Main Classes of Drugs
Jerome Z. Litt, Neil H. Shear in Litt's Drug Eruption & Reaction Manual, 2017
Proton pump inhibitor (PPI)DexlansoprazoleEsomeprazoleLansoprazoleOmeprazolePantoprazoleRabeprazole
Drug-Related Sarcopenia
Kohlstadt Ingrid, Cintron Kenneth in Metabolic Therapies in Orthopedics, Second Edition, 2018
Proton pump inhibitors such as pantoprazole, esomeprazole, and omeprazole contribute to sarcopenia as an adverse effect of long-term use.16 These drugs are known for their use in treating acid-related disorders such as reflux, heartburn, and ulcers. Long-term use of these medications, particularly at higher doses, is a well-established contributor to hip fractures in older adults.17 Less known is the association with sarcopenia which may be from the same mechanism. Lowering pH in the gastrointestinal tract reduces calcium absorption leading to osteoporosis risk. Lowering pH also changes the microbiome to a likely more proinflammatory milieu. Impaired absorption of protein is critical for sarcopenia. Dietary intake of protein is emphasized, but this is only part of the process; the protein must also be absorbed. It is broken down in the stomach to facilitate absorption in the small intestine, but insufficient stomach acid results in a net reduction in protein intake.
The patient with an upper GI bleed
Andrew Stewart, Rory Mackinnon in Pocket On Call, 2015
Suspect peptic ulcer disease (PUD) with an upper GI bleed associated with epigastric pain, previous history of gastritis/ulceration, or recent treatment with NSAIDs. Commence treatment as follows:IV proton pump inhibitor (PPI): Consider for all patients in this category, some units prefer PPIs to be commenced following OGD. Increasing gastric pH will stabilize blood clots, thus reducing further bleeding. The drug of choice is usually pantoprazole delivered either as a regular bolus dose or as a continuous intravenous infusion. Therapy is usually continued for several days post-endoscopy.
Fedratinib, the first selective JAK2 inhibitor approved for treatment of myelofibrosis – an option beyond ruxolitinib
Published in Expert Review of Hematology, 2022
Chandan Saha, Claire Harrison
Fedratinib is rapidly absorbed following single oral dose with peak plasma concentration achieved 2 to 4hours following the administration of Fedratinib 400 mg once daily. The pharmaco*kinetic (PK) studies show a first-order absorption incorporating a lag time and first-order elimination [15,32,33]. Plasma Fedratinib levels reached steady state within 15days of once-daily dosing [30]. Fedratinib is metabolized by cytochrome P450 enzymes [15] (CYP3A4, CYP2C19) and, hence, dose reductions, even in some cases, avoiding co-administration of cytochrome P450 inhibitors may be necessary [34]. Fedratinib is a weak inhibitor of CYP2D6, and a moderate inhibitor of CYP2C19 and CYP3A4 [35]. Gastric acid suppression by co-administration of pantoprazole did not affect Fedratinib pharmaco*kinetics significantly [36]. Fedratinib is mainly excreted in feces [37], and the half-life was found to be 41hours [15]. PK is not significantly affected by age (between 20 and 95years), sex, race (White and Asian), body weight (between 40 and 135 kg), mild to moderate liver dysfunction, or mild renal dysfunction [15]. However, moderate (creatinine clearance 30–59 mL/min) or severe (creatinine clearance 15–29 mL/min) renal impairment increases Fedratinib exposure significantly, mandating a dose reduction for severe renal impairment [15,38].
Black esophagus: a case series and literature review of acute esophageal necrosis
Published in Scandinavian Journal of Gastroenterology, 2018
C. R. Lamers, W. G. N. Mares, D. J. Bac
A 24-year-old male presented to our emergency department with nausea, vomiting and progressive retrosternal pain. Physical examination revealed epigastric tenderness. Laboratory analysis revealed hemoglobin of 9.8 mmol/L—decreased to 8.2 mmol/L the next day—white blood cell count of 17.4/nL, serum creatinine of 87 μmol/L, urea of 9.6 mmol/L, glucose of 6.9 mmol/L, and albumin of 55 g/L. EGD showed a circumferential necrotizing esophagitis with edema, ulcerations, and purulent exudates involving the distal half of the esophagus and abruptly stopping at the gastro-esophageal junction (Figure 1.2). Biopsies of the esophageal mucosa revealed severe necrotizing inflammation. Additional tests for CMV and fungi were negative. Abdominal ultrasound was unremarkable. Patient was treated with pantoprazole. The next day the patient felt much better and he was discharged. Six months after discharge, a repeat EGD showed an unremarkable esophagus.
Stereoselective and nonstereoselective pharmaco*kinetics of rabeprazole – an overview
Published in Xenobiotica, 2018
Ranjeet Prasad Dash, Rana Rais, Nuggehally R. Srinivas
Chemically, the PPIs are substituted benzimidazoles and due to its acid labile nature designed as enteric-coated tablets or capsules intended for absorption after bypassing stomach. In 1989, omeprazole was the first PPI to get an approval in the United States. In the next decade, oral formulations of lansoprazole and pantoprazole were approved (Friedlander et al., 2010). Rabeprazole was first launched in Japan and is now available in over 70 countries (Goh et al., 2000). Rabeprazole was the first PPI approved in the United States with a 7-day course of treatment for Helicobacter Pylori eradication (Goh et al., 2000). Lansoprazole was the first PPI to be approved for pediatric use and pantoprazole got the approval as the first intravenous PPI therapy (Friedlander et al., 2010). Esomeprazole, the first enantiomer PPI, was approved for use in 2001, which was developed with an objective to overcome the issues of high hepatic clearance and low bioavailability associated with omeprazole (Olbe et al., 2003). Recently, in 2009, the second enantiomer PPI, dexlansoprazole, got the approval and it is available as a modified release formulation intended for prolonged release and extended acid suppression (Vakily et al., 2009).
