Related Experiment Videos

Hyperhomocysteinemia in patients with Cushing's syndrome

Massimo Terzolo1, Barbara Allasino, Sandra Bosio

  • 1Dipartimento di Scienze Cliniche e Biologiche, Medicina Interna I, Università di Torino, 10100 Torino, Italy. terzolo@usa.net

Insights

Active Cushing's syndrome elevates serum homocysteine levels and lowers folate. Remission restores homocysteine to normal, suggesting hypercortisolism drives this metabolic change and potential cardiovascular risk.

Area of Science:

  • Endocrinology
  • Metabolic Disorders
  • Clinical Biochemistry

Background:

  • Cushing's syndrome is characterized by hypercortisolism, leading to various metabolic disturbances.
  • Hyperhomocysteinemia is a known risk factor for cardiovascular disease.
  • The role of homocysteine metabolism in Cushing's syndrome is not fully understood.

Purpose of the Study:

  • To investigate serum homocysteine concentrations and methylene tetrahydrofolate reductase (MTHFR) C677T polymorphism in patients with Cushing's syndrome.
  • To compare homocysteine levels in active disease, remission, and healthy controls.
  • To explore the association between homocysteine, cortisol, and folate levels.

Main Methods:

  • Serum homocysteine and folate levels were measured.
  • MTHFR C677T gene polymorphism was analyzed.
  • Patients included 41 with active Cushing's syndrome and 16 in remission.
  • 105 healthy blood donors served as controls.

Main Results:

  • Patients with active Cushing's syndrome exhibited significantly higher homocysteine and lower folate levels compared to controls and those in remission.
  • Homocysteine levels were positively correlated with midnight serum cortisol and negatively with serum folate.
  • No significant difference in MTHFR genotype distribution was observed between groups.

Conclusions:

  • Active hypercortisolism is associated with hyperhomocysteinemia and reduced serum folate.
  • Homocysteine levels normalize upon remission of Cushing's syndrome.
  • Hyperhomocysteinemia may contribute to the prothrombotic state and cardiovascular risk in Cushing's syndrome.

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...
Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers01:19

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers

Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
Hyperosmolar Hyperglycemic State01:21

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State, or HHS, is a serious and life-threatening complication of type 2 diabetes mellitus. It is characterized by three main features: severe hyperglycemia, profound dehydration, and elevated serum osmolality, all occurring without significant ketoacidosis.HHS typically develops in older adults or individuals with limited access to fluids. This may result from illness, cognitive impairment, or medications such as diuretics or corticosteroids. These factors reduce...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...