{"paper_id":"4b38bd43-1a58-4ea1-934b-2649c3a4e0d9","body_text":"Int. J. Med. Sci. 2026, Vol. 23 \n \n \nhttps://www.medsci.org \n3453 \nInternational Journal of Medical Sciences\n \n2026; 23(11): 3453-3463. doi: 10.7150/ijms.140803 \nReview \nAdolescent and Early-Onset Adenomyosis: \nPhenotypes, Diagnostic Challenges, and Fertility-\nConscious Care \nShuhong Yang1,2,3, Yuling Chen1,2,3, Xiangyi Ma1,2,3 \n1. Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technolo gy, Wuhan, Hubei, \n430030, China.  \n2. National Clinical Research Center for Obstetrical and Gynecological Diseases, Wuhan, Hubei, 430030, China.  \n3. Key Laboratory of Cancer Invasion and Metastasis, Ministry of Education, Wuhan, Hubei, 430030, China.  \n Corresponding author: Prof. Xiangyi Ma, Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science \nand Technology 1095 Jiefang Ave, Wuhan 430030, People’s Republic of China. Tel: +86 02783663351; Fax: +86 02783663351; Email addresses: \nxyma@tjh.tjmu.edu.cn; ORCID: https://orcid.org/0000 -0003-3414-6158. \n© The author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License (https: //creativecommons.org/licenses/by/4.0/). \nSee https://ivyspring.com/terms for full terms and conditions. \nReceived: 2026.07.13; Accepted: 2026.09.18; Published: 2026.10.02 \nAbstract \nAdolescent and early-onset adenomyosis is increasingly recognized in symptomatic young patients, but \nits clinical significance remains uncertain. This narrative review synthesizes English-language literature on \nadolescent and early-onset adenomyosis, distinguishing direct adolescent and young-adult evidence from \nsupportive evidence derived from adult populations. Current data suggest that adenomyosis-like imaging \nfeatures may be identified in adolescents with severe dysmenorrhea, heavy menstrual bleeding, c hronic \npelvic pain, or coexisting endometriosis. Early disease often appears as subtle diffuse inner- myometrial \nchange, focal lesions, or cystic/juvenile forms rather than the classic diffuse adult phenotype. Ultrasound \nis the first-line imaging modality, whereas MRI is reserved for equivocal findings, atypical cystic lesions, \nsuspected congenital anomalies, or endometriosis overlap. Management requires a stepwise, symptom -\noriented approach that considers future reproductive options and avoids unnecessary u terine \nintervention. Overall, adolescent adenomyosis should be considered in patients with severe or \ntreatment-resistant menstrual symptoms, while uncertain imaging findings should not be \noverinterpreted. \nKeywords: Adenomyosis; adolescence; dysmenorrhea; endometriosis; fertility  \n1. Introduction \nSevere dysmenorrhea, heavy menstrual bleeding, \nand chronic pelvic pain during adolescence are often \nattributed to functional menstrual symptoms or \nprimary dysmenorrhea [1, 2]. This interpretation may \ndelay evaluation for underlying gynecological disease, \nparticularly when symptoms are persistent, disabling, \nor poorly responsive to first -line analgesic treatment \n[3-5]. In this context, adenomyosis has received \nincreasing attention as a possible yet underrecognized \ncontributor to severe menstrual symptoms in \nadolescents and young women [6]. \nAdenomyosis has traditionally been regarded as \na disorder of later reproductive life, largely because \nearlier descriptions were based on hysterectomy \nspecimens and adult surgical series. However, wider \nuse of high-resolution pelvic ultrasound and magnetic \nresonance imaging has challenged this age -based \nconcept. Imaging studies now suggest that \nadenomyosis-like features may be detected before \nadulthood or in early reproductive life, particularly in \npatients with severe dysmenorrhea, heavy menstrual \nbleeding, pelvic pain, or coexisting endometriosis. \nYoung age alone should therefore not exclude \nadenomyosis from the differential diagnosis. \nThe clinical significance of adolescent \nadenomyosis remains uncertain. Unlike classic adult \nphenotype, early -onset adenomyosis may present as \nsubtle junctional -zone abnormalities, focal inner -\n \nIvyspring  \nInternational Publisher \n\nInt. J. Med. Sci. 2026, Vol. 23 \n \nhttps://www.medsci.org \n3454 \nmyometrial lesions, or cystic phenotypes rather than \ndiffuse uterine enlargement. These findings may be \noverlooked when clinicians rely on the traditional \nadult template, but they may also be overinterpreted \nwhen isolated imaging signs are considered witho ut \nsymptom burden or developmental context. This \ndiagnostic tension is particularly relevant in \nadolescents because age -specific imaging thresholds \nhave not been established. \nThe evidence base is also heterogeneous. Many \nstudies include both adolescents and young adult \nwomen, whereas much of the mechanistic and \nreproductive literature is derived from adult \npopulations. It remains unclear whether adenomyosis \nrecognized during ad olescence represents an early \nstage of the adult disease spectrum, a distinct early-\nonset phenotype, or a heterogeneous group of \nconditions with different trajectories. Natural history, \noptimal diagnostic criteria, treatment response, and \nlong-term reprodu ctive implications remain poorly \ndefined. \nTo address this heterogeneity, this review uses \n“adolescent adenomyosis” as an operational term for \nadenomyosis or adenomyosis -like imaging findings \nidentified during adolescence, generally \ncorresponding to patients aged 10 –19 years according \nto the WHO de finition of adolescence. Because no \nuniversally accepted age threshold exists for “early -\nonset adenomyosis,” we use this broader term to \ninclude adolescent cases and adenomyosis recognized \nin young women near the transition from adolescence \nto adulthood, particularly when symptoms or imaging \nfeatures suggest onset early in reproductive life. \nAccordingly, evidence from cohorts spanning \nadolescence and early adulthood, such as patients \naged 12– 25 or 13– 25 years, is interpreted as mixed \nadolescent/young-adult evidence, whereas studies in \nyoung nulligravid women aged up to 30 years are \nconsidered supportive young -adult evidence rather \nthan strictly adolescent evidence. \nThis review provides a clinically oriented \nsynthesis of adolescent and early- onset adenomyosis. \nWe distinguish direct adolescent evidence from \nsupportive inference derived from young adult and \nbroader reproductive- age populations, and focus on \nepidemiologic signals, early phenotypes, diagnostic \npitfalls, imaging interpretation, management \nprinciples, and fertility- conscious longitudinal care. \nOur aim is to support earlier recognition of clinically \nmeaningful disease while avoiding overdiagnosis and \ninappropriate extrapolation from adult adenomyosis. \n2. Literature identification strategy \nThis review was designed as a clinically oriented \nnarrative review of adolescent and early -onset \nadenomyosis. PubMed, Embase, and Web of Science \nwere searched for English-language articles published \nup to March 5, 2026. The search focused on four core \nconcepts: adenomyosis; adolescence or early -onset \ndisease; symptoms and comorbidity; and diagnosis, \nmanagement, or reproductive implications. The \ndatabase-specific search strategies are provided in \nSupplementary Table S1. \nArticles were considered eligible if they provided \nclinically relevant information on adolescent or early-\nonset adenomyosis, including disease burden, \nsymptoms, imaging phenotypes, adenomyosis–\nendometriosis overlap, differential diagnosis, \nmanagement, follow-up, reproductive implications, or \nrelevant mechanisms. Direct adolescent evidence was \nprioritized; mixed adolescent/young -adult studies \nwere interpreted as supportive early -onset evidence, \nand adult studies were used only when adolescent -\nspecific data w ere unavailable. After duplicate \nremoval, titles and abstracts were screened by two \nauthors, followed by full -text assessment of \npotentially relevant articles. Disagreements were \nresolved through discussion with the senior author. \nSupplementary Figure S1 summarizes the literature \nidentification process but should not be interpreted as \na PRISMA flow diagram; no formal risk- of-bias \nassessment or quantitative synthesis was performed. \n3. Epidemiologic signals and early \nclinical phenotypes \n3.1 Disease burden in symptomatic \nadolescents and young women \nThe population-level epidemiology of adolescent \nadenomyosis remains poorly defined. Most available \nestimates come from imaging- based studies of \nsymptomatic adolescents and young women \nevaluated in referral settings. Reported prevalence \nfigures should therefore be interpreted as indicators of \ndisease burden in selected clinical populations rather \nthan as estimates of adenomyosis prevalence in the \ngeneral adolescent population. \nEven with this limitation, current evidence \nsuggests that adenomyosis is not uncommon among \nhighly symptomatic young patients. In a cohort of 267 \nadolescents aged 12 –20 years with severe \ndysmenorrhea, Exacoustos et al. reported \nultrasonographic signs sugge stive of endometriosis \nand/or adenomyosis in 106 patients (39.7%), with \nadenomyosis identified in 47 patients, corresponding \nto 17.6% of the total cohort [7]. In a cross -sectional \nstudy of patients aged 13–25 years with dysmenorrhea \nand/or heavy menstrual bleeding, Vannuccini et al. \nidentified adenomyosis in 27.4% of cases using \nMorphological Uterus Sonographic Assessment \n\nInt. J. Med. Sci. 2026, Vol. 23 \n \nhttps://www.medsci.org \n3455 \n(MUSA) criteria, suggesting that symptom clustering \nmay help identify early-onset disease [5]. \nEvidence syntheses support this signal while \nemphasizing heterogeneity. Vercellini et al. reported a \nweighted pooled adenomyosis prevalence of 20.7% \n(95% CI, 11.5–31.6; I²=94.8%) across six imaging-based \nstudies in symptomatic adolescents and young \nwomen, with subgroup estimates of 16.9% (95% CI, \n8.8–27.0; I²=91.2%) in adolescents and 29.7% (95% CI, \n17.5–43.5; I²=85.6%) in young women. These data \nsuggest that adenomyosis -related imaging findings \nare not uncommon in selected symptomatic \npopulations, but they  do not provide a reliable \nestimate of population prevalence in adolescents [8, 9]. \nEarlier MRI -based evidence also suggested that \nadenomyosis-related junctional -zone changes may \nemerge relatively early in reproductive life, \nparticularly in women with endo metriosis, although \nthese data were not derived from strictly adolescent \ncohorts [10]. However, differences in diagnostic \ncriteria, imaging expertise, symptom selection, and \nage grouping limit direct comparison across studies. \nCurrent data therefore do not establish the true \nprevalence of adolescent adenomyosis, but they do \nindicate a clinically meaningful disease signal in \nyoung patients with severe menstrual symptoms. The \nkey studies informing current understanding are \nsummarized in Table 1, and imaging-based prevalence \nstudies are summarized in Supplementary Table S2. \n3.2 Early, focal and cystic phenotypes \nEarly-onset adenomyosis appears to differ from \nthe classic adult phenotype derived from \nhysterectomy-based and advanced surgical series. In \nadolescents and young women, adenomyosis is more \noften described as mild, focal, or cystic rather than as \ndiffuse bulky myometrial involvement [12, 13, 18, 19]. \nThis distinction is clinically important because under -\nrecognition in younger patients may reflect not only \nlow clinical suspicion, but also a mismatch between \nearly disease morphology and the traditional adult \nimage of adenomyosis. \n \nTable 1. Key studies on adolescent and early-onset adenomyosis. \nStudy Evidence source/Population Diagnostic modality Key contribution \nExacoustos et al. 2025 [7] Direct adolescent cohort; 267 \nadolescents with severe dysmenorrhea \nUltrasound Adenomyosis was identified in 47 of 267 adolescents with severe \ndysmenorrhea, supporting targeted ultrasound evaluation in \nhighly symptomatic patients. \nWilk et al. 2025 [8] Review-level adolescent evidence Literature review of \nadolescent studies \nSummarized prevalence, symptoms, and diagnostic pathways of \nadolescent adenomyosis and reinforced that the disease is likely \nunderrecognized \nVercellini et al. 2025 [9] Mixed adolescent/young-adult \nevidence synthesis \n \nImaging-based studies Reported a weighted pooled prevalence of 20.7% with high \nheterogeneity, supporting a disease-burden signal in selected \nsymptomatic adolescents and young women. \nMartire et al. 2024 [1] Review-level adolescent supportive \nevidence \nLiterature review Framed adolescent adenomyosis as a challenging diagnosis with \ncomplex management and highlighted the need for age- specific \napproaches \nVannuccini et al. 2024 [5] Mixed adolescent/young-adult \nevidence \nUltrasound using \nMUSA criteria \nDemonstrated that adenomyosis can be identified in \nsymptomatic adolescents/young women, particularly when \ndysmenorrhea and heavy menstrual bleeding coexist  \nZannoni et al. 2024 [11] Mixed adolescent/young-adult study \nof patients with pelvic pain \nClinical and imaging-\nbased assessment \nHighlighted adenomyosis–endometriosis overlap in young \npatients with pelvic pain. \nExacoustos et al. 2022 [12] 43 adolescents aged 12–20 years with \nultrasonographically diagnosed \nadenomyosis \nUltrasound Adenomyosis was predominantly mild to moderate, with no \nsevere cases identified; the outer myometrium and posterior \nuterine wall were the most commonly affected sites.  \nBrosens et al. 2015 [13] Supportive evidence on cystic \nadenomyosis in younger women \nImaging and pathology \nliterature \nDescribed uterine cystic adenomyosis as a phenotype mainly \naffecting younger women. \nMansouri et al. 2015 [14] Adolescent case series MRI before and after \nhormonal suppression \nReported regression of MRI-visible adenomyosis after hormonal \nsuppression in adolescents \nHo et al. 2008[15]; Ho et al. \n2009 [16]; Branquinho et al. \n2012 [17] \nAdolescent case reports Ultrasound, MRI, \nand/or pathology \nReported adenomyotic cysts or juvenile cystic adenomyoma in \nadolescent girls, indicating that early disease may present as \nfocal or cystic lesions \nDietrich 2010 [4] Early narrative-review supportive \nevidence \nLiterature review Summarized the early evidence on adolescent adenomyosis and \nemphasized diagnostic difficulty in teenagers \nTakeuchi et al. 2010 [18] Juvenile cystic adenomyoma case \nseries; 9 cases \nImaging, laparoscopy, \nhistopathology \nDescribed diagnosis, laparoscopic treatment, and pathology of \njuvenile cystic adenomyoma \nItam et al. 2009 [3] Adolescent case report and literature \nreview \nImaging and clinical \ndiagnosis \nOne of the earliest reports highlighting that adenomyosis can \noccur during adolescence and may present with severe \ndysmenorrhea \nNotes: Evidence source/population indicates whether each study provides direct adolescent evidence, mixed adolescent/young -adult evidence, review-level evidence, or \ncase-based supportive evidence. Case reports and case series were included to illustrate early fo cal or cystic phenotypes, not to estimate prevalence. Abbreviations: MRI, \nmagnetic resonance imaging; MUSA, Morphological Uterus Sonographic Assessment. \n \n\nInt. J. Med. Sci. 2026, Vol. 23 \n \n \nhttps://www.medsci.org \n3456 \nAmong adolescent studies, adenomyosis is more \ncommonly classified as mild or moderate, whereas \nsevere diffuse disease appears relatively uncommon \n[12]. Supportive evidence from young nulligravid \nwomen aged 18–30 years points in the same direction, \nsuggesting that adenomyosis -like changes may \nemerge early in reproductive life and may already be \nassociated with dysmenorrhea and heavier menstrual \nbleeding [20]. Although such young adult data cannot \nbe treated as adolescent -specific evidence, they \nprovide trans itional support for the concept that \nadenomyotic changes may precede the age range in \nwhich the disease has historically been diagnosed. \nPhenotypically, adolescent and early- onset \nadenomyosis may be conceptualized as three broad \npatterns: subtle diffuse inner- myometrial change, \nfocal inner-myometrial lesions, and cystic or juvenile \nadenomyotic lesions. This framework is useful \nbecause pheno types may influence symptom profile, \ndifferential diagnosis, imaging interpretation, and \ntreatment intensity [12, 13]. Juvenile cystic \nadenomyoma and related cystic lesions may present \nwith severe dysmenorrhea and disproportionate pain \ndespite localized disease [13, 15-18]. \nThe predominance of mild, focal, and cystic \ndisease should not be interpreted as evidence that all \nearly lesions inevitably progress to diffuse adult \nadenomyosis. Rather, current findings support a more \ncautious interpretation: adolescent adenomyosis likely \nrepresents a spectrum of early phenotypes with \nincompletely characterized trajectories. The main \nvalue of phenotype recognition lies in improving \ndiagnostic accuracy, avoiding both under -recognition \nand overdiagnosis, and aligning management \nintensity with the likely burden of disease. The early \nphenotypic spectrum and its clinical implications are \nsummarized in Figure 1. \n3.3 Comorbidity and key differential diagnoses \nAdenomyosis in adolescents frequently coexists \nwith other gynecological disorders, most notably \nendometriosis [1, 7, 8, 21, 22]. This overlap is clinically \nimportant because it may increase symptom severity, \ncomplicate imaging interpretation, and influence  \ntreatment planning. In adolescent and early -onset \ncohorts, severe dysmenorrhea, chronic pelvic pain, \nand suspected or confirmed endometriosis repeatedly \nemerge as the main clinical context in which \nadenomyosis is identified. \n \n \nFigure 1. Early phenotypic spectrum and clinical implications of adolescent adenomyosis. ACUM, accessory cavitated uterine malformation . Created with BioRender.com. \n \n\n\nInt. J. Med. Sci. 2026, Vol. 23 \n \n \nhttps://www.medsci.org \n3457 \nIn one adolescent cohort reported by Exacoustos \net al., approximately 44% of adolescents diagnosed \nwith adenomyosis were found to have at least one \nconcomitant pelvic endometriotic lesion [12]. \nLikewise, Zannoni et al. reported a high burden of \nboth adenom yosis and endometriosis in adolescents \nand young women with pelvic pain, with a significant \nassociation between ovarian endometriosis and \nadenomyosis [11]. These findings suggest that the two \ndisorders may share common pathogenic mechanisms \nor developmental pathways. \nAt the same time, diagnostic assessment in \nadolescents should remain attentive to important \ndifferential diagnoses. Accessory cavitated uterine \nmalformation (ACUM), juvenile cystic adenomyoma, \nand congenital uterine anomalies may mimic \nadenomyosis on imagi ng and may also present with \nsevere progressive dysmenorrhea [23 -26]. This is \nespecially relevant in younger patients because cystic \nlesions and unusual uterine morphology may be over-\nattributed to adenomyosis if imaging is interpreted \nwithout adequate dev elopmental and anatomic \ncontext. \nFor this reason, comorbidity assessment and \ndifferential diagnosis should be considered together in \nadolescent practice. The key clinical question is not \nsimply whether adenomyosis is present, but whether \nthe patient’s symptoms and imaging findings are best \nexplained by isolated adenomyosis, adenomyosis with \nendometriosis overlap, or an alternative structural \ncondition requiring a different management pathway. \nThis broader diagnostic frame is essential to avoid \nboth under -recognition of overlap disease and \nmisclassification of congenital or cystic lesions as \nadenomyosis. \n4. Biological plausibility and \nmechanistic heterogeneity \nThe pathogenesis of adenomyosis remains \nincompletely understood and is likely multifactorial. \nAltered uterine peristalsis, tissue injury and repair, \nhormonal dysregulation, inflammation, and fibrotic \nremodeling may contribute to disease initiation and \nprogression. Different anatomical phenotypes, \nincluding diffuse, focal, cystic, inner -myometrial, \nouter-myometrial, and endometriosis -associated \ndisease, may therefore arise through partially distinct \npathways rather than through a single uniform \nmechanism [27, 28].  \nJunctional-zone dysfunction and tissue injury -\nrepair models provide one plausible explanation for \nearly inner -myometrial disease, linking severe \ndysmenorrhea, uterine biomechanics, and subtle \ninner-myometrial or focal imaging changes [27, 28]. \nOther propos ed mechanisms, including metaplastic \ntransformation, stem/progenitor -cell differentiation, \nand outside -to-inside extension in endometriosis-\nassociated phenotypes, may help explain focal, cystic, \nouter-myometrial, or overlap disease [28-30].  \nHowever, the adolescent relevance of these \nmechanisms remains inferential. Most mechanistic \nand molecular studies are based on adult tissue or \nsurgical populations with established disease. \nTherefore, current pathophysiological models should \nbe interpreted as biologically plausible explanations \nfor early-onset phenotypes rather than as adolescent -\nspecific evidence.  \n5. Diagnosis in adolescents: from clinical \nsuspicion to imaging interpretation \nThe diagnosis of adenomyosis has shifted from \npostoperative histopathological confirmation to non-\ninvasive recognition based on symptoms and imaging. \nThis shift is particularly relevant in adolescents and \nyoung women, in whom earlier identification may \nimprove symptom control and reduce delayed \nrecognition of underlying gynecological disease. At \nthe same time, diagnosis in this age group remains \nchallenging because menstrual pain is often \nnormalized, imaging findings may be subtle, and age-\nspecific diagnost ic thresholds have not been fully \nestablished. Diagnostic evaluation should therefore be \nregarded as a structured, risk -based process rather \nthan a single imaging event. Symptom severity, \nresponse to first -line treatment, suspected \nendometriosis overlap, a nd imaging phenotype all \ncontribute to diagnostic confidence. \n5.1 Clinical red flags \nThe most important clinical clue is severe \ndysmenorrhea. In adolescent cohorts with ultrasound-\ndiagnosed adenomyosis, dysmenorrhea is reported in \nmost patients, often in highly symptomatic referral \nsettings [8, 12]. Imaging findings suggestive of \nendometriosis and/or adenomyosis have also been \nidentified in a substantial proportion of adolescents \nwith severe dysmenorrhea, indicating that marked \nmenstrual pain should not automatically be regarded \nas functional or “normal” [7, 31]. \nHeavy menstrual bleeding is another important \nsignal. In symptomatic adolescents and young \nwomen, adenomyosis appears to be identified more \noften when dysmenorrhea and heavy menstrual \nbleeding coexist than when pain is considered alone [5, \n32]. Other featu res that should prompt earlier \nevaluation include poor response to first -line \nanalgesics, chronic pelvic pain outside menstruation, \nrecurrent school or activity impairment, and \nsymptoms suggestive of coexisting endometriosis. \nFamily history may provide add itional context, but \n\nInt. J. Med. Sci. 2026, Vol. 23 \n \nhttps://www.medsci.org \n3458 \ncurrent evidence is indirect and should not be treated \nas diagnostic [22, 33, 34]. In practice, it is the pattern of \nsevere, persistent, treatment -resistant symptoms —\nespecially when accompanied by heavy menstrual \nbleeding or chronic pelvic pain —that should  trigger \ntargeted imaging assessment. The main clinical red \nflags prompting targeted evaluation are summarized \nin Figure 2. \n5.2 Ultrasound, MRI, and phenotype-aware \ninterpretation \nUltrasound should remain the first -line imaging \nmodality for suspected adolescent adenomyosis \nbecause it is accessible, repeatable, and capable of \nidentifying subtle or focal myometrial abnormalities \nwhen performed by experienced operators [35 -37]. Its \nvalue in adolescents lies not only in detecting diffuse \ndisease, but also in recognizing subtle inner -\nmyometrial changes, focal lesions, and cystic \nphenotypes that may be more typical of early- onset \ndisease [5, 12]. The ultrasound route should also be \nindividualized. Transabdominal ultrasound is usually \nthe initial approach, particularly in younger or \nsexually inactive patients, whereas transvaginal, \ntransrectal, or transperineal approaches may be \nconsidered selectively according to sexual history, \npatient acc eptability, local practice, and operator \nexpertise [38].  \nAccording to the revised Morphological Uterus \nSonographic Assessment (MUSA) consensus, direct \nfeatures include myometrial cysts, hyperechogenic \nislands, and echogenic subendometrial lines or buds, \nwhereas indirect features include globular uterus, \nasymmetrical myometrial thickening, fan -shaped \nshadowing, translesional vascularity, and an irregular \nor interrupted junctional zone [39]. Because diagnostic \nperformance remains operator- dependent, \nstandardized acquisition and reporting are essential \n[36, 40]. In adolescents, direct features or multiple \nconcordant findings in a highly symptomatic patient \nmay increase diagnostic confidence, whereas isolate d \nindirect or equivocal findings should prompt cautious \ninterpretation, expert review, or interval reassessment. \nMRI has a complementary role when ultrasound \nfindings are inconclusive, lesion phenotype is atypical, \nor the differential diagnosis includes congenital \nanomalies, cystic lesions, or deep infiltrating \nendometriosis [37, 41 -43]. Typical MRI features \ninclude junctional-zone thickening or irregularity, \npoorly defined low -signal-intensity myometrial areas \non T2-weighted imaging, and cystic change in selected \nphenotypes. In adolescents, MRI is most useful when \nsevere pelvic pain persists despite non -diagnostic \nultrasound, when outer -myometrial disease or \nendometriosis overlap is suspected, or when \ndifferentiation from congenital uterine anomalies is \nrequired [44, 45]. However, MRI should not be used as \na routine second -line test for all adolescents with \ndysmenorrhea. Cost, access, and the lack of robust age-\nspecific thresholds limit its role as a screening \nmodality. It is best used as a targeted problem-solving \ntool. \n \n \nFigure 2. Clinical red flags prompting targeted evaluation of suspected adolescent  adenomyosis. Abbreviations: HMB, heavy menstrual bleeding; MRI, magnetic resonance \nimaging. Created with BioRender.com. \n\n\nInt. J. Med. Sci. 2026, Vol. 23 \n \n \nhttps://www.medsci.org \n3459 \n5.3 Emerging adjuncts, diagnostic pitfalls, and \noverdiagnosis \nElastography, artificial intelligence, and \nradiomics may eventually refine image -based \nassessment of adenomyosis, but they should currently \nbe regarded as investigational adjuncts rather than \nroutine tools in adolescent diagnostic pathways. \nElastography is biologically plausible because \nadenomyosis is associated with fibrosis and \nmyometrial remodeling, and adult studies suggest \nthat tissue stiffness may help distinguish adenomyosis \nfrom normal myometrium or correlate with symptom \nburden [46 -49]. Similarly, artificial intelligence and \nradiomics have shown promise in adult ultrasound \nand MRI datasets, but most models have been \ndeveloped in tertiary -care populations with \nestablished disease, and their thresholds, \ngeneralizability, and clinical value in adolescents \nremain uncertain [50, 51]. \nEarlier recognition also increases the risk of \noverdiagnosis. In adolescents, this risk is especially \nimportant because the uterus is still developing, \nimaging findings may be subtle or nonspecific, and \nthresholds for pathologic versus physiologic \nmyometrial variation remain insufficiently defined. \nOne major pitfall is over -attributing severe \ndysmenorrhea to adenomyosis based on isolated \nindirect or equivocal imaging findings. The opposite \nproblem is failure to recognize early disease because it \ndoes not resemble the classic diffuse adult phenotype. \nA balanced diagnostic strategy therefore requires \ncorrelation between symptom severity, imaging \nphenotype, and differential diagnosis rather than \nreliance on a single sign or label. \nInterobserver variability remains another \nchallenge. Even with revised MUSA terminology, \nreproducibility of some ultrasound features is \nimperfect, highlighting the need for standardized \nacquisition, reporting, and reader training [39, 52]. \nDifferential dia gnosis must also remain broad, \nparticularly in adolescents with severe progressive \ndysmenorrhea and atypical cystic or structural \nfindings. Overall, current evidence supports a risk -\nbased diagnostic model: adolescents with severe \nsymptoms, direct MUSA feat ures, multiple \nconcordant imaging features, or overlap disease \nwarrant closer evaluation and follow -up, whereas \nmild symptoms with isolated or equivocal findings \nmay justify observation and reassessment. This \napproach acknowledges both the clinical importa nce \nof adolescent adenomyosis and the uncertainty \nsurrounding its earliest imaging manifestations. \n6. Management of adolescent adenomyo-\nsis: symptom-oriented longitudinal \ncare with attention to future \nreproductive options \nManagement of adolescent adenomyosis should \nbe individualized and proportionate. Unlike \nmanagement in older adults, treatment in adolescents \nmust address symptom relief, bleeding control, long-\nterm adherence, avoidance of overtreatment, and \npreservation of  future reproductive options. Because \nadolescent-specific therapeutic evidence remains \nlimited, management should be guided by symptom \nburden, imaging phenotype, suspected overlap \ndisease, treatment response, and patient priorities, \nwith cautious extrapola tion from adult adenomyosis, \nadolescent dysmenorrhea or endometriosis, and \nbroader chronic pelvic pain care. \n6.1 Stepwise medical management \nFor most adolescents, initial treatment is \nconservative and symptom- oriented. Non -steroidal \nanti-inflammatory drugs (NSAIDs) are appropriate \nfirst-line therapy for mild or moderate dysmenorrhea, \nas recommended in adolescent dysmenorrhea \nguidance [53, 54]. This approach is especially \nreasonable when imaging findings are uncertain or \nwhen symptoms remain manageable without long -\nterm suppression. \nWhen symptoms are recurrent, severe, or \ninsufficiently controlled, hormonal suppression \nbecomes the main therapeutic option. Combined \nhormonal contraceptives and progestins are \ncommonly used on the basis of adolescent \ndysmenorrhea/endometriosis guidance an d \nextrapolation from adult adenomyosis management, \nwhereas gonadotropin- releasing hormone agonists \nshould be reserved for selected refractory cases \nbecause of bone-health concerns and the need for add-\nback therapy [53, 55, 56]. Small adolescent case -series \nevidence also suggests that hormonal suppression \nmay reduce MRI -visible adenomyosis in selected \npatients, but this remains low-level evidence [14]. \nTreatment selection should also consider \ntolerability, bleeding pattern, expected duration of \nuse, adherence, contraceptive needs, bone health, and \nendocrine maturation. Medical therapy should \ntherefore be presented as an adjustable longitudinal \nstrategy rather than as a fixed long -term solution for \nall patients. \n6.2 Refractory or complex disease \nPersistent symptoms despite appropriate first -\nline treatment should prompt reassessment rather \nthan automatic escalation. In adolescents, refractory \nsymptoms may reflect coexisting endometriosis, \n\nInt. J. Med. Sci. 2026, Vol. 23 \n \nhttps://www.medsci.org \n3460 \npelvic floor dysfunction, central pain amplification, \npoor adherence, treatment intolerance, or an \nalternative structural diagnosis. Treatment response \nshould therefore be interpreted cautiously: \nimprovement in bleeding or cyclic dysmenorrhea after \nhormonal suppression may reflect suppression of \nendometrial, adenomyotic, or endometriotic activity, \nwhereas persistent acyclic pelvic pain, bowel or \nurinary symptoms, or functional impairment should \nraise suspicion of coexisting endometriosis or mixed \npain mecha nisms. Recent longitudinal evidence on \nadenomyosis with coexisting endometriosis also \nsupports individualized follow -up according to \nsymptom evolution, imaging phenotype, treatment \nexposure, and reproductive priorities [57]. \nManagement should therefore inc lude review of the \noriginal diagnosis, reassessment of symptom pattern, \nexpert imaging review when needed, and evaluation \nfor overlap disease [2]. \nFor patients with disabling pain, recurrent \nfunctional impairment, or suspected mixed pain \nmechanisms, management may extend beyond \nuterine-directed therapy to include pelvic floor \nphysical therapy, pain education, psychological or \nbehavioral support, and multidisciplinary pain care, \nconsistent with broader chronic pelvic pain guidance \n[58]. The key principle is that refractory adolescent \nadenomyosis should not be managed solely as a \nuterine imaging abnormality; pain mechanisms and \nfunctional consequences also need attention. \n6.3 Selected intervention and longitudinal \nfollow-up \nSurgical or interventional treatment should be \nreserved for carefully selected adolescents with focal \ncystic lesions or juvenile cystic adenomyoma \nrefractory to medical treatment, as supporting \nevidence is limited to case reports and small case series \n[18]. In such cases, uterus -sparing laparoscopic \nexcision may be considered when severe symptoms \npersist despite appropriate medical therapy and when \nexpert imaging identifies a discrete lesion. Potential \nrisks, including uterine scarring, recurrence, and \nuncertain reproductive consequences, should be \ndiscussed before intervention. \nHigh-intensity focused ultrasound and other \nnon-invasive techniques have been explored as \nfertility-preserving approaches in adenomyosis, but \nadolescent evidence remains very limited. These \nmodalities should currently be regarded as selective or \ninvestigational rather than routine care for young \npatients [59]. \nLongitudinal follow -up is central to adolescent \ncare. Symptoms, menstrual pattern, treatment \ntolerance, imaging phenotype, overlap disease, and \nreproductive priorities may all change over time. \nFollow-up should therefore include planned \nreassessment rather than a one -time treatment \ndecision. During transition to adult care, patients with \nsuspected or confirmed adenomyosis should ideally \nhave a cle ar summary of symptom history, imaging \nfindings, prior treatments, treatment response, and \nunresolved concerns. This is particularly important for \nthose with persistent pain, repeated imaging \nabnormalities, suspected endometriosis overlap, or \nfuture fertility concerns. \nOverall, current evidence supports a stepwise \nand fertility- conscious model: medical treatment for \nmost symptomatic adolescents, broader \nmultidisciplinary assessment for refractory or \ncomplex disease, and invasive treatment only for \nselected focal or cystic lesions. This approach balances \nsymptom control with caution, avoids unnecessary \nintervention, and preserves future reproductive \noptions. A symptom- and phenotype-based diagnostic \nand management pathway for suspected adolescent \nadenomyosis is summarized in Figure 3. \n7. Discussion \nAdolescent and early -onset adenomyosis is best \napproached as a clinically relevant but still \nincompletely defined condition. The available \nevidence supports considering adenomyosis in \nadolescents and young women with severe or \ntreatment-resistant dysmenorr hea, heavy menstrual \nbleeding, chronic pelvic pain, or coexisting \nendometriosis. At the same time, early imaging \nfindings cannot be interpreted in isolation. Their \nclinical meaning depends on symptom burden, \nphenotype, developmental context, and alternativ e \ndiagnoses. \nThis distinction is important in daily practice. \nSome adolescents with persistent symptoms may be \nunder-investigated because adenomyosis is still \nperceived as a disease of older reproductive age. \nOthers may be overdiagnosed when subtle or \nequivocal myometr ial findings are treated as \ndefinitive disease. A risk- based approach is therefore \nmore appropriate than a simple positive -or-negative \ndiagnostic label. Multiple concordant imaging features \nin a highly symptomatic patient carry different clinical \nweight fr om an isolated finding in a mildly \nsymptomatic adolescent. \nFertility counselling is another area where \ncaution is essential. Adult studies have linked \nadenomyosis with infertility, implantation failure, \npoorer assisted- reproduction outcomes, and adverse \nobstetric events, particularly in patients with \nendometriosis overlap or specific imaging phenotypes \n[60-62]. Different phenotypes may also carry different \n\nInt. J. Med. Sci. 2026, Vol. 23 \n \nhttps://www.medsci.org \n3461 \nreproductive implications, although this evidence is \nmainly derived from adult, infertility, or assisted -\nreproduction populations [63]. Available studies \nsuggest that symptomatic and diffuse adenomyosis \nmay be more strongly associated with reduced clinical \npregnancy or live -birth rates and increased \nmiscarriage risk after in vitro fertilization than \nasymptomatic adenomyosis [64]. Recent subtype -\nbased evidence also suggests that internal or mixed \nadenomyosis may be associated with lower live -birth \nrates and higher early pregnancy loss after frozen \nembryo transfer, whereas external adenomyosis may \nhave less apparent impact [65]. Disease burden and \nlesion localization may therefore be relevant when \ncounselling young patients, particularly those with \nprogressive imaging findings, coexisting \nendometriosis, or future fertility concerns [66, 67]. \nHowever, these observations should not be directly \nextrapolated to adolescents; instead, they support \ncautious counselling, avoidance of unnecessary \nuterine intervention, and longitudinal documentation \nof symptoms, imaging findings, and treatment \nresponse. \nA strength of this review is that it separates direct \nadolescent evidence from evidence extrapolated from \nyoung adult or broader adult populations. This \ndistinction matters because applying adult \nadenomyosis data too directly to adolescents may \nexaggerate diagnostic certainty, treatment \nimplications, or reproductive risk. The review also \nbrings together epidemiologic signals, early \nphenotypes, biological plausibility, diagnostic \nchallenges, management principles, and fertility -\nconscious care within a life-course framework. \n \n \nFigure 3. Symptom- and phenotype-based diagnostic and management pathway for suspected adolescent or early -onset adenomyosis. Direct and indirect \nMUSA features should be interpreted in clinical context, because isolated indirect or equivocal findings may be nonspecific i n adolescents. Abbreviations: ACUM, accessory \ncavitated uterine malformation; CPP, chronic pelvic pain; CUAs, c ongenital uterine anomalies; HMB, heavy menstrual bleeding; MRI, magnetic resonance imaging; MUSA, \nMorphological Uterus Sonographic Assessment; NSAIDs, non- steroidal anti-inflammatory drugs; US, ultrasound. Created with BioRender.com. \n\n\nInt. J. Med. Sci. 2026, Vol. 23 \n \n \nhttps://www.medsci.org \n3462 \nThe limitations mainly reflect the state of the \nliterature. Most studies are cross -sectional, imaging-\nbased, and drawn from symptomatic or referral \npopulations. Adolescents are often analyzed together \nwith young adult women, making it difficult to define \ntrue prevalence, natural history, and phenotype-\nspecific outcomes in strictly adolescent cohorts. \nTreatment evidence is limited, and most management \nstrategies remain extrapolated from adult adeno -\nmyosis, adolescent dysmenorrhea, endometriosis, or \nchronic pelvic pain care. Mechanistic and reproductive \ndata are also largely adult-derived. \nFuture studies should move beyond earlier \ndetection alone. Prospective multicenter cohorts with \nstandardized symptom assessment, ultrasound and \nMRI reporting, and long-term follow-up are needed to \ndetermine which early lesions are clinically \nmeaningful. Age -conscious diagnostic criteria may \nhelp distinguish disease from normal developmental \nvariation or equivocal myometrial findings. Further \nwork should also clarify whether focal, diffuse, cystic, \ninner-myometrial, outer- myometrial, or \nendometriosis-associated phenotypes differ in \nsymptom persistence, treatment escalation, \nprogression, and reproductive outcomes. \nOverall, the key question is not simply whether \nadenomyosis can be detected earlier, but which \nadolescents require closer follow -up and which \nmanagement strategies improve long -term pain \ncontrol, bleeding patterns, quality of life, and \nreproductive outcomes. \nSupplementary Material \nSupplementary figure and tables.  \nhttps://www.medsci.org/v23p3453s1.pdf \nAcknowledgements \nThe authors thank the researchers and clinicians \nwhose work has advanced the understanding of \nadolescent and early-onset adenomyosis. \nAuthor contributions \nS.Y. and X.M. conceived the review and defined \nits scope. S.Y. and Y.C. designed the review \nframework and interpreted the literature. S.Y. drafted \nthe first version of the manuscript. 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