ADA-SCID affects 1 in 200,000 to 1 in 1 million newborns around the world1

What is ADA-SCID? 

ADA-SCID is an inherited condition that mainly affects immune systems causing recurrent and opportunistic fungal, bacterial and viral infections, low white blood cell count (lymphopenia), and failure to thrive. It is often fatal if left untreated.1-3

When is ADA-SCID diagnosed?

Most ADA-SCID patients become symptomatic and get diagnosed before 6 months of age. The earliest symptoms of ADA-SCID include pneumonia, chronic diarrhea, widespread skin rashes, slowed growth, and/or developmental delay. Some people with ADA-SCID will develop symptoms later in life. The symptoms in the late-onset form are typically milder than in the form that occurs in infancy.

ADA-SCID may be identified by newborn screening in some countries and regions.2,4

How is ADA-SCID treated?

Treatments for ADA-SCID include enzyme replacement therapy (ERT), haematopoietic stem cell transplant (HSCT) and gene therapy (GT).2 Please consult your local health care provider if you are suspicious or diagnosed with ADA-SCID.

Life with ADA-SCID

Living with an immune deficiency can make living in the outside world a challenge. But with the right treatment and management, it is possible.

References:
  1. Hershfield M. Adenosine Deaminase Deficiency. 2006, Oct 3. [Updated 2017 Mar 16]. In: Adam MP, Ardinger HH, Pagon RA et al., editors. Seattle WA: University of Washington. Accessed online at: https://www.ncbi.nlm.nih.gov/books/NBK1483/
  2. Whitmore KV, Gaspar HB. Adenosine deaminase deficiency – more than just an immunodeficiency. Front Immunol 2016;7:1-13.
  3. Sauer AV, Brigida I, Carriglio N, Aiuti A. Autoimmune dysregulation and purine metabolism in adenosine deaminase deficiency. Front Immunol 2012; 3:1-19.
  4. Great Ormond Street Hospital for Children. Severe combined immunodeficiency (SCID). Accessed online at: https://www.gosh.nhs.uk/conditions-and-treatments/conditions-we-treat/severe-combined-immunodeficiency-scid/
  5. van der Burg M, Mahlaoui N, Baspar HB, Pai SY. Universal newborn screening for severe combined immunodeficiency (SCID). Front Pediatr 2019; 7:1-5.

Here’s what goes on inside the body of someone with ADA-SCID:4,5

1. Every day, cells divide in your body. This is a normal part of life for all people.

2.  ADA is an important enzyme in the purine salvage pathway. ADA exists in all human tissues and the highest levels and activity are found in the lymphoid system. ADA is responsible to break down irreversible deamination of adenosine and 2’deoxyadenosine into inosine and 2’deoxyinosine respectively.4

3.  In ADA SCID, absent or impaired
ADA function leads to the accumulation of the toxic metabolites adenosine (Ado), 2’deoxyadenosine (dAdo) and deoxyadenosine triphosphate (dATP).4,5

4.  Increased level of dAdo and dATP block the normal DNA synthesis and repair and increased level of Ado leads to disruption of immune response in a variety of body tissues. As the lymphoid tissues have the highest level of ADA enzyme, ADA SCID is  associated with abnormal lymphoid development and function which is essential for your body to fight off infections.4,5 

5. ADA-SCID is also associated with non-immune system effects such as skeletal abnormalities, neurodevelopmental affects, pulmonary manifestations, organ damage, bone marrow abnormalities, rare skin tumours, and liver and kidney disease.2,4

When ADA isn’t working correctly, the immune system can’t fight off infection (immunodeficient). This leads to common signs of ADA-SCID, which are usually diagnosed in infants.1

There are three different types of ADA-SCID, each with different symptoms:

Signs and symptoms of ADA-SCID:1,2*

ADA-deficient Severe Combined Immunodeficiency Disease (SCID)2

Affecting: Most common form

Age at diagnosis (most):
<6 months1

Most common symptoms:2
Failure to thrive
Opportunistic infections
Chronic diarrhea
Skin rashes
Recurrent pneumonia
Non-infectious lung disease

Additional symptoms:2
Pulmonary dysfunction
Growth delays
Skeletal abnormalities
Bone marrow abnormalities
Abnormal liver function
Neurological abnormalities
Skin tumours

Delayed/Late-onset ADA Deficiency2

Affecting: 15-20% of children

Age at diagnosis (most):
1 to 10 years2,4

Most common symptoms:2
Chronic ear infections
Sinus infections
Upper respiratory infections
Palmar/plantar warts
Chronic  pulmonary insufficiency (leaky heart valve)
Autoimmune illnesses
Allergies

Additional symptoms:2
Papilloma viral infections
Growth delays

Partial ADA Deficiency2

Affecting: Very rare form

Age at diagnosis:
Any2

Presentation:2
Individuals with very low or absent ADA activity in erythrocytes but greater ADA activity in nucleated cells, have normal immune function.

*Some lung abnormalities in ADA-SCID, as well as in other types of severe combined immune deficiency (SCID), may be caused by metabolic insufficiency.1

If left untreated, ADA-SCID becomes life-threatening within the first one to two years of life.1,2 It’s crucial to get the disease diagnosed and initiate treatment as early as possible.

Learn more about how ADA-SCID is diagnosed and treated.

References:
  1. Whitmore KV, Gaspar HB. Adenosine deaminase deficiency – more than just an immunodeficiency. Front Immunol 2016;7:1-13.
  2. Hershfield M. Adenosine Deaminase Deficiency. 2006, Oct 3. [Updated 2017 Mar 16]. In: Adam MP, Ardinger HH, Pagon RA et al., editors. Seattle WA: University of Washington. Accessed online at: https://www.ncbi.nlm.nih.gov/books/NBK1483/
  3. Sauer AV, Brigida I, Carriglio N, Aiuti A. Autoimmune dysregulation and purine metabolism in adenosine deaminase deficiency. Front Immunol 2012; 3:1-19.
  4. Flinn AM, Gennery AR. Adenosine deaminase deficiency: A review. Orphanet Journal of Rare Diseases 2018;13;1-7.
  5. Kohn DB, Hershfield M, Puck JM, Aiuti A, Blincoe A, Gaspar B et al. Consensus approach for the management of severe combined immune deficiency caused by adenosine deaminase deficiency. J Allergy Clin Immunol 2019;143(3):852-63.

ADA-SCID can be diagnosed with:2

A blood test that measures ADA enzyme activity

Diagnosis of ADA-SCID is usually established by demonstrating absent or very low (<1% of normal) ADA activity in red blood cells (RBC), accompanied by elevated levels of adenosine and dAdo in plasma, or dried blood spots (DBS).2

Genetic testing for an ADA gene mutation

Genetic testing is also used to confirm a diagnosis via a blood test.

Genetic testing is to confirm bi-allelic mutations in the gene. This involves examining a person's DNA, the chemical database that carries instructions for the body's functions. Genetic testing can reveal mutations in your genes that may cause illness or disease.2

What your genes say about your risk of ADA-SCID

People born with ADA-SCID have two copies of a gene variant – one from each parent. While the parents may both carry one copy of the gene variant, they usually do not experience any signs or symptoms of the disorder.

Two parents, each with 1 gene variant, have a:

25%

chance of having a child unaffected by
ADA-SCID1

50%

chance of having a child who has 1 defective ADA gene 

25%

chance of having a child with 2 defective ADA genes who may be affected by ADA-SCID1

Family planning

Knowing a person’s family history can help doctors decide to screen before birth. For example, unexplained infant death or infant death due to infection could be a suspicion of ADA-SCID within the family.

If you or someone in your family has ADA-SCID, other family members may be at risk.

Your doctor can help you with how to talk to your family about getting tested.

Learn more about how ADA-SCID is treated.

References:
  1. Whitmore KV, Gaspar HB. Adenosine deaminase deficiency – more than just an immunodeficiency. Front Immunol 2016;7:1-13.
  2. Hershfield M. Adenosine Deaminase Deficiency. 2006, Oct 3. [Updated 2017 Mar 16]. In: Adam MP, Ardinger HH, Pagon RA et al., editors. Seattle WA: University of Washington. Accessed online at: https://www.ncbi.nlm.nih.gov/books/NBK1483/
  3. Great Ormond Street Hospital for Children. Severe combined immunodeficiency (SCID). Accessed online at: https://www.gosh.nhs.uk/conditions-and-treatments/conditions-we-treat/severe-combined-immunodeficiency-scid/

Insert text here...

Please consult your physician about treatment for ADA-SCID as practice and treatment options may vary from country to country

Always consult your local physician if you or your family member is suspicious of ADA-SCID.

Newly diagnosed

Learning that your newborn child has ADA-SCID can be a shock. It’s perfectly normal to feel confused and afraid. After all, ADA-SCID is probably not a medical condition you’ve even heard of until now. Learn more about ADA-SCID and find tips and tools to help you best care for your baby. Be sure to speak to your healthcare provider if you have any concerns.

Life after treatment

After treatment, talk to your healthcare team about the ways to advocate your child to navigate the world through the lens of ADA-SCID. Your child must learn to navigate the world through the lens of ADA-SCID. It is essential to attend regular check-ups for monitoring as per their physician’s advice. Certain adjustments and considerations must be made for your child, and continue as they transition into adulthood. 

Managing mental health

Having a baby with
ADA-SCID can be a stressful, scary and traumatic experience for parents and caregivers. It is important to take time to focus on your mental health and remember that you are not alone. Connect with others in the SCID community for support and don’t hesitate to reach out to your doctors if you have any concerns.

Early treatment

Although the diagnosis can be overwhelming, it’s important to treat as early as possible.

Infection precautions

Reducing the germs your child is exposed to is essential.

Telling your family and friends

Letting your family and friends know that your child has ADA-SCID and explaining things like isolation can be helpful.

These organisations and online communities provide valuable tools, information, and support for you and your family.

You are now leaving ADA-SCIDinfo.com

Links to other websites are provided as a resource.

CONTINUE TO EXTERNAL SITESTAY ON CURRENT PAGE