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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...
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...
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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...
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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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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

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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...

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A Novel Method: Super-selective Adrenal Venous Sampling
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Published on: September 15, 2017

Subclinical Cushing's syndrome.

Massimo Terzolo1, Silvia Bovio, Anna Pia

  • 1Dipartimento di Scienze Cliniche e Biologiche, Medicina Interna I, A.S.O. San Luigi, Università di Torino, Italy. terzolo@usa.net

Arquivos Brasileiros De Endocrinologia E Metabologia
|January 23, 2008
PubMed
Summary

Subclinical Cushing's syndrome (CS) is increasingly found due to adrenal incidentalomas. Management of this cortisol excess condition remains empirical, with options including surgery or observation and metabolic treatment.

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Area of Science:

  • Endocrinology
  • Oncology
  • Radiology

Background:

  • Subclinical Cushing's syndrome (CS) diagnosis is rising due to incidental adrenal masses found via advanced imaging.
  • Adrenal incidentalomas, often cortical adenomas, are common, with 5-20% exhibiting autonomous cortisol secretion.
  • Current diagnostic criteria for subclinical CS are debated, lacking a gold standard.

Purpose of the Study:

  • To review the current understanding and diagnostic challenges of subclinical Cushing's syndrome.
  • To discuss the association between subclinical CS and metabolic comorbidities.
  • To explore current management strategies for subclinical CS.

Main Methods:

  • Literature review of studies on adrenal incidentalomas and subclinical CS.
  • Analysis of diagnostic criteria and reported prevalence rates.
  • Examination of associated metabolic conditions and treatment outcomes.

Main Results:

  • Subclinical CS is linked to increased rates of hypertension, obesity, impaired glucose tolerance, diabetes, and hyperlipidemia.
  • Long-term complications and definitive evidence of clinical impact are still under investigation.
  • Management approaches include adrenalectomy or conservative observation with metabolic syndrome treatment.

Conclusions:

  • Subclinical CS is a growing clinical concern with established metabolic associations.
  • Further research is needed to clarify long-term outcomes and establish diagnostic consensus.
  • Treatment strategies for subclinical CS require further validation and standardization.