Salicylates and Hypoglycemia

Abstract

DURING the past 18 months we have seen three patients who developed hypoglycemia in association with salicylate ingestion. The purpose of this paper is to emphasize the importance of considering and recognizing this association. It was possible to perform extensive studies on only one of these patients (case 1) ; this case will be presented in some detail and the other two only briefly. Report of Cases CASE 1.\p=m-\This 22-month-old white male was the product of a term pregnancy which was complicated by toxemia and abruptio placenta. His birth weight and length were 1.5 kg (31/2 lb) and 41 cm (16 inches), respectively. The first 48 hours of life were complicated by respiratory distress, recurrent apneic spells, and generalized seizures. A blood sugar value at this time was 4 mg%. The hypoglycemia was adequately controlled with hydrocortisone therapy. At 2 weeks of age, the patient developed unexplained jaundice, associated with hepatosplenomegaly, which cleared spontaneously. Phenobarbital therapy, instituted at 48 hours of age, was discontinued at 5 months of age; at 13 months of age, tapering of the dose of hydrocortisone was begun because of the initial appearance of cushingoid features. On three occasions, at 16, 18, and 20 months of age, respectively, a single generalized seizure occurred. Each of these seizures was asso¬ ciated with an upper respiratory infection; blood and spinal fluid glucose levels were normal at these times. The patient's mental and motor development have been normal, with the exception of delayed walking without support because of residual spasticity in the right lower extremity. The physical examination at 21 months of age was normal with the exception of a first degree hypospadias and the spasticity of the leg. His linear growth from birth has been at a constant rate below the third percentile. The laboratory studies performed through 21 months of age had not yielded a specific cause for his hypoglycemia. When the patient was 21 months of age, the history was obtained that the mother had been administering to the patient 60 to 150 mg of aspirin daily since the age of 5 months for "irritability, teething, sleeplessness, etc." The question then arose whether this patient's hypo¬ glycemia might be related to salicylate ingestion, and he was admitted to the Clinical Research Center to investigate the possibility.The data presented in Fig 1 and 2 were obtained during two aspirin-response tests performed during this hospitalization and another one three weeks later. The patient's nutritional status was normal for the two control and test periods, and ketonuria was absent. The aspirin was administered after an eight-hour fast, and the fast was continued until the end of the control and test periods. At the times of these tests, the patient was receiving 4 mg of hydrocortisone daily, administered orally in four equal fractions ; the iden¬ tical dose and dosage schedule were maintained during the control and test periods. Aspirin, 300 mg in 250 ml of water, and 250 ml of water were given by g...

The effect of 3-methyl salicylic (0-cresotinic) acid on plasma insulin and glucose tolerance in diabetic and non-diabetic subjects

“…Although effective oral antidiabetic agents have been available for several years now, none are without some risk or side-effect. The major risk, particularly in the elderly, is the development of hypoglyeaemia and the advantage of salicylates is that whilst they may lower blood sugar and abolish glycosuria and even moderate ketonuria, they do not produce hypoglycaemia (always excepting acute salicylate intoxication, in which hypoglycaemia has been reported (Barnett et al., 1942;Cotton and Fahlberg, 1964) and the rare idiosyncrasy (Limbeck et al, 1965)). Their effectiveness, however, seems to depend on high plasma salicylate concentrations, which has meant the administration of large doses, with inevitably the appearance of other troublesome side-effects, notably tinnitus, deafness, bleeding from gastric erosions, and metabolic stimulation.…”

Delayed Diagnosis Salicylate Toxicity With Confirmed Cerebrospinal Fluid Salicylate Concentration: A Case Report of Altered Mental Status Without Neuroglycopenia and With Coagulopathy

“…Additionally, neuroglycopenia, also known as hypoglycorrhachia, has been noted to occur in salicylate-poisoned animals [ 1 , 2 , 7 ]. Although infrequently documented in humans, neuroglycopenia is believed to be a cause of altered mental status in salicylate-poisoned humans [ 1 , 5 , 8 ]. Multiple other abnormalities can occur as a complication of salicylate toxicity, including salicylate-induced coagulopathy.…”