# When the Transition Goes Wrong: A Rare Case of Diabetic Ketoalkalosis After Transitioning to Tirzepatide in Insulin-dependent Type 2 Diabetes

**Authors:** Waleed Sultan, Jeanne Spencer

PMC · DOI: 10.7759/cureus.87031 · Cureus · 2025-06-30

## TL;DR

A rare case of diabetic ketoalkalosis occurred in a patient with type 2 diabetes after switching to tirzepatide, emphasizing the need for careful monitoring during medication transitions.

## Contribution

This paper reports a rare case of diabetic ketoalkalosis following a transition to tirzepatide in insulin-dependent type 2 diabetes.

## Key findings

- A 57-year-old patient developed diabetic ketoalkalosis after switching to tirzepatide.
- The condition was managed successfully with fluids, electrolytes, and insulin.
- The case underscores the importance of gradual insulin tapering and close monitoring during medication transitions.

## Abstract

Type 2 diabetes mellitus (T2DM) often requires pharmacological management, with newer agents like glucagon-like peptide-1 (GLP-1) receptor agonists (GLP-1 RA) and dual gastric inhibitory polypeptide (GIP)/GLP-1 receptor agonists offering metabolic and cardiovascular benefits. However, transitioning from insulin therapy to these agents can lead to rare complications, such as diabetic ketoalkalosis, a metabolic disturbance marked by simultaneous ketosis and alkalosis.

We report an unusual case of diabetic ketoalkalosis, a mixed acid-base disorder, in a 57-year-old female patient with insulin-dependent T2DM following a switch to Mounjaro (tirzepatide). The patient presented with nausea, vomiting, elevated anion gap, ketosis, and a slightly alkalotic venous pH. This was attributed to insulin deficiency and vomiting-induced acid loss and bicarbonate retention. Management with fluids, electrolytes, and insulin led to rapid recovery. This case highlights the need for gradual insulin tapering and close monitoring while transitioning from insulin therapy to GIP/GLP-1 receptor agonists.

## Linked entities

- **Diseases:** Type 2 diabetes mellitus (MONDO:0005148)

## Full-text entities

- **Genes:** GIPR (gastric inhibitory polypeptide receptor) [NCBI Gene 2696] {aka PGQTL2}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, GIP (gastric inhibitory polypeptide) [NCBI Gene 2695], GCG (glucagon) [NCBI Gene 2641] {aka GLP-1, GLP1, GLP2, GRPP}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}
- **Diseases:** nausea (MESH:D009325), gastric acid loss (MESH:D005764), Diabetic Ketoalkalosis (MESH:D003920), dehydrated (MESH:D003681), T2DM (MESH:D003924), DKA (MESH:D016883), -cell dysfunction (MESH:D002292), confusion (MESH:D003221), polyuria (MESH:D011141), acid-base disorder (MESH:D000137), Insulin-dependent (MESH:D003922), vomiting (MESH:D014839), Insulin deficiency (MESH:D007333), acidosis (MESH:D000138), metabolic disease (MESH:D008659), insulin-dependent type 2 diabetes mellitus (MESH:C565100), beta-cell failure (MESH:D051437), acid loss (MESH:D011015), weight loss (MESH:D015431), ketoacidosis (MESH:D007662), Metabolic alkalosis (MESH:D000471), hypoglycemia (MESH:D007003), hyperglycemia (MESH:D006943)
- **Chemicals:** glucose (MESH:D005947), bicarbonate (MESH:D001639), beta-hydroxybutyrate (MESH:D020155), RA (-), blood glucose (MESH:D001786), ketone (MESH:D007659), C-peptide (MESH:D002096)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

7 references — full list in the complete paper: https://tomesphere.com/paper/PMC12310415/full.md

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Source: https://tomesphere.com/paper/PMC12310415