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Hypocalcemic Seizure in an Adolescent withObesity and AutismDepartment of Pediatrics. Lincoln Medical andMental Health Center, Bronx NY. Weill-Cornell Medical College, New York, NY Case    A 12-year-old Hispanic girl withsevere autism spectrum disorder (ASD), intellectual disability, and obesitypresented to the emergency department (ED) in the middle of winter with anepisode of unprovoked, tonic-clonic seizure that lasted 8 minutes.  Upon arrival to the ED she was afebrile 97.6°F , pulse 110/min, respiratory rate 20/min, blood pressure 103/56 mmHg, O2 Sat97% on room air, weight was 63.

6 kg (95th %), height was 155 cm (61st%) and Body Mass Index (BMI) was 26.4 (96th %). During examinationshe was alert and awake. There was no facial dysmorphism and no findings ofrickets.

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The neurological exam showed no focal deficits, tremors, or other involuntarymovements. Tanner stage of puberty was 4. She showed limited social interactions and her communication skillswere limited to use of short phrases and significant echolalia. Past medical history was remarkable for beingthe product of a twin pregnancy and premature delivery at 24 weeks ofgestation. Since the patient was 3 years old, her diet consisted exclusively offrench fries with ketchup and Doritos® (corn chips), water and Sunny-Delight® (anorange flavored, sugar-containing beverage). For years, the mother hadunsuccessfully made numerous attempts to expand the child’s diet. Because ofthis limited intake a nutritional drink (Pediasure®) was used as a supplementfor several years. It was discontinued two years prior to this episode becauseof the child’s worsening obesity.

Her exposure to sunlight was limited because of her difficultbehaviors coupled with long harsh winters.  The laboratory evaluation was remarkable forsevere hypocalcemia, very low levels of Vitamin D and secondaryhyperparathyroidism (Table 1). The rest of the blood work was within normallimits.   Table 1   On admission Normal values Calcium (mg/dL) 6.

0 8.4-10.5 Ionized Calcium(mg/dL) 3.4 4.5-5.3 PTH (Pg/ml) 309.9 14-72 Vit D (ng/dl) < 0.4 30-100 Magnesium (mg/dL) 2.

0 1.6-2.5 Phosporus (mg/dL) 4.1 2.7-4.5 TSH (IU/ml) 3.31 0.

27-4.20 Albumin (g/dL) 2.7 3.7-5.1 Total Protein (g/dL) 5.2 6.3-8.

2 ALT (U/L) 30 13-56 AST (U/L) 22 15-37 Hemoglobin (g/dL) 12.7 12-15 Hematocrit (%) 37.2 35-49 RDW (%) 14.2 12-15  She received IV infusion of Calcium gluconatefollowed by oral calcium glubionate 150 mg TID (115 mg/5ml) and ergocalciferol 8,000IU daily. She was responsive to the management andremained seizure-free without anticonvulsants.  Upon discharge, Vitamin D and calcium weremixed with ketchup. Her diet, which continued to consist of fries, Doritos® andPediasure®, was restarted.

Behavioral interventions continued to be used toexpand the repertoire of food. Upon follow up 3 weeks later, Vit D was 20.7ng/ml, the rest of the laboratory tests were within normal limits, and sheremained asymptomatic. Discussion Autism spectrum disorder (ASD) is a group of complex, heterogeneousneurodevelopmental conditions characterized by impairments in socialinteraction and social communication.

The etiology of ASD is multifactorial,based on the interplay of genetic predisposition and environmental influences. ASD isusually diagnosed in early childhood when the developmental trajectory of thechild becomes atypical.  For an autismspectrum disorder to be diagnosed, the child must fulfill criteria based on theDSM 5 (Diagnosis and Statistical Manual version 5)1. There must bepersistent deficits in social communication and social interaction acrossmultiple contexts including 1) deficits in social-emotional reciprocity, 2)deficits in nonverbal communicative behaviors used for social interaction and3) deficits in developing, maintaining, and understanding relationships. Thechild must also show at least 2 features of restricted, repetitive patterns ofbehavior, interests, or activities, presenting as 1) stereotyped or repetitivemotor movements, use of objects, or speech; 2) insistence on sameness,inflexible adherence to routines, or ritualized patterns of verbal or nonverbalbehavior; 3) highly restricted, fixated interests that are abnormal inintensity or focus and 4) hyper or hypo-reactivity to sensory input or unusualinterest in sensory aspects of the environment1.

 This lastfeature, hypo or hyperreactivity to sensory inputs is commonly seen in ASD, andhas become a diagnostic criteria since it was included in the DSM 5. Among awide range of atypical behaviors, children with ASD often have atypical feedingbehaviors, of which food selectivity is the most common 2,3,4. Forthe most part, even autistic children with food selectivity achieve growthadequacy2. Children with more severe autism and challengingbehaviors may have increased food selectivity and this can cause significant stressfor the families 2,4 .  Foodselectivity may include food refusal, eating a decreased variety of food, or ahigh frequency of a single food. Diets may be selectively rich in protein orstarch or have sensory aspects like particular textures or flavors 5.There are many theories about the possible reasons for selective diets,including sensory sensitivity3. These feeding difficulties may leadto nutritional deficiencies, including Vitamin D Deficiency (VDD) and irondeficiency anemia 6.

 VDD during pregnancy or early childhood has been proposed as a possibleenvironmental trigger in the pathogenesis of ASD7. Specific geneticpolymorphism found in some children with ASD encode the vitamin D bindingprotein. Several clinical trials have demonstrated that Vitamin Dsupplementation can improve core symptoms in children with ASD8.   Vitamin D is a pro-hormone, a normal level of which is necessary foradequate calcium absorption from the gut. In a vitamin D deficient state, the intestinalabsorption of calcium decreases significantly causing hypocalcemia. Phosphateabsorption decreases with calcium absorption too. When ionized calciumdecreases, it stimulates Parathyroid Hormone (PTH) secretion which increasescalcium reabsorption from the renal tubules and activates 1-?-hydroxylaseenzyme increasing an active version of 1,25(OH)2 vitamin D. Hyperparathyroidismalso increases the loss of renal phosphorous.

Decrease in calcium-phosphorusproduct results in decreased bone mineralization leading to osteopenia, whichincreases the risk for bone deformities and fractures. Skin is a major contributor of circulating vitamin D, which issynthesized from its exposure to ultraviolet B (UV-B) radiation. So naturalsunscreen, melanin pigmentation, and the use of artificial sunscreen affectsits production. Other causes of decreased skin production of vitamin D include skincovering such ethnic clothing, limited exposure to sun in winter months, or tofear of skin cancer. Vitamin D is present in oily fish, cod liver oil, dairyproducts, and vitamin D fortified food or drinks. Children and adolescents whoavoid nutrition rich in vitamin D naturally become at high risk for itsdeficiency. The suggested requirement for Vit D is 400 IU/d (IU=25 ng) ininfants 0 to 1 year old, and 600 IU/d in children older than 1 year.

 The current Endocrine Society clinical practice guideline9recommends screening for VDD in at-risk individuals such as obese children; African-Americanand Hispanic children; pregnant and lactating women; children with physicalfindings of rickets, chronic kidney disease, hepatic failure, malabsorptionsyndromes; and patients on medication like anticonvulsants, glucocorticoids,  antifungals such as ketoconazole, andmedications for AIDS. ASD and other developmental delays are not quoted as riskfactors for VDD screening. The recommended screening method is to measure serumcirculating 25-hydroxyvitamin D 25(OH)D level by a reliable essay9.  Vitamin D deficiency is defined as a 25(OH)Dbelow 20 ng/ml and insufficiency as a 25(OH)D  of 21 to 29 ng/ml 9. The prevalence ofvitamin D deficiency increases with weight: among healthy-weight, overweight, obese, and severely obese children was21%, 29%, 34%, and 49%, respectively10. VDD isalso oftendecreased in children with autism and other neurodevelopmental conditions likeepilepsy 11,12.

In addition, lack of sun exposure on the easterncoast of North America during winter puts children at higher risk for Vitamin Ddeficiency 13. Clinical features of vitamin D deficiency range from asymptomatic tobone pain, irritability, delay in motor development, rickets in growingchildren or osteomalacia in adults. Hypocalcemic seizures as a presenting signof VDD is commonly reported in infancy14 but rarely seen inadolescents  15 ,  periods of higher metabolic demand of calcium. An extreme deficiency of Vitamin D, after thecalcium storage has been depleted, can lead to hypocalcemic seizures. Theseoccur mostly in the newborn period. A case of hypocalcemic seizure in a girl with Down syndrome,celiac disease and VDD secondary to malabsorption was also reported recently16. Seizures as an initial presentation of Vitamin D Deficiency are uncommonin older children17,and are rare overall: a recent British publication reports a frequencyof 3.

49 per million children ages 0-15 (95% CI: 2.81-4.26) in the UK andIreland17. In thisstudy, South Asian andBlack ethnic groups were at the highest risk of symptomatic VDD, but autismwith a restricted diet was also noted in only 2 white adolescents with hypocalcemicseizures17.  Our case is a rare case of a first afebrileseizure as a manifestation of hypocalcemia secondary to severe vitamin Ddeficiency in a light-skin adolescent female with autism, intellectual disability,and obesity with food restrictions.  Sinceher diet was extremely restricted, the use of a nutritional supplementation waslikely the main or only food source of Vitamin D for this child. Ourspeculation is that the discontinuation of the nutritional supplement(Pediasure), her only source lead to vitamin D deficiency and eventually causeda hypocalcemic seizure.

There are no records of previous Vit D levels in thepatient before she presented to our emergency department. Her diet had notimproved with the behavioral approaches informally tried by the family andschool. However, there are studies reporting that interdisciplinary feedingprograms successfully improve challenging feeding behaviors 18 andthis was offered to the mother.  Conclusion  Hypocalcemic seizures due to Vitamin D deficiency secondary to dietaryrestriction are rare in children beyond the neonatal period. A higher level ofalertness must be maintained in the presence of dietary restrictions inchildren with developmental disabilities. Current endocrine societypractice guidelines do not include autism or other developmental disorder as anindication for screening for VDD.

Further studies are therefore needed to establishthe connection between autism spectrum disorder and Vitamin D deficiency.   References: American Psychiatric Association. (2013). Diagnostic and statistical manualof mental disorders (5th ed.) Washington, DC Postorino V, Sanges V,Giovagnoli G, Fatta LM, De Peppo L, Armando M, Vicari S, Mazzone L.

Clinicaldifferences in children with autism spectrum disorder with and without foodselectivity. Appetite 2015 Sep; 92:126-32. doi: 10.1016/j.appet.2015.05.

016 Cermak SA, Curtin C, Bandini LG. Food selectivity and sensorysensitivity in children with autism spectrum disorders. Journal of theAmerican Dietetic Association. 2010;110(2):238-246. doi:10.1016/j.jada.2009.

10.032 Prosperi M, Santocchi E,Balboni G, Narzisi A, Bozza M, Fulceri F, Apicella F, Igliozzi R, Cosenza A,Tancredi R, Calderoni S, Muratori F. Behavioral Phenotype of ASD Preschoolerswith Gastrointestinal Symptoms or Food Selectivity. J Autism Dev Disord (2017) 47: 3574. doi:10.

1007/s10803-017-3271-5. Bandini LG, Anderson SE, Curtin C, Cermak S, Evans EW, Scampini R,Maslin M, Must A. Food selectivity in children with autism spectrum disordersand typically developing children. TheJournal of pediatrics. 2010 Aug 31;157(2):259-64. Bener A, Khattab AO, Bhugra D,Hoffman GF. Iron and Vitamin D levels among autism spectrum disorders children.Ann Afr Med 2017 Oct-Dec; 16 (4); 186-191.

doi: 10.4103/aam.aam_17_17. Kocovska E, Fernell E,Billsteadt E, MInnis H, Gillberg C.

Vitamin D and autism: clinical review. Res Dev Disabil 2012 Sep-Oct;33(5):1541-50. doi: 10.1016/j.ridd.2012.

02.015. Jia F, Shan L, Wang B, Li H,Miao C, Xu Z, Lin CP, Saad K. Bench to bedside review: Possible role of vitaminD in autism spectrum disorder. PsychiatryRes 2017 Dec 6;260:360-365. doi:10.

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005. Holick MF, Binkley NC,Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Hassan Murad M, Weaver CM.Evaluation, Treatment, and Prevention of Vitamin D Deficiency: an EndocrineSociety Clinical Practice Guideline. J Clin Endocrinol Metab. 2011Jul;96(7):1911-30. doi: 10.1210/jc.2011-0385.

 Turer CB, Lin H, Flores G. Prevalence of vitamin Ddeficiency among overweight and obese US children. Pediatrics. 2013 Jan 1;131(1):e152-61. doi:10.1542/peds.

2012-1711. Sonmez FM, Donmez A, Namuslu M,Canbal M, Orun E. Vitamin D Deficiency in Children with Newly DiagnosedEpilepsy. J Child Neurol 2015 Oct 30(11): 1428-32. doi: 10.1177/0883073814566627. Favero de Souza Tostes MH,Polonini HC, Gattaz WF, Barbosa NR, Baptista EB.

Low serum levels of25-hydroxyvitamin D (25-OHD) in children with autism. Trends Psychiatry Psychother 2012;34(3) 161-163.  Hanley DA1, Davison KS. Vitamin Dinsufficiency in North America. J Nutr.2005 Feb;135(2):332-7. Vuletic B, Markovic S,Igrutinovic Z, Vladimir R, Raskovic Z, Simovic A. Case report of an infant withsevere vitamin D deficiency rickets manifested as hypocalcemic seizures SrpArh Celok Lek 2016 Jan-Feb; 144 (1-2):90-3.

 Narchi H, ElJamil M, Kulaylat N. Symptomatic rickets in adolescence. Archives of Diseasein Childhood.

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 Basatemur E, Sutcliffe A; Incidenceof hypocalcemic seizures sue to vitamin D deficiency in Children in the UnitedKingdom and Ireland. J Clin Endocrinol Metab 2015; 100 (1): E91-E95.doi: 10.1210/jc.2014-2773.

doi:10.1210/jc.2014-2773.  Laud RB, Girolami PA, BoscoeJH, Gulotta CS. Treatment Outcomes for Severe Feeding Problems in Children withAutism Spectrum Disorder. Behavior Modif 2009 Sep; 33(5):520-36.

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