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Related Concept Videos

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...
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...
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...
Sympathetic Pathways: Collateral Ganglia and Adrenal Medulla01:27

Sympathetic Pathways: Collateral Ganglia and Adrenal Medulla

The sympathetic pathways of the collateral ganglia and adrenal medulla serve unique but interconnected roles in the sympathetic response.
Collateral Ganglia
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The greater splanchnic nerve, formed by the...
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...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...

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Subclinical phaeochromocytoma.

Massimo Mannelli1, Jacques W M Lenders, Karel Pacak

  • 1University of Florence, Dept. Clinical Pathophysiology, Viale Pieraccini 6, 50139 Florence, Italy. m.mannelli@dfc.unifi.it

Best Practice & Research. Clinical Endocrinology & Metabolism
|August 7, 2012
PubMed
Summary

Subclinical phaeochromocytomas are often undiagnosed neural crest tumors. These silent tumors can cause serious health consequences due to unpredictable catecholamine release, highlighting the need for increased awareness and screening.

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Area of Science:

  • Endocrinology
  • Oncology
  • Genetics

Background:

  • Phaeochromocytomas and paragangliomas are neural crest-derived tumors, frequently undiagnosed due to non-specific symptoms or silent presentations.
  • The clinical presentation varies based on catecholamine and peptide release, with hypertension being a common but not universal sign.

Purpose of the Study:

  • To review the characteristics and diagnostic challenges of subclinical phaeochromocytomas.
  • To emphasize the potential for serious health consequences from undiagnosed tumors.

Main Methods:

  • Literature review of autopsy studies, clinical presentations, and genetic associations.
  • Analysis of tumor secretory capacity, biochemical phenotypes, and genetic mutations (e.g., SDHB).

Main Results:

  • Subclinical phaeochromocytomas may present with minimal or absent symptoms due to low or intermittent catecholamine secretion, dopamine production, or non-secretory activity.
  • Tumors associated with SDHB mutations often exhibit subclinical behavior, poor differentiation, low catecholamine content, and malignancy.
  • Adrenoceptor desensitization can mask high catecholamine levels, leading to a subclinical presentation.

Conclusions:

  • Subclinical phaeochromocytomas are often discovered incidentally or through genetic screening.
  • Undiagnosed phaeochromocytomas, regardless of secretory activity or benign nature, pose significant risks, including death from abrupt catecholamine release.