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 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...
Cirrhosis I: Introduction01:23

Cirrhosis I: Introduction

Cirrhosis is a chronic, irreversible liver disease characterized by the widespread replacement of healthy liver tissue with fibrotic scar tissue and the formation of regenerative nodules.Etiology of cirrhosisCirrhosis results from sustained liver injury that triggers progressive fibrosis and structural remodeling. The underlying causes are diverse, encompassing common and less frequent clinical conditions. Regardless of the origin, all causes lead to chronic inflammation, hepatocyte loss, and...
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...
Esophageal Achalasia01:27

Esophageal Achalasia

Esophageal achalasia is a chronic neurogenic disorder characterized by impaired relaxation of the lower esophageal sphincter (LES) and absent or ineffective peristalsis in the distal esophagus. This leads to a functional obstruction without a physical blockage, despite significant disruption of esophageal motility.EtiologyAchalasia is caused by degeneration of the myenteric (Auerbach's) plexus, specifically the loss of inhibitory ganglion cells that produce vasoactive intestinal peptide (VIP)...
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...

You might also read

Related Articles

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

Sort by
Same author

Differential Transthyretin Stabilization in Patients With Wild Type and Variant Transthyretin Amyloidosis.

JACC. CardioOncology·2026
Same author

Evaluation of the Current ATTR-CM Treatment Landscape via a Mathematical Model of TTR Dissociation and Amyloid Formation.

CPT: pharmacometrics & systems pharmacology·2026
Same author

A qPCR-based algorithm for the diagnosis of classic and non-classic Turner syndrome.

The Indian journal of medical research·2026
Same author

Correlation between DPP-4 Gene Expression and T-Cell Subset Marker Genes in Chronic Liver Disease Patients in Eastern India: An Observational Study.

Indian journal of endocrinology and metabolism·2026
Same author

Myonecrosis Masquerading at an Unusual Site: A Diagnostic Dilemma.

AACE endocrinology and diabetes·2026
Same author

Acoramidis, Serum Transthyretin, and Cardiovascular Outcomes in Transthyretin Amyloid Cardiomyopathy: Insights From the ATTRibute-CM Trial.

Journal of cardiac failure·2026

Related Experiment Video

Updated: May 22, 2026

Endoscopic Endonasal Trans-sphenoidal Approach: Minimally Invasive Surgery for Pituitary Adenomas
07:43

Endoscopic Endonasal Trans-sphenoidal Approach: Minimally Invasive Surgery for Pituitary Adenomas

Published on: January 17, 2018

Acromegaly without acral changes: A rare presentation.

Nilanjan Sengupta1, Uma Sinha, Keshab Sinha Roy

  • 1Department of Endocrinology, Nilratan Sircar Medical College, Kolkata, India.

Indian Journal of Endocrinology and Metabolism
|May 26, 2012
PubMed
Summary
This summary is machine-generated.

This case study highlights an unusual presentation of acromegaly in an elderly woman. Despite typical facial changes, she lacked acral enlargement, emphasizing the need for high diagnostic suspicion.

Keywords:
Acral enlargementacromegalypituitary hyperplasia

Related Experiment Videos

Last Updated: May 22, 2026

Endoscopic Endonasal Trans-sphenoidal Approach: Minimally Invasive Surgery for Pituitary Adenomas
07:43

Endoscopic Endonasal Trans-sphenoidal Approach: Minimally Invasive Surgery for Pituitary Adenomas

Published on: January 17, 2018

Area of Science:

  • Endocrinology
  • Internal Medicine
  • Clinical Case Reports

Background:

  • Acromegaly is typically characterized by acral enlargement and coarse facial features, resulting from excess growth hormone (GH).
  • Diagnosis often relies on clinical signs and biochemical confirmation of elevated GH and insulin-like growth factor-1 (IGF-1).

Observation:

  • A short, elderly female presented with a 10-year history of developing acromegalic facies but no acral overgrowth.
  • She had well-controlled primary hypothyroidism, mild insulin resistance, and systemic hypertension, with no visual field defects.
  • Biochemical tests confirmed high serum IGF-1 and elevated, nonsuppressed GH levels.
  • Brain MRI showed pituitary hyperplasia without a detectable adenoma, and no ectopic source of GH or GHRH was identified.

Findings:

  • Biochemically confirmed acromegaly with typical facies and short stature, but notably lacking acral overgrowth and a pituitary adenoma.
  • The patient's presentation was atypical, challenging conventional diagnostic criteria for acromegaly.
  • Longstanding disease activity occurred without the expected physical manifestations or a clear tumor source.

Implications:

  • This case underscores the importance of considering acromegaly even when classic signs like acral enlargement are absent.
  • Atypical presentations necessitate a high degree of clinical suspicion and thorough biochemical evaluation.
  • The findings suggest that acromegaly can manifest and persist without overt physical overgrowth or identifiable pituitary adenomas, complicating diagnosis.