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Hereditary Epidermolysis Bullosa — Types

Group of inherited mechanobullous disorders characterized by skin and mucosal fragility with blistering after minor trauma, classified by ultrastructural cleavage level into simplex (intraepidermal), junctional (lamina lucida), dystrophic (sublamina densa), and Kindler syndrome (mixed level).

Written by: Saygı Hospital Health Guide Editorial Board
Last updated:

This content has been compiled by the Saygı Hospital Health Guide Editorial Board and is periodically reviewed by a specialist physician.

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What is Hereditary Epidermolysis Bullosa — Types?

Hereditary epidermolysis bullosa (EB) is a clinically and genetically heterogeneous group of inherited mechanobullous disorders affecting approximately 1 in 50,000 births. The unifying feature is skin and mucosal fragility leading to blister formation with minimal mechanical trauma. The classification is based on the ultrastructural level of skin cleavage, which corresponds to specific mutated structural proteins of the dermo-epidermal junction.

EB simplex (EBS) accounts for 70% of cases. Cleavage is intraepidermal (basal keratinocytes). Most cases are autosomal dominant with mutations in keratin 5 (KRT5) or keratin 14 (KRT14). Subtypes include EBS-Weber-Cockayne (localized to hands/feet, mild), EBS-Köbner (generalized intermediate), and EBS-Dowling-Meara (generalized severe with herpetiform clusters). Junctional EB (JEB) is autosomal recessive with cleavage in the lamina lucida due to mutations in laminin-332 (LAMA3, LAMB3, LAMC2) or α6β4 integrin (ITGA6, ITGB4); severity ranges from lethal Herlitz JEB (often fatal in infancy) to non-Herlitz forms.

Dystrophic EB (DEB) involves sublamina densa cleavage from mutations in type VII collagen (COL7A1). Dominant DEB (DDEB) is mild-moderate with scarring blisters. Recessive DEB (RDEB) ranges from severe generalized (RDEB-sev gen, with mutilating scarring, mitten-deformity pseudosyndactyly, growth failure, esophageal strictures, malnutrition, anemia, and aggressive squamous cell carcinoma) to intermediate forms. Kindler EB (KEB) involves mixed cleavage levels from FERMT1 (kindlin-1) mutations and presents with blistering, photosensitivity, and progressive poikiloderma. Diagnosis combines clinical history, immunofluorescence antigen mapping (decreased or absent staining of specific protein), transmission electron microscopy (TEM, gold standard for cleavage level), and genetic testing. Management is multidisciplinary: meticulous wound care with non-adherent dressings, infection prevention, nutritional optimization, anemia management, contracture prevention, and squamous cell carcinoma surveillance. Beremagene geperpavec (B-VEC, Vyjuvek), a topical herpes simplex virus-based gene therapy delivering COL7A1, was FDA-approved 2023 for RDEB.

Symptoms

Skin fragility with blister formation after minor trauma
Erosions and ulcers, often on hands, feet, knees, elbows
Mucosal involvement (oral, esophageal — strictures in DEB)
Nail dystrophy or absence (anonychia in severe forms)
Scarring (DEB) versus non-scarring (EBS, JEB) blistering
Pseudosyndactyly (mitten deformity in severe RDEB)
Growth failure, anemia, malnutrition (severe RDEB)

Risk Factors

Family history of EB (autosomal dominant in most EBS, DDEB)
Consanguinity (JEB, RDEB autosomal recessive)
Specific genetic mutations: KRT5/14 (EBS), LAMA3/LAMB3/LAMC2 (JEB), COL7A1 (DEB), FERMT1 (Kindler)
De novo mutations in dominant forms (10-30%)
Onset typically at birth or early infancy
Heat or friction triggers blistering
Genetic counseling indicated for affected families

When to See a Doctor?

If you experience any of the following symptoms, seek medical attention promptly:

  • Newborn with blistering or skin fragility
  • Infant with poor wound healing or recurrent skin breakdown
  • Family history of EB with planned pregnancy
  • Suspicious blistering pattern triggered by minor trauma
  • Failure to thrive in child with skin fragility
  • Esophageal stricture symptoms (dysphagia) in known DEB
  • New skin ulcer or non-healing wound in known RDEB (rule out SCC)

Treatment Methods

01
Multidisciplinary EB specialty center care
02
Meticulous wound care with non-adherent dressings (Mepilex, Mepitel)
03
Topical antibiotics for superficial infection, systemic for deeper
04
Nutritional optimization with high-calorie/high-protein diet, iron supplementation
05
Pseudosyndactyly prevention with hand splinting and surgical separation when needed
06
Beremagene geperpavec (B-VEC, Vyjuvek) — topical gene therapy for RDEB (FDA 2023)
07
Squamous cell carcinoma surveillance in RDEB (annual whole-body skin examination)

Which Department to Visit?

You can visit our Dermatoloji department for these complaints. Our specialist physicians will create the most suitable treatment plan for you.

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Health Disclaimer: The information on this page is prepared for general informational purposes only. It does not replace medical diagnosis and treatment. Please consult your physician for your complaints. Saygı Hospital does not accept responsibility for actions taken based on the information on this page.