What are the causes and treatment options for chronic telogen effluvium?

Chronic Telogen Effluvium: Causes and Treatment

Primary Causes

Chronic telogen effluvium (CTE) is most commonly triggered by physiological stress, nutritional deficiencies (particularly zinc and vitamin D), thyroid dysfunction, medications, and inflammatory conditions, though many cases remain idiopathic despite thorough evaluation. 1, 2

Nutritional Deficiencies

• Zinc deficiency is significantly associated with CTE, with serum zinc levels being lower in CTE patients compared to controls, and the Cu/Zn ratio serving as a significant predictor of CTE 3
• Vitamin D deficiency is extremely common (72.2% of screened TE patients), though its direct causative role remains unclear 2
• Iron deficiency anemia occurs in only 6.2% of TE patients when properly screened with ferritin and complete blood count 2
• Vitamin B12 deficiency is found in 30.7% of screened patients 2
• Folate (4.4%) and selenium abnormalities are less common, though selenium levels are paradoxically higher in CTE patients 2, 3

Endocrine and Systemic Causes

• Thyroid dysfunction is present in only 4.6% of TE patients, making routine screening of limited yield unless clinically indicated 2
• Physiological stress from surgery, trauma, severe illness, or emotional stress can trigger the telogen shift 1
• Medications and drug reactions are important reversible causes 1

Important Clinical Caveat

Nutritional deficiencies are not as common as traditionally believed in TE patients, and indiscriminate supplementation without documented deficiency is not evidence-based. 3 A detailed history focusing on recent stressors (within 3-6 months prior to hair loss onset), medication changes, and systemic symptoms is more diagnostically valuable than reflexive laboratory ordering 1, 2

Diagnostic Approach

Clinical Diagnosis

• CTE is defined by >6 months of increased telogen hair shedding without visible mid-frontal scalp hair loss (Sinclair stage 1) and no hair follicle miniaturization on scalp biopsy if performed 4
• Hair pull test should be positive, with easy extraction of telogen hairs 1
• Dermoscopy can identify telogen hairs and exclude other diagnoses like alopecia areata 5

Selective Laboratory Testing

The most cost-effective approach based on prevalence data:

1. First-tier tests (highest yield):

   • Serum ferritin (most frequently ordered at 82.3% of cases) and complete blood count to assess for iron deficiency anemia 2
   • Serum zinc level (significantly lower in CTE patients) 3
   • TSH only if clinical signs of thyroid disease are present 2

2. Second-tier tests (if first-tier normal and symptoms persist):

   • Vitamin D level (deficient in 72.2% but unclear causative role) 2
   • Vitamin B12 level (deficient in 30.7%) 2
   • Cu/Zn ratio (significant predictor of CTE) 3

3. Avoid routine testing for:

   • Biotin (no difference between CTE patients and controls) 3
   • Selenium (paradoxically higher in CTE patients) 3
   • ANA titers unless systemic lupus is suspected 2

Treatment Strategies

Address Underlying Causes First

• Correct documented nutritional deficiencies with targeted supplementation 2
• Iron replacement is the most frequently prescribed treatment (37.5% of prescriptions) when deficiency is confirmed 2
• Vitamin D replacement is commonly prescribed, particularly in women, though evidence for efficacy is limited 2
• Discontinue causative medications if identified 1

Pharmacological Treatment

Oral minoxidil (0.25-2.5 mg daily) significantly reduces hair shedding in CTE, with mean hair shedding score reductions of 1.7 at 6 months and 2.58 at 12 months (p<0.001). 4 This represents the strongest treatment evidence available, though it is based on a single retrospective study without placebo control.

Oral Minoxidil Protocol

• Starting dose: 0.25-1 mg daily, titrated based on response and tolerability 4
• Duration: Minimum 6 months for assessment, with continued benefit at 12 months 4
• Monitoring: Blood pressure at baseline and follow-up (mean change: -0.5 mmHg systolic, +2.1 mmHg diastolic) 4
• Common side effects: Facial hypertrichosis (36% of patients), managed with waxing or laser hair removal if bothersome; transient postural dizziness (5.6%); ankle edema (2.8%) 4
• Contraindications: Significant cardiovascular disease, pregnancy 4

Topical Minoxidil Alternative

5% topical minoxidil applied twice daily increases terminal hair count by 12.55 hairs/cm² at 4 weeks and 11.20 hairs/cm² at 12 weeks, with nearly 70% of patients showing improvement of ≥2 grades in hair wash test. 6 This is an off-label use with minimal adverse events and may be preferred for patients concerned about systemic effects 6

Adjunctive Treatments

• Corticosteroids may be used in select cases, though evidence is limited 1
• Novel topical formulations containing caffeine, niacinamide, panthenol, dimethicone, and acrylate polymer show promise but lack robust evidence 1

Critical Management Principles

Natural History Consideration

TE typically self-resolves within 3-6 months once the triggering factor is eliminated, making it essential to distinguish between active treatment effects and natural resolution. 6 This spontaneous recovery complicates interpretation of treatment efficacy in uncontrolled studies 4, 6

Psychological Impact

The substantial hair shedding causes significant psychological stress despite the self-limited nature of the condition 6. Early intervention with topical minoxidil may provide reassurance and reduce anxiety during the recovery period 6

Treatment Algorithm

1. Identify and eliminate triggering factors through detailed history 1, 2
2. Perform selective laboratory testing based on clinical suspicion (ferritin, CBC, zinc) 2, 3
3. Correct documented deficiencies with targeted supplementation 2
4. Consider minoxidil therapy (oral 0.25-2.5 mg daily or topical 5% twice daily) for persistent shedding beyond 3 months or severe psychological distress 4, 6
5. Reassess at 6 months with hair wash test or phototrichogram 6

Common Pitfalls to Avoid

• Avoid indiscriminate vitamin/mineral supplementation without documented deficiency, as nutritional deficiencies are less common than traditionally believed 3
• Do not routinely screen thyroid function unless clinical signs are present (only 4.6% prevalence) 2
• Recognize that vitamin D deficiency is common but its causative role is unproven, making routine supplementation of questionable benefit 2, 3
• Remember that biotin and selenium testing have no diagnostic value in CTE 3