A 72-hour fasting test is conducted to evaluate adult patients presenting with recurrent episodes of spontaneous fasting hypoglycemia. Match each of the following biochemical profiles (all obtained at the time of symptomatic hypoglycemia with plasma glucose < 45 mg/dL) with the most likely underlying etiology.
- Insulin 45 µU/mL (High), C-peptide 0.1 ng/mL (Low), Proinsulin <5 pmol/L (Low), Negative hypoglycemic drug screenExogenous insulin administration
- Insulin 35 µU/mL (High), C-peptide 3.8 ng/mL (High), Proinsulin 55 pmol/L (High), Negative hypoglycemic drug screenInsulinoma (pancreatic beta-cell tumor)
- Insulin 42 µU/mL (High), C-peptide 4.0 ng/mL (High), Proinsulin 12 pmol/L (Normal), Positive hypoglycemic drug screenSulfonylurea or meglitinide surreptitious ingestion
- Insulin 2 µU/mL (Low), C-peptide 0.1 ng/mL (Low), Beta-hydroxybutyrate 0.1 mmol/L (Low), Elevated IGF-II:IGF-I ratioNon-islet cell tumor hypoglycemia (NICTH)
- Insulin 2 µU/mL (Low), C-peptide 0.1 ng/mL (Low), Beta-hydroxybutyrate 4.5 mmol/L (High), Cortisol 2.5 µg/dL (Low)Primary adrenal insufficiency
Answer
The correct matches require distinguishing insulin-mediated vs non-insulin-mediated hypoglycemia, identifying the source of excess insulin (endogenous vs exogenous), and utilizing beta-hydroxybutyrate to differentiate causes of appropriately suppressed insulin.
Each match correctly pairs the underlying pathophysiology with its exact biochemical signature during a fasting state. Exogenous insulin lacks C-peptide; insulinomas secrete insulin/C-peptide/proinsulin; sulfonylureas mimic insulinomas but yield a positive drug screen; NICTH suppresses ketones and insulin via IGF-II; and adrenal insufficiency features low cortisol, low insulin, but high ketones due to unsuppressed lipolysis.
Step-by-Step Solution
Key Concept
Evaluation of fasting hypoglycemia requires a stepwise analysis of insulin, C-peptide, drug screens, and beta-hydroxybutyrate to pinpoint the exact physiological failure point.