Postnatal Acetaminophen and Potential Risk of Autism Spectrum Disorder among Males

Bittker, Seth; Bell, Kathleen R.

doi:10.3390/bs10010026

Cited by 11 publications

(10 citation statements)

References 53 publications

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“…Interestingly, very recently, it has been demonstrated that post-natal use of acetaminophen before the age of two is associated with an increase in the risk of ASD in male children [ 28 ], further confirming our previous results.…”

Section: Acetaminophen Use May Increase the Risk For Asd Which Cousupporting

confidence: 91%

Endocannabinoid System Dysregulation from Acetaminophen Use May Lead to Autism Spectrum Disorder: Could Cannabinoid Treatment Be Efficacious?

Schultz

Gould

Antonucci³

et al. 2021

Molecules

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Persistent deficits in social communication and interaction, and restricted, repetitive patterns of behavior, interests or activities, are the core items characterizing autism spectrum disorder (ASD). Strong inflammation states have been reported to be associated with ASD. The endocannabinoid system (ECS) may be involved in ASD pathophysiology. This complex network of lipid signaling pathways comprises arachidonic acid and 2-arachidonoyl glycerol-derived compounds, their G-protein-coupled receptors (cannabinoid receptors CB1 and CB2) and the associated enzymes. Alterations of the ECS have been reported in both the brain and the immune system of ASD subjects. ASD children show low EC tone as indicated by low blood levels of endocannabinoids. Acetaminophen use has been reported to be associated with an increased risk of ASD. This drug can act through the ECS to produce analgesia. It may be that acetaminophen use in children increases the risk for ASD by interfering with the ECS.This mini-review article summarizes the current knowledge on this topic.

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Section: Acetaminophen Use May Increase the Risk For Asd Which Cousupporting

confidence: 91%

Endocannabinoid System Dysregulation from Acetaminophen Use May Lead to Autism Spectrum Disorder: Could Cannabinoid Treatment Be Efficacious?

Schultz

Gould

Antonucci³

et al. 2021

Molecules

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“…Paracetamol has been furthermore advocated for the pharmacological closure of a patent ductus arteriosus in very preterm infants, although its efficacy is not superior to oral ibuprofen [2,3]. Follow-up examinations of preterm infants at 2 and 5 years of age currently do not point to altered neurodevelopmental outcome following postnatal paracetamol administration [71][72][73], while analysis of data from a survey among parents on 1515 US children found an increased risk of ASD following postnatal paracetamol administration before age two in boys but not in girls [74]. As a matter of concern, none of the trials employing paracetamol for closure of a patent ductus arteriosus in preterm infants registered with www.clinicialtrials.gov list ADHD and ASD as secondary outcome.…”

Section: Postnatal Use Of Paracetamol In Term and Preterm Newborn Infantsmentioning

confidence: 99%

Paracetamol (Acetaminophen) and the Developing Brain

Bührer

Endesfelder

Scheuer

et al. 2021

IJMS

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Paracetamol is commonly used to treat fever and pain in pregnant women, but there are growing concerns that this may cause attention deficit hyperactivity disorder and autism spectrum disorder in the offspring. A growing number of epidemiological studies suggests that relative risks for these disorders increase by an average of about 25% following intrauterine paracetamol exposure. The data analyzed point to a dose–effect relationship but cannot fully account for unmeasured confounders, notably indication and genetic transmission. Only few experimental investigations have addressed this issue. Altered behavior has been demonstrated in offspring of paracetamol-gavaged pregnant rats, and paracetamol given at or prior to day 10 of life to newborn mice resulted in altered locomotor activity in response to a novel home environment in adulthood and blunted the analgesic effect of paracetamol given to adult animals. The molecular mechanisms that might mediate these effects are unknown. Paracetamol has diverse pharmacologic actions. It reduces prostaglandin formation via competitive inhibition of the peroxidase moiety of prostaglandin H2 synthase, while its metabolite N-arachidonoyl-phenolamine activates transient vanilloid-subtype 1 receptors and interferes with cannabinoid receptor signaling. The metabolite N-acetyl-p-benzo-quinone-imine, which is pivotal for liver damage after overdosing, exerts oxidative stress and depletes glutathione in the brain already at dosages below the hepatic toxicity threshold. Given the widespread use of paracetamol during pregnancy and the lack of safe alternatives, its impact on the developing brain deserves further investigation.

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“…However, information on long‐term outcome of large cohorts of preterm infants exposed to paracetamol with the attempt to endorse early closure of the ductus arteriosus is lacking. Unfortunately, this is a matter of urgency since there are several reports linking paracetamol exposure during pregnancy or in the neonatal period with adverse outcomes including autism spectrum disorder, attention deficit hyperactivity disorder, lower IQ and language delay 10–20 …”

Section: Introductionmentioning

confidence: 99%

Prophylactic low‐dose paracetamol for ductal closure and neurodevelopmental outcome in very preterm infants

et al. 2023

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Aim:To investigate the direct effect of prophylactic low-dose paracetamol administration for ductal closure on neurodevelopmental outcome in very preterm infants who did not receive ibuprofen or surgical ligation for treatment of a patent ductus arteriosus. Methods: Infants < 32 gestational weeks born 10/2014-12/2018 received prophylactic paracetamol (paracetamol group, n = 216); infants born 02/2011-09/2014 did not receive prophylactic paracetamol (control group, n = 129). Psychomotor (PDI) and mental (MDI) outcome were assessed using Bayley Scales of Infant Development at 12 and 24 months corrected age.Results: Our analyses showed significant differences in PDI and MDI at age 12 months (B = 7.8 (95% CI 3.90-11.63), p < 0.001 and B = 4.2 (95% CI 0.81-7.63), p = 0.016). At age 12 months, the rate of psychomotor delay was lower in the paracetamol group (OR 2.22, 95% CI 1.28-3.94, p = 0.004). There was no significant difference between the rates of mental delay at any time-point. All group differences remained significant after adjustment for potential confounders p < 0.001,, p = 0.013, PDI < 85 12 months OR 2.65 (95% CI 1.44-4.87), p = 0.002). Conclusion:We found no impairment of psychomotor and mental outcome at age 12 and 24 months in very preterm infants after prophylactic low-dose paracetamol administration.

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Postnatal Acetaminophen and Potential Risk of Autism Spectrum Disorder among Males

Cited by 11 publications

References 53 publications

Endocannabinoid System Dysregulation from Acetaminophen Use May Lead to Autism Spectrum Disorder: Could Cannabinoid Treatment Be Efficacious?

Endocannabinoid System Dysregulation from Acetaminophen Use May Lead to Autism Spectrum Disorder: Could Cannabinoid Treatment Be Efficacious?

Paracetamol (Acetaminophen) and the Developing Brain

Prophylactic low‐dose paracetamol for ductal closure and neurodevelopmental outcome in very preterm infants

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