Dangerous Drug Combinations
People with diabetes often have a number of coexisting health problems. So in addition to insulin or diabetes pills, other drugs are often needed to control these problems — statins for high cholesterol, diuretics or beta-blockers for high blood pressure, antidepressants for depression or neuropathy pain, and a daily aspirin to prevent a heart attack. But some drugs are not supposed to be taken simultaneously, and doctors and pharmacists don’t always notice when a person is taking dangerous or risky drug combinations. What can happen to you if you take several drugs that are not supposed to be taken together? This article explains why and how medicines can interact and what a drug interaction may mean for you and your health care. The scope of the problem Surprisingly, most drug reactions are caused by a small group of commonly prescribed drugs. The nonsteroidal anti-inflammatory drugs (such as ibuprofen), anticoagulants, diuretics, and drugs to treat diabetes are on this list. Adverse drug reactions may add as much as $130 billion a year to the cost of health care in the United States. A significant portion of adverse drug reactions are caused by interacting drugs. This is a huge problem and much research and effort is going into trying to reduce the incidence and risk of these interactions. It is estimated that people over 65 take an average of seven drugs at any one time to treat a variety of illnesses. With this amount of medicine use, the probability that a person will take two prescribed drugs that may interact with one another is very high. In a recent study done in six European countries, investigators reviewed the medicines taken by about 1600 people and found that 46% were taking at least one pair of drugs that could interact. (Studies that include people Continue reading >>
Metformin Suppresses Pregnane X Receptor (pxr)-regulated Transactivation Of Cyp3a4 Gene
Metformin suppresses pregnane X receptor (PXR)-regulated transactivation of CYP3A4 gene We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Metformin suppresses pregnane X receptor (PXR)-regulated transactivation of CYP3A4 gene Lucie Krausova, Lucie Stejskalova, [...], and Petr Pavek Metformin is widely used in the treatment of type-2 diabetes. The pleotropic effects of metformin on glucose and lipid metabolism have been proposed to be mediated by the activation of AMP-activated protein kinase (AMPK) and the subsequent up-regulation of small heterodimer partner (SHP). SHP suppresses the functions of several nuclear receptors involved in the regulation of hepatic metabolism, including pregnane X receptor (PXR), which is referred to as a master regulator of drug/xenobiotic metabolism. In this study, we hypothesize that metformin suppresses the expression of CYP3A4, a main detoxification enzyme and a target gene of PXR, due to SHP up-regulation. We employed various gene reporter assays in cell lines and qRT-PCR in human hepatocytes and in Pxr/ mice. We show that metformin dramatically suppresses PXR-mediated expression of CYP3A4 in hepatocytes. Consistently, metformin significantly suppressed the up-regulation of Cyp3a11 mRNA in the liver and intestine of wild-type mice, but not in Pxr/ mice. A mechanistic investigation of the phenomenon showed that metformin does not significantly up-regulate SHP in human hepatocytes. We further demon Continue reading >>
Evidence-based Prioritisation And Enrichment Of Genes Interacting With Metformin In Type 2 Diabetes
, Volume 60, Issue11 , pp 22312239 | Cite as Evidence-based prioritisation and enrichment of genes interacting with metformin in type 2 diabetes There is an extensive body of literature suggesting the involvement of multiple loci in regulating the action of metformin; most findings lack replication, without which distinguishing true-positive from false-positive findings is difficult. To address this, we undertook evidence-based, multiple data integration to determine the validity of published evidence. We (1) built a database of published data on genemetformin interactions using an automated text-mining approach (n=5963 publications), (2) generated evidence scores for each reported locus, (3) from which a rank-ordered gene set was generated, and (4) determined the extent to which this gene set was enriched for glycaemic response through replication analyses in a well-powered independent genome-wide association study (GWAS) dataset from the Genetics of Diabetes and Audit Research Tayside Study (GoDARTS). From the literature search, seven genes were identified that are related to the clinical outcomes of metformin. Fifteen genes were linked with either metformin pharmacokinetics or pharmacodynamics, and the expression profiles of a further 51 genes were found to be responsive to metformin. Gene-set enrichment analysis consisting of the three sets and two more composite sets derived from the above three showed no significant enrichment in four of the gene sets. However, we detected significant enrichment of genes in the least prioritised category (a gene set in which their expression is affected by metformin) with glycaemic response to metformin (p=0.03). This gene set includes novel candidate genes such as SLC2A4 (p=3.241004) and G6PC (p=4.771004). We have described a se Continue reading >>
Kombiglyze Xr (metformin,saxagliptin) Dosage, Indication, Interactions, Side Effects | Empr
Select the drug indication to add to your list Saxagliptin, metformin HCl (ext-rel); 5mg/500mg, 5mg/1000mg, 2.5mg/1000mg; tabs. Adjunct to diet and exercise in type 2 diabetes when treatment with both saxagliptin and metformin is appropriate. Not for treatment of type 1 diabetes or diabetic ketoacidosis. Individualize; titrate based on response. Swallow whole. Take once daily with evening meal. Not currently treated with metformin: initially 5mg/500mg daily. Previously on metformin alone: Kombiglyze XR dose should provide current metformin dose. Max saxagliptin 5mg/day and metformin ext-rel 2000mg/day. Renal impairment (eGFR 3045mL/min/1.73m2): not recommended; (eGFR <45mL/min/1.73m2): max saxagliptin 2.5mg/day. Concomitant strong CYP3A4/5 inhibitors: max 2.5mg/1000mg daily. Severe renal impairment (eGFR <30mL/min/1.73m2). Metabolic acidosis, diabetic ketoacidosis. Increased risk of metformin-associated lactic acidosis in renal or hepatic impairment, concomitant use of certain drugs (eg, cationic drugs), 65yrs of age, undergoing radiological contrast study, surgery and other procedures, hypoxic states, and excessive alcohol intake; discontinue if lactic acidosis occurs. Discontinue at time of, or prior to intravascular iodinated contrast imaging in patients with eGFR 3060mL/min/1.73m2, history of hepatic impairment, alcoholism, heart failure, or will be given intra-arterial contrast; reevaluate eGFR 48hrs after procedure and restart therapy if renally stable. Suspend therapy if dehydration occurs or before surgery. Avoid if clinical or lab evidence of hepatic disease. Assess renal function prior to starting and periodically thereafter; more frequently in elderly or if eGFR <60mL/min/1.73m2. Consider risks/benefits in patients with known risk factors for heart failure; Continue reading >>
Drug Interactions Of Medications Commonly Used In Diabetes
When patients are diagnosed with diabetes, a large number of medications become appropriate therapy. These include medications for dyslipidemia, hypertension, antiplatelet therapy, and glycemic control. So many medications can be overwhelming, and it is imperative that patients are thoroughly educated about their drug regimen. Patients have many concerns when multiple medications are started, including prescribing errors, the cost of medications, and possible adverse effects. Significantly, 58% of patients worry that they will be given medications that have drug interactions that will adversely affect their health.1 These worries are not unfounded given that several highly publicized drugs have been withdrawn from the U.S. market in the past several years because of adverse effects from drug interactions. Terfenadine, mibefradil, and cisapride have all been withdrawn from the market specifically because of drug-drug interactions. When terfenadine or cisapride were given with a strong inhibitor of their metabolism, torsades de pointes, a life-threatening drug-induced ventricular arrhythmia associated with QT prolongation, could occur.2 Cisapride, for gastroparesis or gastrointestinal reflux disease, and mibefradil, for hypertension, were prescribed for many patients with diabetes. An adverse drug interaction is defined as an interaction between one or more coadministered medications that results in the alteration of the effectiveness or toxicity of any of the coadministered medications. Drug interactions can be caused by prescription and over-the-counter medications, herbal products or vitamins, foods, diseases, and genetics (family history). The true incidence of drug interactions is unknown because many are not reported, do not result in significant harm to patients, o Continue reading >>
Kombiglyze Xr (saxagliptin-metformin) Dosing, Indications, Interactions, Adverse Effects, And More
Indicated as adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus who are already treated with sitagliptin or metformin and have inadequate glycemic control on sitagliptin or metformin alone Individualize starting dose based on patients current regimen Adjust dose according to effectiveness and tolerability; not to exceed daily dose of 5 mg/2000 mg Inadequately controlled on metformin alone 2.5-5 mg/day saxagliptin PO plus current dose of metformin Inadequately controlled on saxagliptin alone 500 mg/day metformin PO plus 5 mg/day PO saxagliptin Coadministration with strong CYP3A4/5 inhibitors: Not to exceed 2.5 mg/day saxagliptin or 1000 mg/day metformin eGFR 30-45 mL/min/1.73 m: Not recommended to initiate treatment Monitor eGFR at least annually or more often for those at risk for renal impairment (eg, elderly) If eGFR falls below 45mL/min/1.73 m while taking metformin, risks and benefits of continuing therapy should be evaluated If eGFR falls below 30 mL/min/1.73 m: while taking metformin, discontinue the drug Initial and maintenance dosing should be conservative due to possibility of decreased renal function. Adjust dose gradually and conservatively considering effectiveness and tolerability Inadequately controlled on metformin alone 2.5-5 mg/day saxagliptin PO plus current dose of metformin Do not administer to patients >80 years before assessing renal function and determined to be normal Inadequately controlled on saxagliptin alone 500 mg/day metformin PO plus 5 mg/day PO saxagliptin Do not administer to patients >80 years before assessing renal function and determined to be normal Concomitant administration with strong CYP3A4/5 inhibitors Not to exceed 2.5 mg/day saxagliptin or 1000 mg/day metformin Do not administer t Continue reading >>
Rcsb Pdb - 5g5j: Crystal Structure Of Human Cyp3a4 Bound To Metformin
139187 Biological Macromolecular Structures Enabling Breakthroughs in Research and Education Global Symmetry: Cyclic - C2( 3D View ) Biological assembly 1 assigned by authors and generated by PISA (software) This is version 1.1 of the entry. See complete history . Heme Binding Biguanides Target Cytochrome P450-Dependent Cancer Cell Mitochondria. The mechanisms by which cancer cell-intrinsic CYP monooxygenases promote tumor progression are largely unknown. CYP3A4 was unexpectedly associated with breast cancer mitochondria and synthesized arachidonic acid (AA)-derived epoxyeicosatrienoic acids ... The mechanisms by which cancer cell-intrinsic CYP monooxygenases promote tumor progression are largely unknown. CYP3A4 was unexpectedly associated with breast cancer mitochondria and synthesized arachidonic acid (AA)-derived epoxyeicosatrienoic acids (EETs), which promoted the electron transport chain/respiration and inhibited AMPK. CYP3A4 knockdown activated AMPK, promoted autophagy, and prevented mammary tumor formation. The diabetes drug metformin inhibited CYP3A4-mediated EET biosynthesis and depleted cancer cell-intrinsic EETs. Metformin bound to the active-site heme of CYP3A4 in a co-crystal structure, establishing CYP3A4 as a biguanide target. Structure-based design led to discovery of N1-hexyl-N5-benzyl-biguanide (HBB), which bound to the CYP3A4 heme with higher affinity than metformin. HBB potently and specifically inhibited CYP3A4 AA epoxygenase activity. HBB also inhibited growth of established ER+ mammary tumors and suppressed intratumoral mTOR. CYP3A4 AA epoxygenase inhibition by biguanides thus demonstrates convergence between eicosanoid activity in mitochondria and biguanide action in cancer, opening a new avenue for cancer drug discovery. Department of Medic Continue reading >>
Metformin Pathways: Pharmacokinetics And Pharmacodynamics
Metformin pathways: pharmacokinetics and pharmacodynamics aDepartment of Genetics, Stanford University Medical Center, Stanford University, Stanford bDepartment of Bioengineering, Stanford University Medical Center, Stanford University, Stanford aDepartment of Genetics, Stanford University Medical Center, Stanford University, Stanford bDepartment of Bioengineering, Stanford University Medical Center, Stanford University, Stanford cDepartment of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, California, USA Correspondence to Teri E. Klein, PhD, Department of Genetics, Stanford University Medical Center, Stanford University, 1501 California Ave, Palo Alto, CA 94304, USA Tel: + 1 650 725 0659; fax: + 1 650 725 3863; [email protected] The publisher's final edited version of this article is available at Pharmacogenet Genomics See other articles in PMC that cite the published article. Metformin is a first-line therapy for type 2 diabetes mellitus (T2DM, formerly non-insulin-dependent diabetes mellitus), and is one of the most commonly prescribed drugs worldwide. As a biguanide agent, metformin lowers both basal and postprandial plasma glucose (PPG) [ 1 , 2 ]. It can be used as a monotherapy or in combination with other antidiabetic agents including sulfonylureas, -glucosidase inhibitors, insulin, thiazolidinediones, DPP-4 inhibitors as well as GLP-1 agonists. Metformin works by inhibiting the production of hepatic glucose, reducing intestinal glucose absorption, and improving glucose uptake and utilization. Besides lowering the blood glucose level, metformin may have additional health benefits, including weight reduction, lowering plasma lipid levels, and prevention of some vascular complications [ 3 ]. As the prevalence o Continue reading >>
Interactions Between Linagliptin-metformin Oral And Linagliptin-strong-p-gp-or-cyp3a4-inducer
Your medicine may speed up how quickly your body processes linagliptin. The amount of linagliptin in your blood may decrease and it may not work as well at treating your diabetes. What you should do about this interaction: Make sure your healthcare professionals (e.g. doctor or pharmacist) know that you are taking these medicines together or if you have used apalutamide, carbamazepine, enzalutamide, fosphenytoin, lumacaftor, phenobarbital, phenytoin, primidone, rifampin, St. John's wort, or tipranavir in the previous six weeks. Your doctor may want to change your diabetes medicine or have you monitor your blood sugars more closely during your therapy and for several weeks after completing therapy with your other medicine.Your healthcare professionals may already be aware of this interaction and may be monitoring you for it. Do not start, stop, or change the dosage of any medicine before checking with them first. 1.Tradjenta (linagliptin) US prescribing information. Boehringer Ingelheim International GmbH August, 2015. 2.This information is based on or an extract from the UW Metabolism and Transport Drug Interaction Database (DIDB) Platform, Copyright University of Washington 1999-2014.. Continue reading >>
Drug Interaction List
Cimetidine hydrochloride (USP); Cimetidine hydrochloride (TN) Erythromycin (JP17/USP/INN); EM; Akne-mycin (TN); Eryc (TN); Erygel (TN); Pce (TN); Staticin (TN); T-stat (TN) (P) Enzyme: CYP3A4 / CYP inhibition: CYP3A4 CYP3A7 Rifampin (USP); Rifampicin (JP17/INN); Rifadin (TN); Rimactane (TN) (P) Enzyme: CYP3A4 / CYP inhibition: CYP3A4 / CYP induction: CYP2C9 CYP2D6 Acyclovir (USP); Aciclovir (JP17/INN); Aciclovir granules (JP17); Aciclovir ophthalmic oinment (JP17); Aciclovir tablets (JP17); Sitavig (TN); Zovirax (TN) Budesonide (JAN/USAN/INN); Entocort EC (TN); Pulmicort (TN); Rhinocort (TN); Uceris (TN) (P) Enzyme: CYP3A4 / CYP inhibition: CYP3A4 Carbamazepine (JP17/USP/INN); Equetro (TN); Tegretol (TN) (P) Enzyme: CYP3A4 / CYP inhibition: CYP3A4 / CYP induction: CYP3A4 Carvedilol (JAN/USAN/INN); Artist (TN); Coreg (TN) (P) Enzyme: CYP2D6 CYP2C9 CYP3A4 CYP1A2 / CYP inhibition: CYP3A4 CYP2D6 CYP2C9 CYP1A2 Clarithromycin (JP17/USP/INN); CAM; Biaxin (TN) (P) Enzyme: CYP3A4 / CYP inhibition: CYP3A4 Diazepam (JP17/USP/INN); Diastat (TN); Valium (TN) (P) Enzyme: CYP3A4 / CYP inhibition: CYP3A4 Digoxin (JP17/USP); Lanoxicaps (TN); Lanoxin (TN) Fentanyl (JAN/USAN/INN); Duragesic (TN); Subsys (TN) (P) Enzyme: CYP3A4 / CYP inhibition: CYP3A4 CYP3A5 CYP3A7 Itraconazole (JP17/USAN); Itrizole (TN); Sporanox (TN) (P) Enzyme: CYP3A4 / CYP inhibition: CYP3A4 Theophylline (JP17); Elixophyllin (TN); Quibron-t (TN); Theo-24 (TN); Theodur G (TN); Theolair (TN); Uniphyl (TN) (P) Enzyme: CYP1A2 / CYP inhibition: CYP1A2 Valacyclovir hydrochloride (USAN); Valaciclovir hydrochloride (JP17); Valtrex (TN) Nifedipine (JP17/USP/INN); Adalat (TN); Afeditab CR (TN); Procardia (TN) (P) Enzyme: CYP3A4 / CYP inhibition: CYP3A4 CYP3A5 Quetiapine fumarate (JP17/USAN); Seroquel (TN) (P) Enzyme: CYP3A4 / Continue reading >>
Food–drug Interactions
US Pharm. 2007;32(3)93-98. Perhaps the most common question patients ask about their medication, aside from "Why does this medication cost so much?" is, "Should I take this with or without food?" In most cases, upon looking in the package insert or drug information resource, the pharmacist discovers that most drugs in question may be administered without regard to meals. However, some food products are fortified with vitamins and/or minerals that can interact with certain drugs. Therefore, the more appropriate question to ask is, "Which foods should I avoid taking with my medications?" Furthermore, many patients consume mega-vitamins and supplements with known drug interactions, yet they are often unaware of these interactions. The purpose of this article is to equip pharmacists with a better understanding of drug–food interactions. This article differs from traditional reviews on this topic because the food substance is categorized individually, with the interacting drugs discussed under each heading. While there are hundreds of drug–nutrient interactions reported in the literature, the aim here is to focus on those that are more common and clinically significant. Grapefruit Juice One of the most well known food–drug interactions is grapefruit juice and the HMG-CoA reductase inhibitors, more commonly known as statins. Grapefruit juice, in large quantities (32 oz. or more per day), can inhibit the cytochrome P450 3A4 (CYP3A4) enzyme and increase blood levels of drugs metabolized by this pathway, such as certain statin drugs.1,2 Note that this interaction applies to grapefruit juice, not the whole fruit itself. Furthermore, not all statins exhibit this interaction: Only atorvastatin (Lipitor), simvastatin (Zocor), and lovastatin (Mevacor) are metabolized by the CYP Continue reading >>
Metformin Suppresses Pregnane X Receptor (pxr)-regulated Transactivation Of Cyp3a4 Gene.
Biochem Pharmacol. 2011 Dec 1;82(11):1771-80. doi: 10.1016/j.bcp.2011.08.023. Epub 2011 Sep 6. Metformin suppresses pregnane X receptor (PXR)-regulated transactivation of CYP3A4 gene. Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Kralove, Charles University in Prague, Heyrovskeho 1203, Hradec Kralove, CZ-500 05, Czech Republic. Metformin is widely used in the treatment of type-2 diabetes. The pleotropic effects of metformin on glucose and lipid metabolism have been proposed to be mediated by the activation of AMP-activated protein kinase (AMPK) and the subsequent up-regulation of small heterodimer partner (SHP). SHP suppresses the functions of several nuclear receptors involved in the regulation of hepatic metabolism, including pregnane X receptor (PXR), which is referred to as a "master regulator" of drug/xenobiotic metabolism. In this study, we hypothesize that metformin suppresses the expression of CYP3A4, a main detoxification enzyme and a target gene of PXR, due to SHP up-regulation. We employed various gene reporter assays in cell lines and qRT-PCR in human hepatocytes and in Pxr(-/-) mice. We show that metformin dramatically suppresses PXR-mediated expression of CYP3A4 in hepatocytes. Consistently, metformin significantly suppressed the up-regulation of Cyp3a11 mRNA in the liver and intestine of wild-type mice, but not in Pxr(-/-) mice. A mechanistic investigation of the phenomenon showed that metformin does not significantly up-regulate SHP in human hepatocytes. We further demonstrate that AMPK activation is not involved in this process. We show that metformin disrupts PXR's interaction with steroid receptor coactivator-1 (SRC1) in a two-hybrid assay independently of the PXR ligand binding pocket. Metformin also inhibited vitamin D re Continue reading >>
Metformin Suppresses Pregnane X Receptor (pxr)-regulated Transactivation Of Cyp3a4 Gene
Metformin is widely used in the treatment of type-2 diabetes. The pleotropic effects of metformin on glucose and lipid metabolism have been proposed to be mediated by the activation of AMP-activated protein kinase (AMPK) and the subsequent up-regulation of small heterodimer partner (SHP). SHP suppresses the functions of several nuclear receptors involved in the regulation of hepatic metabolism, including pregnane X receptor (PXR), which is referred to as a "master regulator" of drug/xenobiotic metabolism. In this study, we hypothesize that metformin suppresses the expression of CYP3A4, a main detoxification enzyme and a target gene of PXR, due to SHP up-regulation. We employed various gene reporter assays in cell lines and qRT-PCR in human hepatocytes and in Pxr(-/-) mice. We show that metformin dramatically suppresses PXR-mediated expression of CYP3A4 in hepatocytes. Consistently, metformin significantly suppressed the up-regulation of Cyp3a11 mRNA in the liver and intestine of wild-type mice, but not in Pxr(-/-) mice. A mechanistic investigation of the phenomenon showed that metformin does not significantly up-regulate SHP in human hepatocytes. We further demonstrate that AMPK activation is not involved in this process. We show that metformin disrupts PXR's interaction with steroid receptor coactivator-1 (SRC1) in a two-hybrid assay independently of the PXR ligand binding pocket. Metformin also inhibited vitamin D receptor-, glucocorticoid receptor- and constitutive androstane receptor (CAR)-mediated induction of CYP3A4 mRNA in human hepatocytes. We show, therefore, a suppressive effect of metformin on PXR and other ligand-activated nuclear receptors in transactivation of the main detoxification enzyme CYP3A4 in human hepatocytes. Do you want to read the rest of this Continue reading >>
Ampk Is Not Required For The Effect Of Metformin On The Inhibition Of Bmp6-induced Hepcidin Gene Expression In Hepatocytes
AMPK is not required for the effect of metformin on the inhibition of BMP6-induced hepcidin gene expression in hepatocytes Scientific Reportsvolume7, Articlenumber:12679 (2017) The biguanide metformin is used for its antidiabetic effect for many years but how metformin acts remains poorly understood and controversial. AMP-activated protein kinase (AMPK), a protein kinase that plays a key role in maintaining energy homeostasis, is assumed to be one of the prime targets of metformin. However, since our demonstration that AMPK is not required for the beneficial effects of metformin on the control of glycemia, the list of AMPK-independent actions of metformin is rapidly increasing. Given the conflicting results on the effects of metformin we sought, using our genetic mouse models deficient in the catalytic subunits of AMPK, to determine whether this kinase is involved in the effects of metformin on the expression of the iron-regulatory hormone hepcidin, as recently proposed. Here we demonstrate, using different approaches, either isolated hepatocytes that lack AMPK, or direct AMPK activators, that, AMPK activation is not necessary for metformin to inhibit BMP6-induced hepcidin gene expression. These results may shed new lights on the increasingly recognized AMPK-independent metformins molecular action, an important area of current research. In a recent study, Kim et al. reported an interesting finding of transcriptional regulation of the iron-regulatory hormone hepcidin expression by the antidiabetic biguanide drug metformin 1 . Hepcidin plays a critical role in the control of systemic iron balance by coordinating the major fluxes of iron into blood plasma through the regulation of intestinal iron absorption, delivery of recycled iron from macrophages, and release of store Continue reading >>
- Renal Handling of Ketones in Response to Sodium–Glucose Cotransporter 2 Inhibition in Patients With Type 2 Diabetes
- Early-onset and classical forms of type 2 diabetes show impaired expression of genes involved in muscle branched-chain amino acids metabolism
- Gene Therapy for Type 1 Diabetes: Preclinical Promise
Clinically And Pharmacologically Relevant Interactions Of Antidiabetic Drugs
Go to: Introduction Patients with type 2 diabetes mellitus (T2DM) often do not suffer solely from symptoms of increased blood glucose levels. In the majority of cases, several comorbidities are present with the need of additional pharmacological treatment. Concomitant diseases such as hypertension and high blood lipids can lead to both microvascular and macrovascular complications [Cornier et al. 2008]. Moreover, central nervous disorders such as depression are increased in patients with T2DM compared with the general population [Anderson et al. 2001]. Multifactorial pharmacotherapy significantly reduces the risk of cardiovascular (CV) mortality [Gaede et al. 2008], but an increasing number of medications taken by the patients leads to a higher risk of adverse drug effects and interactions [Freeman and Gross, 2012; Amin and Suksomboon, 2014; Rehman et al. 2015; Valencia and Florez, 2014; Peron et al. 2015]. Applying a multifactorial pharmacotherapy approach, it is important to consider cytochrome P-450 (CYP) enzyme interactions [De Wildt et al. 1999; Dresser et al. 2000], altered absorption properties [Fleisher et al. 1999] and transporter activities [Lin and Yamazaki, 2003]. Furthermore, nutrition [Fleisher et al. 1999], herbal supplements [Rehman et al. 2015] and other parameters such as patient’s age and gender [Meibohm et al. 2002; Mangoni and Jackson, 2004] are of importance when the drug interaction risk of a pharmacological therapy is assessed. This article provides a short review of the pharmacokinetic and pharmacodynamic properties of antidiabetic drugs and their clinically relevant interactions with common medications which are frequently used to treat diabetic comorbidities. Literature searches included PubMed and Scopus databases using the Medical Subject Continue reading >>
