Alopecia Areata: Clinical Presentation, Investigation and Management in Outpatient Practice
- Mayta

- 7 hours ago
- 3 min read
1️⃣ Presentation
A patient presents with:
Sudden onset patchy hair loss
One or multiple well-demarcated smooth bald patches
No pain
No scaling
No scarring
No erythema
On examination:
Smooth round or oval patches
“Exclamation mark hairs” at margins (short broken hairs that taper proximally)
Possible nail pitting
🧠 Pathophysiology:Alopecia areata is an autoimmune T-cell–mediated attack on the hair follicle, specifically targeting the anagen phase follicle.The follicle remains viable → therefore non-scarring and potentially reversible.
Common associations:
Autoimmune thyroid disease
Vitiligo
Atopic disease
Type 1 diabetes

2️⃣ Management Setting
Based on stable presentation without systemic involvement:
✅ Outpatient Department (OPD)
Alopecia areata is not life-threatening and does not require admission.
3️⃣ Patient Problem List
• Problem 1: Patchy hair loss (suspected Alopecia Areata) • Problem 2: Possible associated autoimmune condition (to be evaluated)
🔬 Laboratory Investigation
According to American Academy of Dermatology (AAD) and UpToDate recommendations:
✅ Routine labs are NOT mandatory in classic alopecia areata.
However, screening for associated autoimmune disease is recommended if clinically indicated.
Labs to Consider:
1️⃣ Thyroid Function Test (TSH, Free T4)
Because alopecia areata is associated with autoimmune thyroid disease.
2️⃣ Anti-TPO antibody
If thyroid abnormal → evaluate autoimmune thyroiditis.
3️⃣ CBC
Rule out iron deficiency or anemia.
4️⃣ Ferritin
Hair growth requires adequate iron stores.
5️⃣ ANA
Only if SLE suspected clinically.
❌ Do NOT send fungal culture unless scaling or infection signs present.
If scaling + broken hairs + lymphadenopathy → think tinea capitis, not alopecia areata.
4️⃣ Plan of Management
Management Setting: OPD
✅ Definitive Treatment
According to American Academy of Dermatology Guidelines
First-line (localized disease <50% scalp involvement):
🔹 Intralesional corticosteroid
Triamcinolone acetonide (2.5–10 mg/mL)Inject intradermally every 4–6 weeks. Reason:
Suppresses autoimmune attack on hair follicle
Highest evidence for localized disease
Superior to topical steroids for small patches
📌 How do % and mg/mL convert?
Remember this formula: 1% = 10 mg/mL
% concentration | mg/mL equivalent |
0.1% | 1 mg/mL |
0.25% | 2.5 mg/mL |
0.5% | 5 mg/mL |
1% | 10 mg/mL |
If patient refuses injection:
Topical clobetasol 0.05%Apply bid for 6–12 weeks
Extensive disease (>50% scalp):
Topical immunotherapy (e.g., DPCP)
Systemic therapy (dermatology referral)
Consider JAK inhibitors (emerging therapy)
❌ Oral steroids are NOT routine first-line
Reason:
High relapse rate
Systemic side effects
Not curative
(Exam pearl: steroids may regrow hair temporarily but relapse common after taper.)
✅ Supportive Treatment
• Psychological support (high emotional burden)
• Cosmetic advice (hair styling, camouflage, wigs)
• Stress reduction (stress can exacerbate autoimmune activity)
5️⃣ Monitoring
• Reassess every 4–6 weeks • Look for vellus hair regrowth • Monitor for steroid-induced skin atrophy • Evaluate progression
🧠 High-Yield Exam Pearl
Alopecia areata:
✔ Smooth bald patch ✔ No scaling ✔ No scarring ✔ Exclamation mark hairs
If scaling present → think tinea capitis
If scarring present → think cicatricial alopecia
📅 Follow-up
Re-evaluate every 4–6 weeks
Continue therapy up to 6 months before labeling treatment failure.
⚠️ Complications to Monitor
• Nail pitting• Progression to alopecia totalis• Progression to alopecia universalis• Psychological distress
🎓 USMLE Style Question
Why don’t we give antifungal?
Because alopecia areata:
❌ Has NO scaling ❌ Has NO infection ❌ Is autoimmune
Giving antifungal would be incorrect unless fungal signs are present.
🔥 Clinical Pearl Mnemonic
“AREATA”
A – Autoimmune R – Round smooth patches E – Exclamation hairs A – Associated thyroid disease T – T-cell mediated A – Anagen follicle attacked





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