Rečové schopnosti u chlapcov s poruchou autistického spektra v súvislosti s reprodukčným zdravím matky, endokrinnými disruptormi a typom pôrodu

Stáhnout PDF English version

Autoři: Klaudia Kyselicová ¹ ; Žofia Baroková ²; Dóra Dukonyová ¹ ; Branislav Bartko ²; Mariia Seliuk ²; Katarína Polónyiová ¹ ; Mária Vidošovičová ¹; Jozef Záhumenský ³ ; Radoslav Beňuš ² ; Daniela Ostatníková ¹
Působiště autorů: Academic Center for Autism Research at the Physiological Institute, Faculty of Medicine, Comenius University in Bratislava, Bratislava, Slovak Republic ¹; Department of Anthropology, Faculty of Natural Sciences, Comenius University in Bratislava, Bratislava, Slovak Republic ²; II. Obstetrics and Gynecology Clinic of the Faculty of Medicine of the UK and Ružinov University Hospital, Bratislava, Slovak Republic ³
Vyšlo v časopise: Ceska Gynekol 2024; 89(5): 360-369
Kategorie: Původní práce
doi: https://doi.org/10.48095/cccg2024360

Souhrn

Ciele: Predkladaný výskum sa zaoberá identifikáciou prenatálnych faktorov vplývajúcich na abnormálny neurovývin a postnatálnu manifestáciu autistického fenotypu v súbore 107 chlapcov (priemerný vek 4,31 ± 2,24). Súbor a metódy: Biologické matky autistických chlapcov poskytli údaje týkajúce sa ich reprodukčného zdravia, infekcií počas gravidity, užívaní orálnej antikoncepcie pred počatím, prípadne užívaním návykových látok pred a počas gravidity a tiež informácie týkajúce sa novorodenca. Následne boli chlapci dia gnostikovaný na poruchy autistického spektra (PAS), pomocou dia gnostických nástrojov ADOS-2 (Autism Dia gnostic Observation Schedule) a ADI-R (Autism Dia gnostic Interview –⁠ Revised). V ADOSE-2 bol zvolený dia gnostický modul podľa rečových schopností dieťaťa, buď Modul 1 –⁠ neverbálny alebo minimálne verbálny chlapci (n = 68) a verbálni chlapci (n = 39). Výsledky: Na základe našich výsledkov, má reprodukčné zdravie matky súvisiace s dĺžkou menštruačného cyklu pred graviditou s autistickým dieťaťom, súvis s mierou rečového postihnutia (p = 0,017), taktiež počet predošlých tehotenstiev (p = 0,026). Matky neverbálnych detí uvádzali kratší cyklus (27,35 dní ± 6,60) ako matky verbálnych detí (30,14 days ± 4,44) a mali viac predošlých tehotenstiev (0,93 ± 1,07 vs. 0,51 ± 0,91). Neuviedli však počet živo narodených detí pred tehotenstvom s autistickým dieťaťom. Deti, ktoré boli neskôr dia gnostikované ako neverbálne, mali dlhší pôrod (od 2 do 48 hod; v priemere 11,13 hod, SD = 9,49), ako verbálne (od 1 do 27 hod, čo bolo v priemere 7,09 hod, SD = 8,91), p = 0,0182. Spôsob pôrodu nezohrával úlohu, ani spôsob počatia (prirodzené vs. umelé). Záver: Skúmanie prenatálnych faktorov v etiológii autizmu z hľadiska rečového vývinu sa javí ako dobrý prístup.

Zdroje

1. World Health Organization. ICD-11 International Classification of Dis eases 11th Revision. 2019 [online]. Available from: https: //icd.who.int/en/.

2. Maltman N, DaWalt LS, Hong J et al. Brief reports: socioeconomic factors associated with minimally verbal status in individuals with ASD. J Autism Dev Disord 2021; 51 (6): 2139–2145. doi: 10.1007/s10803-020-04646-6.

3. Rose V, Trembath D, Keen D et al. The proportion of minimally verbal children with autism spectrum disorder in a community-based early intervention programme. J Intellect Disabil Res 2016; 60 (5): 464–477. doi: 10.1111/jir.12284.

4. National Center on Birth Defects and Developmental Disabilities (NCBDDD). 2024 [online]. Available from: https: //www.cdc.gov/autism/data-research/index.html.

5. Bougeard C, Picarel-Blanchot F, Schmid R et al. Prevalence of autism spectrum disorder and co-morbidities in children and adolescents: a systematic literature review. Front Psychiatry 2021; 27 (12): 744709. doi: 10.3389/fpsyt.2021.744 709.

6. Lyall K, Croen L, Daniels J et al. The changing epidemiology of autism spectrum disorders. Annu Rev Public Health 2017; 38 : 81–102. doi: 10.1146/annurev-publhealth-031816-044318.

7. Hazlett HC, Gu H, Munsell BC et al. Early brain development in infants at high risk for autism spectrum disorder. Nature 2017; 542 (7641): 348–351. doi: 10.1038/nature21369.

8. Shen MD, Kim SH, McKinstry RC et al. Increased extra-axial cerebrospinal fluid in high-risk infants who later develop autism. Biol Psychiatry 2017; 82 (3): 186–193. doi: 10.1016/j.bio psych.2017.02.1095.

9. Folstein S, Rutter M. Infantile autism: a genetic study of 21 twin pairs. J Child Psychol Psychiatry 1977; 18 (4): 297–321. doi: 10.1111/j.1469-7610.1977.tb00443.x.

10. Le Couteur AL, Gottesman I, Bolton P et al. Autism as a strongly genetic disorder evidence from a British twin Study. Psychol Med 1995; 25 (1): 63–77. doi: 10.1017/S0033291700028099.

11. Rosenberg RE, Law JK, Yenokyan G et al. Characteristics and concordance of autism spectrum disorders among 277 twin pairs. Arch Pediatr Adolesc Med 2009; 163 (10): 907–914. doi: 10.1001/archpediatrics.2009.98.

12. Ronald A, Hoekstra RA. Autism spectrum disorders and autistic traits: a decade of new twin studies. Am J Med Genet B Neuropsychiatr Genet 2011; 156B (3): 255–274. doi: 10.1002/ajmg.b.31159.

13. Sandin S, Lichtenstein P, Kuja-Halkola R et al. The familial risk of autism. JAMA 2014; 311 (17): 1770–1777. doi: 10.1001/jama.2014.4144.

14. Kim H, Keifer C, Rodriguez-Seijas C et al. Quantifying the optimal structure of the autism phenotype: a comprehensive comparison of dimensional, categorical, and hybrid models. J Am Acad Child Adolesc Psychiatry 2019; 58 (9): 876.e2–886.e2. doi: 10.1016/j.jaac.2018.09.431.

15. Gaugler T, Klei L, Sanders SJ et al. Most genetic risk for autism resides with common variation. Nat Genet 2014; 46 (8): 881–885. doi: 10.1038/ng.3039.

16. Marro SG, Chanda S, Yang N et al. Neuroligin-4 regulates excitatory synaptic transmission in human neurons. Neuron 2019; 103 (4): 617.e6–626.e6. doi: 10.1016/j.neuron.2019.05.043.

17. Villa CE, Cheroni C, Dotter CP et al. CHD8 haploinsufficiency links autism to transient alterations in excitatory and inhibitory trajectories. Cell Rep 2022; 39 (1): 110615. doi: 10.1016/ j.celrep.2022.110615.

18. Yu TW, Chahrour MH, Coulter ME et al. Using whole-exome sequencing to identify inherited causes of autism. Neuron 2013; 77 (2): 259–273. doi: 10.1016/j.neuron.2012.11.002.

19. Mesman S, Bakker R, Smidt MP. Tcf4 is required for correct brain development during embryogenesis. Mol Cell Neurosci 2020; 106 : 103502. doi: 10.1016/j.mcn.2020.103502.

20. Marotta R, Risoleo M C, Messina G et al. The neurochemistry of autism. Brain Sci 2020; 10 (3): 163. doi: 10.3390/brainsci10030163.

21. De Rubeis S, He X, Goldberg AP et al. Synaptic, transcriptional and chromatin genes disrupted in autism. Nature 2014; 515 (7526): 209–215. doi: 10.1038/nature13772.

22. Manzouri L, Yousefian S, Keshtkari A et al. Advanced parental age and risk of positive autism spectrum disorders screening. Int J Prev Med 2019; 10 (1): 135. doi: 10.4103/ijpvm.ijpvm_25_19.

3. Tioleco N, Silberman AE, Stratigos K et al. Prenatal maternal infection and risk for autism in offspring: a meta-analysis. Autism Res 2021; 14 (6): 1296–1316. doi: 10.1002/aur.2499.

24. Hendricks G, Malcolm-Smith S, Adnams C et al. Effects of prenatal alcohol exposure on language, speech and communication outcomes: A review longitudinal studies. Acta Neuropsychiatr 2019; 31 (2): 74–83. doi: 10.1017/neu. 2018.28.

25. Clausen TD, Mortensen EL, Schmidt L et al. Cognitive function in adult offspring of women with gestational diabetes-the role of glucose and other factors. PLoS One 2013; 8 (6): e67107. doi: 10.1371/journal.pone.0067107.

26. Crump C, Sundquist J, Sundquist K. Preterm or early term birth and risk of autism. Pediatrics 2021; 148 (3): e2020032300. doi: 10.1542/peds.2020-032300.

27. Al-Zalabani AH, Al-Jabree AH, Zeidan ZA. Is cesarean section delivery associated with autism spectrum disorder? Neurosciences (Riyadh) 2019; 24 (1): 11–15. doi: 10.17712/nsj. 2019.1.20180303.

28. Zwaigenbaum L, Szatmari P, Jones MB et al. Pregnancy and birth complications in autism and liability to the broader autism phenotype. J Am Acad Child Adolesc Psychiatry 2002; 41 (5): 572–579. doi: 10.1097/00004583-200205000-00015.

29. Daniels AM, Mandell DS. Explaining differences in age at autism spectrum disorder dia g -⁠ nosis: a critical review. Autism 2014; 18 (5): 583–597. doi: 10.1177/1362361313480277.

30. Lee BK, Magnusson C, Gardner RM et al. Maternal hospitalization with infection during pregnancy and risk of autism spectrum disorders. Brain Behav Immun 2015; 44 : 100–105. doi: 10.1016/j.bbi.2014.09.001.

31. Boukhris T, Sheehy O, Mottron L et al. Antidepressant use during pregnancy and the risk of autism spectrum disorder in children. JAMA Pediatr 2016; 170 (2): 117–124. doi: 10.1001/jamapediatrics.2015.3356.

32. Jung Y, Lee AM, McKee SA et al. Maternal smoking and autism spectrum disorder: meta-analysis with population smoking metrics as moderators. Sci Rep 2017; 7 (1): 4315. doi: 10.1038/s41598-017-04413-1.

33. Zerbo O, Qian Y, Yoshida C et al. Maternal infection during pregnancy and autism spectrum disorders. J Autism Dev Disord 2015; 45 (12): 4015–4025. doi: 10.1007/s10803-013 -⁠ 2016-3.

34. Halliday JL, Muggl E, Lewis S et al. Alcohol consumption in a general antenatal population and child neurodevelopment at 2 years. J Epidemiol Community Health 2017; 71 (10): 990–998. doi: 10.1136/jech-2017-209165.

35. Gardener H, Spiegelman D, Buka SL. Prenatal risk factors for autism: comprehensive meta-analysis. Br J Psychiatry 2009; 195 (1): 7–14. doi: 10.1192/bjp.bp.108.051672.

36. Luo Z, Yang C, Cai T et al. Maternal alcohol consumption during pregnancy and autism spectrum disorder in offspring: a meta-analysis. Rev J Autism Develop Disord 2022; 11 : 265–274. doi: 10.1007/s40489-022-00336-4.

37. Wyper KR, Rasmussen CR. Language impairments in children with fetal alcohol spectrum disorder. J Popul Ther Clin Pharmacol 2011; 18 (2): e364–e376.

38. Jenabi E, Ayub E, Bashirian S et al. Association between previous abortion history and risk of autism spectrum disorders among offspring: a meta-analysis. Clin Exp Pediatr 2023; 66 (2): 70–75. doi: 10.3345/cep.2022.00108.

39. Liu J, He Y, Shen Y et al. Association of attention deficit/hyperactivity disorder with events occurring during pregnancy and perinatal period. Front Psychol. 2021; 12 : 707500. doi: 10.3389/fpsyg.2021.707500.

40. Wang H, Li F, Miao M et al. Maternal spontaneous abortion and the risk of attention-deficit/hyperactivity disorder in offspring: a population-based cohort study. Hum Reprod 2020; 35 (5): 1211–1221. doi: 10.1093/humrep/deaa035.

41. Ji H, Yu Y, Miao M et al. Risk of intellectual disability and maternal history of spontaneous abortion: a nationwide cohort study. Dev Med Child Neurol 2021; 63 (7): 831–838. doi: 10.1111/dmcn.14839.

42. El-Tallawy HN, Farghaly WM, Shehata GA et al. Cerebral palsy in Al-Quseir City, Egypt: prevalence, subtypes, and risk factors. Neuropsychiatr Dis Treat 2014; 8 (10): 1267–1272. doi: 10.2147/NDT.S59599.

43. Hendricks G, Malcolm-Smith S, Adnams C et al. Effects of prenatal alcohol exposure on language, speech and communication outcomes: a review longitudinal studies. Acta Neuropsychiatr 2019; 31 (2): 74–83. doi: 10.1017/neu.2018.28.

44. Roos A, Wedderburn CJ, Fouche JP et al. Central white matter integrity alterations in 2–3-year-old children fol lowing prenatal alcohol exposure. Drug Alcohol Depend 2021; 225 : 108826. doi: 10.1016/j.drugalcdep.2021. 108826.

45. Walton M, Dewey D, Lebel C. Brain white matter structure and language ability in preschool-aged children. Brain Lang 2018; 176 : 19–25. doi: 10.1016/j.bandl.2017.10.008.

ORCID authors

K. Kyselicová 0000-0002-5520-1657

D. Dukonyová 0009-0005-7192-4176

K. Polónyiová 0000-0002-3036-0651

J. Záhumenský 0000-0003-0475-6035

R. Beňuš 0000-0001-5917-1689

D. Ostatníková 0000-0002-4960-5057

Submitted/Doručené: 20. 6. 2024

Accepted/Prijaté: 22. 7. 2024

RNDr. Klaudia Kyselicová, PhD

Physiological Institute

Faculty of Medicine