当前位置: X-MOL 学术BioPsychoSoc. Med. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Iron deficiency anemia, stunted growth, and developmental delay due to avoidant/restrictive food intake disorder by restricted eating in autism spectrum disorder.
BioPsychoSocial Medicine ( IF 2.3 ) Pub Date : 2020-04-10 , DOI: 10.1186/s13030-020-00182-y
Yoshitoki Yanagimoto 1 , Yuko Ishizaki 1 , Kazunari Kaneko 1
Affiliation  

Autism spectrum disorder (ASD) is characterized by impairments in social communication, restricted repetitive and stereotyped patterns of behavior, interests and activities by impairment of imagination, and hyper and hyposensitivity. Food refusal, restricted eating, and problems of eating habits and patterns are more observed in ASD than typical development [1]. Of the characteristics, restricted eating is attributed to restricted behavior and mouth hypersensitivity [2]. Hypersensitivity in patients with ASD often involves the intraoral sense of touch, particularly texture and consistency [3]. Although most cases achieve spontaneous remission [4], severe malnutrition leading to stunted growth can sometimes occur in children with ASD [5, 6].

Cases of children with ASD complicated by restricted eating resulting in severe malnutrition are rarely reported. Here, we report the case of a 2-year-old boy with ASD with severe iron deficiency anemia (IDA) and stunted growth caused by restricted eating.

A 2-year-old boy presented with restricted eating, short stature, and failure to thrive. A local health center had diagnosed his condition as developmental delay and stunted growth. He was unable to eat any solid food and for the previous year had obtained his nutrients from breast milk and vegetable juice. He drank only specific brands of juice (only with his favorite tableware). He was taking no regular medication. Estimated daily energy intake based on dietary habits was approximately 650 kcal/day. His developmental history revealed language delay, obsessions, and repetitive behaviors. According to family history, his older brother had been diagnosed with ASD.

Physical examination revealed his height to be 74 cm (standard deviation [SD], − 3.9) and his weight to be 8.4 kg (SD, − 2.9). In addition, he looked pale and had tachycardia (132 bpm). Laboratory tests revealed severe microcytic hypochromic anemia (hemoglobin, 5.9 g/dL; mean corpuscular volume, 57.8 fL; mean corpuscular hemoglobin, 13.9 pg; serum iron, 14 μg/dL; ferritin, 7.5 ng/dL; TIBC, 447 μg/dL; and UIBC, 380 μg/dL). Two types of developmental assessment were performed. The Kyoto Scale of Psychological Development 2001 [7] revealed a developmental quotient (DQ) of 68. His Pervasive Developmental Disorders Autism Society Japan Rating Scale (PARS) score was 6 (above the ASD cut-off score). A developmental and behavioral pediatrics specialist diagnosed ASD using the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) [8] diagnostic criteria and the PARS score. There was no evidence of suspected child abuse or maltreatment.

Based on these findings, the patient was diagnosed with IDA and malnutrition due to avoidant/restrictive food intake disorder (ARFID) (DSM-5) [8] related to ASD. We orally administered iron supplements (3 mg/kg/day) and enteral nutrients (600kcaL/day); fortunately, he took these by his favorite tableware without resistance. His anemia, nutritional condition, and clinical symptoms improved by treatment within 1 month. Hemoglobin, serum iron, and ferritin had also increased at that time to 10.5 g/dL, 168 μg/dL, and 32 ng/dL, respectively. Iron supplements were finished in 5 months and enteral nutrient were continued for 2 years. In parallel with nutritional replenishment, his height and weight improved to approximately − 1 SD, within the normal range, within 1 year (Fig. 1) [9]. In addition, he started eating a greater variety of foods, and his DQ and nutritional condition improved with nutritional replenishment. Hemoglobin, serum iron, and ferritin at that time had also increased to 12.6 g/dL, 108 μg/dL, and 21.2 ng/dL, respectively, all within the normal range.

Fig. 1
figure1

Clinical course of height, weight and deveropment

Full size image

ARFID is an eating/feeding disturbance caused by apparent lack of interest in eating or food, avoidance based on the sensory characteristics of food, and concern about aversive consequences of eating [8]. Kristoffer reported that cases of ARFID caused by restricted eating or food refusal in ASD need forced nutrition therapy more frequently than those with typical development [10]. We successfully treated a 2-year-old boy with IDA and failure to thrive because of ARFID, which we considered to be caused by restrictive eating behavior and hypersensitivity associated with ASD. Hypersensitivity in patients with ASD often involves the intraoral sense of touch, particularly texture and consistency [3]. In this case, because he was able to drink specific liquids (breast milk and vegetable juice) and liquid forms of enteral nutrients we concluded that the consistency and taste of food and drink restricted his eating habits.

Previous studies have postulated various patterns of restrictive eating and deficiency (e.g., vitamin D deficiency [11]) and suggested that the incidence of iron deficiency is higher in ASD [12, 13]. Hence, restricted eating might lead not only to a lack of energy but also iron deficiency, resulting in IDA. However, there are no previous studies on this topic, except a few case reports and analyses of elemental deficiency in ASD, neither of which mention clinical problems.

He was able to take enteral nutrients without resistance. We think there are two reasons he was able to take enteral nutrients in spite of his severe food restriction. First, he took the nutrients in his favorite tableware. Second, he fortunately preferred the taste of the nutrients. In case of the patients with severe malnutrition, we should choose forced nutrition by nasogastric tube if sufficient nutrients cannot be taken orally..

It is of note that nutritional treatment improved not only his malnutrition and stunted growth but also his food selectivity and developmental delay, suggesting that malnutrition worsens developmental delay and food selectivity. We believe that malnutrition and anemia due to iron deficiency caused hypocirculation in the brain and digestive organs and promoted repetitive eating. As the IDA improved, physical growth and repetitive eating improved.

In conclusion, this case suggests that restricted eating is a risk factor for severe malnutrition, especially in ASD. We recommend that IDA and nutritional condition should be evaluated when an autistic child presents with restricted eating behavior and pallor.

Not applicable.

ASD:

Autism spectrum disorder

IDA:

Iron deficiency anemia

ARFID:

Avoidant/restrictive food intake disorder

  1. 1.

    Zimmer MH, Hart LC, Manning-Courtney P, et al. Food variety as a predictor of nutritional status among children with autism. J Autism Dev Disord. 2012;42:549–56.

    • Article
    • Google Scholar
  2. 2.

    Hubbard KL, Anderson SE, Curtin C, et al. A comparison of food refusal related to characteristics of food in children with autism spectrum disorder and typicaly developing children. J Acad Nutr Diet. 2014;114:1981–7.

    • Article
    • Google Scholar
  3. 3.

    Hubbard KL, Anderson SE, Curtin C, Must A, Bandini LG. A comparison of food refusal related to characteristics of food in children with autism spectrum disorder and typically developing children. J Acad Nutr Diet. 2014;114:1981–7.

    • Article
    • Google Scholar
  4. 4.

    Sharp WG, Berry RC, McCracken C, et al. Feeding problems and nutrient intake in children with autism spectrum disorders: A meta-analysis and comprehensive review of the literature. J Autism Dev Disord. 2013;43:2159–73.

    • Article
    • Google Scholar
  5. 5.

    Keown K, Bothwell J, Jain S. Case report: Nutritional implications of selective eating in a child with autism spectrum disorder. BMJ Case Rep. 2014;2014:bcr2013202581. https://doi.org/10.1136/bcr-2013-202581.

    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  6. 6.

    Tanoue K, Matsui K, Takamasu T. Fried patato diet causes vitamin A deficiency in an autistic child. J Parenter Enteral Nutr. 2012;36:753–5.

    • Article
    • Google Scholar
  7. 7.

    Koyama T, Osada H, Tsujii H, Kurita H. Utility of the Kyoto scale of psychological development in cognitive assessment of children with pervasive developmental disorders. Psychiatry Clin Neurosci. 2009;63:241–3.

    • Article
    • Google Scholar
  8. 8.

    American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Wasington: (DSM 5). American Psychiatric Press; 2013.

    • Google Scholar
  9. 9.

    Isojima T, Kato N, Ito Y, et al. Growth standard charts for Japanese chileren with mean and standard deviation (SD) values based on the year 2000 national survey. Clin Pediatr Endocrinol. 2016;25:71–6.

    • Article
    • Google Scholar
  10. 10.

    Berlin KS, Lobato DJ, Pinkos B, et al. Patterns of medical and developmental comorbidities among children presenting with feeding problems: a latent class analysis. J Dev behave Pediatr. 2011;32:41–7.

    • Article
    • Google Scholar
  11. 11.

    Matsuoka A, Atui K, Matui J, et al. A case of Vitamin D deficiency rickets caused by feeding problems with autism spectrum disorder. J Jpn Pediatr Soc. 2016;120:1637–42.

    • Google Scholar
  12. 12.

    Mari-Bauset S, Llopis-Gonzalez A, Zazpe-Garcia I, et al. Nutritional status of children with autism spectrum disorders (ASDs): a case-control study. J Autism Dev Disord. 2015;45:203–12.

    • Article
    • Google Scholar
  13. 13.

    Sidrak S, Yoong T, Woolfenden S. Iron deficiency in children with global developmental delay and autism spectrum disorder. J Paediatr Child Health. 2014;50:356–61.

    • Article
    • Google Scholar

Download references

We thank Diane Williams, PhD, from Edanz Group (www.edanzediting.com/ac) for editing a draft of this manuscript.

This case report was not supported by any funding.

Affiliations

  1. Department of Pediatrics, Kansai Medical University Medical Center, 10-15 Fumizonocho, Moriguchi, Osaka, 570-8507, Japan
    • Yoshitoki Yanagimoto
    • , Yuko Ishizaki
    •  & Kazunari Kaneko
Authors
  1. Yoshitoki YanagimotoView author publicationsYou can also search for this author in
    • PubMed
    • Google Scholar
  2. Yuko IshizakiView author publicationsYou can also search for this author in
    • PubMed
    • Google Scholar
  3. Kazunari KanekoView author publicationsYou can also search for this author in
    • PubMed
    • Google Scholar

Contributions

Y.Y. and Y.I. cared for the patient and wrote the manuscript. K.K. reviewed the manuscript and supervised the entire study process. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Yoshitoki Yanagimoto.

Ethics approval and consent to participate

Not applicable.

Consent for publication

Written informed consent was obtained from the patient and his parents for publications.

Competing interests

The authors declare that they have no competing interests.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

Verify currency and authenticity via CrossMark

Cite this article

Yanagimoto, Y., Ishizaki, Y. & Kaneko, K. Iron deficiency anemia, stunted growth, and developmental delay due to avoidant/restrictive food intake disorder by restricted eating in autism spectrum disorder. BioPsychoSocial Med 14, 8 (2020). https://doi.org/10.1186/s13030-020-00182-y

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s13030-020-00182-y

Keywords

  • Autism spectrum disorder
  • Avoidant/restrictive food intake disorder
  • Restricted eating
  • Iron deficiency anemia


中文翻译:

由于自闭症谱系障碍者进食受限/避免进食/限制性进食障碍,导致缺铁性贫血,生长发育迟缓和发育延迟。

自闭症谱系障碍(ASD)的特征是社交沟通受损,行为,兴趣和活动受到重复性和刻板印象的限制,想象力受损,超敏和低敏。与典型的发展相比,在ASD中观察到拒食,饮食受限以及饮食习惯和饮食习惯问题[1]。在这些特征中,进食受限归因于行为受限和口部过敏[2]。ASD患者的超敏反应通常涉及口内触觉,尤其是质地和一致性[3]。尽管大多数情况下都能自发缓解[4],但患有自闭症的儿童有时会出现严重的营养不良,导致发育迟缓[5,6]。

很少报告患有自闭症儿童并伴有饮食不当导致严重营养不良的病例。在这里,我们报道了一名2岁男孩患有严重铁缺乏性贫血(IDA)并因进食受限而发育迟缓的ASD病例。

一个2岁男孩的进食受限,身材矮小且无法ive壮成长。当地的一家健康中心将他的病情诊断为发育迟缓和发育迟缓。他无法吃任何固体食物,前一年他从母乳和蔬菜汁中获取了营养。他只喝特定品牌的果汁(只能搭配他最喜欢的餐具)。他没有定期服药。根据饮食习惯估计的每日能量摄入量约为650 kcal /天。他的发展历史显示语言延迟,痴迷和重复行为。根据家族史,他的哥哥被诊断出患有ASD。

身体检查显示他的身高为74厘米(标准偏差[SD],-3.9),体重为8.4公斤(SD,-2.9)。此外,他面色苍白,心动过速(132 bpm)。实验室检查发现严重的小细胞性贫血性贫血(血红蛋白,5.9 g / dL;平均红细胞体积,57.8 fL;平均红细胞血红蛋白,13.9 pg;血清铁,14μg/ dL;铁蛋白,7.5 ng / dL; TIBC,447μg/ dL ;以及UIBC,380μg/ dL)。进行了两种类型的发展评估。《 2001年京都心理发展量表》 [7]显示发育商(DQ)为68。他的普遍性发展障碍自闭症协会日本评定量表(PARS)得分为6(高于ASD截止得分)。发育和行为儿科专家使用《精神障碍诊断和统计手册》(DSM-5)[8]诊断标准和PARS评分诊断为ASD。没有证据表明有虐待儿童或虐待儿童的嫌疑。

基于这些发现,该患者被诊断出患有与ASD相关的回避/限制性食物摄入障碍(ARFID)(DSM-5)[8],并患有营养不良。我们口服铁补充剂(3 mg / kg /天)和肠内营养素(600kcaL /天);幸运的是,他毫不犹豫地用自己喜欢的餐具拿走了这些东西。通过治疗1个月,他的贫血,营养状况和临床症状得到改善。那时血红蛋白,血清铁和铁蛋白也分别增至10.5 g / dL,168μg/ dL和32 ng / dL。铁补充剂在5个月内完成,肠内营养持续2年。在补充营养的同时,他的身高和体重在一年之内在正常范围内提高到大约-1 SD(图1)[9]。此外,他开始吃更多的食物,营养补充改善了他的DQ和营养状况。那时的血红蛋白,血清铁和铁蛋白也分别增至12.6 g / dL,108μg/ dL和21.2 ng / dL,均在正常范围内。

图。1
图1

身高,体重和发育的临床过程

全尺寸图片

ARFID是一种饮食/进食障碍,是由于对饮食或食物明显缺乏兴趣,基于食物的感官特性而回避以及对饮食的厌恶后果引起的关注[8]。克里斯托弗(Kristoffer)报告说,由于ASD进食受限或拒绝进食而引起的ARFID病例比典型发育的病例更需要强迫营养治疗[10]。我们成功治疗了一名2岁男孩IDA并因ARFID而无法failure壮成长,我们认为这是由于进食受限和与ASD相关的超敏反应所致。ASD患者的超敏反应通常涉及口内触觉,尤其是质地和一致性[3]。在这种情况下,

先前的研究提出了各种限制进食和缺乏的模式(例如,维生素D缺乏症[11]),并提示ASD中铁缺乏症的发生率更高[12,13]。因此,进食受限可能不仅会导致精力不足,还会导致铁缺乏,从而导致IDA。但是,除少数病例报告和对ASD元素缺乏的分析外,没有关于该主题的先前研究,都未提及临床问题。

他能够无阻力地摄取肠内营养。我们认为,尽管他严格限制了食物,他还是能够摄取肠内营养,这有两个原因。首先,他从自己喜欢的餐具中吸收了营养。其次,他幸运地喜欢营养的味道。对于严重营养不良的患者,如果不能口服足够的营养,应选择经鼻胃管强制营养。

值得注意的是,营养治疗不仅改善了他的营养不良和生长发育迟缓,而且改善了他的食物选择性和发育延迟,这表明营养不良加剧了发育延迟和食物选择性。我们认为,由于铁缺乏引起的营养不良和贫血会导致大脑和消化器官循环不足,并促进反复进食。随着IDA的改善,身体发育和反复进食得到改善。

总之,该病例表明进食受限是造成严重营养不良的危险因素,特别是在自闭症患者中。我们建议当自闭症儿童的进食行为受到限制且脸色苍白时,应评估IDA和营养状况。

不适用。

ASD:

自闭症谱系障碍

IDA:

缺铁性贫血

ARFID:

回避/限制性食物摄入障碍

  1. 1。

    Zimmer MH,Hart LC,Manning-Courtney P等。食物种类可作为自闭症儿童营养状况的预测指标。J自闭症发展障碍。2012; 42:549–56。

    • 文章
    • 谷歌学术
  2. 2。

    Hubbard KL,Anderson SE,Curtin C等。比较自闭症谱系障碍儿童和典型发育中儿童的食物拒绝与食物特征相关。J Acad食品饮食。2014; 114:1981-7。

    • 文章
    • 谷歌学术
  3. 3。

    哈伯德(KL),安德森(Anderson),科廷(Curtin),穆斯塔(A),班迪尼(Bandini)LG 孤独症谱系障碍儿童和典型发育中儿童与食物特征相关的拒绝食物比较。J Acad食品饮食。2014; 114:1981-7。

    • 文章
    • 谷歌学术
  4. 4。

    Sharp WG,Berry RC,McCracken C等。自闭症谱系障碍儿童的进食问题和营养摄入:荟萃分析和文献综述。J自闭症发展障碍。2013; 43:2159-73。

    • 文章
    • 谷歌学术
  5. 5,

    Keown K,Bothwell J,Jain S.病例报告:自闭症谱系障碍儿童选择性进食的营养意义。BMJ案件代表.2014; 2014:bcr2013202581。https://doi.org/10.1136/bcr-2013-202581。

    • 文章
    • 考研
    • PubMed Central
    • 谷歌学术
  6. 6。

    Tanoue K,Matsui K,Takamasu T.炸土豆饼饮食导致自闭症儿童维生素A缺乏。J父母肠内营养食品。2012; 36:753-5。

    • 文章
    • 谷歌学术
  7. 7。

    Koyama T,Osada H,Tsujii H,Kurita H.《京都议定书》的心理发展量表在普遍性发育障碍儿童的认知评估中的作用。精神病学临床神经科学。2009; 63:241–3。

    • 文章
    • 谷歌学术
  8. 8。

    美国精神病学协会。精神疾病诊断与统计手册。第五版。沃辛顿:(DSM 5)。美国精神病学出版社;2013。

    • 谷歌学术
  9. 9。

    Isojima T,Kato N,Ito Y等。日本chileren的生长标准图,具有根据2000年全国调查得出的均值和标准差(SD)值。临床儿科内分泌。2016; 25:71–6。

    • 文章
    • 谷歌学术
  10. 10。

    柏林KS,Lobato DJ,Pinkos B等。出现喂养问题的儿童的医学和发育合并症的模式:潜在类别分析。J Dev表现儿科。2011; 32:41–7。

    • 文章
    • 谷歌学术
  11. 11。

    Matsuoka A,Atui K,Matui J等。一例由自闭症谱系障碍的进食问题引起的维生素D缺乏性rick病。J Jpn Pediatr Soc。2016; 120:1637–42。

    • 谷歌学术
  12. 12

    Mari-Bauset S,Llopis-Gonzalez A,Zazpe-Garcia I等。自闭症谱系障碍(ASD)儿童的营养状况:一项病例对照研究。J自闭症发展障碍。2015; 45:203–12。

    • 文章
    • 谷歌学术
  13. 13

    Sidrak S,Yoong T,Woolfenden S.全球发育迟缓和自闭症谱系障碍儿童的铁缺乏症。J Paediatr儿童保健。2014; 50:356–61。

    • 文章
    • 谷歌学术

下载参考

感谢Edanz Group(www.edanzediting.com/ac)的Diane Williams博士编辑此手稿的草稿。

该案例报告没有任何资金支持。

隶属关系

  1. 关西医科大学医学中心儿科,大阪府守口市文佐町10-15,大阪570-8507
    • 柳本佳人
    • ,石崎裕子
    •  &Kazunari Kaneko
s
  1. Yanatoki Yanagimoto查看作者出版物您也可以在以下位置搜索该作者
    • 考研
    • 谷歌学术
  2. 石崎裕子查看作者出版物您还可以在以下位置搜索该作者
    • 考研
    • 谷歌学术
  3. Kazunari Kaneko查看作者出版物您也可以在以下位置搜索该作者
    • 考研
    • 谷歌学术

会费

YY和YI照顾病人并撰写了手稿。KK审查了手稿并监督了整个学习过程。所有作者阅读并认可的终稿。

通讯作者

对应于柳本良之。

道德规范的批准和同意参加

不适用。

同意发表

从患者及其父母那里获得了书面知情同意书,以供发表。

利益争夺

作者宣称他们没有竞争利益。

发行人须知

对于出版的地图和机构隶属关系中的管辖权主张,Springer Nature保持中立。

开放存取本文是根据知识共享署名4.0国际许可许可的,该许可允许以任何媒介或格式使用,共享,改编,分发和复制,只要您对原始作者和出处提供适当的信誉,链接到知识共享许可,并指出是否进行了更改。本文的图像或其他第三方材料包含在该文章的知识共享许可中,除非在该材料的信用栏中另有说明。如果该材料未包含在该文章的创用CC许可中,并且您的预期用途未得到法律法规的许可或超出了许可的用途,则您需要直接获得版权所有者的许可。要查看此许可证的副本,请访问http://creativecommons.org/licenses/by/4.0/。

转载和许可

通过CrossMark验证货币和真实性

引用本文

Y.Yanagimoto,Y.,Ishizaki,Y.&Kaneko,K.由于自闭症谱系障碍者进食受限/回避/限制性食物摄入紊乱,导致缺铁性贫血,发育迟缓和发育迟缓。BioPsychoSocial Med 14,14(2020)。https://doi.org/10.1186/s13030-020-00182-y

下载引文

  • 收到

  • 已接受

  • 发表时间

  • DOI https //doi.org/10.1186/s13030-020-00182-y

关键词

  • 自闭症谱系障碍
  • 回避/限制性食物摄入障碍
  • 限制饮食
  • 缺铁性贫血
更新日期:2020-04-10
down
wechat
bug