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Updated: Feb 24, 2026

Induction of Experimental Autoimmune Hypophysitis in SJL Mice
Published on: December 17, 2010
New Molecular, Biological, and Immunological Agents Inducing Hypophysitis
Anna Angelousi1, Eleftherios Chatzellis, Gregory Kaltsas
1Sector of Endocrinology, Department of Pathophysiology, National University of Athens, Athens, Greece.
Hypophysitis, an autoimmune pituitary inflammation, can be triggered by certain cancer immunotherapies like anti-CTLA-4 antibodies. Early diagnosis and hormone replacement are key for managing this rare but significant side effect.
Area of Science:
- Endocrinology
- Immunology
- Oncology
Background:
- Hypophysitis is a rare autoimmune condition affecting the pituitary gland.
- Immunomodulatory drugs, particularly those used in cancer therapy, are increasingly recognized causes.
- Anti-cytotoxic T-lymphocyte-associated antigen-4 (anti-CTLA-4) antibodies are associated with a notable prevalence of hypophysitis.
Purpose of the Study:
- To review current information on hypophysitis induced by novel molecular, biological, and immunological agents.
- To highlight the association between cancer immunotherapies and hypophysitis.
- To discuss diagnostic challenges and management strategies.
Main Methods:
- Literature review of hypophysitis associated with new immunomodulatory and biological agents.
- Analysis of reported prevalence rates for different drug classes.
- Discussion of diagnostic criteria and pathophysiological insights.
Main Results:
- Hypophysitis is a recognized side effect of anti-CTLA-4 antibody therapy (0-18% prevalence).
- Hypophysitis associated with anti-programmed cell death protein-1 (anti-PD-1) antibodies is less frequent (0-0.8%).
- No cases of hypophysitis have been reported with molecular targeted agents.
Conclusions:
- Hypophysitis diagnosis remains primarily clinical, as serological markers are not consistently sensitive.
- The pathophysiology of drug-induced hypophysitis is not fully understood.
- Management typically involves dose adjustment of the causative agent and pituitary hormone replacement therapy.
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