88 was not reported for most of our patients. Furthermore, the choice for histopathology after hysterectomy as a reference standard introduces an element of selection bias. Potentially, our group consisted of women with more severe adenomyosis and thus may have affected the general phenotype. The present study did not conduct a central review of pathology however, and (histological) adenomyosis severity was generally not reported in pathology reports. Therefore this remains hypothetical. Similarly, future validation is needed to confirm the applicability of this model in women without indication for hysterectomy. In clinical practice, our model could be used to calculate the risk of adenomyosis in individual patients. For example, in a 31-year-old woman with a BMI of 19 kg/m2, without history of curettage, with complaints of both dysmenorrhoea and AUB, and an MRI with mean JZ thickness of 8.3 millimetres, a JZ Diff <5 mm, a JZ/MYO >.40, but HSI Foci (Figure 2A), the probability of adenomyosis is 14.9%. In a 35-year-old woman with a BMI of 24 kg/m2, without history of curettage, with complaints of both dysmenorrhoea and AUB, and an MRI with a mean JZ thickness of 24.6 millimetres, a JZ Diff ≥5 mm, a JZ/MYO >.40 and HSI Foci (Figure 2B), this probability increases to 90.3%. In conclusion, we present an MRI-based clinical prediction model for histopathological adenomyosis diagnosis. In future, this tool can be useful for both patients and clinicians, with a potential to reduce morbidity and to contribute to shared decision making. Since patient management depends on several factors, such as age, symptoms, and comorbidity, the clinical use of the predicted risks from the proposed model should still be decided on an individual basis. Thus, before steps are made for use in clinical practice, external validation of the model is needed.
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