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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...
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Adrenal Gland Disorders01:27

Adrenal Gland Disorders

Adrenal gland disorders manifest when the production of adrenal hormones deviates from the norm, resulting in either excessive or insufficient concentrations.
Adrenal insufficiency, characterized by insufficient cortisol and aldosterone production, leads to conditions like Addison's disease. This disorder, affecting the adrenal cortex, exhibits symptoms such as skin bronzing, dehydration, low blood pressure, fatigue, and weight loss. Congenital adrenal hyperplasia, a genetic ailment causing...
Goiter01:27

Goiter

Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...

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Cancer Risk in Acromegaly: Reassessing the Evidence and Impact of Biochemical Control.

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Updated: Jun 19, 2026

Endoscopic Endonasal Trans-sphenoidal Approach: Minimally Invasive Surgery for Pituitary Adenomas
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Acromegaly pathogenesis and treatment.

Shlomo Melmed1

  • 1Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA. Melmed@csmc.edu

The Journal of Clinical Investigation
|November 4, 2009
PubMed
Summary

Acromegaly, caused by excess growth hormone (GH), leads to serious health issues. Effective management of GH and IGF1 levels through surgery, radiation, or novel medications improves patient outcomes and reduces mortality.

Area of Science:

  • Endocrinology
  • Oncology

Background:

  • Acromegaly results from excess growth hormone (GH) hypersecretion, typically due to pituitary adenomas.
  • Elevated GH and IGF1 levels cause disproportionate growth and comorbidities like arthritis and glucose intolerance.
  • Untreated acromegaly significantly increases mortality risk due to cardiovascular, cerebrovascular, and pulmonary dysfunction.

Purpose of the Study:

  • To review the pathogenesis of acromegaly.
  • To discuss current and emerging management strategies for acromegaly.

Main Methods:

  • Review of existing literature on acromegaly.
  • Discussion of surgical, radiological, and pharmacological treatment options.
  • Highlighting novel therapeutic agents in clinical trials.

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Main Results:

  • Somatostatin receptor (SSTR) ligands inhibit GH release and tumor growth.
  • GH receptor antagonists effectively lower IGF1 levels.
  • Novel peptides with polyreceptor affinities show promise in clinical trials.

Conclusions:

  • Effective control of GH and IGF1 hypersecretion is crucial for managing acromegaly.
  • Tumor ablation or stabilization improves comorbidities and reduces mortality.
  • Emerging therapies offer improved treatment options for acromegaly patients.