Autoimmune Endocrine Dysfunctions Associated with Cancer Immunotherapies.
Silvia Martina FerrariPoupak FallahiGiusy EliaFrancesca RagusaIlaria RuffilliArmando PatrizioMaria Rosaria GaldieroEnke BaldiniSalvatore UlisseGiancarlo MaroneAlessandro AntonelliPublished in: International journal of molecular sciences (2019)
Immune checkpoint inhibitors block the checkpoint molecules. Different types of cancer immune checkpoint inhibitors have been approved recently: CTLA-4 monoclonal antibodies (as ipilimumab); anti-PD-1 monoclonal antibodies (as pembrolizumab and nivolumab); and anti-PD-L1 monoclonal antibodies (as atezolizumab, avelumab, and durmalumab). We collect recent published results about autoimmune endocrine dysfunctions associated with cancer antibody immunotherapies. These agents cause a raised immune response leading to immune-related adverse events (irAEs), varying from mild to fatal, based on the organ system and severity. Immune-related endocrine toxicities are usually irreversible in 50% of cases, and include hypophysitis, thyroid dysfunctions, type 1 diabetes mellitus, and adrenal insufficiency. Anti-PD-1-antibodies are more frequently associated with thyroid dysfunctions (including painless thyroiditis, hypothyroidism, thyrotoxicosis, or thyroid storm), while the most frequent irAE related to anti-CTLA-4-antibodies is hypophysitis. The combination of anti-CTLA-4 and anti-PD-1 antibodies is associated with a 30% chance of irAEs. Symptoms and clinical signs vary depending on the target organ. IrAEs are usually managed by an oncological therapist, but in more challenging circumstances (i.e., for new onset insulin-dependent diabetes, hypoadrenalism, gonadal hormones dysfunctions, or durable hypophysitis) an endocrinologist is needed.
Keyphrases
- papillary thyroid
- type diabetes
- immune response
- squamous cell
- multiple sclerosis
- glycemic control
- prostate cancer
- cardiovascular disease
- drug induced
- randomized controlled trial
- cell cycle
- systematic review
- physical activity
- childhood cancer
- metabolic syndrome
- cell proliferation
- inflammatory response
- skeletal muscle