ResearchOct 12, 20260 views

Severe Euglycemic Diabetic Ketoacidosis After Semaglutide-Associated Poor Intake Despite Empagliflozin Discontinuation: A Case Report.

Semaglutide isn’t just another research peptide — it keeps showing up in the case literature. This time, a case report dives into how semaglutide’s well-known gut side effects can intersect with metabolic balance in unexpected ways.

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Int Med Case Rep J

by Niknam K, Niknam T

“Severe Euglycemic Diabetic Ketoacidosis After Semaglutide-Associated Poor Intake Despite Empagliflozin Discontinuation: A Case Report. Niknam K(1), Niknam T(2). Author information: (1)Department of Internal Medicine, Legacy Salmon Creek Medical Center, Vancouver, WA, USA. (2)Department of Pulmonary and Critical Care, Shiraz University of Medical Sciences, Shiraz, Iran. Euglycemic diabetic ketoacidosis (EDKA) may be overlooked when serum glucose is near normal. A 68-year-old woman with long-standing type 2 diabetes developed approximately three weeks of nausea, intermittent vomiting and diarrhea, and minimal oral intake after semaglutide initiation at 0.25 mg once weekly for four weeks followed by 0.5 mg once weekly. Patient and family medication reconciliation indicated that she had stopped empagliflozin, metformin, and pioglitazone approximately two weeks before presentation but continued semaglutide, with the last dose approximately eight days before admission. She presented with weakness, dyspnea, slowed speech, and disorientation. Initial testing showed glucose 132 mg/dL, venous pH 7.13, bicarbonate 9 mmol/L, anion gap 26 mmol/L, and beta-hydroxybutyrate 99.5 mg/dL. She improved with intravenous crystalloid, dextrose-containing fluids, insulin infusion, and electrolyte replacement. The temporal association is consistent with a clinically plausible contribution from semaglutide-associated gastrointestinal intolerance and carbohydrate depletion to EDKA despite reported prior empagliflozin discontinuation. Normal glucose should not delay ketone and acid-base testing when compatible symptoms and poor intake are present. © 2026 Niknam and Niknam. PMCID: PMC13653545 Conflict of interest statement: The authors declare no conflicts of interest.”

Here’s the story: a 68-year-old woman with type 2 diabetes started semaglutide at standard research doses. She quickly ran into nausea, vomiting, and poor oral intake. Her other glucose-lowering compounds — empagliflozin, metformin, and pioglitazone — were discontinued two weeks before she showed up at the hospital. Semaglutide was the only research peptide still in play.

She arrived at the ER confused, weak, and short of breath. Blood tests told the story: normal-range blood glucose (132 mg/dL) but severe acidosis, a big anion gap, and high beta-hydroxybutyrate. Classic euglycemic diabetic ketoacidosis (EDKA) — just with the usual suspects out of the picture. The likely trigger? Extended poor food intake from GI intolerance after semaglutide initiation.

Key takeaways for researchers working with semaglutide or related peptides:

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EDKA can happen even when glucose is normal — don’t skip ketone and acid-base checks when symptoms fit

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GI side effects that reduce carb intake can tip the metabolic scale, especially in those with underlying diabetes

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Discontinuing other glucose modulators doesn’t eliminate risk if calorie intake is low

The patient recovered quickly with fluids, insulin, and electrolytes. The authors point out that the timing fits: semaglutide’s GI impact led to carb depletion, which set the stage for EDKA. This isn’t an indictment — it’s a data point for anyone studying the metabolic ripple effects of GLP-1 research peptides.

Curious about sourcing semaglutide for your own research? Start with the vendor directory. Peptide research keeps revealing new angles.

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