The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration's (FDA's) MedWatch program (800-FDA-1088). If you have reported an interesting, preventable ADR to MedWatch, please consider sharing the account with our readers.
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| http://dx.doi.org/10.1310/hpj5102-115 | DOI Listing |
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Peroxisome proliferator-activated receptor α (PPARα)-dependent regulation of fibroblast growth factor 23 (FGF23).
Pflugers Arch
April 2020
Department of Physiology, University of Hohenheim, Garbenstraße 30, 70599, Stuttgart, Germany.
Bone cells secrete fibroblast growth factor 23 (FGF23), a hormone that inhibits the synthesis of active vitamin D (1,25(OH)D) and induces phosphate excretion in the kidney. In addition, it exerts paracrine effects on other cells including hepatocytes, cardiomyocytes, and immune cells. The production of FGF23 is controlled by different factors including parathyroid hormone, 1,25(OH)D, alimentary phosphate, insulin, inflammation, and AMP-dependent kinase (AMPK) regulation of store-operated Ca entry (SOCE).
View Article and Find Full Text PDFThe Effect of Hypolipidemic Agents on Thyroid Autoimmunity in Women with Hashimoto's Thyroiditis Treated with Levothyroxine and Selenomethionine.
Exp Clin Endocrinol Diabetes
May 2018
Department of Internal Medicine and Clinical Pharmacology, Medical University of Silesia, Katowice, Poland.
Background: Levothyroxine and selenomethionine were found to reduce thyroid antibody titers in patients with Hashimoto's thyroiditis. The same effect was produced by intensive statin therapy. The aim of the present study was to assess whether hypolipidemic agents modulate the impact of thyroid hormone supplementation and selenomethionine on thyroid autoimmunity.
View Article and Find Full Text PDFFenofibrate-Induced Immune Thrombocytopenia; Topical Pramoxine-Induced Anaphylaxis; Nexplanon Delayed Hypersensitivity; Cyclosporine-Induced Cutaneous Pseudolymphoma; Severe Acute Hepatitis with Intravenous Amiodarone; Herpes-like Skin Eruption Due to Fluconazole.
Hosp Pharm
February 2016
Department of Pharmacy Practice, Temple University School of Pharmacy, Philadelphia, Pennsylvania.
The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration's (FDA's) MedWatch program (800-FDA-1088). If you have reported an interesting, preventable ADR to MedWatch, please consider sharing the account with our readers.
View Article and Find Full Text PDFProbable fenofibrate-induced acute generalized exanthematous pustulosis.
Am J Health Syst Pharm
December 2015
Anna E. Power is a medical student, Monash University, Melbourne, Australia, and Summer Vacation Scholar, Centre of Cardiovascular Research & Education (CCRE) in Therapeutics, School of Public Health and Preventive Medicine, Alfred Centre, Melbourne. Linda V. Graudins, B.Pharm., Dip.HospPharm., PGrad.Clinepid., FSHP, is Senior Pharmacist, Pharmacy Department, Alfred Health, Melbourne. Catriona A. McLean, B.Sc., M.B.B.S., FRACPA, M.D., FFSc, is Pathologist, Department of Anatomical Pathology, Alfred Hospital, Melbourne. Ingrid Hopper, M.B.B.S., B.Med.SC., FRACP, is Clinical Pharmacologist, Alfred Health, and National Health and Medical Research Council Postgraduate Scholar, CCRE in Therapeutics, School of Public Health and Preventive Medicine, Alfred Centre.
Purpose: The case of a patient who experienced a severe adverse reaction requiring emergency treatment after a single dose of fenofibrate is described.
Summary: A 58-year-old woman with type 1 diabetes was hospitalized for treatment of an extensive blistering rash on the buttocks and trunk accompanied by fever, hypotension, tachycardia, neutrophilia, impaired renal function, and liver enzyme abnormalities. She reported that two days previously she had developed fever and vomiting four hours after taking her first dose of fenofibrate (145 mg).
Antagonizing Peroxisome Proliferator-Activated Receptor α Activity Selectively Enhances Th1 Immunity in Male Mice.
J Immunol
December 2015
Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada; Toronto General Research Institute, University Health Network, Toronto, Ontario M5G 2M1, Canada; and Women's College Research Institute, Toronto, Ontario M5G 2M1, Canada
Females exhibit more robust Th1 responses than males. Our previous work suggested that this sex disparity is a consequence of higher activity of the androgen-induced gene peroxisome proliferator-activated receptor α (PPARα) in male CD4(+) T cells. The objective of this study was to elucidate the cellular and molecular mechanism of how PPARα inhibits Th1 responses in male mice.
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