Alimentary Tract Hypoglycemia Revisited

\s=b\ Knowing that hypoglycemia and inappropriate plasma insulin levels and insulin-glucose ratios can occur after gastric surgery may prevent unwarranted exploration for insulinoma in patients with alimentary tract hypoglycemia (ATH). Absolute differentiation may be achieved by comparing the insulin-glucose ratios obtained during a 72-hour fast with those obtained during an oral glucose tolerance test. The treatment of ATH is primarily medical, surgery being reserved for those patients in whom diet and drug therapy fails. For such medically intractable patients, reversal of a 10-cm segment of jejunum at the gastroenteric stoma is highly effective in controlling the symptoms of hypoglycemia. (Arch Surg 1983;118:1087-1090) Symptomatic hypoglycemia may occur in the fed or fasting state. Fasting hypoglycemia is most commonly caused by excess insulin from functioning pancreatic betacell tumors, although liver disease, pituitary-adrenal axis insufficiency, and carcinomatosis must be considered in the differential diagnosis.1 On the other hand, alimentary tract hypoglycemia (ATH) is a form of reactive hypoglycemia ini¬ tiated by feeding. It occurs two to three hours after eating and is often a complication of gastric surgery.2 It is charac¬ terized by early rapid glucose absorption and hyperinsulinemia and subsequent hypoglycemia and must be differ¬ entiated from the reactive hypoglycemia of mild adult-onset diabetes mellitus.3 As these disorders involve excessive release of insulin by the pancreatic beta cell, without systematic laboratory investigation the primary fasting hyperinsulinemia of insulinoma can be confused with the secondary reactive hy¬ perinsulinemia of ATH, or pseudoinsulinoma.4 Both may be manifested by profound cerebral dysfunction3,5,6 as well as the typical adrenergic sign-symptom complex associated with hypoglycemia. To add further confusion, an insulinoma has been described that was clinically manifested by reactive rather than fasting hypoglycemia.7 Our approach to a rather difficult case of ATH is described herein. REPORT OF A CASE A 76-year-old man was admitted to Grady Memorial Hospital, Atlanta, with a blood glucose level of 9 mg/dL, after being found unresponsive at home by his wife. He had an extensive history of dizzy spells and spontaneously resolving syncopal spells lasting several minutes. The spells could not be related to meals or diet, although neither the patient nor his family could give accurate histories. The patient had undergone truncal vagotomy, antrectomy, and Billroth II gastrojejunostomy for a bleeding duodenal ulcer five years earlier. He had a history of alcohol abuse and of possible diabetes and hypertension. He was normotensive and asthenie, with no remarkable physical findings except for a reduci¬ ble right inguinal hernia. On neurologic examination, he exhibited deficits in short- and long-term memory that were compatible with dementia, and he walked with a shuffling, narrow-based gait. Aside from the markedly depressed blood glucose level and an SGOT level VA times normal, admission laboratory values were normal. An ECG showed occasional premature ventricular con¬ tractions, and a chest roentgenogram disclosed mild cardiomegaly. A regimen of continuous glucose infusions was started. After admission, the patient experienced several symptomatic hypoglycemie episodes, with blood glucose levels ranging from 19 to 27 mg/dL, despite intravenous (IV) glucose infusion and diet. The relationship of food intake to hypoglycemia was not appreci¬ ated at the time. Thyroid function test findings and the levels of serum cortisol (am and pm), gastrin, growth hormone, and 5-hydroxyindoleacetic acid were all normal. The vitamin B12 level was less than 100 pg/mL. An upper gastrointestinal tract roentgenographic series showed a Billroth II gastrectomy without masses or ulcers. An abdominal computed tomographic scan was normal, but selective celiac and gastroduodenal angiography was suggestive of a "tumor blush" in the head of the pancreas (Fig 1). A liver biopsy specimen showed focal steatosis and hemosiderosis. Glucose-insulin ratios measured during two hypoglycemie epi¬ sodes were 0.2 and 0.3, and a diagnosis of insulinoma was made. Diazoxide therapy was begun, to control the hypoglycemie epi¬ sodes, and the patient was transferred to the surgical service for exploration.