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Pharmacokinetics in Obese Patients: Drug Metabolism and Excretion

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Drug metabolism, a critical process in the liver, involves two primary phases: Phase I reactions and Phase II conjugation. Obesity introduces significant alterations in this metabolic process, primarily due to fatty infiltration of the liver, leading to conditions such as nonalcoholic fatty liver disease (NAFLD). This condition can modify the activities of both Phase I and II enzymes, impacting how drugs are metabolized in obese patients.Phase I metabolism sees variable effects across...
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Drug interactions occur when the pharmacological effect of one drug is altered by another substance, either enhancing or diminishing its activity. The drug whose activity is altered is known as the object drug, and the substance causing the alteration is called the agent drug or the precipitant. The net effects of these interactions are mostly undesirable, leading to decreased effectiveness or increased adverse effects. In rare cases, interactions can be beneficial, such as the enhanced...
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Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
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Obesity significantly alters the pharmacokinetic processes of drug absorption and distribution, presenting unique challenges in medical treatment. The increased fat tissue and decreased lean muscle in obese individuals can significantly affect how drugs are absorbed into the body and distributed across different tissues. This alteration can lead to variances in the effectiveness and safety of medications, necessitating adjustments in dosing or drug selection for obese patients.One notable...
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α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
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Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
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Interaction between Omeprazole and Gliclazide in Relation to CYP2C19 Phenotype.

Tanja Dujic1, Sandra Cvijic2, Amar Elezovic3

  • 1Department of Biochemistry & Clinical Analysis, Faculty of Pharmacy, University of Sarajevo, 71000 Sarajevo, Bosnia and Herzegovina.

Journal of Personalized Medicine
|June 2, 2021
PubMed
Summary

Omeprazole increases gliclazide exposure and hypoglycemia risk, particularly in individuals with specific CYP2C19 enzyme activity. This drug interaction necessitates careful consideration for patients with type 2 diabetes.

Keywords:
CYP2C19adverse drug reactiondrug–drug interactiondrug–drug–gene interactiongliclazidehypoglycemiaomeprazolephysiologically based pharmacokinetic modelingtype 2 diabetes

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Area of Science:

  • Pharmacology
  • Drug Metabolism
  • Clinical Pharmacology

Background:

  • Gliclazide, an antidiabetic medication, is metabolized by CYP2C19.
  • Omeprazole is a potent inhibitor of CYP2C19.
  • Understanding their interaction is crucial for patient safety.

Purpose of the Study:

  • To investigate the pharmacokinetic interaction between omeprazole and gliclazide.
  • To evaluate the impact of CYP2C19 phenotype on this interaction.
  • To assess the clinical risk of gliclazide-induced hypoglycemia with omeprazole co-treatment.

Main Methods:

  • Physiologically-based pharmacokinetic (PBPK) modeling was employed.
  • PBPK models were validated with clinical trial data in healthy volunteers.
  • Real-world data from type 2 diabetes patients (GoDARTS cohort) were analyzed.

Main Results:

  • PBPK simulations predicted increased gliclazide exposure (AUC) with omeprazole, varying by CYP2C19 phenotype.
  • Simulations indicated higher gliclazide AUC with longer omeprazole treatment durations and higher doses.
  • Analysis of type 2 diabetes patients showed a 3.3-fold increased odds of severe hypoglycemia with omeprazole co-administration in specific metabolizer groups.

Conclusions:

  • Omeprazole significantly increases gliclazide exposure, elevating the risk of hypoglycemia.
  • The interaction is influenced by CYP2C19 genetic variations.
  • Clinical monitoring for hypoglycemia is recommended when prescribing omeprazole with gliclazide.