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Zorluk: Çok zorEndocrinology and Metabolism

Match each patient's clinical presentation and laboratory profile, obtained during an episode of documented fasting hypoglycemia, to the most accurate pathophysiologic description of the underlying etiology.

  • A 45-year-old nurse with recurrent hypoglycemia. Labs: Elevated serum insulin, suppressed C-peptide, and undetectable proinsulin.Surreptitious injection of a hypoglycemic agent lacking a connecting peptide
  • A 62-year-old female with recurrent fasting hypoglycemia. Labs: Elevated serum insulin, elevated C-peptide, elevated proinsulin, and a negative oral hypoglycemic secretagogue screen.Autonomous proliferation of neuroendocrine cells lacking normal feedback inhibition
  • A 70-year-old male with dementia presenting with confusion and a blood glucose of 40 mg/dL. Labs: Elevated serum insulin, elevated C-peptide, and a positive oral hypoglycemic secretagogue screen.Ingestion of a compound that artificially closes ATP-sensitive potassium channels on beta cells
  • A 58-year-old male with a large solitary fibrous pleural tumor. Labs: Suppressed serum insulin, suppressed C-peptide, and an elevated IGF-II to IGF-I ratio.Paraneoplastic secretion of a peptide that inappropriately activates peripheral insulin receptors
  • A 34-year-old female with profound fatigue, weight loss, and hyperpigmentation. Labs: Suppressed serum insulin, suppressed C-peptide, and failure of serum cortisol to rise >18 µg/dL.Autoimmune destruction of the adrenal cortex leading to counter-regulatory hormone deficiency

Cevap

The accurate matching pairs exogenous insulin with a lack of connecting peptide, insulinoma with autonomous neuroendocrine proliferation, sulfonylurea ingestion with K-ATP channel closure, Doege-Potter syndrome with paraneoplastic IGF-II secretion, and adrenal insufficiency with counter-regulatory hormone failure.
The diagnostic workup of hypoglycemia relies on measuring insulin, C-peptide, proinsulin, and hypoglycemic agents during a hypoglycemic episode. Exogenous insulin lacks C-peptide. Endogenous hyperinsulinemia (high C-peptide) is split between secretagogue use (positive drug screen, K-ATP channel closure) and insulinoma (negative screen, autonomous tumor). Hypoglycemia with appropriately suppressed insulin points to non-beta cell tumors (IGF-II secretion) or counter-regulatory failure (adrenal insufficiency).

Adım Adım Çözüm

1
Analyze the relationship between insulin and C-peptide in each profile.
Profiles with elevated insulin are either exogenous or endogenous. Profiles with suppressed insulin represent non-insulin-mediated hypoglycemia.
C-peptide is co-secreted 1:1 with endogenous insulin. Its presence or absence differentiates the source of excess insulin.
2
Evaluate the hyperinsulinemic profiles (elevated insulin).
The nurse has low C-peptide, indicating exogenous insulin. The 62-year-old and 70-year-old have high C-peptide, indicating endogenous production.
Exogenous pharmaceutical insulin does not contain C-peptide. Endogenous insulin production (tumors or drugs) secretes both.
3
Differentiate the endogenous hyperinsulinemic profiles.
The 70-year-old has a positive secretagogue screen, indicating sulfonylurea use. The 62-year-old has a negative screen and high proinsulin, indicating an insulinoma.
Sulfonylureas chemically stimulate the beta cells, while insulinomas are autonomous neuroendocrine tumors.
4
Evaluate the hypoinsulinemic (suppressed insulin) profiles.
The 58-year-old with a pleural tumor has elevated IGF-II (Doege-Potter syndrome). The 34-year-old with hyperpigmentation has failed cortisol response (Addison's disease).
Hypoglycemia normally suppresses insulin. If hypoglycemia persists, it is driven by insulin mimics (IGF-II) or a lack of counter-regulatory hormones (cortisol, glucagon, epinephrine).

Anahtar Kavram

Diagnostic differentiation of fasting hypoglycemia using the insulin, C-peptide, and counter-regulatory hormone axis
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