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Ehlers-Danlos Syndrome

How to diagnose, when to refer, and why it matters

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Douglas Ball, MD, DrPH | Clinical Geneticist

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Why this matters today

1

Recognize

when to suspect EDS

2

Decide who needs

testing and/or referral

3

Identify red flags for

vEDS and dangerous conditions

4

Manage EDS and associated conditions in clinic

1

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The EDS Spectrum

Overview

• Ehlers-Danlos Syndromes (EDS) are a group of heritable connective tissue disorders (HCTDs).

• The 2017 International Classification recognizes 13 distinct subtypes.

The Diagnostic Divide

  • Hypermobile EDS (hEDS): is a strictly clinical diagnosis

  • The 12 other subtypes have known causative variants and require molecular confirmation via genetic testing.

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The 13 Types of EDS (2017 Classification)

EDS Subtype

Causative Gene(s)

Inh.

Classical EDS (cEDS)

COL5A1 / COL5A2

AD

Classical-like EDS (clEDS)

TNXB

AR

Cardiac-valvular EDS (cvEDS)

COL1A2

AR

Vascular EDS (vEDS) ⚠ URGENT

COL3A1

AD

Hypermobile EDS (hEDS)

Unknown — multifactorial

AD

Arthrochalasia EDS (aEDS)

COL1A1 / COL1A2

AD

Dermatosparaxis EDS (dEDS)

ADAMTS2

AR

Kyphoscoliotic EDS (kEDS)

PLOD1 / FKBP14

AR

Brittle Cornea Syndrome (BCS)

ZNF469 / PRDM5

AR

Spondylodysplastic EDS (spEDS)

B4GALT7 / B3GALT6 / SLC39A13

AR

Musculocontractural EDS (mcEDS)

CHST14 / DSE

AR

Myopathic EDS (mEDS)

COL12A1

AD/AR

Periodontal EDS (pEDS)

C1R / C1S

AD

Inh. = Inheritance | AD = Autosomal Dominant | AR = Autosomal Recessive | Pink = Urgent evaluation | Blue = No causative gene

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When should you suspect EDS? Joint Clues

• Generalized joint hypermobility or “double-jointed” history

• Atraumatic subluxations / recurrent sprains / frank instability

• Musculoskeletal pain in ≥2 limbs, daily ≥3 months, or widespread chronic pain

• Symptoms start young, persist, and cluster across multiple joints

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When should you suspect EDS? Skin / Tissue Clues

• Soft or velvety skin; mild hyperextensibility

• Unexplained striae, atrophic scars, recurrent hernias

• Bilateral heel piezogenic papules

• Dental crowding with high or narrow palate

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When should you suspect EDS? Systemic Clues

• Positive family history: 3-generation pedigree

• Dysautonomia / orthostatic symptoms / POTS

• Functional GI or bladder disorders, fatigue, anxiety

• MVP or aortic root dilation, especially with other connective tissue signs

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Diagnostic Criteria for hEDS

https://www.ehlers-danlos.com/heds-diagnostic-checklist/

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The Beighton Score — Measuring Joint Hypermobility

Beighton Score Methodology

Score out of 9; each side is evaluated independently.

Age-Adjusted Cut-offs (Malfait 2017)

Strict adherence to cut-offs is required for hEDS diagnosis:

  • 5th Finger: Hyperextends >90°.
  • Thumb: Passively touches the forearm.
  • Elbow: Hyperextends >10°.
  • Knee: Hyperextends >10°.
  • Spine: Palms flat on floor, straight knees.

≥6 for pre-pubertal children and adolescents.

≥5 for pubertal men and women up to age 50.

≥4 for individuals >50 years of age.

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The Beighton Score — Measuring Joint Hypermobility

https://commons.wikimedia.org/wiki/File:Ehlers-Danlos_skala_Beighton%27a.png

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Diagnostic Criteria for hEDS

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Standardizing the Skin Exam

Skin Extensibility

Measured on the volar surface of the mid-non-dominant forearm and neck. Positive cut-offs:

Piezogenic Papules

Herniations of subcutaneous fat in the heel visible upon standing.

>1.5 cm for distal forearms/hands.

>3.0 cm for neck, elbows, and knees.

Must be bilateral to count toward criteria.

https://www.ehlers-danlos.com/skin/

https://share.google/U5aboMzvQbIv0p65n

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Diagnostic Criteria for hEDS

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��Diagnosing hEDS at the bedside

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Criterion 1

Generalized joint hypermobility

• ≥6 pre-pubertal children/adolescents

• ≥5 pubertal adults to age 50

• ≥4 adults >50

If one point below cutoff, historical questions can help.

2

Criterion 2

Two or more of A / B / C

• A: ≥5 systemic features

• B: positive first-degree family history

• C: chronic musculoskeletal pain and/or instability

3

Criterion 3

All prerequisites must be met

• No unusual skin fragility

• Exclude other heritable or acquired CTDs

• Exclude alternative diagnoses that also cause hypermobility

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3-Generation Pedigree

  • Complete family history for 3-generations; patient and their siblings, parents (and aunts and uncles) and grandparents.

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Differential Diagnosis

Hypermobility is a shared phenotype. Consider overlapping connective tissue disorders if severe cardiovascular or skeletal issues exist:

  • The 12 other EDS Subtypes: e.g., Classical, Classical-like, Kyphoscoliotic.
  • Loeys-Dietz Syndrome (LDS): Aggressive arterial aneurysms, bifid uvula, hypertelorism.
  • Marfan Syndrome: Aortic root dilation, ectopia lentis, distinct arachnodactyly.
  • Arterial Tortuosity Syndrome and others.

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Red flags for vEDS and dangerous mimics

vEDS: reasons to escalate quickly

  • Family history of vEDS, arterial rupture, or dissection
  • Arterial rupture or dissection before age 40
  • Unexplained sigmoid colon rupture
  • Third trimester uterine rupture
  • Spontaneous pneumothorax plus other suggestive features
  • Thin translucent skin, easy bruising, abnormal atrophic scars, acrogeria, small-joint hypermobility, characteristic facial appearance, hypoplastic earlobes

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Vascular EDS vs. unaffected controls

Murdock D, Suresh A, Calderon Martinez E ...

Early diagnosis of vascular Ehlers-Danlos syndrome through AI-powered facial analysis: Results from the Montalcino Aortic Consortium. Genetics in Medicine Open, 2025; 3

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Red flags for vEDS and dangerous mimics

Also escalate if the story suggests a higher-risk aortopathy:

    • Loeys-Dietz Syndrome clues (hypertelorism, bifid uvula/cleft palate, clubfoot, aggressive vascular disease).
    • Marfan clues (systemic score pattern, ectopia lentis).
    • Arterial Tortuosity Syndrome / heritable Thoracic Aortic Aneurysm/Dissection clues (marked arterial tortuosity, strong aortic family history).

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POTS: what to evaluate first

POTS (POstural Tachycardia Syndrome) & dysautonomia

• Start with 10-minute standing test after 5 minutes supine; tilt-table if needed. Increase of heart rate by ≥30 (adults) within 10 minutes of standing without drop in BP confirms diagnosis. Orthostatic vitals used to document concurrent orthostasis.

• Basic evaluation may include ECG, CBC/hematocrit, thyroid testing, and echo when symptoms warrant it.

• First-line treatment: fluids, salt, compression, trigger avoidance, medication review, and graded recumbent exercise.

These associations may drive morbidity even though they are not part of the formal hEDS diagnostic criteria.

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MCAS: what to evaluate first

MCAS / hereditary alpha-tryptasemia

• Think about it when recurrent urticaria, flushing, multiple allergies, or anaphylaxis cluster with hypermobility symptoms.

• Serum tryptase can be useful; in the Miami protocol, tryptase >11 ng/mL prompted TPSAB1 copy-number testing for hereditary alpha-tryptasemia.

• Common first-line symptom treatment is stepwise H1 + H2 antihistamines; some patients also use cromolyn, ketotifen, or leukotriene blockers; refer allergy / immunology if severe or unclear.

These associations may drive morbidity even though they are not part of the formal hEDS diagnostic criteria.

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Practical management: PT

Physical therapy

• Start early and focus on strength, stabilization, movement control, and joint protection.

• Prefer low-joint-load activity; start low and go slow.

• Avoid aggressive stretching unless there is a specific functional goal.

Practical clinic pearl: “Stabilize first; stretch only with purpose.”

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Practical management: bracing

Braces / supports

• Consider arch supports (orthoses), proprioceptive braces (like figure-8 ankle brace), compression garments, or off-the-shelf or custom fitted braces (e.g. knee orthoses).

• Use them to improve body awareness and reduce symptom burden — not instead of strengthening.

• Reassess function and avoid “permanent immobilization by default”.

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Practical management: pain

Pain Management Approach

  • Separate instability/mechanical pain from inflammatory or neuropathic pain.
  • Use medications based on pain etiology (i.e. muscle relaxant for muscle spasms).
  • Use multimodal care: PT, pacing, sleep, mental health support, and medication when appropriate.
  • Pain can be more disabling than the Beighton score (in other words, hypermobility is not always painful).

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Genetic Testing Pearls

What testing can — and cannot — do

• hEDS has no confirmatory molecular test yet

• All other EDS subtypes rely on molecular confirmation for a final diagnosis

• In practice, testing is mainly used to exclude alternative diagnoses and identify conditions that change surveillance, surgery, pregnancy, and family screening

TNXB / clEDS caveat

• clEDS is associated with TNXB deficiency

• Testing is difficult because TNXB has a highly homologous pseudogene (TNXA)

• The challenging region is the 3′ end of TNXB, especially exons 32–44

• No method specifically detects TNXB CNVs across all homologous exons; make sure the ordered assay includes TNXB well

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Who needs testing or referral?

Refer / test when the phenotype is not “clean hEDS”

• Arterial event, aortic disease, spontaneous pneumothorax, bowel rupture, or strong vascular family history

• Marfanoid or syndromic features: bifid uvula / cleft palate, hypertelorism, lens issues, severe scoliosis, clubfoot, brittle bones

• Developmental delay, facial dysmorphism, neuromuscular findings, or progressive unexplained course

• Objective connective-tissue signs but incomplete fit for hEDS — especially if management would change with a molecular diagnosis

Why testing matters

26.4%

of patients who met 2017 hEDS criteria in the Miami registry had an alternative or additional diagnosis.

• Connective tissue / skeletal disorders

• Neuromuscular disorders

• Chromosomal abnormalities / CNVs

• Immune disorders and hereditary alpha-tryptasemia

The primary use of genetic testing in hEDS evaluation is to exclude alternative diagnoses.

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EDS Society Algorithm

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Emerging Science InformedAlgorithm

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Take-home Points

• Meeting the 2017 hEDS criteria does not rule out serious genetic conditions.

• Not meeting the 2017 hEDS criteria does not rule out serious genetic conditions.

• Patients with red flags are going to need referral or genetic testing.

• Don’t wait for genetics referral to manage what helps patients now: PT, pain strategy, orthostatic symptoms, mast-cell symptoms, and other targeted referrals.

• Order testing for the differential you need to exclude — especially when management would change.

Key references

1. Malfait F, Francomano C, Byers P, et al. The 2017 international classification of the Ehlers-Danlos syndromes. Am J Med Genet C Semin Med Genet. 2017;175:8-26.

2. Forghani I, See J, McGonigle WC. Hypermobile Ehlers–Danlos Syndrome: Diagnostic Challenges and the Role of Genetic Testing. Genes. 2025;16(5):530.

3. The Ehlers-Danlos Society: https://www.ehlers-danlos.com/

Detailed citations and image attributions are included in slide notes.

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Key Resources

EDS Society — print and use at every encounter. Includes Beighton score guide.

EDS Society Paediatric Working Group — use for patients under 18 or before biological maturity.

Clinical guidance, CME, patient handouts, and specialist referral network.

Marfan screening tools, aortic management guidelines, cardiac referral resources.

Peer-reviewed clinical summaries for all EDS subtypes, Marfan, Loeys-Dietz.

Full open-access article — complete criteria for all 13 EDS subtypes, Beighton tables, skin measurements.