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Dermatology

Alopecia

High EvidenceUpdated: 2025-12-22

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Red Flags

  • Scarring (cicatricial) alopecia - urgent referral to prevent permanent loss
  • Associated systemic symptoms (virilization, weight loss, joint pain)
  • Scalp inflammation (pustules, crusting, boggy swelling)
  • Rapidly progressive universal hair loss
Overview

Alopecia

1. Overview

Alopecia is the general medical term for hair loss. It is a broad category encompassing various etiologies ranging from benign, self-limiting conditions to permanent, scarring disorders. Accurate diagnosis is critical as treatments differ fundamentally between scarring (cicatricial) and non-scarring forms.

Classification

  1. Non-Scarring Alopecia (Hair follicles preserved; potential for regrowth)

    • Androgenetic Alopecia: Pattern hair loss (Male/Female)
    • Alopecia Areata: Autoimmune patchy loss
    • Telogen Effluvium: Stress-reactive shedding
    • Trichotillomania: Traumatic pulling
    • Tinea Capitis: Fungal infection
  2. Scarring (Cicatricial) Alopecia (Hair follicles destroyed; permanent loss)

    • Lichen Planopilaris (LPP)
    • Frontal Fibrosing Alopecia (FFA)
    • Discoid Lupus Erythematosus (DLE)
    • Folliculitis Decalvans

Key Epidemiology

TypePrevalenceDemographics
Androgenetic>50% of men >0yMen > Women; Age-dependent
Areata2% lifetime riskChildren & Young Adults
Telogen EffluviumCommonPost-partum, Post-illness

2. Pathophysiology
┌─────────────────────────────────────────────────────────────────────────────┐
│                       ALOPECIA PATHOPHYSIOLOGY                              │
├─────────────────────────────────────────────────────────────────────────────┤
│                                                                             │
│   ┌─────────────────────────────────────────────────────────────────────┐   │
│   │                    THE HAIR GROWTH CYCLE                            │   │
│   │  1. Anagen (Growth): 2-6 years (85-90% of hairs)                    │   │
│   │  2. Catagen (Transition): 2-3 weeks (<1%)                           │   │
│   │  3. Telogen (Resting): 3 months (10-15%) -> Shedding (Exogen)       │   │
│   └─────────────────────────────────────────────────────────────────────┘   │
│                                    ↓                                        │
│                ┌───────────────────┼────────────────────┐                   │
│                ↓                   ↓                    ↓                   │
│   ┌────────────────────┐  ┌──────────────────┐  ┌──────────────────────┐    │
│   │ ANDROGENETIC       │  │ ALOPECIA AREATA  │  │ TELOGEN EFFLUVIUM    │    │
│   │ (Miniaturization)  │  │ (Autoimmune)     │  │ (Cycle Reset)        │    │
│   └────────────────────┘  └──────────────────┘  └──────────────────────┘    │
│            ↓                       ↓                    ↓                   │
│   • DHT sensitivity    │  • T-cell attack on │  • Stress/Shock triggers │   │
│   • Shortened Anagen   │    hair bulb        │    synchronous entry     │   │
│   • Follicles shrink   │  • "Immune privi-   │    into Telogen          │   │
│     (Miniaturization)  │    lege" collapse   │  • Massive shedding 3    │   │
│   • Terminal -> Vellus │  • Non-scarring     │    months LATER          │   │
│     hairs              │                     │                          │   │
│                        │                     │                          │   │
└────────────────────────┴─────────────────────┴──────────────────────────────┘

Mechanisms by Type

  1. Androgenetic Alopecia (AGA):

    • Dihydrotestosterone (DHT) causes follicular miniaturization in genetically susceptible follicles.
    • Terminal hairs (thick, pigmented) are replaced by Vellus hairs (fine, unpigmented).
  2. Alopecia Areata (AA):

    • CD8+ T-cells attack the hair bulb.
    • Collapse of "immune privilege" of the hair follicle.
    • Hairs enter dystrophic catagen/telogen state but follicles remain intact (reversible).
  3. Scarring Alopecia:

    • Inflammation targets the bulge region (stem cell reservoir).
    • Permanent destruction of stem cells = permanent hair loss.

3. Clinical Features

History Taking

Essential Questions:

  • Shedding vs Thinning? (Hairs coming out in clumps vs scalp becoming more visible?)
  • Duration? (Acute <6 months vs Chronic)
  • Pattern? (Patchy, diffuse, or receding hairline?)
  • Triggers? (Illness, childbirth, stress 3 months ago? New medications?)
  • Symptoms? (Itching, burning, pain? - Red flags for scarring)
  • Hormonal signs? (Acne, hirsutism, irregular periods in women?)

Diagnosis by Pattern

PatternLikely DiagnosisClinical Features
Patchy LossAlopecia AreataSmooth, round patches; Exclamation mark hairs
Tinea CapitisScaly, broken hairs, inflammation (kids)
TrichotillomaniaIrregular borders, hairs of different lengths
Diffuse LossTelogen EffluviumPositive hair pull test, generalized thinning
Female PatternWidening of central part, preserved hairline
RecedingMale PatternM-shape recession, vertex thinning
Frontal Fibrosing"Band" of recession, loss of eyebrows (scarring)

Physical Examination Tools

  • Hair Pull Test: Gently pull ~60 hairs. >10% (6+ hairs) extracted = Active shedding (Telogen effluvium, active AA).
  • Trichoscopy (Dermoscopy): Essential for diagnosis.

Trichoscopy Findings

ConditionKey Findings
Alopecia AreataYellow dots, black dots, exclamation mark hairs
AndrogeneticHair diameter diversity (thick and thin hairs mixed)
Lichen PlanopilarisPerifollicular scaling/erythema, loss of follicular ostia
Tinea CapitisComma hairs, corkscrew hairs

4. Diagnosis

Diagnostic Approach

Usually clinical + trichoscopy. Biopsy reserved for scarring or uncertain cases.

Laboratory Investigations

Standard Screen (for diffuse loss in women):

  • Ferritin: Iron deficiency is a common cause (Target >40-70 ng/mL for growth).
  • TSH: Hypo/Hyperthyroidism cause hair loss.
  • Vitamin D / B12: Optimizing supports growth.
  • Hormonal Profile (FSH/LH/Testosterone/DHEAS): Only if signs of hyperandrogenism (PCOS symptoms).

Scalp Biopsy

  • Indication: Suspected scarring alopecia (LPP, DLE, FFA) to confirm diagnosis and prevent permanent loss.
  • Technique: 4mm punch biopsy. Often 2 samples (horizontal and vertical sectioning).

5. Management Algorithm
┌─────────────────────────────────────────────────────────────────────────────┐
│                         ALOPECIA MANAGEMENT ALGORITHM                       │
├─────────────────────────────────────────────────────────────────────────────┤
│                                                                             │
│   DETERMINE TYPE (Scarring vs Non-Scarring)                                 │
│                          ↓                                                  │
│              ┌──────────────────────────────────────┐                       │
│              │       IS IT SCARRING? (Redness,      │                       │
│              │       Pain, Loss of pores)           │                       │
│              └──────────────────────────────────────┘                       │
│                    ↓ YES (Scarring)           ↓ NO (Non-Scarring)           │
│   ┌──────────────────────────┐  ┌──────────────────────────────────────┐   │
│   │  URGENT DERM REFERRAL    │  │  DIAGNOSE SUBTYPE                    │   │
│   │  Goal: Halt progression  │  │  1. Androgenetic (Pattern)           │   │
│   │                          │  │  2. Areata (Patchy)                  │   │
│   │  • Potent Topical Steroids│  │  3. Telogen Effluvium (Diffuse)      │   │
│   │  • Intralesional Steroid │  └──────────────────────────────────────┘   │
│   │  • Oral: Doxycycline,    │                    ↓                         │
│   │    Hydroxychloroquine    │                                              │
│   └──────────────────────────┘                                              │
│                                                                             │
│             ┌─────────────────────────┼──────────────────────────┐          │
│             ↓                         ↓                          ↓          │
│  ┌────────────────────┐   ┌───────────────────────┐  ┌───────────────────┐  │
│  │ ANDROGENETIC (Men) │   │ ANDROGENETIC (Women)  │  │ ALOPECIA AREATA   │  │
│  │ • Minoxidil 5% Top │   │ • Minoxidil 5% Foam   │  │ • Intralesional   │  │
│  │ • Finasteride 1mg  │   │ • Spironolactone      │  │   Steroids (&lt;50%) │  │
│  │   Oral             │   │   (Anti-androgen)     │  │ • Potent Topical  │  │
│  │ • Hair Transplant  │   │ • Oral Minoxidil      │  │   Steroids        │  │
│  │                    │   │   (Low dose)          │  │ • JAK Inhibitors  │  │
│  └────────────────────┘   └───────────────────────┘  │   (Severe/Totalis)│  │
│                                                      └───────────────────┘  │
│                                                                             │
└─────────────────────────────────────────────────────────────────────────────┘

Management: Androgenetic Alopecia (AGA)

Men:

  1. Topical Minoxidil (5%): Prolongs anagen. Apply BD. Lifelong use.
  2. Oral Finasteride (1mg): 5α-reductase inhibitor. Stops conversion of T to DHT.
    • Efficacy: Stops loss in 90%, regrowth in 60%.
    • Side Effects: Sexual dysfunction (1-2%), reversible.
  3. Hair Transplant: FUE (Follicular Unit Extraction) relocates DHT-resistant hairs from back of head to front.

Women:

  1. Topical Minoxidil (5% Foam): Once daily.
  2. Anti-androgens (Off-label): Spironolactone or Cyproterone Acetate.
  3. Oral Minoxidil (Low dose): 0.25mg-1.25mg daily. Highly effective, avoids messy topicals. Causes hypertrichosis.

Management: Alopecia Areata (AA)

Limited Disease (<50% Scalp):

  • Intralesional Corticosteroids (Triamcinolone): First line. Injected every 4-6 weeks.
  • Potent Topical Steroids: Adjunctive.

Does not respond / Extensive (>50%):

  • JAK Inhibitors (Baricitinib, Ritlecitinib): Breakthrough therapy. Restores hair in severe cases.
  • Topical Immunotherapy (DPCP): Induces allergic contact dermatitis to distract immune system.
  • Systemic Steroids: Bridge therapy only.

Management: Telogen Effluvium

  • Self-limiting: Resolves in 6-12 months once trigger removed.
  • Reassurance: "You are shedding, not going bald."
  • Treat correctable causes: Iron, thyroid, diet.

6. Scarring Alopecias (Brief Overview)

Lichen Planopilaris (LPP):

  • Perifollicular redness and scaling.
  • Treatment: Potent steroids, Hydroxychloroquine.

Frontal Fibrosing Alopecia (FFA):

  • "Clown alopecia" - recession of frontal hairline + eyebrow loss.
  • Post-menopausal women.
  • Treatment: 5α-reductase inhibitors + anti-inflammatories.

7. Prognosis
ConditionPrognosis
Telogen EffluviumExcellent. Complete regrowth expected.
AndrogeneticProgressive without treatment. Treatment maintains, rarely restores full density.
Alopecia Areata80% spontaneous regrowth in 1 year for mild cases. Poor prognosis if: onset in childhood, ophiasis pattern, or totalis/universalis.
ScarringIrreversible loss. Goal is to stop progression. preservation.

8. Complications
  • Psychological Distress: Anxiety, depression, body dysmorphia.
  • Sunburn: Scalp burn risk increased.
  • Social Stigma: Particularly for women and children.

9. Special Considerations

Hair Loss in Children

  • Tinea Capitis: Always rule out fungal infection. Scale + lymphadenopathy. Treat with ORAL antifungals (topicals fail).
  • Alopecia Areata: Common in children. High association with atopy.
  • Trichotillomania: Compulsive pulling. Look for odd shapes and different lengths.

Pregnancy

  • Telogen Gravidarum: physiologic thickening during pregnancy (prolonged anagen), followed by massive shedding 3 months post-partum (Telogen Effluvium).
  • Management: Reassurance. Resolves spontaneously.

10. Key Clinical Pearls

Exam-Focused Points

  1. Exclamation Mark Hairs: Pathognomonic for Alopecia Areata (taper towards scalp).
  2. Scarring vs Non-Scarring: The most important distinction. Look for loss of follicular ostia (smooth shiny scalp = scarring).
  3. Pull Test: Positive (>10% loose) means ACTIVE shedding (TE or active AA/LPP). Negative means stable or AGA.
  4. Ferritin: Target >40-70 ng/mL for optimal hair growth. Normal lab range (e.g., >15) is often too low for hair.
  5. Finasteride: Teratogenic. Women of childbearing potential must not handle crushed tablets or use it (unless on strict contraception).
  6. Tinea Capitis: Must treat with ORAL Griseofulvin/Terbinafine. Creams do not penetrate the hair shaft.

Common Exam Scenarios

  • 30yo woman, diffuse shedding 3 months after having a baby. (Telogen Effluvium).
  • Young man with coins-sized smooth bald patches. (Alopecia Areata).
  • 60yo woman with receding hairline and eyebrow loss. (Frontal Fibrosing Alopecia).

11. Patient Explanation

Why Is My Hair Falling Out?

"Hair loss happens for different reasons.

  1. Genetic (Pattern) Balding: Your hair follicles are sensitive to hormones and shrink over time.
  2. Autoimmune (Alopecia Areata): Your immune system mistakenly attacks the hair root, making it fall out. The root is still alive, so hair can grow back.
  3. Shedding (Telogen Effluvium): Stress, illness, or hormonal shifts 'reset' the clock on your hairs, causing many to fall out at once. This usually happens 3 months after the trigger event."

Will It Grow Back?

"It depends on the type:

  • Shedding (Stress/Post-partum): Yes, it almost always grows back on its own.
  • Alopecia Areata: Yes, often on its own or with steroid injections.
  • Pattern Balding: It won't grow back on its own, but we can stop it from getting worse and sometimes regrow hair with medication."

Do Shampoos Work?

"Most over-the-counter 'hair growth' shampoos do not work. The FDA-approved treatments are Minoxidil and (for men) Finasteride. Ketoconazole shampoo can help slightly by reducing inflammation."


12. Evidence & Guidelines

Key Guidelines

GuidelineOrganizationYearKey Points
Alopecia AreataBritish Association of Dermatologists2012Steroids first line, Immunotherapy for severe
Androgenetic AlopeciaEuropean Dermatology Forum2017Finasteride/Minoxidil evidence based
Scarring AlopeciaBAD2020Early biopsy and aggressive anti-inflammatory Rx

Landmark Trials

BRAVE-AA1 and BRAVE-AA2 (2022):

  • Phase 3 trials for Baricitinib (JAK inhibitor) in severe Alopecia Areata.
  • Showed significant hair regrowth (>80% scalp coverage) compared to placebo.
  • Led to first FDA approval for severe AA.

Finasteride Trials (1998):

  • Long-term (5 year) data showing cessation of hair loss in 90% of men.

Evidence-Based Recommendations

RecommendationEvidence Level
Oral Finasteride for Male AGAHigh
Topical Minoxidil for AGAHigh
Intralesional Steroids for Patchy AAModerate
JAK Inhibitors for Severe AAHigh
PRP (Platelet Rich Plasma)Low/Controversial

13. References
  1. Messenger AG, et al. British Association of Dermatologists' guidelines for the management of alopecia areata 2012. Br J Dermatol. 2012;166(5):916-926.

  2. King B, et al. Two Phase 3 Trials of Baricitinib for Alopecia Areata. N Engl J Med. 2022;386(18):1687-1699.

  3. Kanti V, et al. Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men - short version. J Eur Acad Dermatol Venereol. 2018;32(1):11-22.

  4. Harries MJ, et al. Lichen planopilaris and frontal fibrosing alopecia as model epithelial stem cell diseases. Trends Mol Med. 2018;24(5):435-448.

  5. Adil A, Godwin M. The effectiveness of treatments for androgenetic alopecia: A systematic review and meta-analysis. J Am Acad Dermatol. 2017;77(1):136-141.e5.

Last updated: 2025-12-22

At a Glance

EvidenceHigh
Last Updated2025-12-22

Red Flags

  • Scarring (cicatricial) alopecia - urgent referral to prevent permanent loss
  • Associated systemic symptoms (virilization, weight loss, joint pain)
  • Scalp inflammation (pustules, crusting, boggy swelling)
  • Rapidly progressive universal hair loss

Clinical Pearls

  • Women; Age-dependent |
  • Shedding (Exogen) │ │
  • Vellus │ • Non-scarring │ months LATER │ │

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines