1883-P: Impact of Premenstrual Syndrome on Glycemic Control in Women with Type 1 Diabetes Using Automated Insulin Delivery Systems: Preliminary Results from the DIABETEXX/1 Study

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Introduction and Objective: Although worsening glycemic control during the menstrual cycle (MC) has been reported in type 1 diabetes (T1D), the influence of premenstrual syndrome (PMS) remains poorly defined. Objectives: i) To characterize PMS severity across MC phases; ii) To evaluate associations between PMS severity and glycemic control, (iii) To assess whether higher PMS severity is associated with poorer glycemic.Methods: DIABETEXX/1 is a prospective study (ClinicalTrials.gov ID: NCT06338072) with 21 women with T1D using MiniMed™ 780G. Continuous glucose monitoring (5’ intervals) and insulin delivery data were collected. Premenstrual symptoms were assessed every 48 hours using the Premenstrual Syndrome Questionnaire (PSQ). MC phases were defined by quantitative measurements of gonadotropins, estrone, and pregnanediol from first-morning urine samples every 48 hours.Results: Women had a mean age of 34±10 yrs, T1D duration of 18±10 yrs, and HbA1c of 6.7± 0.5%. PSQ scores varied significantly and non-linearly across the MC, decreasing after menses and progressively increasing toward the luteal phase (LP), P < 0.001. TIR70-180 was lower during the periovulatory and LP compared with the early FP (80±14 and 81±13 vs 86±8%; P = 0.005 and P = 0.026, respectively), accompanied by higher mean glucose, increased glucose AUC, reduced tight TIR70-140, and increased TAR180-250 (all P < 0.05). Although premenstrual symptoms by PSQ increased toward the LP, symptom severity was not consistently associated with adverse glycemic outcomes. Stratification by tertiles of PSQ scores showed no significant differences in glycemic control, including TIR70-180, time above or below range.Conclusion: Although PSQ increase during the LP, their severity is not associated with poorer glycemic control. These findings suggest that menstrual cycle-related physiological changes, rather than symptom severity, drive glycemic variability and should be considered in future AID personalization strategies.

Disclosure

L. Nattero Chávez: None. M. de la Calle de la Villa: None. I. Sala Mira: None. A. Quintero: None. S. de Lope Quiñones: None. N. Albaladejo: None. J.L. Diez: None. J. Bondia: None.

Funding

Grant PID2022-137723OB-C21 funded by MICIU/AEI/10.13039/501100011033 and by “ERDF/EU”.



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