Cocaine use has been generally linked to DKA but whether it’s through its antagonizing effect on insulin action or more indirectly through its association with non-compliance with insulin, or both, is not totally clear.
A retrospective study found cocaine users to account for 14% of all DKA admissions.1 Cocaine users were also less likely than controls to have an intercurrent illness identified as a precipitant for DKA, and more likely to have missed taking insulin prior to admission. Another study also reported active cocaine use to be associated with DKA, but found its effect to be independent of non-compliance. 2
Yet another retrospective study limited to patients admitted with hyperglycemia, found no significant association between active cocaine use and development of hyperglycemic crisis.
There are reasons to believe that cocaine may contribute to DKA. Cocaine has been proposed as a possible precipitant of DKA due to its ability to potentially enhance counterregulatory mechanisms designed to antagonize the effect of insulin by increasing catecholamine and cortisol levels. 1,3
So next time you have a patient with DKA, consider cocaine as a possible precipitant, particularly when the cause of DKA is unclear.
- Warner EA, Greene GS, Buchsbaum MS et al. Diabetic ketoacidosis associated with cocaine use. Arch Intern Med 1998; 158:1799-802. https://www.ncbi.nlm.nih.gov/pubmed/9738609
- Nyenwe E, Loganathan R, Blum S, et al. Active use of cocaine: An independent risk factor for recurrent diabetic ketoacidosis in a city hospital. Endocr Pract 2007;13:22-29. https://www.ncbi.nlm.nih.gov/pubmed/17360297
- Modzelewski KL, Rybin DV, Weinberg JM, et al. Active cocaine use does not increase the likelihood of hyperglycemic crisis. J Clin Transl Endocrinol 2017;9:1-7 http://www.jctejournal.com/article/S2214-6237(16)30056-4/pdf
Contributed in part by Quin L Sievers, Medical Student, Harvard Medical School