• Disease Overview
  • Synonyms
  • Signs & Symptoms
  • Causes
  • Affected Populations
  • Disorders with Similar Symptoms
  • Diagnosis
  • Standard Therapies
  • Clinical Trials and Studies
  • References
  • Programs & Resources
  • Complete Report

White-Sutton Syndrome

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Last updated: 5/14/2024
Years published: 2024


Acknowledgment

NORD gratefully acknowledges Kate Richardson, MS, CGC, McGovern Medical School, UTHealth Houston and V. Reid Sutton, MD, Professor, Molecular & Human Genetics, Baylor College of Medicine, Texas Children’s Hospital, for the preparation of this report.


Disease Overview

Summary

White-Sutton syndrome is a genetic disorder that primarily causes differences in a person’s development. There are also other medical problems observed in people with this disorder including growth, behavior, eye and gastrointestinal problems. Typically, the age of onset is in infancy or in the first three years of life.

This disorder is caused by genetic changes (disease-causing variants) in the POGZ gene which makes the POGZ protein. This protein plays a crucial role in turning genes on and off (gene expression), especially in the brain, but also in other body parts. White-Sutton syndrome is usually caused by a new genetic change (de novo) in the person with symptoms. Rarely, it has been noted to be inherited from a parent.

Treatment is based on the medical problems that are present in an affected person. The important benefits of an early diagnosis include psychosocial support from a patient community, knowledge of what medical problems a person may have over their lifetime and to obtain appropriate therapies (such as speech, occupational, physical and/or applied behavioral analysis) and academic support.

Introduction

White-Sutton syndrome was first described in 2016 by Dr. Janson White and Dr. Reid Sutton who were studying a small group of individuals with neurodevelopmental and behavioral issues. Since it has only been recognized for a few years, this disorder has a wide and evolving spectrum of symptoms. As time passes, we will continue to learn more about how variants in the POGZ gene change a person’s neurodevelopment and what symptoms they can cause.

 

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Synonyms

  • POGZ-related intellectual disability
  • intellectual disability-microcephaly-strabismus-behavioral abnormalities syndrome
  • autosomal dominant intellectual disability 37
  • MRD37
  • WHSUS
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Signs & Symptoms

White-Sutton syndrome has variable expressivity, meaning there is a range of symptoms that can occur in people affected with this condition.

Reported signs and symptoms may include:

  • Neurologic and developmental symptoms that are variable and may include:
    • Varying degrees of intellectual disability
    • Speech delay or troubled speech
      • First words are often spoken at the expected time, but putting words together to form sentences may be delayed until school-age
      • Inability to speak (non-verbal) in some cases
    • Motor delay
    • Clumsiness
    • Difficulty with coordinating movements (such as tying shoes or jumping)
    • Small head size (microcephaly)
    • Weak muscles (hypotonia)
    • Seizures with or without a fever (epilepsy; febrile seizures)
      • Seizures often start between one to four years of age and are well controlled with medication (anti-epileptic drugs)
    • Differences in brain structure or shape (brain malformations) that are often non-specific or cause additional medical problems
  • Behavioral issues including:
    • Autism
    • Biting
    • Aggression
    • Anxiety
    • Hyperactivity
    • Repetitive behaviors
  • Eye problems that can include
    • Lazy eye (strabismus)
    • Decreased vision caused by damage to the retina, the light-sensitive tissue at the back of the eye (called retinal dystrophy)
    • Area of missing tissue in the center of the eye (coloboma)
    • Smaller optic nerve behind the eye that sends signals to the brain (optic nerve hypoplasia)
  • Hearing loss
  • Feeding difficulties
  • Trouble gaining weight (failure to thrive)
  • Constipation
  • Repeating episodes of vomiting or nausea (cyclic vomiting)
  • Recurrent infections (including respiratory, ear and bladder)
  • Being shorter in height than expected based on the family (short stature)
  • Anomalies of the stomach or intestines
    • Twisting of the intestines/bowel (intestinal malrotation)
    • Soft tissue bulges through a weak point in the abdominal muscles (inguinal hernia)
    • Large intestine that slips outside the anus (rectal prolapse)
  • Urologic problems:
    • Kidneys that are shaped differently (dysplastic kidneys)
    • Fluid buildup in the kidney (hydronephrosis)
    • Extra tube (ureter) that carries urine to the bladder (duplicated collecting system)
    • Large ureter (megaureter).
  • Sleep problems such as:
    • Trouble falling asleep
    • Waking up many times during the night
    • Stopping breathing briefly while sleeping (sleep apnea)
  • Birth anomalies (rare) that can include:
    • Hole in the diaphragm, which is the muscle that separates the chest from the abdomen (diaphragmatic hernia)
    • Opening in the roof of the mouth (cleft palate)
    • Anomalies in the shape or structure of the heart (cardiac defects)
    • Genital anomalies such as:
      • Undescended testicles (cryptorchidism)
      • Smaller testicles (hypoplastic testes)
      • Smaller penis (micropenis)
  • Distinctive facial appearance including:
    • Flat back of the head (brachycephaly)
    • Broad forehead
    • Eyes that are far apart (hypertelorism)
    • Long face
    • Small nose
    • Small mouth
    • Small cheeks (malar hypoplasia)
    • Ears that sit lower on the head (low-set ears)
    • Downturned mouth
  • Broad and/or short fingers or toes
  • Extra weight (obesity)
  • Increased flexibility (hypermobility)
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Causes

White-Sutton syndrome is caused by genetic changes (disease-causing variants) in the POGZ gene. Genes are the body’s instruction manual for creating proteins that play critical roles in the body. This POGZ protein plays a crucial role in turning genes on and off (gene expression), especially in the brain, but also in other body parts. When a genetic change in a gene occurs, it causes the protein to stop working in the body. Depending on the function of the protein, it can affect different parts of the body. The medical problems that occur in White-Sutton syndrome happen because there’s not enough of the POGZ protein being made to do its job in the body.  

 

Most changes in the gene are called “stop” variants, meaning that no protein is made from that gene. Other types of variants (missense and splicing) have been reported but are less common than the “stop” variants. To date, no relation between the type of genetic change and the level of severity of the condition has been identified.  

 

White-Sutton syndrome has also been reported to have variable expressivity, meaning there is a range of symptoms that can occur in people affected with this condition. As an example, some individuals have low-normal intelligence whereas others have moderate-severe intellectual disability.  

 

White-Sutton syndrome follows autosomal dominant inheritance. Dominant genetic disorders occur when only a single copy of a disease-causing gene variant is necessary to cause the disease. The gene variant can be inherited from either parent or can be the result of a new (de novo) changed gene in the affected individual that is not inherited. The risk of passing the gene variant from an affected parent to a child is 50% for each pregnancy. The risk is the same for males and females. Typically, most of the genetic changes in POGZ happen for the first time in the affected person (referred to as de novo). This means that it was not inherited from either parent. Rarely, it has been noted to be inherited from a parent. 

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Affected populations

As of 2024, there have been at least 90 patients reported in the medical literature. White-Sutton syndrome is extremely rare. The number of people affected by this disorder is unknown. Rare disorders often go undiagnosed or misdiagnosed, making it extremely difficult to determine their true frequency in the general population. It has been estimated from exome sequencing tests that 1/1000 individuals with intellectual disability and autism have White-Sutton syndrome. With available information currently, males and females as well as all ethnicities are affected equally. Age of onset is typically in infancy.

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Diagnosis

A diagnosis of White-Sutton syndrome is based on DNA testing results that show a disease-causing (pathogenic) variant in the POGZ gene. This disorder cannot be diagnosed based on symptoms alone. White-Sutton syndrome should be considered in any person with developmental delay, intellectual disability, learning difficulties, speech delay and any additional medical problems.

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Standard Therapies

Treatment is based on the medical problems that are present in an affected person. A multidisciplinary team of pediatricians, physicians who specialize in the diagnosis and treatment of neurological disorders (neurologists), speech pathologists, physical therapists, gastroenterologists (stomach doctors) and other healthcare professionals can be involved in care.

Management can include:

  • Speech and language therapy
  • Occupational therapy
  • Physical therapy
  • Applied behavioral analysis (ABA) therapy
  • Neurodevelopmental assessments to assess the patient’s academic ability
  • Gastrointestinal evaluation to assist with growth, constipation and feeding difficulties, if necessary
  • Endocrinology (hormone doctors) for assistance in growth, if necessary
  • Audiology (hearing doctor) to evaluate for hearing loss
  • Antiepileptic medications for seizures, if necessary
  • Sleep study (to evaluate for sleep apnea), if necessary
  • Use of glasses, if necessary

A baseline picture of the heart (echocardiogram) and kidneys (renal ultrasound) are recommended to determine if follow up with a heart doctor (cardiologist) or kidney doctor (nephrologist) is recommended.

Due to the rarity of the disease, there are no treatment trials that have been tested in a large group of patients. There are no standardized treatment protocols or guidelines for affected individuals.

Genetic counseling is recommended for affected individuals and their families. Psychosocial support for the entire family is essential as well.

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Clinical Trials and Studies

Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.

For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:

Toll-free: (800) 411-1222
TTY: (866) 411-1010
Email: [email protected]

Some current clinical trials also are posted on the following page on the NORD website: https://rarediseases.org/living-with-a-rare-disease/find-clinical-trials/

For information about clinical trials sponsored by private sources, in the main, contact: www.centerwatch.com

For more information about clinical trials conducted in Europe, contact: https://www.clinicaltrialsregister.eu/

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References

Assia Batzir N, White J, Sutton VR. White-Sutton Syndrome. 2021 Sep 16. In: Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2024. Available from: https://www.ncbi.nlm.nih.gov/books/NBK573972/ Accessed April 24, 2024.

Assia Batzir N, Posey JE, Song X, et al. Phenotypic expansion of POGZ-related intellectual disability syndrome (White-Sutton syndrome). Am J Med Genet A. 2020;182(1):38-52. doi:10.1002/ajmg.a.61380

Matsumura K, Seiriki K, Okada S, et al. Pathogenic POGZ mutation causes impaired cortical development and reversible autism-like phenotypes. Nat Commun. 2020;11(1):859. Published 2020 Feb 26. doi:10.1038/s41467-020-14697-z

Satterstrom FK, Kosmicki JA, Wang J, et al. Large-scale exome sequencing study implicates both developmental and functional changes in the neurobiology of autism. Cell. 2020;180(3):568-584.e23. doi:10.1016/j.cell.2019.12.036

White J, Beck CR, Harel T, et al. POGZ truncating alleles cause syndromic intellectual disability. Genome Med. 2016;8(1):3. Published 2016 Jan 6. doi:10.1186/s13073-015-0253-0

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Ensuring that patients and caregivers are armed with the tools they need to live their best lives while managing their rare condition is a vital part of NORD’s mission.

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This first-of-its-kind assistance program is designed for caregivers of a child or adult diagnosed with a rare disorder.

Learn more https://rarediseases.org/patient-assistance-programs/caregiver-respite/

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