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Telogen Effluvium (TE)

BASICS

  • Definition: Acute, self-limited diffuse hair loss caused by a shift of a significant proportion of anagen (growth phase) hairs into telogen (resting phase), resulting in increased shedding and noticeable thinning when follicles re-enter anagen.
  • Each follicle independently cycles through anagen (growth), catagen (transformation), and telogen (rest), with most follicles in anagen at any time.

TYPES OF TE

  • Immediate anagen release: Most common; follicles exit anagen prematurely (triggers: high fever, drugs, stress); lasts 3–4 weeks.
  • Delayed anagen release: Prolonged anagen phase followed by synchronized entry to telogen; common postpartum.
  • Short anagen: Shortened anagen phase; speculative; >50% follicles affected.
  • Immediate telogen release: Premature loss of resting club hairs, prompting early entry into anagen.
  • Delayed telogen release: Prolonged telogen phase ends abruptly (often due to increased visible light/seasonal change).

EPIDEMIOLOGY

  • Most cases are subclinical; true incidence unknown.
  • No racial predilection.
  • Females seek care more often (possible overrepresentation).
  • Elderly women: more susceptible after fever, trauma, hemorrhage, or stress.
  • Incidence in children: ~2.7%.
  • Second most common cause of alopecia.

ETIOLOGY AND PATHOPHYSIOLOGY

  • Normal hair cycle: Anagen (~3 years) and telogen (~3 months); normally 10–15% of scalp hairs in telogen.
  • Triggers: External/internal stress → increased telogen hairs; new anagen hairs force telogen hairs out (shedding occurs 2–3 months after trigger).
  • Key mediator: Substance P (neuropeptide) influences catagen entry, apoptosis, and immune response:
    • ↑ Substance P receptor (NK1): premature catagen, inhibits growth
    • ↑ NGF/p75NTR: hair apoptosis
    • ↓ TrkA (growth-promoting)
    • ↑ MHC I/β2-microglobulin: immune privilege loss
    • ↑ TNF-α (mast cell): keratinocyte apoptosis
  • Chronic stress: ↓ Cortisol may enhance effect

RISK FACTORS

  • Infection, trauma, major surgery, thyroid disorder, febrile illness, malignancy
  • Allergic contact dermatitis
  • Iron deficiency, excess vitamin A, protein/calorie restriction, end-stage liver/renal disease
  • Hormonal changes (pregnancy, delivery, estrogen meds)
  • Chronic stress
  • Drug-induced (β-blockers, anticonvulsants, antidepressants, anticoagulants, retinoids, ACE inhibitors)
  • Immunizations

DIAGNOSIS

HISTORY

  • Onset: 2–6 months after trigger (often evident)
  • Symptoms: Noticeable hair loss, collections of hair, or photo evidence
  • Fear: Concern about permanent baldness

PHYSICAL EXAM

  • Scalp: Decreased density (crown, temples)
  • Chronic TE: Rare loss at eyebrows, pubic region
  • Shed hairs: Telogen "club" hairs with small bulb at root end
  • Nails: Rarely, associated changes

DIFFERENTIAL DIAGNOSIS

  • Hypo/hyperthyroidism
  • Alopecia areata
  • Androgenetic alopecia
  • Drug-induced alopecia
  • SLE
  • Secondary syphilis
  • Trichotillomania

DIAGNOSTIC TESTS & INTERPRETATION

  • Mainly clinical diagnosis—history and exclusion of other causes.
  • Labs: CBC, ferritin, TSH, creatinine, iron profile, hepatic enzymes, RPR/VDRL as indicated.
  • Hair pull test: Pulling 25–30 hairs yields <5 club hairs (normal); increased shedding suggests TE.
  • Hair clip test: >10% small-diameter hair shafts = positive for TE.
  • Trichogram: >10% telogen hairs confirms TE.
  • Scalp biopsy: Rare; >12–15% follicles in telogen phase supports TE diagnosis.

TREATMENT

  • TE is benign and self-limited.
  • Identify and correct the underlying cause.
  • Reassure patients: Hair regrowth resumes in 3–6 months; full regrowth in 12–18 months.
  • Nutritional deficiency: Supplement as indicated.

MEDICATION

  • Minoxidil: Can stimulate regrowth, but not always necessary.
  • Oral zinc: May benefit if deficient—supports cell division, inhibits catagen, hedgehog signaling.

COMPLEMENTARY & ALTERNATIVE

  • Multivitamins: Zinc, biotin, iron, vitamins A, C, E, B complex, folic acid, magnesium, amino acids—may help hair loss and quality.
  • Millet extract: (with polar lipids) may improve cell proliferation, scalp dryness, brightness.

ONGOING CARE

DIET

  • Correct nutritional deficiencies.
  • Polyphenols (green tea) may help in animal studies, but human evidence lacking.

PROGNOSIS

  • Excellent. Self-limited; complete regrowth expected within 12–18 months.

CODES

  • ICD-10: L65.0 Telogen effluvium

CLINICAL PEARLS

  • Self-limited, non-scarring alopecia; most cases acute.
  • Caused by premature shift of follicles to telogen phase (resting), then shed.
  • Many causes—emotional, physiologic, drug-induced.
  • Elimination of stressor/trigger is the key; reassurance is crucial.
  • No treatment required—regrowth occurs over time.

REFERENCES

  1. Malkud S. Telogen effluvium.
  2. Karashima T, Tsuruta D, Hamada T, et al. Oral zinc therapy for zinc deficiency effluvium.
  3. Sant’Anna Addor FA, Donato LC, Melo CSA. Comparative evaluation between two nutritional supplements in the improvement of telogen effluvium.