instability (GI), leading to increased mutations and carcinogenesis [1,2,3]
This is due to the compensatory effect in response to decreased acid production, resulting in the destruction of the gastric glands and persistent hypergastrinemia, a denomination for atrophic gastritis [4]
These events may be derived by different mechanisms, a common theme is the involvement of reactive oxygen and nitrogen species (ROS/RNS) in the human stomach and oncoprotein production such as the cytotoxin-associated gene A (CagA) [5]
Summary
Cumulative reports suggest that a high prevalence of gastroesophageal diseases and drug-induced side effects may result in genomic instability (GI), leading to increased mutations and carcinogenesis [1,2,3]. Omeprazole (OME) therapy can alter the bacterial flora of the gastrointestinal tract, leading to malabsorption, enteric infections, and acute or chronic lesions in the stomach. This is due to the compensatory effect in response to decreased acid production, resulting in the destruction of the gastric glands and persistent hypergastrinemia, a denomination for atrophic gastritis [4]. Helicobacter pylori infection and OME monotherapy can cause atrophic gastritis associated with an increased risk of mucosal dysplasia and gastric cancer [4] These events may be derived by different mechanisms, a common theme is the involvement of reactive oxygen and nitrogen species (ROS/RNS) in the human stomach and oncoprotein production such as the cytotoxin-associated gene A (CagA) [5]. Upon understanding the overall fact, this review aimed to sketch a current scenario on the pharmacological effects and toxicogenetic risks of OME therapy in the context of genomic instability and cancer
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