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Prader-Willi Syndrome

para>Sudden death after initiation of growth hormone therapy due to worsening of obstructive sleep apnea has been reported, so before initiating growth hormone, a sleep study should be done (6)[B].
  • Contraindications to growth hormone: weight >225% of ideal, uncontrolled diabetes, respiratory compromise, acute respiratory infection, untreated severe sleep apnea, active cancer, psychosis

  • Hormone replacement during puberty is controversial due to increased risk of stroke with estrogen replacement and worsening of behavioral problems with testosterone replacement.

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    ISSUES FOR REFERRAL


    • All patients should be assessed by an ophthalmologist.
    • Early involvement of physical, speech, and occupational therapy
    • Endocrine referral for discussion of growth hormone replacement and sex hormone therapy

    SURGERY/OTHER PROCEDURES


    • Surgical and hormonal correction of cryptorchidism
    • Tonsillectomy and adenoidectomy may be necessary in those with sleep apnea and especially considered before growth hormone initiation.
    • Results of surgical weight loss procedures are inconsistent, and patients seem to have greater risks than benefits.

    ALERT
    • Patients are at increased risk of respiratory complications during the perioperative period when undergoing adenotonsillectomy, so close monitoring is required.

    • Unusually high complication rates for scoliosis surgery have been reported.

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    ONGOING CARE


    FOLLOW-UP RECOMMENDATIONS


    Patient Monitoring
    • Screen infants for strabismus.
    • Routine monitoring of height, weight, and BMI
    • Screen for diabetes mellitus if BMI is >95th percentile.
    • Monitor for sleep disturbances and obtain sleep study, especially before growth hormone initiation or if concerned about sleep apnea.
    • Evaluate for behavior and psychiatric disturbances at least annually.
    • Monitor for recurrence of cryptorchidism after orchidopexy.
    • Examine annually for scoliosis: If patient is obese, consider radiographs of the spine.
    • Dual energy x-ray absorptiometry (DEXA) scans to monitor bone density starting at age 5 years and every 2 to 3 years thereafter
    • Monitor calcium and vitamin D intake.
    • Specialized group homes are an option for adults with PWS to provide behavior and diet monitoring.

    DIET


    • Oromotor evaluation, swallow study, and thickened high caloric feedings may be needed in neonates/infants; significant dysfunction may warrant gastrostomy or fundoplication.
    • Fundoplication must be used with caution due to tendency to overeat following infancy.
    • When hyperphagia begins, strict supervision of food intake with restricted access to food in home, including locks on refrigerator and cabinets.
    • Food seeking behaviors can lead to issues such as eating garbage, frozen/spoiled food, or potentially toxic items.
    • Regular consultation with dietician

    ALERT

    Monitor eating habits because binge eating can lead to acute gastric dilation, choking episodes, or toxic ingestions, which can lead to death.

    ‚  

    PATIENT EDUCATION


    • Genetic counseling for families of children who have imprinting center deletions, due to the possibility of recurrence in subsequent pregnancies
    • Discuss issues of guardianship, wills, and advocacy by adolescence.
    • Patients can often work in a structured setting with support.

    PROGNOSIS


    • Increased morbidity and mortality due to obesity, diabetes, and hypertension, which can be prevented with good programs
    • With improved treatments, most children live until adulthood and can work.
    • Most experience decline in physical and psychological function with advancing age.

    COMPLICATIONS


    • Obesity-related problems (diabetes, cardiovascular problems, sleep apnea, right-sided heart failure)
    • Thrombophlebitis
    • Skin infections from skin picking

    REFERENCES


    11 Gross ‚  N, Rabinowitz ‚  R, Gross-Tsur ‚  V, et al. Prader-Willi syndrome can be diagnosed prenatally. Am J Med Genet A.  2015;167A(1):80 " “85.22 Gunay-Aygun ‚  M, Schwartz ‚  S, Heeger ‚  S, et al. The changing purpose of Prader-Willi syndrome clinical diagnostic criteria and proposed revised criteria. Pediatrics.  2001;108(5):E92.33 Angulo ‚  MA, Butler ‚  MG, Cataletto ‚  ME. Prader-Willi syndrome: a review of clinical, genetic, and endocrine findings. J Endocrinol Invest.  2015;38(12):1249 " “1263.44 Cassidy ‚  SB, Schwartz ‚  S, Miller ‚  JL, et al. Prader-Willi syndrome. Genet Med.  2012;14(1):10 " “26.55 Deal ‚  CL, Tony ‚  M, H ƒ ¶ybye ‚  C, et al. Growth Hormone Research Society workshop summary: consensus guidelines for recombinant human growth hormone therapy in Prader-Willi syndrome. J Clin Endocrinol Metab.  2013;98(6):E1072 " “E1087.66 Goldstone ‚  AP, Holland ‚  AJ, Hauffa ‚  BP, et al. Recommendations for the diagnosis and management of Prader-Willi syndrome. J Clin Endocrinol Metab.  2008;93(11):4183 " “4197.

    ADDITIONAL READING


    • Allen ‚  K. Managing Prader-Willi syndrome in families: an embodied exploration. Soc Sci Med.  2011;72(4):460 " “468.
    • Bigi ‚  N, Faure ‚  JM, Coubes ‚  C, et al. Prader-Willi syndrome: is there a recognizable fetal phenotype? Prenat Diagn.  2008;28(9):796 " “799.
    • Duker ‚  AL, Ballif ‚  BC, Bawle ‚  EV, et al. Paternally inherited microdeletion at 15q11.2 confirms a significant role for the SNORD116 C/D box snoRNA cluster in Prader " “Willi syndrome. Eur J Hum Genet.  2010;18(11):1196 " “1201.
    • Manning ‚  KE, McAllister ‚  CJ, Ring ‚  HA, et al. Novel insights into maladaptive behaviours in Prader-Willi syndrome: serendipitous findings from an open trial of vagus nerve stimulation [published online ahead of print May 27, 2015]. J Intellect Disabil Res.
    • Miller ‚  JL. Approach to the child with Prader-Willi syndrome. J Clin Endocrinol Metab.  2012;97(11):3837 " “3844.
    • Tauber ‚  M, Mantoulan ‚  C, Copet ‚  P, et al. Oxytocin may be useful to increase trust in others and decrease disruptive behaviours in patients with Prader-Willi syndrome: a randomised placebo-controlled trial in 24 patients. Orphanet J Rare Dis.  2011;6:47.
    • Tuysuz ‚  B, Kartal ‚  N, Erener-Ercan ‚  T, et al. Prevalence of Prader-Willi syndrome among infants with hypotonia. J Pediatr.  2014;164(5):1064 " “1067.

    CODES


    ICD10


    Q87.1 Congenital malform syndromes predom assoc w short stature ‚  

    ICD9


    759.81 Prader-Willi syndrome ‚  

    SNOMED


    Prader-Willi syndrome (disorder) ‚  

    CLINICAL PEARLS


    • PWS is a rare genetic disorder caused by a deletion, UPD, or an imprinting center defect resulting in the absence of expression of a region of the paternal chromosome 15.
    • Characterized by hypotonia in early infancy followed by hyperphagia and behavior problems beginning in toddlerhood or early childhood
    • Although there are clinical diagnostic criteria, genetic testing is the gold standard to confirm the diagnosis.
    • A multidisciplinary approach is necessary to maximize the child 's potential.
    • Weight control is critical to prevent obesity-related morbidity and mortality.
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