Puberty in boys with a history of cryptorchidism

Jorma Toppari

Research Centre for Integrative Physiology and Pharmacology, and Centre for Population Health Research, and In Flames Research Flagship Center, Institute of Biomedicine, University of Turku, Turku, Finland, and Department of Pediatrics, Turku University Hospital, Turku, Finland

Correspondence; Prof Dr med , PhD Jorma Toppari Kiinamyllynkatu 10 20520 Turku Finland

Table of contents

Abstract
Résumé
Paper
References
Author

Abstract

Cryptorchidism—the failure of one or both testes to descend into the scrotum—is the most common genital anomaly in male infants and a salient risk factor for hypogonadism, impaired spermatogenesis, and testicular malignancy later in life. The neonatal hypothalamic–pituitary–testicular (HPT) axis surge (“mini-puberty”) provides a natural stress test of the infant testis, and accumulating prospective evidence shows that boys with cryptorchidism display biochemical signatures consistent with suboptimal Sertoli-cell function already in early infancy. Puberty, however, is orchestrated by a renewed activation of the HPT axis and a rapid expansion of seminiferous tubule mass; how these processes unfold in boys with a history of cryptorchidism is clinically decisive for lifetime reproductive potential. Drawing on Nordic birth cohorts from Denmark and Finland, longitudinal adolescent follow-ups, and contemporary guideline-based care, this paper synthesizes the physiology and clinical course of puberty after cryptorchidism. We summarize (i) geographic variation in cryptorchidism and the “testicular dysgenesis” paradigm; (ii) infant endocrine phenotypes that stratify later risk; (iii) trajectories of pubertal onset and tempo; (iv) testicular growth and hormone dynamics (inhibin B, AMH, FSH, LH, testosterone); (v) modifying effects of laterality, position at diagnosis, spontaneous descent versus orchiopexy, and timing of surgery; and (vi) clinical implications for counselling and follow-up. The weight of evidence indicates that pubertal timing per se is typically normal in prior cryptorchid boys, but testicular growth during puberty is blunted—most clearly in bilateral and formerly non-palpable/abdominal testes—and accompanied by lower inhibin B and modestly higher FSH (with broadly similar serum testosterone), signaling reduced Sertoli-cell mass and germ-cell output. Early orchiopexy (by 6–12 months) and spontaneous descent are associated with more favorable adolescent testicular volume and endocrine profiles than late correction. These insights refine risk stratification and motivate structured, biomarker-informed pubertal surveillance to optimize fertility counselling.

Key words: cryptorchidism, mini puberty, Sertoli cell, treatment

Résumé

La cryptorchidie – absence de descente d’un ou des deux testicules dans le scrotum – est l’anomalie génitale la plus fréquente chez le nourrisson de sexe masculin et un facteur de risque majeur d’hypogonadisme, d’altération de la spermatogenèse et de cancer testiculaire à l’âge adulte. La poussée néonatale de l’axe hypothalamo-hypophyso-testiculaire (HPT), surnommée « mini-puberté », constitue un test de stress naturel pour le testicule du nourrisson. Des données prospectives de plus en plus nombreuses montrent que les garçons atteints de cryptorchidie présentent, dès la petite enfance, des signatures biochimiques compatibles avec un fonctionnement suboptimal des cellules de Sertoli. La puberté, quant à elle, est orchestrée par une nouvelle activation de l’axe HPT et une expansion rapide de la masse des tubes séminifères. Le déroulement de ces processus chez les garçons ayant des antécédents de cryptorchidie est déterminant pour leur potentiel reproductif tout au long de leur vie. S’appuyant sur des cohortes de naissance Nordiques (Danemark et Finlande), des suivis longitudinaux à l’adolescence et les recommandations actuelles en matière de soins, cet article synthétise la physiologie et l’évolution clinique de la puberté après une cryptorchidie. Nous résumons (i) la variation géographique de la cryptorchidie et le paradigme de la « dysgénésie testiculaire » ; (ii) les phénotypes endocriniens infantiles qui stratifient le risque ultérieur ; (iii) les trajectoires d’apparition et de rythme de la puberté ; (iv) la croissance testiculaire et la dynamique hormonale (v) les effets modificateurs de la latéralité, de la position au moment du diagnostic, de la descente spontanée versus l’orchidopexie et du moment de l’intervention ; et (vi) les implications cliniques pour le conseil et le suivi. L’ensemble des données probantes indique que le calendrier pubertaire en lui-même est généralement normal chez les garçons généralement normal chez les garçons ayant présenté une cryptorchidie, mais que la croissance testiculaire pendant la puberté est ralentie – plus particulièrement en cas de cryptorchidie bilatérale et de testicules anciennement non palpables/abdominaux – et s’accompagne d’une diminution de l’inhibine B et d’une légère augmentation de la FSH (avec une testostéronémie globalement similaire), ce qui indique une réduction de la masse des cellules de Sertoli et de la production de cellules germinales. Une orchidopexie précoce (entre 6 et 12 mois) et une descente spontanée sont associées à un volume testiculaire et à des profils endocriniens plus favorables à l’adolescence qu’une correction tardive. Ces observations affinent la stratification des risques et justifient une surveillance pubertaire structurée, basée sur les biomarqueurs, afin d’optimiser le conseil en matière de fertilité.
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1. Introduction: why puberty matters after cryptorchidism

Cryptorchidism affects ~1–9% of term male newborns globally, with pronounced geographic variation even across closely related Nordic populations [1,5]. In the turn of the millenium, harmonized examinations in Copenhagen (Denmark) and Turku (Finland) demonstrated a roughly four-fold higher prevalence in Denmark than Finland, catalyzing the modern “testicular dysgenesis syndrome” (TDS) discourse spanning impaired fetal Leydig/Sertoli function, cryptorchidism, hypospadias, reduced semen quality, and testicular cancer [1,5–7]. Puberty is the life stage when testicular function recovers (or fails to recover) from earlier insults: gonadotropin pulsatility resumes, Sertoli cells complete maturation, the blood-testis barrier consolidates, and spermatogenesis scales up. Consequently, pubertal outcomes in boys with prior cryptorchidism provide an integrated readout of the testis’ biological reserve built during fetal life and “mini-puberty” and modified by surgical timing and postnatal environment.

Historically, concerns in cryptorchidism focused on testicular cancer risk and fertility; however, contemporary longitudinal studies show that the tempo and quality of pubertal testicular growth—rather than age of pubertal onset—best differentiates formerly cryptorchid boys from controls [2,4]. This review organizes current evidence with an emphasis on Nordic prospective cohorts, laboratory phenotypes, and modifiable determinants of testicular growth trajectories.

 

2. From fetal life to mini-puberty: setting the stage for adolescence

2.1. Physiology in brief

Fetal testicular differentiation depends on placental hCG acting via the LH/CG receptor before the fetal pituitary–gonadal loop matures; in the second and third trimesters, fetal pituitary LH/FSH takes over steroidogenic regulation. After birth, an HPT “mini-puberty” (weeks 1–16) features rising LH/FSH, peaking total testosterone (~1–3 months), and robust Sertoli-cell outputs (inhibin B, AMH). This surge supports penile growth, scrotal pigmentation, and testis descent completion, but—critically—also expands Sertoli-cell number, which constrains future spermatogenic capacity. Disruption of this window leaves a durable imprint on adolescent fertility potential [2-4, 6-10].

2.2. Mini-puberty in cryptorchid boys: consistent Sertoli-cell signals

Across birth cohorts that sampled at ~3 months (the compromise time point when FSH/inhibin B are near peak, and LH/testosterone are declining from peak), cryptorchid boys—particularly those with higher-lying testes—exhibit lower inhibin B and/or higher FSH, consistent with a Sertoli-cell deficit; serum testosterone is often comparable to controls, suggesting relatively preserved Leydig-cell steroidogenesis at a population level [11]. In the joint Danish–Finnish cohorts, mini-puberty hormones differed by testis position: suprascrotal/inguinal and non-palpable testes showed the most adverse Sertoli signals compared with boys whose testes were scrotal at exam [11]. These findings align with the pathophysiology whereby impaired Sertoli proliferation is an early, salient lesion in cryptorchidism, with lasting consequences for pubertal Sertoli mass and inhibin B later on [2–4].

3. Epidemiology and natural history relevant to puberty

The Danish–Finnish comparative birth cohorts quantified marked prevalence differences (e.g., ~9% Denmark vs ~2–3% Finland at standardized exams), provided a robust platform for hormone phenotyping during mini-puberty, and enabled tracking of spontaneous descent [1,2,4-7]. Spontaneous descent commonly occurs by 6 months corrected age; persistence beyond this window predicts need for orchiopexy. Guideline statements (Nordic 2007, AUA 2014, EAU/ESPU 2016) converged on recommending orchiopexy by 6–12 months to optimize testicular growth and reduce later risks [3,8,10]. The timing of orchiopexy becomes pivotal for pubertal trajectories: early relocation likely preserves more of the Sertoli/germ-cell niche than late surgery, even though puberty itself reactivates gonadotropin support [3,8-10].

4. Puberty after cryptorchidism: what do longitudinal data show?

4.1. Age at pubertal onset and tempo

Multiple cohorts (including Turku and Copenhagen, with standardized anthropometry and repeated testicular volume assessments) indicate that the calendar age at pubertal onset is not materially delayed in boys with a history of cryptorchidism compared with peers [2,4]. The more discriminating signal is testicular growth velocity once puberty begins. In the Turku study of formerly cryptorchid boys followed across adolescence, testicular volumes at the same Tanner genital stages were smaller than in controls, particularly in bilateral and previously non-palpable/abdominal cases [2,4].

4.2. Testicular volume dynamics: unilateral vs bilateral, spontaneous descent vs orchiopexy

Sadov et al. (2016) and Rodprasert et al. (2022) provided a detailed analysis of pubertal testicular growth in formerly cryptorchid boys versus controls, stratified by important clinical modifiers (laterality, whether descent was spontaneous or surgical, and age at orchiopexy). They reported:

  • Onset: Pubertal onset (clinically defined) was comparable across groups.
  • Growth: Testicular growth during puberty was attenuated in boys with a history of cryptorchidism; disparities were most pronounced in bilateral disease and in those who required surgery (versus spontaneous descent).
  • Endocrine correlates: Seminiferous growth impairment corresponded to lower inhibin B and higher FSH during adolescence; LH/testosterone profiles were broadly similar to controls. [2]

These data operationalize the clinical intuition taught in pediatric endocrinology/urology: puberty does not “fix” a depleted Sertoli pool; rather, pubertal gonadotropin drive unmasks the anatomic constraint as a blunted volumetric trajectory. Replication and extensions of these observations in national registries and clinic-based cohorts support the same direction of effect [10].

4.3. Hormone profiles during adolescence

Sertoli-cell axis (FSH–inhibin B): Relative to controls, formerly cryptorchid adolescents commonly show higher FSH and lower inhibin B, pointing to suboptimal Sertoli mass/germ-cell output. Differences scale with bilateral disease, non-palpable position, and later surgery [2]. This discordant Sertoli signal in the face of normal or near-normal testosterone is the hallmark endocrine phenotype and has direct fertility implications.

Leydig-cell axis (LH–testosterone): Most cohorts report no major difference in serum testosterone at comparable pubertal stages; LH can be slightly higher on average in bilateral/operated groups, but within reference ranges [2]. This suggests that Leydig-cell function—at least as captured by circulating testosterone under pubertal LH drive—is relatively preserved in many formerly cryptorchid boys, even when seminiferous expansion lags.

AMH: Pubertal AMH normally falls as Sertoli cells mature under intratesticular testosterone. AMH patterns in formerly cryptorchid cohorts are heterogeneous, reflecting the interplay of delayed Sertoli maturation and reduced Sertoli mass; AMH is generally not the preferred monitoring biomarker in mid-to-late puberty compared with inhibin B/FSH. [2,3,12]

4.4. Growth references and measurement methods

Testicular volume is best tracked longitudinally using the same method. Orchidometry (Prader beads) remains widely used, but ultrasound provides more precise estimates and can detect modest inter-testis asymmetries important in unilateral disease. Scandinavian pubertal studies have often combined both methods to strengthen inferences and added also ruler measurements [2,4,13].

5. Determinants of pubertal outcome after cryptorchidism

5.1. Laterality and initial position

Bilateral cryptorchidism predicts smaller pubertal testicular volumes, lower inhibin B, and higher FSH compared with unilateral cases and controls [2,4,13]. Within each laterality stratum, higher-lying/non-palpable testes have worse trajectories than suprascrotal/low-inguinal positions, consistent with the gradient of thermal and developmental insult inferred in infancy [2,4,13,14].

5.2. Spontaneous descent vs orchiopexy

Boys with spontaneous descent generally perform better in adolescence than those who required orchiopexy, supporting the concept that spontaneous descent is a biomarker of a more competent testis at baseline. Among the surgically corrected, earlier operation is associated with better pubertal testicular growth and Sertoli-axis labs [13,14].

5.3. Timing of orchiopexy

Nordic and European guidelines recommend orchiopexy between 6 and 12 months, certainly before 18 months, to optimize later testicular growth and fertility potential [3,10]. Adolescent follow-ups confirm that earlier repair tracks with larger pubertal testicular volumes and more favorable inhibin B/FSH than late repair, though surgery cannot fully normalize outcomes in bilateral/non-palpable disease [3,8,13,14].

5.4. Mini-puberty phenotype as a predictor

Inhibin B and FSH measured at ~3 months stratify later risk: lower inhibin B/higher FSH in cryptorchid infants (especially in those with higher-lying testes) predict more attenuated pubertal seminiferous growth and a higher likelihood of adverse adolescent Sertoli-axis profiles [2,13]. Such associations bind infancy to adolescence and rationalize early endocrine testing in persistent cryptorchidism.

6. Mechanistic links: from dysgenesis to pubertal shortfall

Two nonexclusive mechanisms bridge cryptorchid infancy to pubertal outcomes:

  1. Primary testicular dysgenesis (impaired Sertoli/germ-cell programing), reflecting fetal/placental endocrine disruption and/or gene–environment risk. This manifests as deficient mini-puberty Sertoli signals (inhibin B), constraining the maximal proliferative base of the seminiferous epithelium available at puberty [2,13].
  2. Secondary heat/ischemic injury from extra-scrotal position, proportional to height (inguinal → abdominal), duration, and laterality, which cumulatively erodes germ-cell number and Sertoli mass. Earlier relocation limits dose–time exposure and better preserves the prepubertal platform for pubertal expansion [3,8,14].

At puberty, GnRH/LH/FSH activation drives Leydig testosterone and FSH-mediated Sertoli support. If the Sertoli-cell pool is small, FSH rises and inhibin B remains low despite normal LH/testosterone, and testicular volume grows along a shallower slope—the quintessential cryptorchid adolescent signature [2,3,13].

7. Clinical implications for pubertal care

7.1. Who needs structured follow-up?

All boys with bilateral cryptorchidism, non-palpable/abdominal testes, late orchiopexy (>12–18 months), or abnormal mini-puberty labs warrant structured adolescent follow-up (growth, genital staging, testicular volume, and selective labs). Unilateral low-inguinal cases repaired early and boys with spontaneous descent have lower risk but still merit counselling and a baseline pubertal assessment. [2,14]

7.2. What to measure and when?

  • Testicular volume (orchidometer ± ultrasound) during puberty, noting symmetry in unilateral cases.
  • FSH and inhibin B at mid-puberty (e.g., Tanner G3–G4) to appraise Sertoli axis; consider repeat in late puberty if values are borderline.
  • LH/testosterone only if clinical signs suggest hypoandrogenism; routine measurement is less discriminative.
  • AMH is mainly informative prepubertally and in the early stages of puberty; interpret with caution later on. [12]

7.3. Counselling about fertility

The adolescent phenotype (smaller testicular volumes, low inhibin B/high FSH) correlates with reduced adult semen quality in population studies; bilateral cryptorchidism and late surgery carry the highest odds of oligo/azoospermia. Early orchiopexy and spontaneous descent are favorable signs but do not guarantee normal fertility, especially after bilateral disease. Counselling should be realistic and individualized, and in late adolescence/young adulthood, semen analysis provides the definitive assessment. [3,8,10]

8. Controversies and knowledge gaps

  •  Biomarker thresholds: While group differences are consistent, individual-level cut-offs for inhibin B/FSH that predict future infertility lack universal validation.
  • Leydig-cell reserve: Subtle androgen deficiencies may not be captured by total testosterone alone; studies using free testosterone or androgen bioactivity assays are limited and need replication.
  • Ethnic/environmental heterogeneity: The Danish–Finnish contrast underscores environmental contributions, but the specific exposures remain incompletely resolved.
  • Surgery alone vs adjuvant therapy: Whether peri-operative hormonal therapy improves adolescent Sertoli outcomes remains debated; current practice prioritizes timely orchiopexy over GnRH/HCG regimens, given mixed evidence and concerns over down-stream fertility endpoints. [3,8,10]

9. Practical algorithm for adolescent follow-up (risk-tiered)

1.   Risk stratification at or after repair:

  • Low: unilateral, low-inguinal, spontaneous descent or orchiopexy ≤12 months, normal mini-puberty labs.
  • Intermediate: unilateral high-inguinal or non-palpable, orchiopexy 12–18 months, unavailable infant labs.
  • High: bilateral, non-palpable/abdominal, orchiopexy >18 months or staged, abnormal infant inhibin B/FSH.

2.   Monitoring plan:

  • Low: clinical pubertal review; testicular volume at G2/G3; labs if volumes small for stage.
  • Intermediate: testicular volumes + FSH/inhibin B at G3; repeat at G4–G5 if abnormal.
  • High: repeated testicular volumes through mid-puberty; FSH/inhibin B at G2–G3 and G4; consider ultrasound at baseline.

3.   Transition planning:

Late-adolescent/young adulthood semen analysis for intermediate/high-risk groups; endocrine referral if FSH persistently high/inhibin B low or volumes plateau <15–20 mL combined.

This pragmatic approach operationalizes what the longitudinal literature—especially the Copenhagen/Turku experiences—has taught us about the shape of pubertal development after cryptorchidism. [1-4,6,13,14]

10. Conclusion

Boys with a history of cryptorchidism, especially bilateral or non-palpable disease and those repaired after the first year of life, typically enter puberty at the usual age but show constrained testicular growth and a Sertoli-axis signature (low inhibin B, elevated FSH) consistent with reduced seminiferous capacity. These pubertal findings echo endocrine phenotypes already visible during mini-puberty, binding fetal–neonatal events to adolescent outcomes. Early orchiopexy and spontaneous descent are favorable modifiers but do not fully normalize pubertal trajectories in higher-risk subgroups. A risk-tiered, biomarker-informed adolescent follow-up can sharpen counselling about fertility and guide timely referral for semen analysis and adult-care transition. Continued collaboration across Nordic and international cohorts will refine individualized prediction—transforming the epidemiologic signal of cryptorchid infancy into actionable pubertal care.

Declaration Section

a) Ethics Approval and Consent to Participate Investigations were carried out in accordance 326 with the Declaration of Helsinki of 1975, revised in 2008.

b) Consent for publication Not applicable

c) Availability of data and supporting material  Not applicable

d) Competing interests  Author/s declare that they have no competing interests

e) Funding: see manuscript 4,10,12

Acknowledgements

I thank colleagues and collaborators in Copenhagen and Turku for two decades of joint cohort work, and the families who made longitudinal follow-up possible.

References

  1. Holmboe SA, Beck AL, Andersson AM, Main KM, Jørgensen N, Skakkebæk NE, Priskorn L. The epidemiology of cryptorchidism and potential risk factors, including endocrine disrupting chemicals. Front Endocrinol (Lausanne). 2024 Apr 3;15:1343887. doi: 10.3389/fendo.2024.1343887. eCollection 2024.
  2. Rodprasert W, Koskenniemi JJ, Virtanen HE, Sadov S, Perheentupa A, Ollila H, et al. Reproductive Markers of Testicular Function and Size During Puberty in Boys With and Without a History of Cryptorchidism. J Clin Endocrinol Metab. 2022 Nov 25;107(12):3353-3361. doi: 10.1210/clinem/dgac520
  3. Ritzen EM, Bergh A, Bjerknes R, Christiansen P, Cortes D, Haugen SE, et al. Nordic consensus on treatment of undescended testes. Acta Paediatr. 2007;96(5):638–643.
  4. Sadov S, Koskenniemi JJ, Virtanen HE, Perheentupa A, Petersen JH, Skakkebaek NE, et al. Testicular Growth During Puberty in Boys With and Without a History of Congenital Cryptorchidism. J Clin Endocrinol Metab. 2016;101(7):2570–2577.
  5. Boisen KA, Kaleva M, Main KM, Virtanen HE, Haavisto AM, Schmidt IM, et al. Difference in prevalence of congenital cryptorchidism in infants between two Nordic countries. Lancet. 2004;363(9417):1264–1269.
  6. Skakkebaek NE, Rajpert-De Meyts E, Buck Louis GM, Toppari J, Andersson AM, Eisenberg ML, et al. Male reproductive disorders and fertility trends: influences of environment and genetic susceptibility. Physiol Rev 2016 Jan;96(1):55-97. doi: 10.1152/physrev.00017.2015
  7. Main KM, Skakkebaek NE ,Virtanen HE, Toppari J. Genital anomalies in boys and the environment. Best Pract Res Clin Endocrinol Metab. 2010;24(2):279–289.
  8. Kolon TF, Herndon CD, Baker LA, Baskin LS, Baxter CG, Cheng EY, et al.; American Urological Assocation. Evaluation and treatment of cryptorchidism: AUA guideline. J Urol. 2014 Aug;192(2):337-45. doi: 10.1016/j.juro.2014.05.005.
  9. Yiee JH, Saigal CS, Lai J, Copp HL Churchill BM, Litwin MS. Timing of orchiopexy in the United States: a quality-of-care indicator Urology. 2012 Nov;80(5):1121-6. doi: 10.1016/j.urology.2012.08.008
  10. Kuiri-Hänninen T, Sankilampi U, Dunkel L. Activation of the hypothalamic–pituitary–gonadal axis in infancy: mini-puberty. Horm Res Paediatr. 2014;82(2):73–80.
  11. Radmayr C, Dogan HS, Hoebeke P, Kocvara R, Nijman R, Silay S et al. Management of undescended testes: European Association of Urology/European Society for Paediatric Urology Guidelines. J Pediatr Urol. 2016 Dec;12(6):335-343. doi: 10.1016/j.jpurol.2016.07.014 (corrigendum in J Pediatr Urol. 2017 Apr;13(2):239. doi: 10.1016/j.jpurol.2017.02.011).
  12. Suomi AM, Main KM, Kaleva M, Schmidt IM, Chellakooty M, Virtanen HE, et al. Hormonal changes in 3-month-old cryptorchid boys. J Clin Endocrinol Metab. 2006 Mar;91(3):953-8. doi: 10.1210/jc.2004-2318.
  13. Coutant R, Biette-Demeneix E, Bouvattier C, Bouhours-Nouet N, Gatelais F, Dufresne S, et al. Baseline inhibin B and anti-Mullerian hormone measurements for diagnosis of hypogonadotropic hypogonadism (HH) in boys with delayed puberty. J Clin Endocrinol Metab. 2010 Dec;95(12):5225-32. doi: 10.1210/jc.2010-1535.
  14. Kollin C, Stukenborg JB, Nurmio M, Sundqvist E, Gustafsson T, Söder O, et al. Boys with undescended testes: endocrine, volumetric and morphometric studies on testicular function before and after orchidopexy at nine months or three years of age. J Clin Endocrinol Metab. 2012 Dec;97(12):4588-95. doi: 10.1210/jc.2012-2325.

Editorial comment

  1. Impaired mini puberty with decreased LH and testosterone levels affected Ad and Sertoli cell development through positive and negative regulation of morpho regulatory and  apoptotic genes. GnRHa treatment had a repressive effect on most Sertoli cell specific genes, which suggested that Sertoli cells underwent a cellular rearrangement. Gonadotropin-dependent increases in FASLG and GDNF expression drove Sertoli cell proliferation and germ cell self-renewal and supported the transition of gonocytes to Ad spermatogonia, independent of inhibin. Furthermore, reductions in RNA expression of CDKN1B, CALB2, CTSL, CREB1, DMRT1, and WT1 occurred. All these genes are involved in Sertoli cell function and differentiation. This finding suggested that GnRHa induced transcriptional changes in multiple target genes. (Gegenschatz-Schmid K, Verkauskas G, Demougin P, Bilius V, Dasevicius D, Stadler MB, Hadziselimovic F.) Curative GnRHa treatment has an unexpected repressive effect on Sertoli cell specific genes. Basic Clin Androl. 2018 Feb 9;28:2.)
Jorma Toppari portrait

Jorma Toppari

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