# Diabetic Ketoacidosis Associated With the Menstrual Cycle: A Case of Catamenial Diabetic Ketoacidosis

**Authors:** Reza Alavi, Casper Chen, Hector Armando Sanchez Garcia, Obiora Udeozo

PMC · DOI: 10.7759/cureus.99191 · Cureus · 2025-12-14

## TL;DR

A 34-year-old woman with type 1 diabetes experienced recurring diabetic ketoacidosis linked to her menstrual cycle, highlighting the role of hormonal changes in triggering this condition.

## Contribution

This case highlights catamenial diabetic ketoacidosis as a rare but important clinical entity linked to menstrual hormonal fluctuations.

## Key findings

- Recurrent DKA episodes were temporally associated with the patient's menstrual cycle.
- Hormonal changes, particularly luteal-phase progesterone, may contribute to insulin resistance and metabolic decompensation.
- Targeted strategies like insulin dose adjustments or hormonal modulation may help prevent recurrence.

## Abstract

Catamenial diabetic ketoacidosis (DKA) is an uncommon but clinically significant phenomenon characterized by recurrent DKA episodes temporally related to the menstrual cycle. Hormonal fluctuations, particularly luteal-phase progesterone surges that contribute to transient insulin resistance, appear to play a central role in this condition. We present the case of a 34-year-old woman with type 1 diabetes mellitus (T1DM) who developed recurrent DKA episodes coinciding with her menstrual periods. Extensive evaluation ruled out infection, noncompliance, and insulin pump malfunction. A clear temporal association between symptom onset and menstruation was established through review of menstrual and glucose logs. She was treated with intravenous fluids, potassium replacement, and insulin infusion per DKA protocol. Within 24 hours, her anion gap closed, bicarbonate normalized, and she was transitioned to subcutaneous insulin with endocrinology follow-up.

Patterns of glucose dysregulation linked to menstrual hormonal shifts can create cyclical susceptibility to ketosis and metabolic decompensation. In this context, rising luteal-phase progesterone and accompanying hormonal changes may enhance counterregulatory activity and impair glucose utilization. Recognizing this pattern is essential, as targeted strategies such as hormonal modulation or anticipatory insulin dose adjustments may help prevent recurrence. A focused approach that considers individualized physiologic variation can improve diagnostic accuracy and long-term management in affected patients.

## Linked entities

- **Chemicals:** progesterone (PubChem CID 5994), insulin (PubChem CID 70678557), potassium (PubChem CID 813)
- **Diseases:** diabetic ketoacidosis (MONDO:0012819), type 1 diabetes mellitus (MONDO:0005147)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** DKA (MESH:D016883), glucose dysregulation (MESH:D018149), T1DM (MESH:D003922), insulin resistance (MESH:D007333), ketosis (MESH:D007662), infection (MESH:D007239)
- **Chemicals:** progesterone (MESH:D011374), potassium (MESH:D011188), bicarbonate (MESH:D001639), glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

8 references — full list in the complete paper: https://tomesphere.com/paper/PMC12798761/full.md

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Source: https://tomesphere.com/paper/PMC12798761