We report a case of isolated adrenocorticotropin deficiency caused by pembrolizumab. This condition can be fatal, but its rarity causes under-recognition. Oncologists should pay attention to adrenal insufficiency due to pembrolizumab.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8190675 | PMC |
| http://dx.doi.org/10.1002/ccr3.4305 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Functional study of three cases with novel TBX19 variants.
Endocrine
January 2025
Department of Pediatrics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University, Shanghai, China.
Purpose: Congenital isolated adrenocorticotropic hormone deficiency (CIAD) is an autosomal recessive disorder. This study identifies novel TBX19 variants for CIAD patients, explores its possible effect mechanism at the structural, functional and protein levels, and guides clinicians better understand the condition.
Methods: The clinical characteristics of three CIAD children were summarized.
Central Adrenal Insufficiency: Etiology and Diagnostic Approach.
J Clin Res Pediatr Endocrinol
January 2025
İstanbul University, İstanbul Faculty of Medicine, Department of Pediatric Endocrinology, İstanbul, Turkey
Central adrenal insufficiency (CAI) occurs due to a pituitary gland disorder (secondary AI) or hypothalamic dysfunction (tertiary AI). It is a potentially life-threatening condition that has many congenital and acquired causes. Adrenocorticotropic hormone deficiency may be isolated or more commonly it can be accompanied by other pituitary hormone deficiencies or midline defects.
View Article and Find Full Text PDFCongenital isolated adrenocorticotropic hormone deficiency in a newborn caused by mutation: a case report and literature review.
Front Pediatr
November 2024
Department of Neonatology, Lanzhou University Second Hospital, Lanzhou, China.
Background: To investigate the clinical phenotype, genetic characteristics, and prognosis of isolated adrenocorticotropic hormone deficiency in a newborn (IAD, OMIM 201400) caused by mutation of the gene.
Case Presentation: The clinical features, diagnosis, treatment, and prognosis of a newborn with IAD admitted to our hospital were retrospectively analyzed. The patient and his parents were also examined by whole exome sequencing.
Modeling corticotroph deficiency with pituitary organoids supports the functional role of in human pituitary differentiation.
Elife
November 2024
Aix-Marseille University, INSERM, UMR1251, Marseille Medical Genetics, Institut MarMaRa, Marseille, France.
Article Synopsis
- Deficient Anterior pituitary with common Variable Immune Deficiency (DAVID) syndrome is caused by heterozygous mutations leading to adrenocorticotropic hormone deficiency and immune system issues.
- Researchers created pituitary organoids from edited human stem cells to study how specific genetic mutations affect pituitary development and found that these mutations significantly reduced the number of hormone-producing cells called corticotrophs.
- The study identified changes in gene expression related to pituitary development and suggested that the observed mutations have a direct impact on endocrine function, classifying them as pathogenic for pituitary development.
Comparison of Magnetic Resonance Imaging Features Between Programmed Cell Death 1/Programmed Cell Death Ligand 1 Inhibitor-Induced Hypopituitarism and Idiopathic Hypopituitarism in Japanese Subjects.
Cureus
October 2024
Department of Diabetes, Endocrinology and Metabolism, Kawasaki Medical School, Kurashiki, JPN.
Objective Immune checkpoint inhibitor-associated hypopituitarism (ICI-HP) is a rare immune-related adverse event (irAE) of ICIs. This study aimed to identify characteristic pituitary findings on magnetic resonance imaging (MRI) in ICI-HP. Methods This study is a single-center, retrospective, observational study.
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!