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< Back FASD COVID-19 and Weakened Systems This is from a physician out of BC who assesses individuals with FASD and has a daughter with the condition as well. I think this is a nice piece on the increased risk of COVID19 with this population. He gave permission for this to be shared anywhere. April 3, 2020 Rod Densmore, M.D. Prenatal alcohol exposure (PAE) is common but often unrecognized. PAE causes immune dysfunction and increased risk of infections—a serious concern in this time of COVID-19 Fetal Alcohol Spectrum Disorder (FASD) is a condition diagnosed by strict criteria including proven prenatal alcohol exposure (PAE) and markedly significant impairments of function in at least 3 brain domains indicated by scores of minus 2 standard deviations or lower on standardized psychological testing in each domain. (1) Despite these strict diagnostic criteria, FASD has a high prevalence in the general population; it affects 1 in every 25 Canadians. (2) By comparison, 1 in 66 Canadian children is affected by Autism. (3) Popova et al. reported that overall, the estimated prevalence of FASD was 10-40 times higher for specific subpopulations (including adults and youth in correctional systems, children in foster care, special education populations, and psychiatric care populations) compared with the prevalence estimate for the global general population. (4) Specific populations, for instance, incarcerated young adults in a northern Canadian correctional population, have an even higher prevalence of FASD (17.5%; and this rate could have been 31.2% with confirmation of alcohol exposure). (5) Even higher portions of the population have been exposed to alcohol in utero, for example, a recent Australian study found that many women (60.6%) reported consuming alcohol between conception and pregnancy recognition. (6) Amongst children, FASD is very commonly underdiagnosed and misdiagnosed. (7) I know from personal experience working at the only two British Columbia clinics that can provide a diagnosis of FASD for adults that our provincial diagnostic capacity for this age group is very limited (20 or less individuals per year). Such low numbers of adults being diagnosed is discrepant with the published goals of the B.C. Provincial Government’s “Strategic Plan” for FASD—a document, released 12 years ago, that called for increased diagnostic capacity and supports. (8) One aspect of COVID-19 care that may not yet be fully considered by policymakers, physicians and the general population is the extent to which patients with FASD or prenatal exposure to alcohol (PAE) may have a degree of immune compromise. In addition to the humane imperative of providing adequate medical care for society’s most vulnerable patients—a group that includes many individuals with PAE—the general public’s safety may be threatened if a reservoir of COVID-19 infection persists in such an at-risk group. That reservoir could re-infect the general population once the first wave of COVID-19 infections subsides. In 2018 at the 8th International Research Conference on Adolescents and Adults with Fetal Alcohol Spectrum Disorder at UBC in Vancouver I presented these slides in a workshop titled: FASD is a Whole-Body Diagnosis, Part 2: Slide 1) Infections in FASD - Compared to healthy controls, chest and sinus infections are 2-3 x more common and chronic ear infections in adults are reported to be over 100 x more common in FASD (9) - Chronic or recurrent otitis media (middle ear infections) in FASD: 77.3% (10) - Siblings of children with FAS had an increased risk of death due to infectious disease. (11)- Children with FASD have more minor (ear and respiratory) and major (e.g. sepsis) infections; adult animals with PAE have enhanced disease severity of influenza caused by an impaired immune response to that virus. (12)Slide 2) Serious Infections in Fetal Alcohol Syndrome (FAS) discuses an older but detailed study done by Johnson in 1981 (13): Johnson studied 13 seriously ill patients, all of whom had FAS: 5/13 had pneumonia, 2 had meningitis and 1 had sepsis…compared to controls, patients with FAS had a different immune response to their infections; those with FAS had higher eosinophil counts, more abnormal gammaglobulins, diminished immune response to mitogen-induced stimulation and abnormal lymphocyte response to their infections. Slide 3) McGill, et al. (2009) found that mice with prenatal alcohol exposure (PAE) have impaired adaptive immune responses: decreased virus-specific lung CD8 T cells, and reduced production of influenza-specific antibody following influenza infection (14) Since 2018 I’ve become aware of the following information that further corroborates my concerns about immune system impairment for people that have had prenatal alcohol exposure (PAE). PAE is linked to 1) premature delivery and 2) immune system compromise; both these are risk factors for neonatal infections. (15) Even after controlling for low maternal income, smoking, and having a baby that was SGA, the researchers found that the newborns were three times more likely to have a neonatal infection if their mothers drank more than seven drinks per week during pregnancy (16). In addition, animal studies show that alcohol has a direct effect on specific aspects of immune function, particularly in the developing lung. (15)Studies in sheep find that prenatal ethanol exposure disrupts immune function by decreasing in the fetal lung surfactant proteins (SP), which also are known as collectins, particularly SP-A and SP-D (17) In the lung, these proteins are essential mediators of the local immune response in that they modulate the function of dendritic and T cells and facilitate the removal of pathogens by the alveolar macrophage (18) Sorenson et al. 2007). The alveolar macrophage is the resident inflammatory cell that provides the initial defense against foreign and infectious particles and orchestrates the inflammatory process within the lung (19). Alveolar macrophages reside in the lungs’ alveoli and are derived from peripheral circulating blood monocytes (19) As a consequence, anything that affects immune responses of fetal monocytes—for example, exposure to alcohol during pregnancy—may subsequently affect the alveolar macrophage population and the inflammatory environment within the newborn lung (20). Furthermore, substances that directly affect alveolar macrophages can, therefore, affect immunity in the infant's lung. Studies in animals found that fetal alcohol exposure decreases the antioxidant glutathione in the fluid lining the alveolar space and within the resident alveolar macrophages (21). Reductions in glutathione cause oxidative stress in the lung that, in turn, contributes to alveolar macrophage dysfunction and altered alveolar macrophage maturation (21) Bodnar and colleagues reported in 2020 that prenatal alcohol exposure results in activation of ofeotaxin-3, eotaxin, and bFGF. These immunomodulators have all been associated with the pathogenesis of asthma. There are subtle trends for increased asthma rates in children and adolescents with prenatal alcohol exposure, as well as data from animal models showing impairments in the immune environment of the lung (22).Gauthier and colleagues performed a case-controlled analysis of very low birth weight newborns born at Grady Memorial Hospital (Atlanta, GA). Alcohol exposure, as the predictive variable, was assessed by maternal self-report. Early-onset sepsis was 15-fold higher in the alcohol-exposed group compared with findings for the matched control group (23).Libster, et al. studied 3423 children hospitalized for respiratory infection in Buenos Aires, Argentina. Alcohol consumption during the last trimester was reported by 398 mothers (12.4%) and categorized as low (n = 210, 6.5%) or high (n = 188, 5.9%). A greater effect on life‐threatening respiratory infection, defined by low oxygen saturation was observed with higher alcohol intake due to all viruses and specifically RSV in the logistic regression analyses. Alcohol consumption was strongly associated with a life‐threatening disease, particularly in boys whose, adjusted odds ratio rose from 3.67 to 13.52 when their mothers drank alcohol. Alcohol consumption during pregnancy was associated with life‐threatening respiratory infections in boys. (24)Compared to children with no prenatal alcohol exposure, children with FASD were hospitalized more often with otitis media, pneumonia, and bronchitis. Higher amounts of prenatal alcohol exposure resulted in higher rates of infections severe enough to require hospitalization. (25)Reid and colleagues conducted a systematic review of all available literature regarding the effects of PAE on body systems other than the central nervous system. Notwithstanding the need for further study, particularly for older people with FASD, they found that exposure to early‐life adversity differentially impacted the immune system of offspring with PAE compared to controls, such that offspring with PAE showed a lack of responsivity to early‐life adversity. The authors suggested that PAE alters the development of the immune system, leading to inappropriate immune system responses that may be displayed when the system is challenged later in life. (26)Johnson et al found decreased lymphocyte levels because of PAE (13) and Oleson et al found increased levels (27). These apparently discordant results might be explainable because research subjects in each study group had different ethnic backgrounds. Although further study is needed to clarify the situation, initial data suggests PAE alters cellular immunity; specifically, compared to controls, PAE changes T and B lymphocyte response to infection and/or stress. Conditions that influence lymphocyte response to infection are of particular concern because the most common lab abnormality of COVID-19 patients is lymphopenia. (28) Animals exposed to PAE showed decreased levels of pro-inflammatory city lines in the spleen and hypothalamus (29). Lower cytokine levels in the spleen, an important immune organ, and the hypothalamus, an important integrator of immune and endocrine responses, may underlie the increased susceptibility to infection (29). Raineki et al. report: The pattern of early life adversity-induced cytokine changes in animals exposed to prenatal alcohol varied from non-exposed animals. Early-life adversity reduced serum TNF-α, KC/GRO, and IL-10 levels in control but not PAE animals. PAE increased serum CRP, and levels were even higher in pups exposed to adversity. Finally, PAE reduced KC/GRO and increased IL-10 levels in the amygdala. Our results indicate that PAE alters immune system development and both behavioral and immune responses to early-life adversity (30).Subjectively for me, though seven years old, Bodnar and Weinberg’s chapter in the book Neural-Immune Interactions in Brain Function and Alcohol-Related Disorders is the most helpful review of prenatal alcohol exposure-related immune impairment I could access. This is a brief excerpt: Studies on children exposed to alcohol prenatally have demonstrated impairments in immune competence in both innate and adaptive immunity. Adaptive immunity is MHC (major histocompatibility complex) restricted and can be classified as either cellular immunity, mediated by T lymphocytes, or humoral immunity, mediated by B lymphocytes. Innate immunity is not MHC restricted. Through phagocytes such as monocytes, macrophages, and polymorphonuclear leukocytes (PMNL), as well as natural killer cells and mediators such as complement and C-reactive protein, innate immunity provides a first line of defense against many common pathogens. Importantly, interactions between the innate and adaptive components of the immune system are necessary to launch effective immune responses. When controlling for many possible confounds including maternal smoking, low maternal income, and being small for gestational age, high levels of maternal drinking (7 or more drinks per week), specifically during the second trimester, was found to increase the risk of infection by approximately fourfold, compared to that in unexposed newborns. (31) Offspring sired by alcohol-consuming males exhibit decreased locomotor activity, an effect opposite to that seen with maternal alcohol exposure; show poorer adaptation to stress as measured in the forced swim task; and show increased susceptibility to infection (32). Taken together, regrettably, these articles are consistent with prenatal alcohol exposure (PAE) causing a degree of change and impairment of both humoral (involving chemicals such as antibodies and cytokines) and cellular (T and B lymphocytes and other immune cells) immunity. Being over 60 I have a higher risk from COVID-19 infection, so I must be even more careful than the average younger person about practicing prevention including keeping a social distance from others, frequently washing my hands, and staying home. I am also concerned for my patients who have FASD and my daughter who has FAS. Just like older people, those with FASD need to be even more careful in avoiding infection, because their immune systems are less able to deal with severe infection. My goal with this review is to alert other physicians, policy makers and health planners to the increased risk patients with FASD have. Regrettably, few of these patients are diagnosed with FASD so they are unlikely to be able to self-advocate. Screening tools for FASD can be accessed via the Public Health Agency of Canada’s webpage: National Screening Tool Kit for Children and Youth Identified and Potentially Affected by FASD. https://ken.childrenshealthcarecanada.ca/xwiki/bin/view/FASDScreeningToolkit/National+Screening+Tool+Kit+for+Children+and+Youth+Identified+and+Potentially+Affected+by+FASD The following link allows a download of The Asante Centre Youth Probation Officers’ Guide to FASD Screening and Referral: https://static1.squarespace.com/static/5afcc5b9e17ba38be3185853/t/5c76fa7a6e9a7f0763056bb1/1551301249598/Youth+Probation+Officers%27+Guide+to+FASD+Screening+and+Referral+%28Booklet+Format%29.pdf 1. Cook JL, Green CR, Lilley CM, Anderson SM, Baldwin ME, Chudley AE, et al. Fetal alcohol spectrum disorder: a guideline for diagnosis across the lifespan. Can Med Assoc J. February 16, 2016, 188(3) Pages 191-197. 2. CanFASD (Canada FASD Research Network): https://canfasd.ca/topics/prevalence/ 3. Autism Spectrum Disorder among Children and Youth in Canada 2018 A Report of the National Autism Spectrum Disorder Surveillance System: https://www.canada.ca/en/public-health/services/publications/diseases-conditions/autism-spectrum-disorder-children-youth-canada-2018.htmlhttps://www.canada.ca/en/public-health/services/publications/diseases-conditions/autism-spectrum-disorder-children-youth-canada-2018.html 4. Popova S, Lange S, Sheild K, Burd L, Rehm J. Prevalence of fetal alcohol spectrum disorder among special subpopulation: a systematic review and meta-analysis. Addiction. 2019;114 pages 1150-1172 doi:10.1111/add.14598 5. McLachlan K, McNeil A, Pei J, Brain U, Andrew G, Oberlander TF. Prevalence and characteristics of adults with fetal alcohol spectrum disorder in corrections: a Canadian case ascertainment study. BMC Public Health. 2019;19(1):43. Published 2019 Jan 9. doi:10.1186/s12889-018-6292-x 6. McCormack C, Hutchinson D, Burns L, et al. Alcohol Clin Exp Res. 2017;41(2):369‐378) 7. Chasnoff IJ, Wells AM, King L. Misdiagnosis and missed diagnoses in foster and adopted children with prenatal alcohol exposure. Pediatrics. 2015 Feb;135(2):264-70. doi: 10.1542/peds.2014-2171. Epub 2015 Jan 12. 8. https://www2.gov.bc.ca/assets/gov/health/managing-your-health/fetal-alcohol-spectrum-disorder/fetal_alcohol_spectrum_disorder_building_strengths.pdf 9. Himmelreich M, Lutke CJ, Travis E. 2017 Plenary Panel: The Lay of The Land: Final Results of a Health Survey of 500+ Adults with Diagnosed FASD. 7th International Conference on FASD. UBC. Vancouver. March 4, 2017 10. Popova S, Lange S, Sheild K, Mihic A, Chudley AE, Maukherjee RAS, Bekmuradov D, Rehm J. 2016. Comorbidity of Fetal alcohol Spectrum Disorder: a systemic review and meta-analysis. Lancet. 2016 Mar 5; Vol 387 No.10022 pages 978-987 11. Burd L, Klug MG, Martsolf JT. Increased sibling mortality in children with fetal alcohol syndrome. Addict Biol. 2004; 9(2): 179-86 12. Bodnar TS, Hill LA, Weinberg J. Evidence for an immune signature of prenatal alcohol exposure in female rats. Brain Behav Immun. 2016;58:130–141. doi: 10.1016/j.bbi.2016.05.022. 13. Johnson S, Knight R, Marmer DJ, Steele RW. Immune deficiency in fetal alcohol syndrome. Pediatr Res. 1981 Jun;15(6): 908-11 14. McGill J, Meyerholz DK, Edsen-Moore M, et al. Fetal exposure to ethanol has long-term effects on the severity of influenza virus infections. Journal of immunology (Baltimore, Md : 1950). 2009;182(12):7803-7808 15.Gauthier T.W. 2015. Prenatal alcohol Exposure and the Developing Immune System. Alcohol Research: Current Reviews Vol.37, No. 2, Pages 279-285 16. Gauthier TW, Drews-Botsch C, Falek A, et al. Maternal alcohol abuse and neonatal infection. Alcoholism: Clinical and Experimental Research. 2005a;29(6):1035–1043. 17. Lazic T, Wyatt TA, Matic M, et al. Maternal alcohol ingestion reduces surfactant protein A expression by preterm fetal lung epithelia. Alcohol. 2007;41(5):347–355. 18. Sorensen GL, Husby S, Holmskov U. Surfactant protein A and surfactant protein D variation in pulmonary disease. Immunobiology. 2007;212(4–5):381–416. 19. Fels AO, Cohn ZA. The alveolar macrophage. Journal of Applied Physiology. 1986;60(2):353–369. 20. Kramer BW, Ikegami M, Moss TJ, et al. Endotoxin-induced chorioamnionitis modulates innate immunity of monocytes in preterm sheep. American Journal of Respiratory and Critical Care Medicine. 2005;171(1):73–77. 21. Gauthier TW, Ping XD, Harris FL, et al. Fetal alcohol exposure impairs alveolar macrophage function via decreased glutathione availability. Pediatric Research. 2005b;57(1):76–81 22. Bodnar T.S., et al. 2020. Immune network dysregulation associated with child neurodevelopmental delay: modulatory role of prenatal alcohol exposure. Journal of Neuroinflammation. 17:39 pages 1-14 https://doi.org/10.1186/s12974-020-1717-8 23. Gauthier TW, et al. 2004. Is maternal alcohol use a risk factor for early-onset sepsis in premature newborns? Alcohol Vol 33, Issue 2, June 2004, Pages 139-145 24. Libster R, Ferolla FM, Hijano DR, Acosta PL, Erviti A, Polack FP, Network IR. Alcohol during pregnancy worsens acute respiratory infections in children. Acta Paediatr. 2015;104:e494–9. https://doi.org/10.1111/apa.13148 25.Kvigne VL, Leonardson GR, Borzelleca J, Neff-Smith M, Welty TK. Hospitalizations of Children Who Have Fetal Alcohol Syndrome or Incomplete Fetal Alcohol Syndrome. South Dakota Medicine. 2009 Mar;62(3):97, 99, 101-3. 26.Reid N, Moritz KM, Akison LK. Adverse health outcomes associated with fetal alcohol exposure: A systematic review focused on immune‐related outcomes. Pediatr Allergy Immunol. 2019;30:698–707 https://doi.org/10.1111/pai.13099 27. Oleson DR, Magee RM, Donahoe RM, Falek A, Coles CD. Immunity and prenatal alcohol exposure. In: Friedman H, Madden JJ, Klein TW, eds. Drugs of Abuse, Immunomodulation, and Aids. Advances in Experimental Medicine and Biology. Vol 437. Boston, MA: Springer; 1998:255‐264. 28. Ahmad O, Thomas A, Francispragasam M, Ahmad D. Emergency and Critical Care Management of COVID-19. March 24th, 2020 webinar on emergency and critical care. UBC Continuing Professional Development March 24th, 2020. 29. Bodnar TS, Hill LA, Weinberg J. Evidence for an immune signature of prenatal alcohol exposure in female rats. Brain Behav Immun. 2016;58:130‐141. 30. Raineki C, Bodnar TS, Holman PJ, Baglot SL, Lan N, Weinberg J. Effects of early-life adversity on immune function are mediated by prenatal environment: Role of prenatal alcohol exposure. Brain, Behavior and Immunity Volume 66, November 2017, Pages 210-220 https://doi.org/10.1016/j.bbi.2017.07.001 31. Bodnar T, Weinberg J. Chapter 10 Prenatal Alcohol Exposure: Impact on Neuroendocrine-Neuroimmune Networks in C. Cui et al. (eds.), Neural-Immune Interactions in Brain Function and Alcohol Related Disorders, DOI 10.1007/978-1-4614-4729-0_10, © Springer Science+Business Media, New York: 2013 Pages 307-357 32. Abel EL, Hazlett LS, Berk RS, Mutchnick MG. Neuroimmunotoxic effects in off- spring of paternal alcohol consumption. Prog Clin Biol Res. 1990. 325:47–55

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