Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1210/jcem-25-4-457 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Multiple electrolyte disorders triggered by proton pump inhibitor-induced hypomagnesemia: Case reports with a mini-review of the literature.
Clin Nephrol Case Stud
January 2024
Hospital Universitário Cassiano Antonio Moraes, Universidade Federal do Espírito Santo (HUCAM-UFES), Vitória, ES.
Article Synopsis
- Drug-induced hypomagnesemia can have serious and potentially fatal consequences, particularly from long-term use of proton pump inhibitors (PPIs), which impair magnesium absorption in the intestines.
- The mechanisms involve reduced transport of magnesium through specific cellular channels (TRPM6 and TRPM7) and a decrease in paracellular absorption due to downregulated claudins.
- Two cases are highlighted where PPI use led to electrolyte disorders resulting in cardiac arrhythmia, cognitive changes, and seizures, emphasizing the importance of monitoring magnesium levels in high-risk patients.
Acarbose diminishes postprandial suppression of bone resorption in patients with type 2 diabetes.
Bone
May 2023
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark; Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark. Electronic address:
Aims: The alpha-glucosidase inhibitor acarbose is an antidiabetic drug delaying assimilation of carbohydrates and, thus, increasing the amount of carbohydrates in the distal parts of the intestines, which in turn increases circulating levels of the gut-derived incretin hormone glucagon-like peptide 1 (GLP-1). As GLP-1 may suppress bone resorption, acarbose has been proposed to potentiate meal-induced suppression of bone resorption. We investigated the effect of acarbose treatment on postprandial bone resorption in patients with type 2 diabetes and used the GLP-1 receptor antagonist exendin(9-39)NH to disclose contributory effect of acarbose-induced GLP-1 secretion.
View Article and Find Full Text PDFUnexpected serum phosphorus lost in an amniotic fluid embolism patient.
Clin Chim Acta
January 2023
Department of Laboratory Medicine, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu Province 210029, China. Electronic address:
Background: Serum phosphorus concentration reflects body energy equilibrium and functions of the kidney and the coagulation system. It is regulated by serum calcium concentration and parathyroid hormone (PTH).
Case Report: We present a case of constant low concentrations of serum phosphorus in a 34-year-old female who was diagnosed with amniotic fluid embolism (AFE) and was continuously treated with extracorporeal membrane oxygenation (ECMO), continuous renal replacement therapy (CRRT) and blood component transfusion during an observational period of 11 days.
Antagonizing microRNA-19a/b augments PTH anabolic action and restores bone mass in osteoporosis in mice.
EMBO Mol Med
November 2022
Molecular Skeletal Biology Laboratory, Department of Trauma, Hand and Reconstructive Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Postmenopausal bone loss often leads to osteoporosis and fragility fractures. Bone mass can be increased by the first 34 amino acids of human parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP), or by a monoclonal antibody against sclerostin (Scl-Ab). Here, we show that PTH and Scl-Ab reduce the expression of microRNA-19a and microRNA-19b (miR-19a/b) in bone.
View Article and Find Full Text PDFNovel PTH Gene Mutations Causing Isolated Hypoparathyroidism.
J Clin Endocrinol Metab
May 2022
Division of Endocrinology and Diabetes, The Children's Hospital of Philadelphia (CHOP), Philadelphia, Pennsylvania, USA.
Context: Parathyroid hormone (PTH) gene mutations represent a rare cause of familial isolated hypoparathyroidism (FIH). These defects can cause hypoparathyroidism with increased or decreased serum levels of PTH through 1) impaired PTH synthesis; 2) induction of parathyroid cell apoptosis; or 3) secretion of bioinactive PTH molecules. Eight pathogenic mutations of this gene have been described previously.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!