TOPLINE:
Sodium-glucose cotransporter 2 inhibitor (SGLT2i)-associated diabetes ketoacidosis (DKA) in people with type 2 diabetes (T2D) is associated with lower degrees of hyperglycemia over the first 24 hours of treatment than seen in type 1 diabetes (T1D)-associated DKA, potentially leading to hypo- or hyperglycemia if the same insulin infusion protocols are used.
METHODOLOGY:
- Retrospective cohort study comparing natural history and response to treatment for 37 episodes of SGLT2i-associated DKA (n = 27) or ketosis (n = 10) in people with T2D vs 19 episodes of T1D-associated DKA in people of the same age range as the T2D group, identified from endocrine consultation requests in two South Australian tertiary hospitals.
TAKEAWAY:
- Patients with T2D and SGLT2i-associated DKA had milder DKA than T1D-associated DKA (median ketone peak, 5.3 vs 6.5 mmol/L; P = .02).
- The SGLT2i group had delayed resolution compared with the T1D group (median time, 36 vs 18 h; P = .002).
- Weight was higher in the T2D SGLT2i group than the T1D group (81.8 vs 67.7 kg; P = .04) yet patients with SGLT2i DKA received significantly less insulin (intravenous and subcutaneous) in the first 24 hours of treatment compared with the T1D DKA group (median dose, 44.0 vs 87.0 units; P = .01).
- In SGLT2i DKA, changes in ketone levels over the first 24 hours were significantly associated with baseline insulin therapy (P = .002), lower bicarbonate nadir (P = .02), and higher admission plasma glucose (P = .24).
IN PRACTICE:
“T1D DKA is driven by absolute insulin deficiency, leading to ketosis and hyperglycemia. In contrast, SGLT2i DKA occurs due to a reduction in plasma glucose from urinary glucose losses, which reduces insulin secretion and stimulates glucagon secretion, leading to ketosis. Accordingly, plasma glucose levels in SGLT2i DKA are often normal or mildly elevated.” “Despite these differences, the American Association of Clinical Endocrinologists and American College of Endocrinology recommend treatment with the same protocols for both types. This may result in hypoglycemia when patients receive fixed-dose insulin infusion or inadequate insulin dosing and reduced ketone clearance when patients receive dynamic insulin infusions.” “It would be reasonable, based on the evidence and the safety profile of intravenous dextrose, to increase dextrose infusion rates and concentration to allow increased insulin administration and suppression of ketosis.”
SOURCE:
Conducted by Mahesh M. Umapathysivam, DPhil, of Southern Adelaide Diabetes and Endocrine Services, Flinders Medical Centre, Adelaide, South Australia, and colleagues. The study was published online in JAMA Network Open.
LIMITATIONS:
The study was retrospective, and the sample size was small.
DISCLOSURES:
This work has been supported by a Diabetes South Australia (SA) investigator grant and support from the Hospital Research Foundation. Umapathysivam reported receiving grants from Diabetes SA during the conduct of the study and grants from the Australian Diabetes Society funded by AstraZeneca outside the submitted work.
A version of this article first appeared on Medscape.com.