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Dr Snehal Pardeshi, Dermatologist., horizons at wakad, shop no 10 , skyline Road, chaudhari park, wakad, Wakad (2026)

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Horizons At Wakad, Shop No 10 , Skyline Road, Chaudhari Park, Wakad

11/11/2025

DIF Findings in Autoimmune Bullous Disorders

So after studying basic antigens , we know the antibodies target, which results in loss of cell adhesion and the basic skin scaffolding which results in blister formation. We l see how DIF can be used to locate the target of antibodies and so the subsequent disorder.

Direct Immunofluorescence (DIF) helps detect where antibodies are deposited in the skin — this pattern helps us identify the exact disease.
Each autoimmune blistering disorder has a distinct DIF pattern and target antigen.

🔹 Key DIF Findings

🕸️ Fish-net (Intercellular pattern)

Pemphigus vulgaris: IgG & C3 between cells (mainly lower epidermis); target → Desmoglein 3 ± 1

Pemphigus foliaceus: IgG & C3 in upper epidermis; target → Desmoglein 1

🔄 Mixed (Fish-net + Linear BMZ)

Paraneoplastic pemphigus: IgG & C3 both between cells and along BMZ; targets → Desmoglein 1, 3, Desmoplakin, Envoplakin, Periplakin, Plectin

➖ Linear (Along Basement Membrane Zone)

Bullous pemphigoid: Linear IgG, C3; targets → BP180, BP230

Mucous membrane pemphigoid: Linear IgG, C3 ± IgA; targets → BP180, Laminin 332, Integrin α6β4

Pemphigoid gestationis: Linear C3 > IgG; target → BP180 (NC16A domain)

Linear IgA disease: Linear IgA ± C3; target → LAD-1 (fragment of BP180)

EBA: Linear IgG, C3 ± IgA; target → Type VII collagen

💎 Granular (Dermal Papillae)

Dermatitis herpetiformis: Granular IgA ± C3 (“cluster of jewels”); target → Epidermal transglutaminase (TG3)

✅ Quick Recap:

Fish-net → Pemphigus

Linear → Pemphigoid group

Granular → Dermatitis herpetiformis

Mixed → Paraneoplastic pemphigus

11/11/2025

So before proceeding with DIF findings in various vesicobullous disease,we need to first understand the target antigens for antibodies in this autoimmune bullous disorders. The most important antigens are proteins which form desmosomes.

Desmosome is nothing but a junction form of proteins which connects one keratinocyte to other. It provides the connectivity between cells which form the scaffolding of our skin. Let's see various components of this junction.

DESMOSOME (Macula Adherens)

The desmosome is a tiny junction that acts like a button joining one skin cell (keratinocyte) to another.
It gives the skin its strength, stretch resistance, and integrity, preventing cells from separating under pressure.

🔹 Components of desmosome

Desmoglein (1,2,3,4) & Desmocollin (1,2,3)
→ The “glue” between cells (calcium-dependent cadherins) which connect cells.

Plakoglobin & Plakophilin → Link these outer molecules to the inside of the cell.

Desmoplakin → The main anchor connecting to keratin filaments.

Envoplakin, Periplakin & Plectin → Strengthen the junction and connect it with other anchoring systems.

Keratin Filaments → Insert into desmoplakin, linking one cell’s skeleton to the next.

💡 Together, these make the skin tough yet flexible!

🧠 MCQ CORNER

1️⃣ Adhesion molecules in desmosome → Desmoglein, Desmocollin
2️⃣ Main anchoring protein → Desmoplakin
3️⃣ Calcium is needed for → Desmoglein–Desmocollin adhesion
4️⃣ Plakin family proteins → Desmoplakin, Envoplakin, Periplakin, Plectin
5️⃣ Autoantigen in paraneoplastic pemphigus → Plakin family proteins
6. Autoantigen in pemphigus vulgaris - desmoglenin 3 and 1
7. Autoantigen in pemphigus foliaceous- desmoglenin 1

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08/11/2025

DIRECT IMMUNOFLUORESCENCE (DIF) – PRINCIPLE & METHOD

Purpose:
To detect in-vivo bound immunoreactants (IgG, IgA, IgM, C3, Fibrin) in the patient’s skin or mucosa — a gold-standard test for autoimmune blistering and connective tissue diseases.

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⚙️ Principle:

Patient’s tissue already contains autoantibodies deposited in skin.

The biopsy section is incubated with fluorescein-labeled antihuman antibodies.

These bind to the patient’s antibodies → emit apple-green fluorescence under a fluorescence microscope.
✨ This highlights where immune deposits lie — intercellular, linear, or granular.

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🧪 Method (Stepwise):

1️⃣ Site Selection:
Take perilesional, non-ulcerated skin (0.5 cm punch).
→ Lesional skin may destroy immune complexes.

2️⃣ Transport:
Use Michel’s medium or normal saline (❌ never formalin).

3️⃣ Sectioning:
Frozen sections (4–6 μm) are cut using a cryostat.

4️⃣ Incubation:
Apply fluorescein-tagged anti-IgG, IgA, IgM, C3, and Fibrin.

5️⃣ Washing & Microscopy:
Wash excess stain → Examine under fluorescence microscope for characteristic patterns.

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⚠️ Key Precautions

Avoid steroids ≥48 hours before biopsy.

Always take a separate biopsy for H&E and DIF.

Choose a fresh early lesion for best yield.

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🧠 MCQ CORNER

1️⃣ Stain used → FITC-labeled antihuman immunoglobulins
2️⃣ Biopsy site → Perilesional skin
3️⃣ Transport medium → Michel’s medium
4️⃣ Type of microscopy → Fluorescence microscope
5️⃣ Pattern determines → Type of disease (intercellular, linear, granular)

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07/11/2025

KOEBNER PHENOMENON & ITS VARIANTS

Definition:
Appearance of new lesions of a pre-existing dermatosis at sites of trauma, friction, or injury to previously normal skin.

🧠 First described by Heinrich Koebner (1877) in psoriasis patients who developed lesions on tattooed or scratched skin.

⏱ Interval to koebnerization:
Usually 10–20 days, may vary from 3 days to 2 years.

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🔹 Boyd–Nelder Classification of Koebner Phenomenon

1️⃣ True Koebner phenomenon –
Lesions appear after trauma in diseases replicating original histopathology.
➡️ Psoriasis, Lichen planus, Vitiligo

2️⃣ Pseudo-Koebner phenomenon –
Infective inoculation at trauma sites.
➡️ Warts, Molluscum contagiosum, Pyoderma

3️⃣ Occasional / Questionable Koebner –
Rarely reproducible; inconsistent evidence.

4️⃣ Negative Koebner phenomenon –
Failure to reproduce lesions after trauma.

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🔹 Reverse Koebner Phenomenon

Existing lesions disappear at trauma sites (e.g., psoriasis after dermabrasion or surgery).

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🔹 Remote Reverse Koebner Phenomenon

Seen in vitiligo – repigmentation of distant patches following autologous skin grafts.

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🔹 Isotopic Phenomenon (Wolf’s Isotopic Response)

Development of a new, unrelated dermatosis at the site of a healed lesion (commonly post–herpes zoster).
🔬 Examples: Granuloma annulare, LP, sarcoidosis, Kaposi’s sarcoma, SCC, verruca plana, molluscum contagiosum.
💡 Mechanism: Virus-induced local immune and neural dysregulation (locus minoris resistentiae).

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🧠 MCQ CORNER

1️⃣ Koebner described → Psoriasis (1877)
2️⃣ True positive - Psoriasis,lichen planus, vitiligo, pseudo positive in viral infections
3️⃣ Reverse Koebner → Lesions disappear post-trauma, psoriasis
4️⃣ Remote reverse Koebner → Repigmentation of distant vitiligo patches
5️⃣ Isotopic phenomenon → New disease at healed site (Herpes zoster scars)

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04/11/2025

TZANCK SMEAR IN INFECTIOUS DERMATOSES

Purpose:
A rapid cytologic test to identify viral, parasitic, and bacterial infections using characteristic cellular findings.

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🔹 1️⃣ Viral Infections

Herpes simplex / Varicella / Herpes zoster

Multinucleated giant cells

Ground-glass nuclei, chromatin margination, nuclear molding

Ballooning degeneration of keratinocytes
🧠 Mnemonic: M³G → Multinucleation, Molding, Margination, Ground-glass

Molluscum contagiosum

Henderson–Patterson bodies (large intracytoplasmic inclusion bodies)

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🔹 2️⃣ Parasitic Infection

Cutaneous leishmaniasis

Macrophages packed with Leishman–Donovan (LD) bodies

Each LD body = nucleus + rod-shaped kinetoplast

Background: histiocytes, plasma cells, lymphocytes

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🔹 3️⃣ Bacterial / Fungal Lesions

Impetigo / Folliculitis: Neutrophils ± cocci in clusters

Candidiasis: Budding yeast cells, pseudohyphae

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⚡ Quick Recall

Infection Characteristic Cell Key Feature

HSV / VZV -Multinucleated giant cell Ground-glass nucleus
Molluscum Inclusion body -Henderson–Patterson body
Leishmaniasis -Macrophage with LD bodies Nucleus + kinetoplast
Candidiasis -Yeast with pseudohyphae Budding forms
Impetigo -Neutrophils + cocci Bacterial clusters

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🧠 MCQ Corner

1️⃣ Multinucleated giant cells → Herpes simplex/zoster
2️⃣ Henderson–Patterson bodies → Molluscum contagiosum
3️⃣ LD bodies → Leishmaniasis
4️⃣ Yeast + pseudohyphae → Candidiasis
5️⃣ Test used → Giemsa stain (preferred)

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04/11/2025

TZANCK CYTOLOGY – FINDINGS IN VARIOUS DERMATOSES

A simple bedside cytodiagnostic test that reveals characteristic cells across a wide spectrum of skin diseases — from autoimmune to infective, genodermatoses, and tumors.

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🔹 IMMUNOBULLOUS DISORDERS

Pemphigus vulgaris: Acantholytic cells with hazy nucleoli

BP / SJS / Erosive LP: No acantholytic cells; numerous leukocytes

Toxic epidermal necrolysis: Necrotic basal cells, leukocytes, fibroblasts

Staphylococcal scalded skin syndrome: Dyskeratotic acantholytic cells, minimal inflammation

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🔹 INFECTIVE LESIONS

Leishmaniasis: Leishman–Donovan (LD) bodies, Wright’s cells

Herpes simplex / Varicella / Zoster: Ballooning multinucleated giant cells

Molluscum contagiosum: Henderson–Patterson inclusion bodies

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🔹 GENODERMATOSES

Hailey–Hailey disease: Acantholytic cells with normal nucleoli

Darier’s disease: Corps ronds and grains (dyskeratotic keratinocytes)

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🔹 CUTANEOUS TUMORS

Basal cell carcinoma: Clusters of basaloid cells

Squamous cell carcinoma: Isolated atypical squamous cells

Paget’s disease (breast): Paget cells with large pale cytoplasm

Erythroplasia of Queyrat: Poikilokaryosis, naked & clumped nuclei

Mastocytoma: Mast cells with metachromatic granules

Histiocytosis X: Atypical Langerhans cells

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🧠 MCQ CORNER

1️⃣ Henderson–Patterson bodies → Molluscum contagiosum
2️⃣ Corps ronds & grains → Darier’s disease
3️⃣ LD bodies → Leishmaniasis
4️⃣ Acantholytic cells + hazy nucleoli → Pemphigus vulgaris
5️⃣ Dyskeratotic acantholytic cells → SSSS
6️⃣ Paget cells → Paget’s disease of breast

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04/11/2025

1️⃣ Pemphigus Vulgaris (PV)

Type of blister: Suprabasal (intraepidermal)

Findings:

Numerous large, rounded acantholytic (Tzanck) cells

Hyperchromatic nucleus with perinuclear halo

Mourning edge (peripheral chromatin condensation)

Sertoli rosettes (acantholytic cells arranged around inflammatory cells)

Streptocytes (elongated acantholytic cells)

Background: Cellular, with lymphocytes & few eosinophils

Interpretation: Classical positive Tzanck smear for autoimmune acantholysis

🔹 2️⃣ Pemphigus Foliaceus (PF)

Type of blister: Subcorneal

Findings:

Fewer acantholytic cells (smaller, polygonal)

Eosinophilic cytoplasm, less distinct halo

Mourning edge faint or absent

Clean background

Interpretation: Suggestive of superficial acantholysis

🔹 3️⃣ Paraneoplastic Pemphigus (PNP)

Type of blister: Suprabasal

Findings:

Scattered acantholytic cells + necrotic keratinocytes

Mixed inflammatory background (lymphocytes, eosinophils, histiocytes)

Interpretation: Cytology nonspecific — requires DIF and IIF for confirmation.

🔹 4️⃣ Bullous Pemphigoid (BP)

Type of blister: Subepidermal

Findings:

No acantholytic cells

Numerous eosinophils and inflammatory debris

Occasionally neutrophils

Interpretation: Negative Tzanck test for acantholysis

🔹 5️⃣ Linear IgA Disease & Dermatitis Herpetiformis

Type of blister: Subepidermal

Findings:

Predominant neutrophils ± eosinophils

No acantholytic cells

Interpretation: Tzanck smear nonspecific, used only to confirm inflammatory nature

MCQ Corner

1️⃣ Tzanck cells = Acantholytic keratinocytes (PV hallmark)
2️⃣ Negative Tzanck = Bullous pemphigoid, EBA
3️⃣ Cell pattern in PF = Fewer, smaller polygonal acantholytic cells
4️⃣ Mourning edge + halo = Pemphigus vulgaris
5️⃣ Predominant cells in BP = Eosinophils
6️⃣ Predominant cells in DH / LAD = Neutrophils

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Hashtags:

04/11/2025

TZANCK SMEAR – PROCEDURE & PRINCIPLE

Purpose:
A simple bedside cytodiagnostic test to detect acantholysis and viral cytopathic changes in vesiculobullous and pustular disorders.

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⚙️ Principle:

Cells are gently scraped from the floor of a vesicle or bulla and examined microscopically after staining to look for diagnostic cytologic features (e.g., acantholytic cells, giant cells).

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🩺 Procedure Steps

1️⃣ Select a fresh vesicle or bulla — preferably intact and

04/11/2025

AUSPITZ SIGN & GRATTAGE TEST — The Classic Clue in Psoriasis

🔍 Definition:
Auspitz sign refers to pinpoint bleeding spots that appear when the scales of psoriasis are gently scraped off.
It represents the rupture of dilated capillaries in elongated dermal papillae due to suprapapillary thinning of the epidermis.

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⚙️ Grattage Test (Scraping Test)

Purpose:
To demonstrate the Auspitz phenomenon.

Steps:
1️⃣ Select a representative psoriatic plaque.
2️⃣ Gently scrape with a glass slide, blunt scalpel, or curette.
3️⃣ Observe the three characteristic stages:

Stage 1 – Candle Grease Sign: Silvery white scales appear and fall like wax shavings.

Stage 2 – Membrane of Bulkeley: A thin glistening red membrane becomes visible once scales are removed.

Stage 3 – Auspitz Sign: Continued scraping reveals pinpoint bleeding spots where capillaries in dermal papillae are torn.

Caution:
Avoid in oozing, infected, or intertriginous lesions.

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🧬 Pathophysiology

Parakeratosis: Retention of nuclei in stratum corneum → thin, friable scales.

Suprapapillary thinning: Minimal epidermal barrier over dermal papillae.

Dilated, tortuous papillary capillaries: Responsible for pinpoint bleeding.

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📚 Clinical Insights

✅ Seen in: Psoriasis (classic)
⚠️ Also observed in: Darier’s disease, actinic keratosis
❌ Absent in: Inverse, guttate, pustular, erythrodermic psoriasis

🧠 MCQ CORNER

1️⃣ Test used to elicit Auspitz sign → Grattage test
2️⃣ Membrane seen before bleeding → Membrane of Bulkeley
3️⃣ Underlying cause of bleeding → Rupture of capillaries in elongated dermal papillae
4️⃣ Diseases other than psoriasis showing Auspitz sign → Darier’s disease, actinic keratosis
5️⃣ Is Auspitz sign specific for psoriasis? → ❌ No
6️⃣ First step in grattage test → Candle grease sign

03/11/2025

ASBOE–HANSEN SIGN (BULLA SPREAD SIGN) 🌸
Aka Lutz sign

💧 When gentle pressure on a bulla causes it to extend into adjacent unblistered skin, due to epidermal fragility or loss of adhesion.

✨ Asboe–Hansen sign: Pressure on the center of a tense bulla → spreads peripherally
✨ Lutz sign: Pressure on the margin of the bulla → extends beyond marked edge

🩺 Interpretation:

Rounded border → Subepidermal blister (e.g. Bullous pemphigoid)

Irregular border → Intraepidermal blister (e.g. Pemphigus vulgaris)

🔬 Positive in:
Pemphigus vulgaris, Pemphigus foliaceus, Bullous pemphigoid, Dermatitis herpetiformis, EBA, Cicatricial pemphigoid, Bullous drug eruptions, SJS/TEN

🚫 Negative in:
Hailey–Hailey disease, Staphylococcal scalded skin syndrome (due to fragile roof)

💡 Trivia:
Both Asboe–Hansen and Nikolsky signs may be positive in acute bullous lichen planus.
👨‍⚕️ Asboe–Hansen is also remembered for Asboe–Hansen Syndrome — the initial phase of Bloch–Sulzberger syndrome (Incontinentia pigmenti).

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🎯 MCQ Corner
✅ Asboe–Hansen = Bulla spread sign = Lutz sign
✅ Pressure site → Center (Asboe–Hansen), Margin (Lutz)
✅ Round vs. Irregular border → Subepidermal vs. Intraepidermal
✅ Negative in → SSSS, Hailey–Hailey
✅ Asboe–Hansen Syndrome = Early stage of Bloch–Sulzberger syndrome

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03/11/2025

Nikolsky Sign 🩸

Gentle tangential pressure on the skin leads to epidermal detachment, indicating epidermal fragility — from either acantholysis or necrosis, depending on the cause.

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🔹 True Nikolsky sign
Pressure on normal skin → epidermis peels off due to acantholysis
➡️ Intraepidermal split
✅ Seen in Pemphigus vulgaris, Pemphigus foliaceus, SSSS
🚫 Negative in TEN

🔹 Marginal Nikolsky
Pressure at blister edge → extension of erosion
Seen in Pemphigus, SSSS, TEN

🔹 Direct Nikolsky
Pressure near a lesion causes new blister formation → indicates active pemphigus

🔹 Indirect Nikolsky
Pressure on distant normal skin → blister develops elsewhere → extensive pemphigus

🔹 Pseudo-Nikolsky (Sheklakov sign)
Epidermis peels due to necrosis, not acantholysis
➡️ Subepidermal split
✅ Seen in TEN, SJS, severe SSSS, acute GVHD

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❌ Don’t confuse with:
Asboe–Hansen sign → Downward pressure causes blister to extend by fluid spread
🩹 Seen in Bullous pemphigoid

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🧠 MCQ Corner

True Nikolsky → Acantholysis, intraepidermal

Pseudo Nikolsky → Necrosis, subepidermal

Positive in → PV, PF, SSSS

Negative in → BP, EM, TEN (true sign)

Asboe–Hansen → Bullous pemphigoid

Desmoglein-3 → Mucosal PV | Desmoglein-1 → PF

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02/11/2025

Tuberous Sclerosis Complex (TSC)

Autosomal dominant neurocutaneous syndrome caused by mutations in:
🧬 TSC1 (Hamartin, chromosome 9q34)
🧬 TSC2 (Tuberin, chromosome 16p13)
→ Loss of inhibition of mTOR pathway → hamartomatous growths in multiple organs

Mnemonic: “Skin is the mirror of the brain” 🪞

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🌿 Cutaneous Manifestations (Earliest Clues)

• Facial angiofibromas – red papules over nasolabial folds (75%)
• Ash-leaf macules – hypopigmented leaf-shaped macules (90%)
• Shagreen patch – leathery plaque on lumbosacral area (>50%)
• Periungual / subungual fibromas (20–80%)
• Fibrous cephalic plaque (25%)
• Oral findings: gingival fibromas (20–50%), enamel pits (90%)
• Retinal astrocytic hamartoma (40–50%)

🩸 Classic triad: Angiofibromas + Shagreen patch + Ash-leaf macules

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🧩 Systemic Involvement (Organ-wise)

🧠 CNS:
• Cortical tubers, subependymal nodules (80–90%)
• Subependymal giant cell astrocytoma (SEGA) – 10–20%
• Seizures (80–90%), developmental delay, autism, behavior issues

🩺 Renal:
• Angiomyolipomas (75%) – risk of bleeding
• Renal cysts, PKD, rarely RCC (3%)
• TSC2–PKD1 contiguous gene syndrome → early renal failure

❤️ Cardiac:
• Rhabdomyomas – may regress spontaneously
• Detected prenatally or in infancy

🌬️ Pulmonary:
• Lymphangioleiomyomatosis (LAM) – 30%, mainly women
• Multifocal micronodular pneumocyte hyperplasia (40–60%)

🫀 Hepatic:
• Angiomyolipomas, cysts (~30%), mostly asymptomatic

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🧪 Diagnosis

🩻 Neuroimaging: Cortical tubers, subependymal nodules
🧬 Genetic testing: TSC1 / TSC2 mutations
💡 Wood’s lamp: Detects hypomelanotic macules (ash-leaf spots)

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💊 Treatment Highlights

• mTOR inhibitors – Sirolimus, Everolimus (for SEGAs, renal AML, skin lesions)
• Seizure control – Vigabatrin (esp. for infantile spasms)
• Laser therapy – for angiofibromas
• Multidisciplinary follow-up – derm, neuro, nephro, cardio, pulmonology

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Dr Snehal Pardeshi, Dermatologist.

11/11/2025

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