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Fine structure of adrenal cortex in ectopic ACTH syndrome
Endokrinologie
|February 1, 1977
Summary
Ectopic ACTH syndrome caused by pancreatic cancer led to adrenal gland changes. Bilateral adrenalectomy revealed cellular hyperplasia and altered mitochondria, demonstrating adaptability to hormonal stimulation.
Area of Science:
- Endocrinology
- Oncology
- Cell Biology
Background:
- Ectopic ACTH syndrome presents with hypercortisolism due to non-pituitary tumors.
- Pancreatic adenocarcinoma can rarely cause ectopic ACTH syndrome.
- Bilateral adrenalectomy is a treatment option for severe ectopic ACTH syndrome.
Observation:
- A patient with pancreatic adenocarcinoma exhibited ectopic ACTH syndrome.
- Light microscopy showed adrenocortical compact cell hyperplasia and lipid depletion.
- Electron microscopy revealed enlarged cells with abundant smooth endoplasmic reticulum (SER), increased rough endoplasmic reticulum (RER), and prominent Golgi apparatus.
Findings:
- Adrenocortical cell changes, including SER accumulation and interdigitation, were attributed to tumor-secreted ACTH.
- Mitochondria displayed enlargement, pleomorphism, cavitation, and predominantly vesicular cristae, typical of fasciculata cells.
- Some mitochondria showed lamellar cristae, suggesting a transformation towards the vesicular type.
Implications:
- The study highlights the ultrastructural adaptations of the adrenal cortex to chronic ACTH stimulation from ectopic sources.
- It demonstrates mitochondrial plasticity within adrenocortical cells.
- Understanding these cellular changes provides insights into the pathophysiology of ectopic ACTH syndrome.