The results of this study indicate that among the 1,636 AM patients, 61.31% had dysmenorrhea, demonstrating a high incidence rate. In a population-based cohort study in the United States from 2006 to 2015(17), the incidence of dysmenorrhea in adenomyosis was 60.3%, consistent with our results, indicating that AM-related dysmenorrhea is a significant public health concern.
The results of this study confirmed that menorrhagia, concurrent pelvic inflammatory disease, family history of AM, and multiple deliveries are risk factors for dysmenorrhea in AM. Previous studies based on imaging and pathological examinations reported that about one-third of patients were asymptomatic(18–19).Menorrhagia is one of the primary symptoms of AM. The possible mechanism is the invasion of the endometrium into the myometrium and stroma, causing improper uterine contractions during menstruation, increased endometrial surface area, excessive prostaglandin secretion, and excessive estrogen, leading to increased menstrual volume(20). The results of this study indicate that menorrhagia is a risk factor for dysmenorrhea in AM, possibly related to increased uterine contraction intensity, increased prostaglandins, increased tissue pressure, local ischemia, and inflammatory response. This study suggests that pelvic inflammatory disease is related to dysmenorrhea in AM patients, possibly associated with local inflammation, tissue damage, extensive adhesions, hyperplasia, scar formation, and pelvic congestion. Symptoms may include lower abdominal heaviness and pain, worsened by fatigue and around menstruation, easily triggering dysmenorrhea. The mechanism may be related to the imbalance between pro-inflammatory and anti-infective factors(21). Family history of AM is a risk factor for AM dysmenorrhea. It may be due to genetic factors, and it may also be because women adopt similar behaviors or lifestyles from relatives, increasing the risk of dysmenorrhea. Nilufer et al. conducted a meta-analysis using 24 GWAS datasets from multiple countries and regions, finding that endometriosis-related pelvic pain may be associated with genetically mediated increased neural sensitization. As similar diseases, AM and EM are reasonably suspected to have similar genetic potentials(22). The relationship between the number of deliveries and adenomyosis has received extensive research attention. During pregnancy, trophoblast cells continuously invade the myometrium, increasing the risk of disrupting the junctional zone(23). With an increase in the number of pregnancies, the damage to the endometrium-myometrium junctional zone increases, enlarging the lesion area, stimulating more prostaglandins, inflammatory factors, and other substances, easily triggering dysmenorrhea.
Binary logistic regression analysis results indicated that older age at onset, infrequent menstruation, and exercise are protective factors for AM-related dysmenorrhea. This study explored the relationship between age at onset and dysmenorrhea, finding that older age at onset may be a protective factor for AM. Clinical studies have also indicated that the risk of dysmenorrhea decreases by 0.97 times with increasing age(24). The possible reason is that with age, the pain threshold increases and sensitivity to pain decreases. In this study, a long menstrual cycle (≥ 30 days) was a protective factor for dysmenorrhea. The possible reason is that the duration of dysmenorrhea is relatively short, and the long interval between menstruations reduces pain sensitivity. However, some studies have reached opposite conclusions. A meta-analysis of 77 articles suggested that a long menstrual cycle increases the duration of prostaglandin secretion, thereby increasing the severity and duration of dysmenorrhea(25). Other studies have found no significant difference in menstrual cycle between adenomyosis patients with no to mild dysmenorrhea and those with moderate to severe dysmenorrhea(26). The relationship between menstrual cycle and AM-related dysmenorrhea has not yet been conclusively determined and requires further research. Prostaglandins stimulate uterine muscle contractions, causing dysmenorrhea. Studies have reported that high levels of stress inhibit LH and FSH, further damaging follicle development, affecting progesterone release, and thus affecting prostaglandin synthesis, leading to dysmenorrhea(27–29). Stress may also influence PG synthesis by affecting adrenaline and cortisol release, impacting muscle contractions and causing dysmenorrhea(30). Exercise is a protective factor for dysmenorrhea. Moderate exercise can relieve patient stress and reduce the synthesis of prostaglandins in women(31). If intense exercise becomes a source of stress, the severity of dysmenorrhea may increase. Some studies have reported that regular intense exercise may increase the severity of dysmenorrhea, possibly related to the increased frequency, intensity of exercise, and bodily sensitivity, which may also be related to the occupational characteristics of the surveyed population(32).
Adenomyosis, as a chronic disease, seriously affects health services and the socio-economy. Domestic experts(33) have pointed out that adenomyosis should be managed with a long-term management approach. Based on the characteristics of the disease at different stages, a hierarchical management model should be adopted to achieve phased prevention and treatment. Based on the risk factors and protective factors for dysmenorrhea in adenomyosis identified in this study, primary management goals should be achieved for women of reproductive age. At the stage where susceptible individuals are exposed to risk factors but have not yet developed the disease, appropriate measures should be taken to prevent or delay the occurrence of dysmenorrhea in adenomyosis. The following management recommendations are proposed: initiate health education for adenomyosis early to improve awareness of the disease; guide susceptible individuals to improve their lifestyle by adjusting diet, daily routine, emotions, and exercise habits to enhance disease resistance, and fully utilize the advantages of traditional Chinese medicine; and ensure early diagnosis and treatment. For adenomyosis patients meeting the minimum diagnostic criteria, early intervention is needed even if dysmenorrhea has not yet occurred.
Previous studies have often been limited to populations diagnosed with AM through surgery or pathology reports, which are prone to underdiagnosis and selection bias. This study, however, is based on gynecological patients visiting outpatient clinics, diagnosed according to symptoms and ultrasound or MRI reports, with a large sample size and high data reliability, making the epidemiological results closer to the real world. The main limitation of this study is that it is a cross-sectional survey, which cannot accurately establish causality. Additionally, variables such as depression, anxiety, diet, and exercise were not quantified. Future research will further improve experimental design and deepen the study of AM dysmenorrhea.
In summary, this study found the distribution of adenomyosis dysmenorrhea through a cross-sectional survey and conducted logistic regression analysis. The results showed that dysmenorrhea is a common symptom in AM patients. A long disease course, multiple deliveries, menorrhagia, concurrent pelvic inflammatory disease, and family history of AM are risk factors for dysmenorrhea in AM, while older age at onset, infrequent menstruation, and exercise are protective factors. Furthermore, this study established a nomogram model for predicting the probability of dysmenorrhea in AM, used to stratify high- and low-risk populations, develop effective health strategies, alleviate patient suffering, and improve quality of life.