American Journal of Therapeutics 0, 000–000 (2014)

Those Salicylate Cases—How Sweet Are They? Christopher S. Lim, MD,1* Christian B. Marcelo, MD,1 and Sean M. Bryant, MD1,2

Owing to the complex metabolism of salicylates, both hyperglycemia and hypoglycemia have been reported with salicylate poisoning. The aim of this study was to characterize this relationship. Data from the Illinois Poison Center were retrospectively queried over a 5-year period (2008–2012), and patients with a salicylate concentration $30 mg/dL were included. Hypoglycemia and hyperglycemia were defined as glucose concentrations ,55 and .140 mg/dL, respectively. Of the 160 patients included, most were normoglycemic (81%) and 19% were hyperglycemic. No patient experienced hypoglycemia. Our study indicates that hypoglycemia may be a very rare occurrence in the setting of salicylate poisoning. Clinicians must remain vigilant, regardless of the glucose concentration, when entertaining salicylism as an etiology in appropriate patients. Keywords: aspirin, salicylate, glucose, hypoglycemia, hyperglycemia, poisoning, overdose, toxicity

INTRODUCTION Medical toxicology and emergency medicine texts submit contradictory expectations regarding glucose concentrations in the context of salicylate poisoning.1,2 There are several case reports describing either hypoglycemia or hyperglycemia in the setting of salicylate poisoning.3–6 However, there are no larger studies describing the correlation between glucose and salicylate concentrations, and it is the aim of this study to further characterize this relationship.

MATERIALS AND METHODS Using Crystal Reports (Version 11.0), all salicylate cases reported to our regional poison center (RPC) over a 5-year period (2008–2012) were retrospectively

1

Department of Emergency Medicine, Toxikon Consortium, Cook County Hospital (Stroger), Chicago, IL; and 2Illinois Poison Center, Chicago, IL. The authors have no conflicts of interest to declare. *Address for correspondence: Department of Emergency Medicine, Toxikon Consortium, Cook County Hospital (Stroger), 1900 W Polk St, 10th Floor, Chicago, IL 60605. E-mail: [email protected] 1075–2765  2014 Lippincott Williams & Wilkins

queried. Those cases where the salicylate concentration was reported to be $30 mg/dL, and a serum glucose concentration was recorded, were included. Abnormalities in glucose concentration were defined according to standard Endocrine Society Guidelines. Hypoglycemia was defined as a concentration ,55 mg/dL, and hyperglycemia as a concentration .140 mg/dL. Patient medical history (eg, history of diabetes), time of ingestion, and nature of ingestion (acute vs. chronic) was not reported.

RESULTS A total of 1418 salicylate exposures were managed during the 5-year period. Cases of interest included 160 patients where a documented salicylate concentration of $30 mg/dL and a glucose concentration were reported. Within our study group, salicylate concentrations ranged from 30 to 118 mg/dL (average 54 mg/dL) and serum glucose concentrations ranged from 63 to 674 mg/dL (average 122 mg/dL) (Figure 1). Most patients (130 or 81%) were normoglycemic and 30 patients (19%) were classified as hyperglycemic. None of the patients in this series were defined as hypoglycemic. The highest salicylate concentration was 118 mg/dL and had a corresponding glucose concentration of 140 mg/dL. Additionally, the lowest www.americantherapeutics.com

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Lim et al

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FIGURE 1. Salicylate concentration correlated with glucose concentration.

salicylate concentration was 30 mg/dL with a corresponding glucose concentration of 100 mg/dL.

DISCUSSION Because of the complex metabolic processes that occur during poisoned states, both hypoglycemia and hyperglycemia have been reported in the setting of salicylate toxicity.3–6 Hyperglycemia is attributed to impaired tissue utilization in the early phase of toxicity.7 Several mechanisms proposed for hypoglycemia include increased insulin secretion: impairment of gluconeogenesis, increased glucose utilization by tissue and secondary to inhibition of oxidative phosphorylation.4,5 Although the relationship of glucose concentrations in salicylate-poisoned patients may vary, these data reveal a propensity toward normoglycemia followed by hyperglycemia. None of our patients were hypoglycemic. We highlight, however, a slight trend of increased salicylate concentrations corresponding with higher glucose concentrations. Although salicylate toxicity may alter glucose metabolism in multiple ways, glucose measurements should be interpreted with caution in this setting and may have no correlation with the severity of poisoning. These data are limited in several ways. Every patient reported to our RPC with salicylate poisoning did not

American Journal of Therapeutics (2014) 0(0)

have glucose concentrations reported in the RPC record. Because of this, our numbers are limited. Additionally, the timing and correlation of these laboratory values in each particular patient was problematic and difficult to ascertain from the medical record. Pertinent medical history of disorders altering glucose metabolism (eg, diabetes) was not consistently documented and not taken into consideration in our series. Finally, separating patients into groups based on acute versus chronic poisoning was challenging in this cohort. A prospective study may help better define the relationship between salicylate poisonings and corresponding glucose concentrations. When appropriate, physicians must remain vigilant in keeping salicylism in the differential diagnoses of poisoned patients regardless of glucose concentration. Our data may, in fact, mirror what is appreciated in many populations of poisoned patients (ie, frequency of hyperglycemia), and further inquiry into glycemic states in salicylate–poisoned patients warrants study, especially whether or not there is any true relationship to hypoglycemia.

REFERENCES 1. Marx JA, Hockberger RS, Walls RM. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 7th ed. Philadelphia, PA: Mosby Elsevier; 2010. 2. Nelson LS, Lewin NA, Howland MA, et al. Goldfrank’s Toxicologic Emergencies. 9th ed. The McGraw-Hill Companies; 2011. 3. Cotton EK, Fahlberg VI. Hypoglycemia with salicylate poisoning. Am J Dis Child. 1964;108:171–173. 4. Raschke R, Arnold-Capell PA, Richeson R, et al. Refractory hypoglycemia secondary to topical salicylate intoxication. Arch Intern Med. 1991;151:591–593. 5. Maurer RA, Winter ME, Koo J, et al. Refractory hypoglycemia: a complication of topical salicylate therapy. Arch Dermatol. 1994;130:1455–1457. 6. Bideci A, Yesilkaya E. Salicylate intoxication masquerading as diabetic ketoacidosis in a child. Pediatr Int. 2008; 50:605. 7. Temple AR. Acute, chronic effects of aspirin toxicity and their treatment. Arch Intern Med. 1981;141:364–369.

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Copyright ª Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Those Salicylate Cases-How Sweet Are They?

Owing to the complex metabolism of salicylates, both hyperglycemia and hypoglycemia have been reported with salicylate poisoning. The aim of this stud...
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