Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
Cushing Syndrome I: Introduction01:26

Cushing Syndrome I: Introduction

Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the syndrome.Exogenous...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Hypothyroidism II: Pathophysiology01:23

Hypothyroidism II: Pathophysiology

Hypothyroidism is a disorder characterized by insufficient production of thyroid hormones, which regulate metabolism, energy balance, and multiple organ systems.TypesHypothyroidism is classified based on the level of dysfunction. Primary hypothyroidism results from intrinsic thyroid gland dysfunction, causing reduced hormone production despite normal or increased stimulation. Secondary hypothyroidism arises from inadequate thyroid-stimulating hormone (TSH) secretion by the pituitary. Tertiary...
Hypothalamic-Pituitary Axis01:37

Hypothalamic-Pituitary Axis

The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
Graves' Disease I: Introduction01:28

Graves' Disease I: Introduction

Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Primary hyperparathyroidism: review and recommendations on evaluation, diagnosis, and management. A Canadian and international consensus.

Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA·2016
Same author

Effect of concomitant vitamin D deficiency or insufficiency on lumbar spine volumetric bone mineral density and trabecular bone score in primary hyperparathyroidism.

Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA·2016
Same author

Low vitamin D levels have become less common in primary hyperparathyroidism.

Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA·2015
Same author

Relationship of bone mineralization density distribution (BMDD) in cortical and cancellous bone within the iliac crest of healthy premenopausal women.

Calcified tissue international·2014
Same author

Lentivirus-mediated α-melanocyte-stimulating hormone overexpression in the hypothalamus decreases diet induced obesity in mice.

Journal of neuroendocrinology·2013
Same author

Endothelial function in mild primary hyperparathyroidism.

Clinical endocrinology·2012
Same journal

Mitochondria produce lactate to vent redox pressure.

Trends in endocrinology and metabolism: TEM·2026
Same journal

Beyond fat storage: neuronal lipid droplets regulate whole-body metabolism.

Trends in endocrinology and metabolism: TEM·2026
Same journal

HDL resuscitates cells from ferroptosis.

Trends in endocrinology and metabolism: TEM·2026
Same journal

2-Methylbutyrylcarnitine (2MBC).

Trends in endocrinology and metabolism: TEM·2026
Same journal

Decoding growth hormone actions on human growth plate stem cells.

Trends in endocrinology and metabolism: TEM·2026
Same journal

Androgen loss backfires: Brain gate for tumor immunity.

Trends in endocrinology and metabolism: TEM·2026
See all related articles

Related Experiment Video

Updated: Jul 6, 2026

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis
10:52

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis

Published on: December 17, 2010

Hypothalamic-pituitary sarcoidosis.

P U Freda1, S J Silverberg, K D Post

  • 1Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.

Trends in Endocrinology and Metabolism: TEM
|November 1, 1992
PubMed
Summary
This summary is machine-generated.

Sarcoidosis can cause hypopituitarism due to granulomatous pituitary infiltration, leading to various hormonal deficiencies. Neurologic symptoms often improve with corticosteroids, but hormonal issues typically persist.

More Related Videos

Induction of Experimental Autoimmune Hypophysitis in SJL Mice
10:38

Induction of Experimental Autoimmune Hypophysitis in SJL Mice

Published on: December 17, 2010

Related Experiment Videos

Last Updated: Jul 6, 2026

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis
10:52

Preparation of Mouse Pituitary Immunogen for the Induction of Experimental Autoimmune Hypophysitis

Published on: December 17, 2010

Induction of Experimental Autoimmune Hypophysitis in SJL Mice
10:38

Induction of Experimental Autoimmune Hypophysitis in SJL Mice

Published on: December 17, 2010

Area of Science:

  • Endocrinology
  • Neurology
  • Immunology

Background:

  • Sarcoidosis is an inflammatory disease that can affect multiple organs.
  • Granulomatous infiltration of the pituitary and hypothalamus is a known complication of sarcoidosis.
  • Hypopituitarism can result from this infiltration, impacting anterior pituitary function.

Purpose of the Study:

  • To describe the spectrum of hypopituitarism in patients with sarcoidosis.
  • To outline associated neurological manifestations.
  • To discuss the impact of corticosteroid therapy on these conditions.

Main Methods:

  • Review of clinical data from patients diagnosed with sarcoidosis and hypopituitarism.
  • Assessment of anterior pituitary hormone levels.
  • Evaluation of neurological and visual deficits.

Main Results:

  • Patients exhibited varying degrees of anterior pituitary insufficiency, from selective deficiencies to panhypopituitarism.
  • Diabetes insipidus was a frequent finding.
  • Cranial neuropathies, aseptic meningitis, and visual field defects were common neurological manifestations.

Conclusions:

  • Hypopituitarism is a significant complication of neurosarcoidosis.
  • While neurological deficits may respond to corticosteroids, hormonal deficiencies often require long-term management.
  • Comprehensive endocrine and neurological evaluation is crucial for affected patients.