Secondary or Compensatory Hypoglycemia.

Abstract

In contrast with true hypoglycemia, of which insulin hypoglycemia is an example, we suggest the term secondary or compensatory hypoglycemia for those conditions in which an initial rise in blood sugar is followed by a fall below normal. McGuigan and Ross 1 state that many investigators have reported a hyperglycemia, while others working with the same substance have demonstrated a hypoglycemia. Santos 2 finds that secretin exerts a hypoglycemic action in man, dog and rabbit. Lambert and Hermann, 3 however, show that injection of secretin causes transient hyperglycemia, followed by hypoglycemia. Such differences in observation may be due to the quantity of reserve glycogen in the animal, or to the time of withdrawal of the blood for analysis, after injection of the biologic mixture or compound under investigation.

We postulate that any biologic condition or chemical substance giving rise to persistent hyperglycemia may eventually produce hypoglycemia. Josephs 4 has demonstrated that the hyperglycemia developed during anesthesia results in post-anesthetic hypoglycemia. According to Herold, 5 a high blood sugar during obstetrical labor is followed by post-partum hypoglycemia. Maud L. Menten 6 has reported that the soluble toxic products of the enteritidis-paratyphoid B group produce an initial hyperglycemia and a secondary hypoglycemia. Taya 7 has shown that a rise in temperature causes an increase in blood sugar concentration, followed by a fall below normal. Geiger 8 maintains that spontaneous fall of fever is accompanied by a hypoglycemia.

Adrenalin, known to cause a marked rise in blood sugar, is also capable of producing hypoglycemia. According to György and Herzberg, 9 the initial hyperglycemia occasioned by adrenalin is finally superseded by hypoglycemia. The latter results from depletion of the glycogen stores incident upon the, increased glycogenolysis and increased glucose consumption. Collens, Shelling and Byron 10 found that ligating the hepatic artery causes a total depletion of the glycogen reserves of the body.