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Rheumatoid Arthritis (RA) is a chronic inflammatory disease leading to joint inflammation and destruction. Treatment of RA includes the use of conventional (cs), biologic (b) disease-modifying anti-rheumatic drugs (DMARDs), and oral or intraarticular (IA) glucocorticoids (GCs). All different classes of drugs have shown to halt disease progression in clinical studies. In real life, a physician has more options than just adding or switching to a new ts/bDMARD if any kind of DMARDs has failed. They can modify or optimize the therapy with concomitant csDMARDs, and oral or IA-GC can be added to the treatment regimen. The EULAR states that therapeutic adjustment including the "optimization of csDMARDs dose or route of administration or intra-articular injections of GCs" is recommended. Thus, a new therapeutic agent can be embedded in a whole strategy with parallel optimization of the csDMARD and GC treatment. The idea of treating to target (T2T) for the treatment of RA patients has been around since the late 1990s. Many clinical studies (Ticora, BsSt, Camera) have demonstrated the superiority of a T2T approach. When I talk to physicians, I understand that most of them only rarely inject joints with GC. Therefore, I would like to create an issue on the T2T approach in reality including primary data, reviews, and real-life data demonstrating the general opinion and execution of T2T in treating RA.

Medicine --- rheumatoid arthritis --- sleep --- sleep disorders --- pain --- osteoporosis --- fracture --- fracture risk assessment tool --- treat-to-target --- certolizumab pegol --- csDMARDs --- glucocorticoids --- intra-articular injections --- DAS 28 --- ACR response --- HAQ-DI --- TNFα --- golimumab --- efficacy --- tolerability --- immunogenicity --- methotrexate --- posology --- titration --- oral route --- subcutaneous route --- bioavailability --- effectiveness --- periodontitis --- periodontal disease --- anti-citrullinated protein autoantibodies --- rheumatoid factor --- smoking --- medication --- Porphyromonas gingivalis --- Rheumatoid arthritis --- matrix metalloproteinase 3 --- infliximab --- pharmacogenomics --- anti-TNF --- personalized medicine --- baricitinib --- disease-modifying antirheumatic drugs --- pain perception --- outcomes research --- patient perspective --- Rheumatoid Arthritis --- therapy --- DMARD --- MTX --- Tumor Necrosis Factor-Alpha Inhibitors --- ankylosing spondylitis --- biosimilar --- switching --- synovial fibroblasts --- cytokine --- osteoclast --- herbal medicine --- methylation --- next-generation sequencing --- recovery of function --- fatigue --- productivity --- tofacitinib --- oral --- Th1.17 --- IL-17A --- IFN-γ, CD73 --- adenosine --- psoriatic arthritis --- regulation --- pseudoerosions --- hand --- foot --- ultrasonography --- radiography --- computed tomography --- magnetic resonance imaging --- n/a

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Rheumatoid Arthritis (RA) is a chronic inflammatory disease leading to joint inflammation and destruction. Treatment of RA includes the use of conventional (cs), biologic (b) disease-modifying anti-rheumatic drugs (DMARDs), and oral or intraarticular (IA) glucocorticoids (GCs). All different classes of drugs have shown to halt disease progression in clinical studies. In real life, a physician has more options than just adding or switching to a new ts/bDMARD if any kind of DMARDs has failed. They can modify or optimize the therapy with concomitant csDMARDs, and oral or IA-GC can be added to the treatment regimen. The EULAR states that therapeutic adjustment including the "optimization of csDMARDs dose or route of administration or intra-articular injections of GCs" is recommended. Thus, a new therapeutic agent can be embedded in a whole strategy with parallel optimization of the csDMARD and GC treatment. The idea of treating to target (T2T) for the treatment of RA patients has been around since the late 1990s. Many clinical studies (Ticora, BsSt, Camera) have demonstrated the superiority of a T2T approach. When I talk to physicians, I understand that most of them only rarely inject joints with GC. Therefore, I would like to create an issue on the T2T approach in reality including primary data, reviews, and real-life data demonstrating the general opinion and execution of T2T in treating RA.

rheumatoid arthritis --- sleep --- sleep disorders --- pain --- osteoporosis --- fracture --- fracture risk assessment tool --- treat-to-target --- certolizumab pegol --- csDMARDs --- glucocorticoids --- intra-articular injections --- DAS 28 --- ACR response --- HAQ-DI --- TNFα --- golimumab --- efficacy --- tolerability --- immunogenicity --- methotrexate --- posology --- titration --- oral route --- subcutaneous route --- bioavailability --- effectiveness --- periodontitis --- periodontal disease --- anti-citrullinated protein autoantibodies --- rheumatoid factor --- smoking --- medication --- Porphyromonas gingivalis --- Rheumatoid arthritis --- matrix metalloproteinase 3 --- infliximab --- pharmacogenomics --- anti-TNF --- personalized medicine --- baricitinib --- disease-modifying antirheumatic drugs --- pain perception --- outcomes research --- patient perspective --- Rheumatoid Arthritis --- therapy --- DMARD --- MTX --- Tumor Necrosis Factor-Alpha Inhibitors --- ankylosing spondylitis --- biosimilar --- switching --- synovial fibroblasts --- cytokine --- osteoclast --- herbal medicine --- methylation --- next-generation sequencing --- recovery of function --- fatigue --- productivity --- tofacitinib --- oral --- Th1.17 --- IL-17A --- IFN-γ, CD73 --- adenosine --- psoriatic arthritis --- regulation --- pseudoerosions --- hand --- foot --- ultrasonography --- radiography --- computed tomography --- magnetic resonance imaging --- n/a

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This book serves to highlight the pharmacokinetics/drug–drug interactions and mechanistic understanding in relation to the drug-metabolizing enzymes and drug transporters.This book presents a series of drug metabolism and transport mechanisms that govern the pharmacokinetic features of therapeutic drugs as well as natural herbal medicines. It also covers the pharmacokinetic interactions caused by inhibiting or inducing the metabolic or transport activities under disease states or the coadministration of potential inhibitors. It also deals with microenvironmental pharmacokinetic profiles as well as population pharmacokinetics, which gives new insights regarding the pharmacokinetic features with regard to drug metabolism and transporters.

Medicine --- Pharmaceutical industries --- tofacitinib --- dose-dependent pharmacokinetics --- hepatic and intestinal first-pass effect --- rats --- catalposide --- in vitro human metabolism --- UDP-glucuronosyltransferase --- sulfotransferase --- carboxylesterase --- celecoxib --- drug–drug interaction --- fluorescence --- HPLC --- metabolism --- repaglinide --- HSG4112 --- anti-obesity agent --- stereoselectivity --- pharmacokinetics --- compound K --- protopanaxadiol (PPD) --- biliary excretion --- intestinal metabolism --- Carthamus tinctorius extract --- notoginseng total saponins --- comparative pharmacokinetic study --- large volume direct injection --- compatibility mechanism --- mertansine --- human hepatocytes --- cytochrome P450 --- UDP-glucuronosyltransferases --- sodium-glucose cotransporter 2 (SGLT2) inhibitors --- DWP16001 --- kidney distribution --- inhibition mode --- diabetes --- transporter-enzyme interplay --- influx transporter --- efflux transporter --- physiologically based pharmacokinetic model --- cytochrome P450 enzymes --- tiropramide --- healthy Korean subjects --- modeling --- population pharmacokinetic --- quercetin --- breast cancer resistance protein --- inhibitor --- prazosin --- sulfasalazine --- kinetic analysis --- food–drug interactions --- Caco-2 --- EpiIntestinal --- first-pass --- P-gp --- BCRP --- drug transporter --- CYP3A4 --- oral availability --- automatization --- drug absorption --- drug dosing --- head-and-neck cancer --- real-time measurements --- taxanes --- tissue engineering --- UHPLC-MS/MS --- metformin --- verapamil --- drug interaction --- organic cation transporter 2 --- renal excretion --- acute renal failure --- gentamicin --- cisplatin --- hepatic CYP3A1(23) --- creatinine clearance --- renal clearance --- nonrenal clearance --- tofacitinib --- dose-dependent pharmacokinetics --- hepatic and intestinal first-pass effect --- rats --- catalposide --- in vitro human metabolism --- UDP-glucuronosyltransferase --- sulfotransferase --- carboxylesterase --- celecoxib --- drug–drug interaction --- fluorescence --- HPLC --- metabolism --- repaglinide --- HSG4112 --- anti-obesity agent --- stereoselectivity --- pharmacokinetics --- compound K --- protopanaxadiol (PPD) --- biliary excretion --- intestinal metabolism --- Carthamus tinctorius extract --- notoginseng total saponins --- comparative pharmacokinetic study --- large volume direct injection --- compatibility mechanism --- mertansine --- human hepatocytes --- cytochrome P450 --- UDP-glucuronosyltransferases --- sodium-glucose cotransporter 2 (SGLT2) inhibitors --- DWP16001 --- kidney distribution --- inhibition mode --- diabetes --- transporter-enzyme interplay --- influx transporter --- efflux transporter --- physiologically based pharmacokinetic model --- cytochrome P450 enzymes --- tiropramide --- healthy Korean subjects --- modeling --- population pharmacokinetic --- quercetin --- breast cancer resistance protein --- inhibitor --- prazosin --- sulfasalazine --- kinetic analysis --- food–drug interactions --- Caco-2 --- EpiIntestinal --- first-pass --- P-gp --- BCRP --- drug transporter --- CYP3A4 --- oral availability --- automatization --- drug absorption --- drug dosing --- head-and-neck cancer --- real-time measurements --- taxanes --- tissue engineering --- UHPLC-MS/MS --- metformin --- verapamil --- drug interaction --- organic cation transporter 2 --- renal excretion --- acute renal failure --- gentamicin --- cisplatin --- hepatic CYP3A1(23) --- creatinine clearance --- renal clearance --- nonrenal clearance

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

This book serves to highlight the pharmacokinetics/drug–drug interactions and mechanistic understanding in relation to the drug-metabolizing enzymes and drug transporters.This book presents a series of drug metabolism and transport mechanisms that govern the pharmacokinetic features of therapeutic drugs as well as natural herbal medicines. It also covers the pharmacokinetic interactions caused by inhibiting or inducing the metabolic or transport activities under disease states or the coadministration of potential inhibitors. It also deals with microenvironmental pharmacokinetic profiles as well as population pharmacokinetics, which gives new insights regarding the pharmacokinetic features with regard to drug metabolism and transporters.

tofacitinib --- dose-dependent pharmacokinetics --- hepatic and intestinal first-pass effect --- rats --- catalposide --- in vitro human metabolism --- UDP-glucuronosyltransferase --- sulfotransferase --- carboxylesterase --- celecoxib --- drug–drug interaction --- fluorescence --- HPLC --- metabolism --- repaglinide --- HSG4112 --- anti-obesity agent --- stereoselectivity --- pharmacokinetics --- compound K --- protopanaxadiol (PPD) --- biliary excretion --- intestinal metabolism --- Carthamus tinctorius extract --- notoginseng total saponins --- comparative pharmacokinetic study --- large volume direct injection --- compatibility mechanism --- mertansine --- human hepatocytes --- cytochrome P450 --- UDP-glucuronosyltransferases --- sodium-glucose cotransporter 2 (SGLT2) inhibitors --- DWP16001 --- kidney distribution --- inhibition mode --- diabetes --- transporter-enzyme interplay --- influx transporter --- efflux transporter --- physiologically based pharmacokinetic model --- cytochrome P450 enzymes --- tiropramide --- healthy Korean subjects --- modeling --- population pharmacokinetic --- quercetin --- breast cancer resistance protein --- inhibitor --- prazosin --- sulfasalazine --- kinetic analysis --- food–drug interactions --- Caco-2 --- EpiIntestinal --- first-pass --- P-gp --- BCRP --- drug transporter --- CYP3A4 --- oral availability --- automatization --- drug absorption --- drug dosing --- head-and-neck cancer --- real-time measurements --- taxanes --- tissue engineering --- UHPLC-MS/MS --- metformin --- verapamil --- drug interaction --- organic cation transporter 2 --- renal excretion --- acute renal failure --- gentamicin --- cisplatin --- hepatic CYP3A1(23) --- creatinine clearance --- renal clearance --- nonrenal clearance