Autosomal Dominant Preaxial Polydactyly–Upper-Back Hypertrichosis Syndrome

Autosomal dominant preaxial polydactyly–upper-back hypertrichosis syndrome is a very rare genetic condition. “Autosomal dominant” means a single changed copy of the gene region from either parent can cause the condition. “Preaxial polydactyly” means extra digits on the thumb side of the hands or the big-toe side of the feet. “Upper-back hypertrichosis” means there is a stripe or patch of thick hair that runs from the hairline down the middle of the upper back. Most children are otherwise healthy. Limb differences can include a triphalangeal thumb (a thumb with three bones), a duplicated thumb, an extra ray on the thumb side, fusion between the first and second fingers, a big or duplicated great toe, or fusion between the first and second toes. The extra hair typically extends from the back of the head to the middle of the back. Age of onset is at birth. Inheritance is autosomal dominant, and the condition is ultra-rare. Genetic Rare Diseases Center+2Orpha+2

Autosomal dominant preaxial polydactyly–upper-back hypertrichosis syndrome is a genetic condition that runs in families in an autosomal dominant pattern (one changed copy of a gene is enough to cause it). Babies are typically born with extra thumbs or big toes on the inner (preaxial) side and may have webbing between the first and second digits. They also tend to have a stripe or patch of dense hair from the back of the neck down to the mid-back. The condition is extremely rare (estimated <1 per 1,000,000). Symptoms begin at birth (neonatal onset). Global Genes+3Orpha+3Genetic Rare Diseases Center+3

In the first reported family, researchers found a tiny DNA deletion near the SHH (Sonic Hedgehog) gene, a master switch that helps hands, feet, and hair follicles form. That deleted piece sits far “upstream” of the SHH gene and behaves like a silencer (a brake). Losing the brake likely mis-timed SHH signals during limb and hair development, producing extra preaxial digits and localized upper-back hair. This explains why the condition affects both fingers/toes and hair growth. PMC+2PubMed+2

Research in an affected family shows a small deletion (about 2 kilobases) located ~240 kilobases upstream of the SHH (Sonic Hedgehog) gene that likely removes a regulatory “silencer,” causing mis-timed or mis-placed SHH activity during limb and hair-follicle development. SHH is a key signal for forming digits; mis-regulation can create preaxial extra digits. The same mis-regulation may drive the upper-back hair stripe. PMC+1

Other names

You may also see the disorder listed as:

• Autosomal dominant preaxial polydactyly–upperback hypertrichosis (without the hyphen or with spacing variants).

• ORPHA:476119 (Orphanet identifier) or MONDO:0018777 in disease ontologies and databases. Orpha+1

Types

There is no official, universally adopted subtype system for this syndrome. However, clinicians often describe phenotypic sub-patterns to document the range of features:

1. Hand-dominant pattern: limb differences mostly in the hands (e.g., triphalangeal thumb, duplicated thumb, thumb-index syndactyly), plus the classic upper-back hair stripe. Genetic Rare Diseases Center

2. Foot-dominant pattern: changes mainly in the feet (e.g., large/duplicated hallux, hallux-second-toe syndactyly), plus the hair stripe. Genetic Rare Diseases Center

3. Combined hand-and-foot pattern: both upper and lower limb findings with the hair stripe. Genetic Rare Diseases Center

4. Mild hair, mild limb pattern: subtle upper-back hair with minimal digit differences (illustrates variable expressivity seen in autosomal-dominant traits). Genetic Rare Diseases Center

Causes

Important note: In this rare syndrome, one established cause is known (a regulatory defect affecting SHH). The list below starts with the proven mechanism, then explains additional biologic mechanisms inferred from closely related preaxial polydactyly biology (especially SHH regulatory architecture). I’m explicit about what is proven for this syndrome and what is extrapolated from related conditions.

1. Proven: small upstream deletion removing an SHH “silencer.” A ~2 kb deletion ~240 kb upstream of SHH likely removes a silencer, lifting brakes on SHH at the wrong time/place in embryos. This is the only mechanism directly demonstrated in AD-PPD-UBH to date. PMC+1

2. Mis-regulation of SHH due to altered cis-regulatory elements (general concept). Limb patterning relies on enhancers/silencers; disrupting them can mis-activate SHH and create preaxial extra digits (principle shown across polydactyly research). PMC

3. Position effect from structural variants near SHH. Inversion/duplication/rearrangement can reposition enhancers/silencers and change SHH expression domains (known in polydactyly biology; potential mechanism here). PMC

4. Copy-number change encompassing SHH regulatory DNA. Gains/losses of enhancer blocks can boost or blunt SHH locally (established in SHH-related limb malformations generally). PMC

5. TAD (topologically associating domain) boundary disruption. Altered 3D genome folding can make distant enhancers contact SHH inappropriately, shifting limb patterning (shown in limb malformation models). PMC

6. Mutations in the limb enhancer ZRS (precedent from preaxial polydactyly). Classic preaxial polydactyly often involves ZRS variants; while ZRS variants are not reported for the combined hair-back stripe in this specific syndrome, the biology shows how enhancer changes drive thumb-side extra digits. PMC

7. Regulatory SNPs/indels in other SHH enhancers. Multiple enhancers govern when/where SHH turns on; subtle sequence changes could perturb timing/levels (general mechanism from enhancer biology). PMC

8. Complex rearrangements (e.g., insertions) inserting new enhancers. Inserted DNA can carry ectopic enhancer activity near SHH (general limb-malformation mechanism). PMC

9. Chromatin modification defects in the SHH locus. If chromatin can’t adopt the right “open/closed” states, enhancer control may fail (concept supported in developmental genetics reviews). PMC

10. Long-range silencer malfunction beyond the reported 2-kb site. Other silencers likely exist; losing them could mimic the same mis-expression pattern (inference from the proven silencer deletion). PMC

11. Regulatory hub disruption during hair-follicle morphogenesis. SHH also regulates follicle development; mis-activation along the midline may underlie the hair stripe (biological rationale). PMC

12. Embryonic mosaicism of a regulatory lesion. If a regulatory mutation occurs after fertilization, some tissues (limb buds, dorsal skin) may be affected variably—explaining asymmetric findings in some families (general genetic principle). PMC

13. Modifier variants elsewhere in hedgehog pathway (e.g., GLI proteins). Background variants can amplify or buffer the effect of primary SHH mis-regulation (inference from pathway biology). PMC

14. Noncoding RNA changes affecting SHH domain. lncRNAs/microRNAs in the locus can fine-tune expression; alterations may modify penetrance (general mechanism from gene-regulation literature). PMC

15. Epigenetic imprinting effects (rare). Parent-of-origin methylation patterns may modulate enhancer activity, potentially shaping variability (inference from epigenetic regulation principles). PMC

16. Environmental perturbations do not cause the syndrome but may shape severity. While the root cause is genetic, early developmental influences could modify expressivity (general concept in congenital limb anomalies). PMC

17. Germline structural variant breakpoints near SHH. Breakpoints that rewire enhancer contacts can recreate preaxial polydactyly patterns (shown in polydactyly case series). PMC

18. Altered enhancer insulation by CTCF/cohesin changes. If insulation fails, off-target enhancer activity can “leak” into SHH (mechanism known in enhanceropathies). PMC

19. Regulatory sequence conservation loss. Variants that erase conserved transcription-factor binding motifs within limb enhancers/silencers can shift SHH (general mechanism). PMC

20. Undiscovered non-SHH pathways with similar phenotype. While SHH regulation is central, other loci could theoretically produce the same hand/foot + hair pattern; current evidence, however, points to SHH regulatory mis-expression. PMC

Symptoms and signs

1. Extra thumb-side finger(s) (preaxial polydactyly of the hand). The extra digit may be well-formed or partially formed; the thumb may look wider or split. Function can range from normal to limited. Genetic Rare Diseases Center

2. Triphalangeal thumb. The thumb has three small bones instead of two, appearing longer or finger-like and sometimes affecting grip. Genetic Rare Diseases Center

3. Duplicated thumb. Two thumbs arise from the preaxial side; surgeons later decide whether and how to reconstruct for best function. Genetic Rare Diseases Center

4. Thumb–index web fusion (syndactyly I–II). The skin or soft tissue between the first two fingers may be fused, influencing fine motor tasks. Genetic Rare Diseases Center

5. Extra big-toe side ray or large hallux. The great toe can be very big, partially duplicated, or have extra bones; this can affect footwear and gait. Genetic Rare Diseases Center

6. Hallux–second-toe syndactyly. Webbing between the first two toes can alter balance or shoe comfort. Genetic Rare Diseases Center

7. Upper-back hair stripe (dorsal midline hypertrichosis). Hair extends from the posterior hairline to mid-back; it is benign but cosmetically noticeable. Genetic Rare Diseases Center

8. Symmetry can vary. One hand/foot can be more affected than the other; even within families, features differ (variable expressivity). Genetic Rare Diseases Center

9. Normal growth and development otherwise. Reports emphasize limb/skin findings; no consistent internal organ issues are described. Genetic Rare Diseases Center

10. Feeding/infancy usually normal. The condition is present at birth but does not usually affect feeding or general newborn health. Genetic Rare Diseases Center

11. Pain is uncommon in infancy. Discomfort later may relate to calluses or shoe fit when feet are involved. Genetic Rare Diseases Center

12. Functional hand issues depend on anatomy. Triphalangeal or duplicated thumbs may change pinch strength, fine motor coordination, or handwriting tasks. Genetic Rare Diseases Center

13. Footwear challenges. Large or duplicated hallux can make finding comfortable shoes difficult; pressure points may form. Genetic Rare Diseases Center

14. Skin-care concerns for the hair patch. Thick hair can trap sweat, causing itch or folliculitis in hot climates; hair removal is optional and cosmetic. Osmosis

15. Psychosocial impact. Visible differences in hands/feet or back hair can lead to self-consciousness; supportive counseling can help. (General consideration for visible congenital differences.) PMC

Diagnostic tests

A. Physical examination 

1. Detailed newborn/child exam by a dysmorphologist. Confirms the pattern of thumb-side extra digits, any webbing, and the characteristic upper-back hair distribution; documents symmetry and severity. Genetic Rare Diseases Center

2. Hand function assessment. Checks pinch, grasp, range of motion, and opposability to plan therapy or surgery if needed. (Standard hand evaluation in limb malformations.) PMC

3. Foot and gait evaluation. Looks for shoe-wear problems, pressure points, balance, and walking pattern changes caused by hallux anomalies. (Standard ortho evaluation.) PMC

4. Skin/hair mapping of the back. Notes width, length, and density of the hair stripe; helps track changes or guide cosmetic discussions. Genetic Rare Diseases Center

5. Family history and pedigree review. Because inheritance is autosomal dominant, multiple affected members across generations can appear; this supports the diagnosis and guides genetic counseling. Genetic Rare Diseases Center

B. “Manual” clinical tests 

6. Standardized hand measurements. Anthropometric measures (digit lengths, web space) help plan reconstruction and monitor outcomes. (General limb-difference practice.) PMC

7. Grip and pinch dynamometry. Quantifies strength for therapy planning and post-surgical follow-up. (General ortho/hand standards.) PMC

8. Range-of-motion goniometry. Measures joint angles in thumbs/fingers and first ray of the foot to tailor therapy. (General practice.) PMC

9. Gait analysis (clinical). Observational analysis (step length, stance) to see if hallux anomalies cause compensations; advanced lab gait analysis if needed. (General ortho approach.) PMC

10. Photographic documentation. Standardized photos of hands/feet/back aid follow-up and family counseling. (General practice in congenital malformation clinics.) PMC

C. Laboratory / pathological / genetic tests

11. Targeted testing of the SHH upstream regulatory region. Looks for the reported ~2-kb deletion ~240 kb upstream of SHH (e.g., high-resolution CNV testing or targeted sequencing). This is the most specific test when clinical features fit. PMC

12. Chromosomal microarray (CMA). Detects copy-number changes near SHH that might disrupt enhancers/silencers; a first-line genomic test in many clinics. (General genomic standard.) PMC

13. Whole-genome sequencing (trio if possible). Captures noncoding variants and structural breakpoints affecting SHH regulatory elements; WGS outperforms exome for enhanceropathies. (General genomic evidence.) PMC

14. Targeted enhancer sequencing (e.g., ZRS). While ZRS variants are a classic cause of preaxial polydactyly, they have not been shown to cause the hair-stripe pattern; still useful in the differential when the phenotype is atypical. PMC

15. qPCR/MLPA for small CNVs across SHH regulatory blocks. Complements CMA to catch small deletions/duplications that might be missed. (General method.) PMC

16. Long-read sequencing or optical mapping (specialized). Helps resolve complex rearrangements or TAD-boundary disruptions around SHH. (Emerging clinical research tools.) PMC

D. Electrodiagnostic tests 

17. Nerve conduction studies/EMG—usually not indicated. The syndrome affects limb patterning and hair, not peripheral nerves. These tests are reserved only if another nerve disorder is suspected. (General clinical reasoning.) PMC

18. Somatosensory evoked potentials—rarely, for differential diagnoses only. Used when neurologic conditions are being considered; not part of routine work-up here. (General principle.) PMC

E. Imaging tests 

19. Plain radiographs of hands and feet. Define bone number/shape (e.g., triphalangeal thumb, extra preaxial ray), guide surgical planning, and document growth. (Standard imaging in polydactyly). PMC

20. Ultrasound or MRI (selected cases). Ultrasound can characterize newborn soft-tissue/bone; MRI helps when complex soft-tissue anatomy must be mapped before surgery. CT is rarely needed due to radiation. (General limb-difference imaging practice.) PMC

Non-pharmacological treatments (therapies & other measures)

1. Genetic counseling — Families learn inheritance (50% chance per pregnancy) and options. Purpose: informed planning and testing. Mechanism: explains autosomal dominant risk and SHH-related biology. Orpha+1

2. Surgical planning clinic (multidisciplinary) — Team review (hand surgeon, anesthesiologist, therapist). Purpose: plan the safest timing and technique. Mechanism: aligns surgery with growth milestones to optimize outcomes. PMC

3. Thumb (or hallux) duplication reconstruction — Tailored procedures (e.g., resection of extra ray, reconstruction of ligaments/tendons, sometimes “on-top plasty”). Purpose: improve function, pinch, and appearance. Mechanism: restore a single stable, well-aligned digit. PMC+1

4. Wassel-guided surgical strategy — Using X-rays to classify duplication (Types I–VII) before surgery. Purpose: choose the right technique. Mechanism: the level of duplication predicts what to remove/reconstruct. PMC

5. Optimal timing of hand surgery (usually around 7–12 months) — Earlier than school age, often within the first year. Purpose: support normal motor development and growth. Mechanism: surgery before pathological growth patterns set in, but after anesthetic risks decline. PMC+1

6. Syndactyly release where present — Separation of fused first web space with local flaps and grafts. Purpose: improve spread and function of thumb/index. Mechanism: restores independent movement and proper web depth. PMC+1

7. Post-op splinting and hand therapy — Gentle splints and guided exercises. Purpose: maintain alignment, reduce scarring, regain range. Mechanism: controlled motion and scar management. PMC

8. Long-term follow-up for revision risk — Some children need secondary procedures as they grow. Purpose: correct residual angulation or instability. Mechanism: serial exams catch changes early. Jhandsurg

9. Laser hair reduction (alexandrite 755 nm) — In-clinic laser that targets melanin in follicles. Purpose: reduce upper-back hair density long-term. Mechanism: selective photothermolysis heats follicle/bulge stem cells to limit regrowth. FDA Access Data+1

10. Laser hair reduction (diode 808–810 nm) — Common alternative when alexandrite is less suitable. Purpose: similar to #9. Mechanism: wavelength also absorbed by melanin for follicle damage. PMC

11. Laser hair reduction (Nd:YAG 1064 nm) — Useful for darker skin types. Purpose: safer option with deeper penetration. Mechanism: targets follicle melanin with lower epidermal melanin absorption. PMC

12. Intense pulsed light (IPL) hair reduction — Broad-spectrum light devices, some FDA-cleared (510(k)). Purpose: reduce hair in suitable skin/hair types. Mechanism: filtered light heats pigmented follicles. FDA Access Data

13. Electrolysis — Follicle-by-follicle destruction with electric current. Purpose: permanent removal of individual hairs not responsive to lasers (e.g., very light hairs). Mechanism: thermal/chemical injury to the follicle. (Background on hypertrichosis management.) NCBI

14. Skin cooling and sun protection around laser sessions — SPF and avoidance of tanning. Purpose: reduce burns, pigment changes. Mechanism: minimizes epidermal melanin activation and post-inflammatory hyperpigmentation. PubMed

15. Dermatology grooming plan — Safe shaving/depilatories with patch testing. Purpose: short-term control between laser sessions. Mechanism: mechanical or chemical hair shaft removal without affecting root permanently. NCBI

16. Psychosocial support — Address self-image and social concerns. Purpose: reduce anxiety/stigma related to visible differences. Mechanism: counseling, support groups. (Hypertrichosis and limb differences often benefit from counseling.) NCBI

17. Peri-anesthetic pediatric pathways — Age-appropriate fasting, pain control. Purpose: safe surgery in infants/toddlers. Mechanism: standardized pediatric anesthesia protocols (aligned with timing data). PMC

18. Scar care after hand surgery — Silicone gel/sheets and massage. Purpose: flatter, softer scars; better motion. Mechanism: hydration/pressure modulates collagen remodeling after syndactyly release. PMC

19. Home exercise and caregiver training — Simple range-of-motion and play-based tasks. Purpose: embed therapy in daily life. Mechanism: frequent, gentle movement supports tendon glide and joint mobility. PMC

20. Transition planning to adolescence/adulthood — Reassess function and cosmetic goals as activities change. Purpose: decide on any late revisions or hair-reduction touch-ups. Mechanism: periodic multidisciplinary review. Jhandsurg

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Medicines

There are no FDA-approved drugs specifically for “autosomal dominant preaxial polydactyly–upper-back hypertrichosis syndrome.” Treatment is surgical and device-based (e.g., lasers) plus supportive care. For the hair-growth component, the only FDA-approved pharmacologic product that directly slows hair growth is topical eflornithine 13.9% cream (brand Vaniqa)—approved for facial hair reduction in women. It’s sometimes considered off-label by dermatologists for other areas in carefully selected cases; however, safety/benefit must be individualized, especially in children. FDA Access Data+1

Eflornithine 13.9% cream (Vaniqa®)

Class: Ornithine decarboxylase inhibitor (slows hair growth). Dose/Use: Thin layer twice daily to affected area (per label for adult women’s facial hair). Onset/Time: Improvements often by 8 weeks; hair returns toward baseline about 8 weeks after stopping. Purpose: Reduce the speed and thickness of unwanted hair, making other methods (e.g., shaving/laser) easier. Mechanism: Inhibits polyamine synthesis in follicles, slowing matrix keratinocyte proliferation. Common side effects: Temporary stinging/burning, acne, rash, folliculitis; avoid mucosal contact. Note: US market availability has varied; check local availability. Off-label use requires specialist oversight—especially for non-facial sites or pediatric patients. FDA Access Data+1

Because the condition’s core problem is congenital limb formation (not inflammation or a metabolic pathway we can “block”), systemic drugs do not correct the digit patterning. That is why the high-value interventions are hand/foot surgery and hair-reduction devices rather than pills. PMC+1

Multiple alexandrite (755 nm), diode (≈810 nm), and Nd:YAG (1064 nm) lasers and IPL systems hold FDA 510(k) clearances for long-term or permanent hair reduction. These devices act by selective photothermolysis—melanin absorbs light, converts it to heat, and damages the follicle/bulge stem cells. Your dermatologist chooses wavelength by hair/skin type for safety and efficacy. PMC+4FDA Access Data+4FDA Access Data+4

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Dietary molecular supplements

There are no supplements that fix SHH-related limb patterning or reliably reverse congenital hypertrichosis. If families use supplements, they should be framed as general skin/hair health support, not cures, and checked for safety in children. Below are commonly discussed nutrients with general rationale (not disease-modifying). Always review with your clinician.

1. Protein (adequate dietary intake) — Supports wound healing after surgery and normal hair keratin formation; deficiency can worsen hair quality. Typical pediatric dosing = dietary planning, not pills. (General hypertrichosis care background.) NCBI

2. Biotin — Popular for hair quality; evidence for excess hair reduction is lacking; high doses can interfere with lab tests. Use only if deficient. NCBI

3. Vitamin D — Broad skin/immune support; correct deficiencies to support healing. Not disease-specific. NCBI

4. Vitamin C — Collagen co-factor; helpful in wound healing after reconstructive surgery. PMC

5. Zinc — Supports epithelial repair; supplement only if deficient. NCBI

6. Omega-3 fatty acids — General anti-inflammatory benefits for skin; not specific to hypertrichosis. NCBI

7. Copper/iron (if deficient) — Correcting deficiency prevents brittle hair; supplementation only when labs indicate. NCBI

8. Probiotics — Sometimes used to support skin barrier/immune tone; not disease-modifying. NCBI

9. Silicon (orthosilicic acid) — Marketed for hair strength; evidence modest; avoid in children unless directed. NCBI

10. Hydration/electrolytes — Adequate fluids aid skin elasticity and healing. NCBI

Important: None of these supplements reduce congenital upper-back hair or alter SHH-driven limb development. They are adjuncts at best and should be clinician-guided, especially in children. NCBI

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Immunity booster / regenerative / stem-cell drugs

There are no FDA-approved “immunity boosters,” regenerative medicines, or stem-cell drugs that treat this syndrome. Hand/foot differences result from developmental patterning before birth, so postnatal “regenerative” drugs do not re-pattern digits. Efforts should focus on surgical correction and rehabilitation. Lasers/devices—not drugs—address hypertrichosis. PMC+1

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Surgeries

1. Excision of accessory thumb with reconstruction — Removes the extra digit and repairs ligaments/tendons to create one stable thumb. Why: improve pinch, function, and symmetry. PMC

2. On-top plasty / partial transfer — Transfers the best parts of duplicated digits (e.g., nail/phalangeal segment) to build a single, stronger thumb. Why: optimize motion and appearance when neither duplicate is ideal alone. PMC

3. First web space deepening and syndactyly release — Separates fused skin between thumb and index, adds skin flaps/grafts to deepen the web. Why: restore span for grasp and fine motor tasks. PMC+1

4. Osteotomy or joint realignment — Corrects angulation or malalignment as the child grows. Why: improve stability and function; reduce pain or deformity. Jhandsurg

5. Hallux (big toe) duplication correction — Similar principles applied to feet to improve gait, shoe wear, and comfort. Why: prevent pressure points and enable normal walking. Journal of Materials Chemistry A

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Prevention & safety tips

1. Early referral to pediatric hand/foot and dermatology teams—best outcomes with planned timing. PMC

2. Avoid tanning before/after laser hair procedures to reduce burn risk. PubMed

3. Sun protection on treated skin (SPF, clothing). PubMed

4. Adhere to post-op splinting/therapy to prevent stiffness. PMC

5. Watch for scar problems (raised, tight scars) and seek care early. PMC

6. Use devices with proper FDA clearance and trained operators. FDA Access Data+1

7. Patch-test depilatories to avoid irritant dermatitis on the back. NCBI

8. Maintain healthy nutrition for wound healing. PMC

9. Psychosocial support for child and family to address self-image. NCBI

10. Plan long-term follow-ups into adolescence for function and cosmetic goals. Jhandsurg

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When to see doctors

• Right after birth/diagnosis: Pediatrician should refer to pediatric hand/foot surgeon and genetics for counseling. Early plans often lead to better hand function. PMC

• Before 1 year of age: Surgical consult to discuss timing (often 7–12 months for thumb duplication; individualized for syndactyly). PMC+1

• Dermatology visit when hair causes distress or skin issues—discuss laser options and timing; assess skin type and risks. PMC

• Any time there’s pain, stiffness, visible deformity progression, skin color change after laser, or scar problems—seek care promptly. PMC

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What to eat / what to avoid

Eat:

• A balanced diet with adequate protein (fish, eggs, dairy/legumes), fruits/vegetables (vitamins C, A), and whole grains to support incision healing and skin integrity after surgery. Hydrate well. PMC

Avoid or limit:

• New supplements without clinician advice, particularly in children.

• Sun exposure and tanning around laser sessions (higher burn/pigment risk).

• Harsh depilatories or abrasive scrubs on sensitive post-laser skin. PubMed

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Common questions

1. Is this condition hereditary? Yes—autosomal dominant; each child of an affected parent has a 50% chance. Orpha

2. What causes it? A regulatory change near SHH that alters limb and hair-follicle development signals. PMC

3. How rare is it? Extremely rare (<1 in 1,000,000). Orpha

4. When does it show up? At birth (neonatal). Genetic Rare Diseases Center

5. Are there lab tests? Mostly imaging (X-rays) and genetic testing when available. PMC

6. Can medicines fix extra digits? No—surgery is needed for function/appearance. PMC

7. Can medicines stop the back hair? Only topical eflornithine slows hair growth (approved for women’s facial hair); other sites/ages are off-label decisions. FDA Access Data

8. Do lasers really work? Yes—multiple FDA-cleared lasers/IPL reduce hair long-term by selective photothermolysis. FDA Access Data+1

9. What are laser risks? Temporary redness, swelling, pigment change; minimized by choosing correct device for skin type and avoiding sun. PubMed

10. When is hand surgery done? Often 7–12 months; syndactyly release timing varies with web space and finger lengths. PMC+1

11. Will my child need more than one surgery? Possibly; some need revisions during growth. Jhandsurg

12. Will hair come back after stopping eflornithine? It tends to approach baseline ~8 weeks after stopping. FDA Access Data

13. Is there a cure? No cure to change embryologic patterning, but surgery + lasers provide excellent functional and cosmetic outcomes. PMC+1

14. Does diet help? Only as support for wound healing and general health; it does not change the genetic cause. PMC

15. Should we screen relatives? Offer genetic counseling/testing to at-risk relatives planning pregnancies. OrphN

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: October 04, 2025.

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