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Postprandial (reactive) hypoglycemia

F John Service, MD, PhD
Adrian Vella, MD
Section Editor
David M Nathan, MD
Deputy Editor
Jean E Mulder, MD


Hypoglycemic disorders cause symptoms primarily in the postprandial or fasting states and rarely in a chaotic fashion unrelated to food ingestion or deprivation. Some disorders that cause hypoglycemia predominantly in the postprandial state are the noninsulinoma pancreatogenous hypoglycemia syndrome (NIPHS), postgastric bypass hypoglycemia, and insulin autoimmune hypoglycemia (table 1). It is important to appreciate that sometimes patients are unable to differentiate fasting from postprandial occurrences of hypoglycemia, and some disorders can produce both fasting and postprandial hypoglycemia.

The diagnosis, evaluation, and management of patients with hypoglycemic symptoms that predominantly occur in the postprandial state will be reviewed here. Other causes of hypoglycemia and the diagnostic approach to hypoglycemia are discussed separately. (See "Hypoglycemia in adults: Clinical manifestations, definition, and causes" and "Hypoglycemia in adults without diabetes mellitus: Diagnostic approach".)


Postprandial (reactive) hypoglycemia — Postprandial or reactive hypoglycemia is a descriptor of the timing of hypoglycemia (within four hours after meals) and is not a diagnosis per se. Its presence requires an evaluation to determine the cause of hypoglycemia.

The term reactive hypoglycemia is often erroneously used to describe a functional or idiopathic disorder observed in patients with nondescript postprandial symptoms and no biochemical evidence of hypoglycemia after ingestion of a high carbohydrate meal and with resolution of symptoms after dietary modification [1-3] (see 'Postprandial syndrome' below). The danger in considering postprandial (reactive) hypoglycemia as a disease itself, rather than a descriptor of the timing of hypoglycemia, is the failure to search for the underlying cause of the hypoglycemia.

Postprandial syndrome — In the remote past, patients with symptoms suggestive of increased sympathetic activity (anxiety, weakness, tremor, perspiration, or palpitations) occurring after meals were considered to have functional hyperinsulinism or functional hypoglycemia, as a reaction to the ingestion of food. The diagnosis was based upon reproduction of the patient's hypoglycemia symptoms in association with a blood glucose value of <50 mg/dL (2.8 mmol/L) after an oral glucose tolerance test (OGTT) [4]. However, the value of an OGTT in diagnosing reactive hypoglycemia has been discredited based upon the following observations:

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Literature review current through: Nov 2017. | This topic last updated: Oct 20, 2016.
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  1. Scheen AJ, Lefèbvre PJ. [Reactive hypoglycaemia, a mysterious, insidious but non dangerous critical phenomenon]. Rev Med Liege 2004; 59:237.
  2. Brun JF, Fedou C, Mercier J. Postprandial reactive hypoglycemia. Diabetes Metab 2000; 26:337.
  3. Virally ML, Guillausseau PJ. Hypoglycemia in adults. Diabetes Metab 1999; 25:477.
  4. Permutt MA. Postprandiol hypoglycemia. Diabetes 1976; 25:719.
  5. Lev-Ran A, Anderson RW. The diagnosis of postprandial hypoglycemia. Diabetes 1981; 30:996.
  6. Johnson DD, Dorr KE, Swenson WM, Service FJ. Reactive hypoglycemia. JAMA 1980; 243:1151.
  8. Hofeldt FD, Dippe S, Forsham PH. Diagnosis and classification of reactive hypoglycemia based on hormonal changes in response to oral and intravenous glucose administration. Am J Clin Nutr 1972; 25:1193.
  9. Chalew SA, McLaughlin JV, Mersey JH, et al. The use of the plasma epinephrine response in the diagnosis of idiopathic postprandial syndrome. JAMA 1984; 251:612.
  10. Hogan MJ, Service FJ, Sharbrough FW, Gerich JE. Oral glucose tolerance test compared with a mixed meal in the diagnosis of reactive hypoglycemia. A caveat on stimulation. Mayo Clin Proc 1983; 58:491.
  11. Charles MA, Hofeldt F, Shackelford A, et al. Comparison of oral glucose tolerance tests and mixed meals in patients with apparent idiopathic postabsorptive hypoglycemia: absence of hypoglycemia after meals. Diabetes 1981; 30:465.
  12. Buss RW, Kansal PC, Roddam RF, et al. Mixed meal tolerance test and reactive hypoglycemia. Horm Metab Res 1982; 14:281.
  13. Lefebvre PJ, Andreani D, Marks V. Statement on 'post-prandial' or 'reactive' hypoglycemia. In: Hypoglycemia, Andreani D, Marks V, Lefebvre PJ (Eds), Raven Press, New York 1987. p.79.
  14. Snorgaard O, Binder C. Monitoring of blood glucose concentration in subjects with hypoglycaemic symptoms during everyday life. BMJ 1990; 300:16.
  15. Palardy J, Havrankova J, Lepage R, et al. Blood glucose measurements during symptomatic episodes in patients with suspected postprandial hypoglycemia. N Engl J Med 1989; 321:1421.
  16. Simpson EJ, Holdsworth M, Macdonald IA. Ambulatory blood glucose measurement, dietary composition and physical activity levels in otherwise healthy women reporting symptoms that they attribute to hypoglycaemia. Br J Nutr 2006; 95:1127.
  17. Ford CV, Bray GA, Swerdloff RS. A psychiatric study of patients referred with a diagnosis of hypoglycemia. Am J Psychiatry 1976; 133:290.
  18. Anthony D, Dippe S, Hofeldt FD, et al. Personality disorder and reactive hypoglycemia. A quantitative study. Diabetes 1973; 22:664.
  19. Gilbert, JAL, Dunlap, DM. Hypoglycaemia following partial gastrectomy. BMJ 1947; 2:330.
  20. Leichter SB, Permutt MA. Effect of adrenergic agents on postgastrectomy hypoglycemia. Diabetes 1975; 24:1005.
  21. Wiznitzer T, Shapira N, Stadler J, et al. Late hypoglycemia in patients following vagotomy and pyloroplasty. Int Surg 1974; 59:229.
  22. Service GJ, Thompson GB, Service FJ, et al. Hyperinsulinemic hypoglycemia with nesidioblastosis after gastric-bypass surgery. N Engl J Med 2005; 353:249.
  23. Basu A, Service FJ, Yu L, et al. Insulin autoimmunity and hypoglycemia in seven white patients. Endocr Pract 2005; 11:97.
  24. Service FJ, Natt N, Thompson GB, et al. Noninsulinoma pancreatogenous hypoglycemia: a novel syndrome of hyperinsulinemic hypoglycemia in adults independent of mutations in Kir6.2 and SUR1 genes. J Clin Endocrinol Metab 1999; 84:1582.
  25. Faludi G, Bendersky G, Gerber P. Functional hypoglycemia in early latent diabetes. Ann N Y Acad Sci 1968; 148:868.
  26. Centers for Disease Control (CDC). Toxic hypoglycemic syndrome--Jamaica, 1989-1991. MMWR Morb Mortal Wkly Rep 1992; 41:53.
  27. Froesch ER. Essential fructosuria and hereditary fructose intolerance. In: The Metabolic Basis of Inherited Disease, Stanbury JB, Wyngaarden JB, Fredrickson DS (Eds), McGraw-Hill, New York 1978. p.121.
  28. O'Keefe SJ, Marks V. Lunchtime gin and tonic a cause of reactive hypoglycaemia. Lancet 1977; 1:1286.
  29. Joffe BI, Roach L, Baker S, et al. Failure to induce reactive hypoglycaemia by drinking a starch-based alcohol beverage (sorghum beer). Ann Clin Biochem 1981; 18:22.
  30. Shen J, Gaglia J. Hypoglycemia following pancreas transplantation. Curr Diab Rep 2008; 8:317.
  31. Ozgen AG, Hamulu F, Bayraktar F, et al. Long-term treatment with acarbose for the treatment of reactive hypoglycemia. Eat Weight Disord 1998; 3:136.
  32. Lefebvre PJ, Scheen AJ. The use of acarbose in the prevention and treatment of hypoglycaemia. Eur J Clin Invest 1994; 24 Suppl 3:40.
  33. Gérard J, Luyckx AS, Lefèbvre PJ. Acarbose in reactive hypoglycemia: a double-blind study. Int J Clin Pharmacol Ther Toxicol 1984; 22:25.
  34. Renard E, Parer-Richard C, Richard JL, et al. Effect of Miglitol (Bay m1099), a new alpha-glucosidase inhibitor, on glucose, insulin, C-peptide and GIP responses to an oral sucrose load in patients with post-prandial hypoglycaemic symptoms. Diabete Metab 1991; 17:355.