Bioderma Congress Reports WCPD 2025

Reports written by Dr Maria Florencia Martinez (Pediatrician & Pediatric dermatologist, Argentina)

Psoriasis and seborrheic dermatitis

Speaker: Enrique Salvador Rivas Zaldivar (Guatemala)

Introduction

• The talk focused on the clinical and dermatoscopic differentiation between scalp psoriasis and seborrheic dermatitis in children and adolescents, both common diagnoses seen in pediatric dermatology.
• Special attention was given to scalp hyperkeratosis, which is frequently encountered and may represent various underlying conditions:
  • Most commonly: Atopic dermatitis and seborrheic dermatitis
  • Other considerations: Scalp Psoriasis and Tinea capitis

  • Less frequent but important systemic diseases: Dermatomyositis and Langerhans cell histiocytosis

Clinical Features: Psoriasis vs. Seborrheic Dermatitis

Even histology can be inconclusive in some overlapping presentations.
That’s where dermatoscopy (trichoscopy) becomes essential.

Trichoscopy: A Non-Invasive Diagnostic Aid

Vascular Patterns – The Key Differentiator:

• Zoom level matters: 10x is often not enough to see vessels clearly, 50x magnification is preferred.
• Gel application (e.g., ultrasound gel) is recommended to avoid flush artifacts that may distort vascular visualization.

Classification of Scalp Psoriasis Patterns

(Bruni et al., 2021)

1. Plaque Psoriasis – Classic well-demarcated red plaques with scaling
2. Thin Scale Psoriasis – Subtle erythema, fine scale
3. Sebopsoriasis – Overlap appearance with greasy scale
4. Psoriatic Cap – Thick scale buildup without overt erythema
5. Pityriasis Amiantacea Type – Common in children, adherent scales surrounding hair shafts
6. Cicatricial Psoriasis – Rare, with scarring features
7. Pustular Psoriasis – Very rare in the pediatric scalp

Clinical Subtypes of Seborrheic Dermatitis by Age

• Infants: Cradle cap
• Younger children: Fold involvement (retroauricular, perioral)
• School-aged: Often associated with atopic dermatitis
• Adolescents: Often worsened by acne, hormonal changes, and oily skin

Contributing factor: Malassezia spp. overgrowth in all age groups

Study Reference: Prof. Kim (Korea, 2011)

• Validated the use of vascular pattern analysis via trichoscopy to distinguish between psoriasis and SD.
  • Psoriasis: red dots and globules, glomerular vessels, twisted red loops
  • Seborrheic Dermatitis: arborizing vessels, atypical red vessels 

Take-Home Points

• Scalp psoriasis and seborrheic dermatitis can be hard to distinguish clinically, especially in children.
• Trichoscopy is a key tool to avoid misdiagnosis and reduce unnecessary biopsies.
• Main differentiator = Vascular pattern:
  • Psoriasis → glomerular, regular red dots
  • SD → blurry, arborizing vessels
• Always consider extra-scalp clues: nail changes, extensor plaques (psoriasis), facial fold involvement, and AD background (SD).

References:

- Bruni F, et al. Clinical and trichoscopic features in various forms of scalp psoriasis. J Eur Acad Dermatol Venereol. 2021 Sep;35(9):1830-1837.

- Silverberg NB. Scalp hyperkeratosis in children with skin of color: diagnostic and therapeutic considerations. Cutis. 2015 Apr;95(4):199-204

- Waśkiel-Burnat A et al. Differential diagnosis of red scalp: the importance of trichoscopy, Clinical and Experimental Dermatology, 2024, Setp; 49 (9): 961–968

- Kim GW et al. Dermoscopy can be useful in differentiating scalp psoriasis from seborrhoeic dermatitis. Br J Dermatol. 2011 Mar;164(3):652-6

Tinea capitis and pediculosis

Speaker: Arturo Lopez Yañez Blanco (Mexico)

Tinea capitis

The speaker began with a general overview of tinea capitis emphasizing that it's a fungal scalp infection mainly affecting children (98%), caused by dermatophytes of the Trichophyton and Microsporum genera.

Epidemiology & Clinical Forms

The etiological agents vary by region: M canis, T tonsurans, M audouinii, T mentagrophytes, T verrucosum. 

Two main clinical forms:

Diagnostic Tools

• Clinical examination
• Microscopy
• Wood’s lamp 
• Molecular methods 
• Trichoscopy (important tool emphasized throughout):

Triad of signs (hair loss, scaly patches, peritoneal involvement) = high predictive value (95%).

Differential Diagnosis: 

• Lupus
• Alopecia areata
• Seborrheic Dermatitis 
• Dissecting cellulitis 

Treatment Recommendations

• Systemic antifungals are essential.
• Griseofulvin (20-25 mg/k/d during 8-12 weeks longer is culture is positive) and Terbinafine (3-6 mg/k/d during 4 weeks (Tricophyton) to 8-12 weeks (Microsporum)) recommended first-line.
• Choice depends on fungal culture result and drug availability.
• Topical agents recommended as adjuvant therapy (twice weekly).
• Remove fomites 
• Household screening and treatment are crucial to prevent recurrence.

Common parental questions addressed:

• School return: after treatment initiation.
• No need for haircuts or use of hats.

Tracing contact in school is essential.

• Measures at home: avoid sharing personal items, boil and sanitize possible fomites for 5 minutes, pets should be examined. 

Pediculosis capitis

Introduction

• Ectoparasitic infection of the hairs and scalp 
• Public global health problem
• Affects children aged 6–12 years.
• Females more affected.
• Transmission: direct contact (lice don't jump or fly).
• Examination revealed white nodes, prompting evaluation for nits vs. pseudo-nits.
  
  Differential Diagnosis

Trichoscopic Differences

True nits: brown with oval heads.

Pseudonits: translucent, grayish, black tips.

Clinical Signs

• Occipital/cervical pruritus
• Lymphadenopathy
• Fast-moving lice, difficult to spot (can move ~23 cm/min)
• May co-occur with other scalp conditions (e.g., alopecia areata)
• Complications: secondary bacterial infection

Treatment

No major new treatments. Conventional therapy remains effective.

Education for parents about lice behavior and contagion is essential.

References:

• Vargas-Navia N et al. Tiña Capitis en niños. Revista chilena de pediatría. 2020:91(5), 773-783
• Kinoshita-Ise M, et al. Update on trichoscopy: Integration of the terminology by systematic approach and a proposal of a diagnostic flowchart. J Dermatol. 2022 Jan;49(1):4-18.
• Aqil N, et al. A prospective study of tinea capitis in children: making the diagnosis easier with a dermoscope. J Med Case Rep. 2018 Dec 28;12(1):383
• Lacarrubba F, et al. Trichoscopy in the Differential Diagnosis of Pseudonits. Skin appendage disorders. 2019: 5; 142-145

Effluvium in pediatric population

Speaker: Cecilia Navarro Tuculet (Argentina) 

Pediatric telogen effluvium – causes, diagnosis, and management

Introduction:

• Telogen effluvium (TE) is a form of diffuse non-scarring hair loss caused by an abnormal shift in follicular cycling leading to premature shedding.
• Incidence in Children: Data on pediatric TE is limited; most studies have been conducted on adults. Point prevalence of TE in children is 2.7%.

Types of Telogen Effluvium:

1. Acute TE
   • Develops within 2-3 months of the inciting factor.
   • Self-limited and resolve within 3 months.
2. Chronic TE
   • Persistent shedding for over 6 months.

Common Triggers of Telogen Effluvium in Children:

• Emotional Stress
• Chronic illness (e.g., rheumatic, collagen, vascular diseases)
• Acute Illness (e.g., viral infections, febrile conditions)
• Nutritional Deficiencies (low ferritin, zinc, vitamin D)
• Endocrine Disorders (thyroid disease, androgen excess)
• Medications (e.g., anticoagulants, beta-blockers, retinoids)
• Infectious Diseases (e.g., post-COVID, dengue outbreak)
• Inflammatory Scalp Conditions (e.g., seborrheic dermatitis)
• Eating Disorders (e.g., rapid weight loss)

Prevalence in Pediatric Population:

• Acute TE: Common after viral infections like COVID-19 and dengue.
• Chronic TE: Frequently triggered by nutritional deficiencies, especially low ferritin and zinc.

Diagnosis and Evaluation:

1. History and Physical Exam:
   • Assess duration, rate, location, and extent of hair loss.
   • Associated symptoms: pain, tenderness, pruritus.
   • Hair care behavior: grooming or use of hair care products. 
   • Differentiate hair shedding from breakage.
2. Scalp Exam:
   • Evaluate: erythema, scales, pustules, papules, erosions, excoriations.
   • Hair Pull test 
   • Hair loss pattern is typically diffuse, especially in the bitemporal area.
   • Dermoscopy: Empty follicles and upright regrowing hairs of normal thickness; differentiation from androgenetic alopecia using hair shaft diameter variability.

3. Additional Tests:
   • Scalp Biopsy: To distinguish TE from other conditions (e.g., alopecia areata).
   • Trichogram: To assess the proportion of telogen vs. anagen hairs.
   • Hair Collection: Useful to quantify and track the hair loss over time.

Differential Diagnosis:

• Anagen Effluvium: Hair loss from chemotherapy or toxins (over 80% of scalp hair).
• Androgenetic Alopecia: Characterized by miniaturized hairs.
• Diffuse Alopecia Areata: Diffuse hair thinning with possible exclamation-point hairs.
• Loose Anagen Syndrome: Easily extracted hair, typically in blonde females.
• Structural hair disorders: weakening of the hair shafts. 

Management:

1. Reassurance and Avoidance of Triggers:
   • TE is usually self-limiting and requires removal of inciting factors.
   • Psychological Support for emotional distress is crucial.
2. Treatment Options:
   • Minoxidil: Its use in children is uncertain. Not first-line therapy.
   • TE typically resolves after 2-3 months of active shedding, followed by stabilization and regrowth within 6-12 months.
3. Prognosis:
   • TE is generally self-limiting. Once triggers are addressed, hair regrowth is typically seen within 6-12 months.

Take-Home Messages:

1. Key Triggers: Emotional stress, febrile illness, and nutritional deficiencies.
2. Patient Evaluation: Inquire about hair styling and rule out traction alopecia.
3. Diagnosis: Use dermoscopy to differentiate between TE and other forms of alopecia.
4. Management: Provide reassurance; minimize trigger exposure and offer psychosocial support.
5. Prognosis: TE is self-limiting; improvement expected within 6-12 months.

References: 

• Chen V, et al.  Etiology, management, and outcomes of pediatric telogen effluvium: A single-center study in the United States. Pediatric dermatology. 2023; 2023 (1): 120-124
• Thomas M, et al. A Single Centre Retrospective Review of Nutritional Deficiencies Associated With Telogen Effluvium in the Paediatric Population in Canada. J Cutan Med Surg. 2022;26 (4): 420-421
• Kim HS, et al Braids or Pony-Tail-Associated Traction Alopecia in Female Children. Ann Dermatol. 2019 Feb;31(1):117-119.

Loose anagen syndrome versus short anagen syndrome

Speaker: Arturo Lopez Yañez Blanco (Mexico) 

Introduction:

• Although both SAS and LAHS are present with short hair in children, they are distinct disorders.
• They may appear similar but differ in pathophysiology, clinical findings, and diagnostic features.

Short Anagen Syndrome (SAS)

Definition:

• Benign disorder due to shortened anagen phase.
• It leads to an inability to grow long scalp hair.

Epidemiology:

• Primarily affects Caucasian females, aged 2–6 years.

Pathophysiology:

• Shortened anagen phase → hair does not grow long before transitioning to telogen.
• WNT10A gene mutation in ~40% (suggestive of autosomal dominant pattern).

Clinical Features:

• Hair appears short, sparse, and thin.
• Often, it affects bilateral frontoparietal scalp.
• May be associated with:
• Inner scleroderma
• Nail changes (e.g. micronychia)
• Trichodysplasia síndromes
• No hair fragility or breakage.
• It can significantly impact psychosocial well-being.

Diagnostic Findings:

• Pull test: Negative or mildly positive.
• Trichoscopy: Normal.
• Haircut test: Conical tips.
• Trichogram: Increased telogen hairs, anagen:telogen ratio reversed (e.g. 1:2).
• Microscopy: Normal anagen hairs.

Loose Anagen Hair Syndrome (LAHS)

Definition:

• Hair shedding disorder due to defective anchoring of anagen hairs in the follicle.

Epidemiology:

• Typically affects female children, ages 6–10 years.
• May be underdiagnosed in males.

Pathophysiology:

• Defective keratinization of the inner root sheath.
• Poor adhesion between outer and inner root sheaths.
• Linked to keratin gene mutations.

Clinical Features:

• Diffuse hair loss, especially in occipital and parietal areas.
• Hair easily and painlessly extracted.
• Associated conditions: Noonan syndrome, trichorhinophalangeal syndrome.
• May lead to psychological distress.

Diagnostic Findings:

• Pull test: Positive and painless.
• Trichoscopy:
• Vellus hair and slightly pigmented hairs
• Dirty dots
• Scalp scales 
• Cadaveric hair
• Granular rectangular structures
• Trichogram: Loose anagen hairs with ruffled cuticles, "pockey stick" morphology.
• Microscopy: Confirms disrupted inner root sheath.

Differential Diagnosis:

• SAS (normal or thin hair diameter)
• Telogen effluvium (regrowing hairs, single hair follicular units) 
• Diffuse alopecia areata (black and yellow dots, broken hairs)
• Androgenetic alopecia (anisotrichosis, vellus hairs, single hair follicular units, perifollicular pigmentation)

Treatment and Management (Both Conditions):

• Reassurance and education of parents.
• Spontaneous improvement often occurs with age.
• For selected cases with psychosocial impact:
• Topical minoxidil 2–5%,
• Oral minoxidil: max 0.02 mg/kg/day
• Supportive care:
• Gentle grooming
• Camouflage
• Counseling

Comparison Table: SAS vs. LAHS

Clinical presentation:

• Scarring alopecia
• Perifollicular erythema
• Scaling
• Atrophic areas
• Follicular hyperkeratosis
• Predominantly in vertex and parietal regions

Treatment:

Secondary Cicatricial Alopecia – Hair Transplantation

• Study included 13 children with post-burn scalp alopecia (10 males, 3 females).
  • Hair transplantation shown to be Safe and effective for secondary cicatricial alopecia

Differential Diagnosis: Congenital Triangular Alopecia (CTA)

• A non-cicatricial and benign alopecia, usually first noted in infancy or early childhood.
• Can mimic cicatricial alopecia due to trichoscopic overlap.

Clinical characteristics:

• Triangular, oval, or lancet-shaped patches
• Apex typically oriented toward the vertex

Take-Home Messages

• Early diagnosis is essential to prevent progression and improve long-term outcomes.
• Lichen planopilaris (LPP) is the most frequent primary cicatricial alopecia in pediatric populations (~11 years average age).
• Secondary alopecia, especially post-burn, can be managed with hair transplantation.
• Conditions like congenital triangular alopecia must be considered in differential diagnosis to avoid mismanagement.
• More clinical and epidemiological studies are needed in the pediatric population.

References: 

• Carmichael AR, et al. Cicatricial Alopecia in the Pediatric Population: A Case Series and Review of the Literature. Pediatr Dermatol. 2025 Jan 29. doi: 10.1111/pde.15864. Epub ahead of print
• Papierzewska M, et al. Lichen Planopilaris in Children: A Systematic Review. Pediatr Dermatol. 2025 Jan-Feb;42(1):22-30.
• Wang J, et al. Application of Autologous Hair Transplantation Technique in Children with Cicatricial Alopecia. Adv Ther. 2023 Sep;40(9):4024-4031.
• Starace M, et al. Atypical Presentation of Congenital Triangular Alopecia: A Case Series in Italy. Dermatol Pract Concept. 2020 Oct 26;10(4):e2020122

My most challenging cases

Speaker: Lizet Rojano Fritz (Colombia)

Case 1: Tinea Capitis + Trichotillomania

Key Point:
Consider dual diagnoses in pediatric alopecia. Always confirm tinea capitis via culture.

Trichoscopy – Findings by Condition

Case 2: Inactive Linear Morphea – Hair Transplant

Key Point:

Hair transplantation can be effective in inactive morphea with no ongoing inflammation.

Case 3: Trichorhinophalangeal Syndrome Type I (TRPS I)

Key Point:
In congenital hypotrichosis, always assess for syndromic features and genetic testing.

Final Clinical Takeaways

• Multiple pathologies may coexist in pediatric alopecia (e.g., tinea + trichotillomania).
• Culture remains the gold standard for Tinea capitis diagnosis.
• Hair transplantation is a valid treatment for inactive linear morphea.
• Genetic evaluation is critical when hair loss presents dysmorphic features.

References: 

• Rudnicka L, et al. Atlas of Thrichoscopy. 
• Sonthalia S, et al. Linear Patch of Alopecia in a Child: Trichoscopy Reveals the Actual Diagnosis. Skin Appendage Disord. 2019 Nov;5(6):409-412
• Saceda-Corralo D, Tosti A. Trichoscopic Features of Linear Morphea on the Scalp. Skin Appendage Disord. 2018 Jan;4(1):31-33.
• Glaser DH, et al. Linear Scleroderma of the Head - Updates in management of Parry Romberg Syndrome and En coup de sabre: A rapid scoping review across subspecialties. Eur J Rheumatol. 2020 Feb;7(Suppl1):S48-S57

Androgenetic alopecia

Speaker: Luis Sanchez Dueñas (Mexico)

General Overview

• Pathophysiology: Miniaturization of hair follicles due to susceptibility to androgens (not elevated serum androgens).
• Paradox: Androgens promote terminal hair in some regions (beard, axilla, etc.) but cause miniaturization in scalp due to receptor sensitivity 
• Key areas of scalp involvement:
  • Males: Frontal-temporal and vertex
  • Females: Crown

In Children & Adolescents

• Onset after adrenarche (ages 6–9) due to adrenal androgen (DHEA) production
• Clinical pattern in males often resembles female pattern (MAGA-F)
• Inflammation may be more frequent in pediatric biopsies
• Trichoscopic features mirror adult patterns but with earlier onset

Trichoscopy

• Main differentiator: Hair diameter variability 
  (not seen in telogen effluvium or alopecia areata)

Epidemiology & Clinical Data

• Youngest reported case: 6 years old
• Sex distribution: Male predominance overall
• Family history: Present in ~75% of pediatric cases
• Common comorbidity: Acne, insulin resistance

Associated Conditions (Comorbidities)

• Endocrine:
  • Non-classical congenital adrenal hyperplasia
  • Insulin resistance (frequent)
  • Thyroid dysfunction
• Metabolic:
  • Obesity
  • Metabolic syndrome
• Mental Health:
  • Depression
  • Anxiety
  • Social withdrawal
• Cutaneous:
  • Acne
  • Seborrhea
  • Hirsutism

Referral & Workup Recommendations

Differential Diagnosis: Telogen effluvium, Alopecia areata, trichotillomania 

Treatment Algorithm (Not Officially Approved)

First-line (Both sexes):

• Topical Minoxidil 2% - 5%

If partial response:

• Add low-dose oral minoxidil:
  • Females: 0.25–0.5 mg/day
  • Males: 1–2.5 mg/day

Adjuncts:

• Topical/oral Finasteride (Males/Females)
• Oral Spironolactone (Females only)

Advanced therapy (if poor response):

• Females: Oral Finasteride 2.5 mg
• Males: Oral Finasteride 1 mg

Adverse Events Noted

Clinical Cases

• Telogen effluvium may precede androgenetic alopecia
• Association with acne, dermatitis, and metabolic disorders is frequent 
• Case example: Insulin resistance aggravates alopecia flare

Take-Home Messages

• AGA in children/adolescents is underdiagnosed and underreported
• Often associated with systemic androgen sensitivity → Requires systemic evaluation
• Trichoscopy is the cornerstone for early diagnosis
• Treat early to prevent irreversible follicular loss
• Strong need for multidisciplinary approach

References: 

• Gomes TF, et al. Pediatric androgenetic alopecia: an updated review. J Dtsch Dermatol Ges. 2023 Jan;21(1):19-25.
• Gonzalez ME, et al. Androgenetic alopecia in the paediatric population: a retrospective review of 57 patients. Br J Dermatol. 2010 Aug;163(2):378-85
• Tosti A, et al. Androgenetic alopecia in children: report of 20 cases. Br J Dermatol. 2005 Mar;152(3):556-9
• Griggs Jet al. Pediatric androgenetic alopecia: A review. JAAD. 2021;85 (5): 1267 - 1273

Alopecia areata

Speaker: Sonia Ocampo-Garza (Mexico)

General Overview

• Type: Non-scarring, autoimmune alopecia
• Pediatric onset: ~20% of cases begin in childhood
• Course: Chronic, unpredictable, with high relapse rates
• Spontaneous regrowth: ~50% within 1 year
• Impact: Significant psychological burden and ↓ quality of life
• Evidence: No preventive or curative treatment; limited RCTs

Clinical Classification and Management Strategy

Topical and Intralesional Corticosteroids

• Topical: High-potency (e.g. clobetasol) effective vs. low-potency (hydrocortisone)
  → Clobetasol: 85% ≥50% regrowth vs. Hydrocortisone: 33% (at 24 weeks)
• Intralesional Triamcinolone:
  • Recommended in children >10 years with localized disease
  • Usual doses: 2.5, 5, 10 mg/mL
  • 5 mg/mL preferred (higher regrowth vs. 2.5 mg/mL)
  • Max: ≤20 mg per session
  • Injection depth: Bulb-level, unlike superficial injection in scarring alopecias

Systemic Corticosteroids

• Preferred: Oral dexamethasone or betamethasone mini pulses
  • Dose: 0.1 mg/kg, 2 days/week
  • ↓ Side effects, ↓ relapse vs. daily/oral IM

Minoxidil

Methotrexate

• Dose: 0.2–0.4 mg/kg/week + folic acid
• Age range studied: 8–18 years
• Response: 50% regrowth in 5/40 patients
• Discontinue if no response after 6–9 months

Hydroxychloroquine

• Limited evidence
• 9 patients: 5 responders, 4 non-responders
• Mean SALT score improvement: 3.2

Topical Immunotherapy

Agents:

• SACV (Squaric acid dibutyl ester)
• DPCP (Diphenylcyclopropenone)

Protocol:

1. Sensitize with 2% solution on small area
2. After 2–3 weeks: initiate treatment with 0.0001–0.001%
3. Gradual titration to induce mild dermatitis
4. If there is no regrowth after 6 months, discontinue

Adverse Events:

• Contact dermatitis, vesicles, lymphadenopathy, edema, pigmentary changes, flu-like symptoms

JAK Inhibitors

• Recurrence: High after discontinuation
• Limitation: High cost, limited long-term safety data

Treatment Summary by Pattern and Activity

Take-Home Messages

• Choose therapy based on age and disease extent
• Avoid discontinuation before 3–6 months
• First-line: Topical corticosteroids + Minoxidil
• Consider oral mini pulses for extensive or rapidly progressing cases
• JAK inhibitors and immunotherapy: viable for severe cases
• Limited evidence for pediatric populations — interpret cautiously

References: 

• Garnacho Saucedo G, et al. Treatment of alopecia areata in children. Piel. 2016; 31 (8): 582-588
• Lenane P, et al. Clobetasol propionate, 0.05%, vs hydrocortisone, 1%, for alopecia areata in children: a randomized clinical trial. JAMA Dermatol. 2014 Jan;150(1):47-50.
• Chu, T et al. Benefit of different concentrations of intralesional triamcinolone acetonide in alopecia areata: An intrasubject pilot study. JAAD. 2015; 73 (2): 338 – 340
• de Nicolas-Ruanes B, et al. Low-dose oral minoxidil for treatment of androgenetic alopecia and telogen effluvium in a pediatric population: A descriptive study. J Am Acad Dermatol. 2022 Sep;87(3):700-702

Topical therapy update

Speaker: Lawrence Eichenfield (USA)

Opening Remarks and Clinical Context

Despite recent advances in systemic agents, topical care remains foundational in AD management, even in patients on systemic treatment.

Topical therapy includes:

• General skin care (e.g., moisturization, barrier repair)
• Topical corticosteroids
• Calcineurin inhibitors
• Newer non-steroidal agents

A critical point raised is that new topical agents are typically studied against vehicles, rather than active comparators like corticosteroids, and usually as monotherapy, which doesn’t reflect real-world practice where combination therapy is common.

The speaker's core message to patients is to aim for long-term disease control, defined as:

• Minimal rash
• Minimal itch
• Minimal sleep disturbance

Wrestling with Steroid Phobia: The Topical steroid withdrawal phenomenon

Topical corticosteroids remain first-line treatment in many cases. 

Steroid phobia is discussed with a notable shift from concern about atrophy to a growing belief in "topical steroid addiction" (TSA). The speaker highlights the video “Skin on Fire” as an example of this messaging. (https://www.youtube.com/watch?v=GuaBbsL1qKA)

While topical steroid withdrawal syndrome (TSW) is a recognized phenomenon, particularly in adults (rare in pediatric population) with long-term use, the concept of widespread topical steroid addiction lacks evidence. 

A Swedish internet survey of self-identified TSW patients (recruited via Facebook) reported:

• Common symptoms: burning, pruritus, neuropathic sensations
• Some were still using topical corticosteroids
• High psychosocial burden including school/work absenteeism

Challenges in Comparing Topical Agents

• Meta-analysis limitations due to inconsistent outcome measures and population variability 
• A Cochrane network meta-analysis on topicals identified: 
• Very potent corticosteroids are the most effective
• Low-dose tacrolimus surprisingly ranked second, based on a small 30-patient study

Real-World Corticosteroid Effectiveness

Clinical trial data may overstate perceived effectiveness. In a study of BID mid-potency corticosteroids for 4 weeks:

• 25% of patients achieved clear/almost clear
• 15% reached EASI-90
• About one-third had ≥4-point itch reduction

These results reflect modest short-term efficacy even for traditional agents, reinforcing the need for novel therapies.

Newer Non-Steroidal Topical Therapies

1. Topical Ruxolitinib (JAK1/2 Inhibitor)

• Formulation: 1.5% cream
• Approved in the U.S. for patients 12+ years, with studies down to age 2
• Rapid antipruritic effect
• In phase 2, superior to triamcinolone 0.1% for IGA success and EASI-75
• Well-tolerated with low stinging/burning; systemic absorption limits use to ≤20% BSA

Pediatric Data: In 2–12-year-olds, ~56% achieved clear/almost clear with BID application.

2. Tapinarof (Aryl Hydrocarbon Receptor Agonist)

• Approved for ages 2+
• Mechanism: AHR activation reduces oxidative stress, inhibits T-resident memory cells
• Phase 3 study: ~46% clear/almost clear; mean baseline BSA = 17%
• Well-tolerated, even on sensitive skin
• Unique AE: Follicular events, possibly due to keratinocyte upregulation

Long-term data:

• 1-year study: 82% reached clear/almost clear with intermittent use
• No systemic absorption; no BSA restrictions

3. Crisaborole (Topical PDE4 Inhibitor)

• Approved ≥3 months of age
• Shown to be safe and effective for long-term daily use (1 year)
• Used for mild-to-moderate AD

4. Roflumilast (PDE4 Inhibitor)

• In AD studies: ~30% clear/almost clear after QD for 4 weeks
• Extension trial: Twice-weekly proactive use-maintained remission for ~281 days
• Good tolerability and long-term safety data emerging

5. Delgocitinib (Pan-JAK Inhibitor)

• Approved in some regions for chronic hand eczema
• Demonstrates good results in clinical and QoL metrics
• May have broader dermatologic applications in the future

Clinical Implications and Future Direction

Current Topical Options

• Steroids remain first-line, but usage varies due to safety concerns and access
• Calcineurin inhibitors (tacrolimus/pimecrolimus) remain valuable
• New non-steroidals are expanding options, especially for sensitive skin areas and steroid-phobic patients

Cost and Access Challenges

• Many new agents are cost-prohibitive, which limits routine use
• Insurance access varies significantly

Combination Therapy and Real-World Practice

• While trials study monotherapy, in practice we combine topical agents
• There's increasing interest in proactive therapy to maintain remission
  • Tacrolimus and roflumilast have data supporting this approach
  • Tapinarof has shown drug-free remission lasting 60–80 days in some patients

Closing Thoughts

• The landscape of topical therapy for AD is evolving rapidly
• There is now a broader armamentarium of steroid-sparing options with novel mechanisms
• The challenge lies in determining optimal integration, balancing:
  • Efficacy
  • Safety
  • Cost-effectiveness
  • Patient preferences

References: 

• Buethe MG, et al. Topical The rapy fo r A topic Dermatitis. What is New and the New Paradigm. Dermatol Clin. 2024; 42 (4): 569-575
• Kleinman E, et al. What's New in Topicals for Atopic Dermatitis?. Am J Clin Dermatol. 2022;23 (5): 595-603
• Alsterholm M et al. Topical Steroid Withdrawal in Atopic Dermatitis: Patient-reported Characterization from a Swedish Social Media Questionnaire. Acta Derm Venereol. 2025;3:105
• Lax SJ, et al. Topical anti-inflammatory treatnebts for eczcema: network meta-analysis (Review). Cochrane database Syst Rev. 2024;8 (8):Cd015064. 
• Simpson EL, et al. Long-Term Safety and Efficacy with Roflumilast Cream 0.15% in Patients Aged ≥6 Years with Atopic Dermatitis: A Phase 3 Open-Label Extension Trial. Dermatitis. 2025. Epub ahead of print.

Systemic treatment: eligibility criteria, medication choice

Speaker: Carsten Flohr (United Kingdom)

While advanced therapies in atopic dermatitis (AD) are gaining prominence, conventional systemic treatments remain foundational. This presentation addresses the strategic use of both conventional and newer systemic treatments, framed through clinical evidence and a detailed case study.

Key Discussion Points

• Indications for initiating systemic therapy in AD
• Selection and practical use of conventional agents (methotrexate, cyclosporine)
• Introduction and positioning of advanced therapies (biologics and JAK inhibitors)
• Highlight the importance of progression and individualization of therapy. 

Pathophysiological Considerations and Disease Burden

Atopic dermatitis is characterized by a chronic itch-scratch cycle that perpetuates inflammation. Exacerbating factors must be managed before initiating systemic therapy:

• Food and respiratory allergies
• Psychological comorbidities (anxiety, depression)
• Recurrent skin infections

Effective management should include:

• Intensive topical therapy
• Multidisciplinary support (including psychological input)
• Education and behavioral interventions
• Consideration of patch testing where indicated

Conventional Systemic Therapies

Methotrexate

• Commonly used as a first-line systemic in UK practice (off-label)
• Mechanisms include folate antagonism and modulation of JAK/NF-κB pathways
• Demonstrated durable efficacy in the TREAT trial
• Dosing: 0.4–0.5 mg/kg/week, without need for test dosing
• Subcutaneous administration can improve efficacy and reduce GI side effects
• Common side effect: nausea (managed with daily folic acid except on dosing day)
• Rare but monitored risk: bone marrow suppression

Cyclosporine

• Offers rapid disease control but limited by rebound and long-term safety concerns
• Mechanism: T-cell inhibition
• Nephrotoxicity and hypertension are primary risks, although recent biomarker studies show no significant renal impact in trial participants
• Often used short-term, with tapering or transition to other agents

Transition to Advanced Therapies

Following suboptimal or complicated responses to conventional agents, advanced therapies may be introduced.

Dupilumab

• Approved for AD and asthma, offering a targeted IL-4/IL-13 blockade
• Strong safety profile
• Notable concern: increased frequency of herpetic infections in a subset of patients

JAK Inhibitors (e.g., baricitinib, upadacitinib, abrocitinib)

• Broader cytokine inhibition, with rapid pruritus control
• Higher risk of infections; patient selection is key
• Flexibility in dosing (e.g., 15 vs 30 mg for upadacitinib) allows for individualized approaches

Evidence-Informed Decision-Making

Network meta-analyses (NMAs) provide comparative efficacy and safety data for systemic treatments. One application of this is the clinical decision-support platform [EczemaTherapies.com], designed to:

• Compare therapies on outcomes such as EASI, pruritus NRS, and DLQI/CDLQI
• Present GRADE-based interpretations
• Facilitate shared decision-making with patients

Combination Therapy in Complex Cases

For patients with multifaceted disease courses or limitations to monotherapy, combination regimens may be necessary. 

Case Study Overview:

A patient with severe, early-onset AD (EASI >50 at age 10) demonstrated:

• Dependence on potent topical corticosteroids
• Recurrent bacterial and viral infections, including HSV
• High comorbidity burden (asthma, allergic rhinitis, psychological distress)
• Partial or unsustained response to methotrexate and cyclosporine
• Adverse effects limiting conventional therapy use
• After the recurrence of HSV on dupilumab monotherapy, treatment was adjusted
• Combined therapy with dupilumab (200 mg Q2W) and upadacitinib (15 mg/day) was initiated
• Prophylactic valacyclovir successfully prevented viral reactivation
• Patient achieved long-term stability and substantial improvement in quality of life

This treatment approach is now published in Pediatric Dermatology as an example of advanced therapeutic integration.

Clinical Practice Considerations

• Methotrexate remains the preferred first-line systemic option in many settings
• Cyclosporine is useful for acute control but has limitations in maintenance
• Advanced agents offer greater precision and patient-tailored outcomes but require close monitoring and infrastructure
• Guidelines and NMAs support rational sequencing but do not yet provide strict hierarchies; clinical judgment remains essential
• Combination therapies may be considered in severe or refractory cases under close supervision

Final Reflection

Optimal management of atopic dermatitis requires a nuanced balance between guideline-based strategies, emerging evidence, and real-world complexities. The therapeutic landscape is expanding rapidly, and with it, the opportunity to tailor interventions based on disease severity, comorbidities, and patient preferences—always with a multidisciplinary approach at the center.

References: 

• Noda S et al. The translational revolution and use of biologics in patients with inflammatory skin diseases. J Allergy Clin Inmunol. 2015;135(2):423-336
• Gandhi NA et al. Targeting key proximal drivers of type 2 inflammation in disease. Nat Rev Drug Discov. 2016;15(1): 35-50 
• Flohr C, et al. Efficacy and safety of ciclosporin versus methotrexate in the treatment of severe atopic dermatitis in children and young people (TREAT): a multicentre parallel group assessor-blinded clinical trial. Br J Dermatol. 2023 Nov 16;189(6):674-684
• Wollenberg A, et al. European guideline (EuroGuiDerm) on atopic eczema: part I - systemic therapy. J Eur Acad Dermatol Venereol. 2022 Sep;36(9):1409-1431
• Drucker AM, et al. Systemic Immunomodulatory Treatments for Atopic Dermatitis: Living Systematic Review and Network Meta-Analysis Update. JAMA Dermatol. 2024;160(9):936–944.

Approach to patients with suboptimal response to systemic treatment

Speaker: Elaine Siegfried (USA)

Key Themes:

• Patient selection is critical to avoid treatment failure
• Recognition of phenotype and endotype is essential
• Multiple patient-specific factors affect treatment response
• High complexity in non-responders, often requiring individualized strategies

Initial Evaluation and Patient Stratification

Checklist Prior to Initiating Systemic Therapy:

Phenotyping & Endotyping

Recognized Subtypes:

• Classical atopic dermatitis
• Contact dermatitis (irritant/allergic/mixed)
• Psoriasis or psoriasiform dermatitis
• Urticarial variants
• Nutritional/immunodeficiency-associated dermatoses

Biomarkers and Labs

Defining and Assessing Treatment Response

Clinical Metrics:

Common Causes of Treatment Failure

Treatment Adjustment Strategies

Meta-Analysis Summary

• JAK inhibitors (high dose) show superior efficacy compared to low dose and dupilumab
• Higher efficacy comes with increased adverse effects
• Studies vary in duration and population (mostly adult-centric)

Conclusion

• Treatment failures in pediatric AD are multifactorial and require understanding of endotype, phenotype, and patient context.
• 10% of patients account for most time and complexity.
• A flexible, personalized, data-informed approach is essential to optimizing outcomes.

References: 

• Talasila S, et al. Analysis of publicly available adverse events reported for pediatric patients treated with Janus kinase inhibitors. Pediatr Dermatol. 2024 Nov-Dec;41(6):1040-1046.
• Fyhrquist N, et al. Endotypes of atopic dermatitis. J Allergy Clin Immunol. 2025 Mar 5:S0091-6749(25)00260-X
• Bieber T. Disease modification in inflammatory skin disorders: opportunities and challenges. Nat Rev Drug Discov. 2023 Aug;22(8):662-680.
• Bieber T. The paradigm shift in drug development for atopic dermatitis: Addressing the variables of the equation leading to disease modification. Ann Allergy Asthma Immunol. 2025 Feb;134(2):144-150.
• Liao Q, et al. Comparative efficacy and safety of dupilumab versus newly approved biologics and JAKi in pediatric atopic dermatitis: A systematic review and network meta-analysis. PLoS One. 2025 Feb 24;20(2):e0319400

The future of atopic dermatitis

Speaker: Amy S. Paller (USA)

Advances and Predictions in Atopic Dermatitis (AD)

1. Topical Therapies: Evolving Options

• Calcineurin Inhibitors (e.g., Tacrolimus, Pimecrolimus)
  • ~25 years of clinical use; safety profile well understood
  • Effective for maintenance and use in sensitive areas
  • Burning/stinging can be reduced by:
    • Pre-treatment with topical corticosteroids
    • Use of chilled formulations
• New Non-Steroidal Topicals:
• Microbiome-Based Topicals:
  • Ongoing research into commensal organisms (e.g., S hominis)
  • Goal: reduce S aureus colonization

2. Novel Targets and Pathways

• OX40/OX40L Inhibitors (Type 2 immune pathway)
  • Target T-cell co-stimulation
  • Potential for longer remission post-treatment
  • May enable less frequent dosing
• Multi-Target Biologics (Bispecifics/Trispecifics)
  • Combining IL-4Rα, IL-13, IL-31, IL-18 targets
  • Greater efficacy potential via polycytokine blockade
• IL-31 Pathway
  • Nemolizumab shows rapid itch reduction

3. Drug Delivery Innovations

• Challenges with Biologics:
  • Injection pain is a major barrier in pediatrics
  • Strategies for pain reduction:
    • Distraction techniques (VR, music, toys)
    • Cuddling techniques
    • Warming or room-temp medication
    • Topical anesthetics
• Emerging Technologies:

4. Systemic Therapies: Present and Future

• Dupilumab (IL-4Rα blocker):
  • Durable responses in some pediatric patients
  • Some maintain remission after stopping therapy
• Selective JAK Inhibitors (e.g., Upadacitinib, Abrocitinib)
  • Fast-acting oral options
  • Broader immunosuppressive profile; long-term safety still under investigation
• Small Molecule IL-23 Inhibitors (e.g., Icotrokinra)
  • Successful in psoriasis; early AD trials ongoing

5. Itch as a Therapeutic Frontier

• Itch Pathways:

• Objective Itch Monitoring:
  • Acoustic and movement sensors to distinguish:
    • Scratching vs. rubbing vs. random motion

• Biofeedback wearables show promise in reducing nocturnal scratching

6. Remote Monitoring & Digital Trials

Remote Clinical Trials:                                          

Feasible with:                                                       

• Telemedicine                                                     
• High-res photography                                      
• Real-time PROs                                                
• Sensorized wearables                                               

Wearable Technology:

Tracks:

• Itch/scratch activity
• Sleep disturbance
• Skin hydration, TEWL, erythema, thickness
• Microbial density

Examples:

• Programmable wearable TEWL sensor: collects hourly data non-invasively
  • Miniaturized skin sensors developed at Northwestern University

8. Next-Gen Technologies:

• Skin Lipidomics:
  • Stratum corneum ceramides as predictors for:
    • Disease development in infants
    • Therapy responsiveness
  • Potential to guide topical ceramide replacement or filaggrin enhancement therapy

Summary of Future Directions

References: 

• Puar N, et al. New treatments in atopic dermatitis. Ann Allergy Asthma Immunol. 2021 Jan;126(1):21-31
• Gallo RL, et al. Staphylococcus aureus: The Bug Behind the Itch in Atopic Dermatitis. J Invest Dermatol. 2024 May;144(5):950-953
• Au C-Y, et al. Sensorised Glove to Detect Scratching for Patients with Atopic Dermatitis. Sensors. 2023; 23(24):9782
• Tsoi LC, et al. Noninvasive Tape-Stripping with High-Resolution RNA Profiling Effectively Captures a Preinflammatory State in Nonlesional Psoriatic Skin. J Invest Dermatol. 2022 Jun;142(6):1587-1596
• Rinnov MR, et al. Skin biomarkers predict development of atopic dermatitis in infancy. Allergy. 2023 Mar;78(3):791-802

Nail surgery in children: Practical tips for success

Speaker: Jane Bellet (USA)

Key Concepts & Tips

1. Nail Anatomy Review:

• Know your landmarks: The lunula and proximal nail fold overlie the nail matrix, the key site for many biopsies.
• Nail matrix is thin—depth matters, as you reach bone quickly.

2. When to Biopsy:

• Same rule as skin lesions: If you'd biopsy it on the skin (e.g., for diagnostic uncertainty, management guidance, or concern), biopsy it on the nail.
• Don’t fear nail dystrophy post-biopsy— “the nail is already abnormal.”
• Atypical nail pigmentation should not be ignored (e.g., longitudinal melanonychia).

3. Pediatric Considerations:

• Anatomy is the same as adults, but logistics differ:
  • Anesthesia is always needed (often general for younger patients).
  • Post-op behavior (kids run, play, etc.).
• Choose digit carefully if optional—avoid thumbs/great toes if possible.

4. Pre-op Planning:

• Schedule time generously (1 hour recommended).
• Ensure child eats pre-procedure (to reduce vasovagal risk, unless under General Anesthesia).
• Mark lesion pre-anesthesia to guide biopsy, especially if nail is avulsed.

5. Anesthesia Techniques:

• Always perform a block, even under general.
• Choose between:
  • True digital block (base of finger/toe).
  • Distal digital block (most common).
  • Wing block.
• Use ropivacaine or lidocaine w/epi (limit volume to 3 mL to avoid ischemia).
• Emphasize difference between pressure vs pain during procedures.

6. Tourniquet Options: bloodless field

• Sterile glove roll-down (DIY).
• Penrose drain (distal to proximal, then clamp).
• T-Ring Tourniquet: Preferred; uniform pressure but expensive.

7. Common Procedures:

A. Punch Biopsy:

• For narrow lesions (<3 mm).
• Option to punch through soft nail or 
  after partial nail avulsion.

B. Partial Proximal Nail Avulsion:

• Cut across plate near proximal fold, lift with 
  hemostat.
• Enables better access to matrix or bed.

C. Nail Matrix Shave Excision:

• Preferred for lesions >3 mm wide.
• Steps:
  1. Avulse nail proximally.
  2. Score lesion.
  3. Shave in parallel to plate.
  4. Trim nail edge to avoid spicules.
  5. Return plate segment, suture skin to nail (e.g., 5-0 Vicryl Rapide).
• No sutures needed in the matrix defect itself

Risk Factors

• IL-17 inhibitors → ↑ Candida infections
• Moccasin-type tinea pedis
• Nail trauma (e.g., crushed toenails)

Clinical Variants

• Similar to adults:
  • Distal lateral subungual onychomycosis (DLSO) 
  • Proximal subungual onychomycosis (PSO)
  • Superficial white onychomycosis (SWO)
  • Total dystrophic onychomycosis

• Endonyx Onychomycosis:    
  • No inflammation, no onycholysis, no subungual hyperkeratosis
  • Milky white discoloration, primarily fingernails
  • Often misdiagnosed (e.g., as alopecia areata, psoriasis)
  • Caused by endothrix dermatophytes (commonly T. soudanense)

Diagnosis

• Specimen collection tip: Use a small curette — works better than scraping.
• Diagnostic tools:

Dermoscopy clues:

• Onychomycosis → frond-like distal edges
• Helps differentiate from psoriasis or trauma
  • KOH prep: Low sensitivity, but quick and bedside
  • Staining → ↑ sensitivity
  • PAS stain on histology
  • PCR: High sensitivity, $$$ expensive in the U.S.
  • Confocal microscopy: Non-invasive, still experimental
  • AI image analysis: In development
  • Culture: Gold standard (especially to identify non-dermatophyte molds)

Treatment

Topical:

• Preferred if:
  • Disease is limited to distal nail
  • Matrix not involved
• More effective in children than adults
• Expensive options in U.S. (e.g., efinaconazole, tavaborole)
• Don’t forget to treat coexisting tinea elsewhere

Systemic:

• Required for matrix or full nail involvement
• Terbinafine:
  • “Crush between two spoons”
  • Mix with sweet food (e.g., honey, syrup)
  • Avoid acidic foods (↓ drug efficacy)
• Dermatophytoma (biofilm-like mass in nail):
  • Linear or round, difficult to treat
  • Often requires combination therapy
  • Nail curetting/splitting may help penetration of topical agents

Organisms

• Similar to adults:
  • Trichophyton rubrum (most common)
  • T. tonsurans, T. mentagrophytes
  • Candida: More common in infants and fingernails
  • ↑ Reports of non-dermatophyte molds 
    (e.g., Scopulariopsis, Fusarium, etc.)

 Special Considerations

• Fingernail-only disease in infants → consider Candida
• Nail of the fourth toenail can be an isolated site of onychomycosis

Systemic associations:

• Down syndrome
• Sarcoidosis
• Immunodeficiency syndromes

Clinical Subtypes

Clinical Cases

• Case 1:

5-year-old boy with progressive nail roughness, previously treated with various topicals without improvement.

• No underlying dermatoses
• Final diagnosis: Idiopathic trachyonychia
• Treatment: Calcipotriol and corticosteroids for 10 months — no improvement
• Spontaneous resolution noted two years later

• Case 2:

4-year-old girl with a history of atopic dermatitis

• Nail roughness, cuticular hyperkeratosis, and pitting
• Treated with calcipotriol + topical corticosteroids
• Marked improvement within 4 months

Key Takeaways

• Trachyonychia is usually idiopathic and self-limited in children
• Always evaluate for associated skin or systemic conditions
• Treatment is often not necessary; reassurance and follow-up are key
• Biopsies are discouraged unless diagnosis is uncertain
• Set expectations early — cosmetic recovery can take months to years

References: 

• Chernoff KA, et al. Nail disorders: Kids are not just little people. Clin Dermatol. 2016 Nov-Dec;34(6):736-741.
• Gordon KA, et al. Trachyonychia: a comprehensive review. Indian J Dermatol Venereol Leprol. 2011 Nov-Dec;77(6):640-5
• Haber JS, et al. Trachyonychia: Review and Update on Clinical Aspects, Histology, and Therapy. Skin Appendage Disord. 2017 Jan;2(3-4):109-115
• Lim S, et al. Dermoscopic Evaluation of Inflammatory Nail Disorders and Their Mimics. Acta Dermato-Venereologica. 2021; 101(9), adv00548
• Starace M, et al. Trachyonychia: a retrospective study of 122 patients in a period of 30 years. J Eur Acad Dermatol Venereol. 2020 Apr;34(4):880-884.
• Pradhan S, et al. Trachyonychia in Children: A Comprehensive Review with Recent Updates. Indian Journal of Paediatric Dermatology:2024: 25(2):88-93

Congenital/Inherited nail deformities

Speaker: Lourdes Navarro Campoamor (Spain)

Key Concepts Presented

Diagnostic Importance of Nails in Children

• Nail abnormalities can be early diagnostic clues.
• Nails may be the first or only sign of certain systemic or congenital diseases.
• Close clinical observation is key, particularly in subtle or underdiagnosed conditions.

Congenital Nail Abnormalities 

Congenital hypertrophy of the lateral nail fold

• Involves abnormal interaction between the nail plate and surrounding soft tissues.
• Often asymptomatic but may present with distal inflammation and excessive nail growth.
• Nails typically show a trapezoidal shape.

Congenital malalignment of the toenail

• Defined by lateral dislocation of the nail plate due to improper alignment.
• Clinical features include trapezoidal nail plate, transverse grooves, chromonychia (brown, white, green), and onycholysis.
• Pathogenesis is unclear, but spontaneous realignment occurs in about 50% of cases.

Congenital anonychia

• Partial (Gene mutation of WNT pathway) or total absence of nails 
• Non-Syndromic
  Syndromic: Nail patella Sme, Cooks Sme, Hypohidrotic ectodermal dysplasia

Iso-Kikuchi Syndrome

• A rare congenital nail dystrophy usually affects one or both index fingers.
• Most frequently presents as micronychia, with variable nail morphology.
• Pathogenesis: 
  • Drugs during pregnancy
  • Ischemic events
  • Mesodermal malformations
  • Variants Wnt pathway

Genetic/Syndromic Nail Disorders

Nail-Patella Syndrome

• Inheritance: Autosomal dominant/De novo variants 12% 
• Gene Involvement: LMX1B gene
• Classic Tetrad:
  • Pattelar and elbow dysplasia
  • Posterior iliac horns
  • Nail dysplasia (95%): bilateral symmetrical, ulnar side, triangular lunula, swan necking, micronychia, anonychia
  • Others: 
    • Renal involvement
    • Eyes (glaucoma, microcornea, congenital cataract)
• Clinical Recommendations:
  • Clinical + radiographic exam
  • Anual Screening for renal disease and glaucoma 

Pachyonychia Congenita

• Inheritance: Autosomal dominant/De novo variants 30%
• Gene Involvement: KRT6/16/17
• Classic Triad:
  • Focal palmoplantar keratoderma
  • Hypertrophic nail dystrophy
  • Plantar pain 
• Treatment:
  • Conservative: Topical (Urea 40% - Salicylic or Lactic Acid)
  • Systemic retinoids, analgesic, botulinum toxin A, mTOR/EGFR inhibitors, Statins, 

Tuberous Sclerosis Complex 

• Ungual fibromas (Koenen tumors) – 15-50% 
  • Major diagnostic criterion
  • Toenails, longitudinal nail grooves

Darier Disease     

• Nail changes (95%)
  • Longitudinal red/white streaks, distal wedge-shaped subungual keratosis, V shaped notch

Important Diagnostic Notes

Melanonychia & Fibromas

• Ungual fibromas are frequently observed (50–52% of cases in some cohorts)
• Melanonychia (brown/black discoloration) may or may not be associated with fibromas
• Asymptomatic melanonychia should not be ignored, particularly in pediatrics

Summary Table: Common Nail Findings in Pediatric Disorders

Closing Remarks from Speaker

• Many nail disorders in pediatrics are underdiagnosed.
• Nails can reflect early developmental abnormalities or systemic conditions.
• Clinical suspicion and knowledge of these entities aid in early diagnosis and management.

References: 

• Peña-López S, et al. Iso-Kikuchi syndrome with Y-shaped bifurcation of the distal phalanx of the index fingers. J Dtsch Dermatol Ges. 2020 Oct;18(10):1173-1174
• Tognetti L, et al. A novel mutation in LMX1B gene in a newborn with nail-patella syndrome: Clinical and dermoscopic findings. Pediatr Dermatol. 2020 Nov;37(6):1205-1206
• Curtis KL, et al. Pachyonychia congenita: Spectrum of cutaneous disease. J Am Acad Dermatol. 2024 Nov;91(5):1021-1025