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Summary Table

Domain	Detail
Risk Factors	Patients receiving cytotoxic chemotherapy, radiation to the scalp, or those with heavy metal exposure (thallium, arsenic). Less commonly, severe protein malnutrition or autoimmune conditions
Etiology	Direct toxic injury to rapidly dividing hair matrix keratinocytes during the anagen (active growth) phase of the hair cycle
Patient Presentation	Acute, diffuse, dramatic hair loss beginning 1 to 3 weeks after initiation of chemotherapy or toxic exposure. Often involves eyebrows, eyelashes, and body hair
Classic Physical Exam	Diffuse, non-scarring alopecia with >80% scalp hair affected. Hair shafts fracture at or near the scalp surface. No erythema, scaling, or scarring
Key Diagnostic Results	Trichogram shows dystrophic anagen hairs with tapered, pencil-point proximal ends. Trichoscopy reveals black dots (cadaverized hairs) and Pohl-Pinkus constrictions
Management	Primarily supportive; hair regrows 1 to 3 months after removing the offending agent. Scalp hypothermia (cooling caps) during chemotherapy is the main preventive intervention. Topical minoxidil may accelerate regrowth
Keywords	"Diffuse hair loss after chemotherapy," "pencil-point fracture," "dystrophic anagen hairs," "Pohl-Pinkus constriction," "black dots on dermoscopy," "non-scarring alopecia"

1. Pathophysiology

The hair follicle cycle consists of three phases: anagen (active growth, lasting 2 to 7 years), catagen (regression, 2 to 3 weeks), and telogen (resting, 2 to 3 months). At any given time, approximately 85 to 90% of scalp hairs are in anagen. This is a critical number to internalize because it explains why anagen effluvium causes such dramatic hair loss: the toxic insult hits the vast majority of follicles simultaneously.

Hair matrix keratinocytes in the anagen bulb are among the most rapidly proliferating cells in the human body, with a mitotic rate approaching every 12 to 72 hours. This proliferative rate makes them exquisitely vulnerable to any agent that targets dividing cells. Cytotoxic chemotherapy drugs, particularly alkylating agents (cyclophosphamide), antimetabolites (methotrexate, 5-fluorouracil), anthracyclines (doxorubicin), and taxanes (paclitaxel, docetaxel), all exert their effect by disrupting DNA synthesis or mitotic spindle function. When these agents reach the hair bulb via the blood supply, they abruptly halt mitotic activity in the matrix cells.

The result is a structural failure of the growing hair shaft. The abrupt cessation of matrix cell division causes a focal narrowing in the shaft called a Pohl-Pinkus constriction. This weakened segment cannot support the mechanical stress of normal hair growth and daily activity, so the shaft fractures at or near the scalp surface. This is fundamentally different from telogen effluvium, in which hair is pushed prematurely from anagen into the telogen resting phase and then shed as an intact club hair. In anagen effluvium, the hair never completes its cycle; it simply breaks.

The onset of hair loss is 1 to 3 weeks after the toxic exposure, reflecting the time needed for the structurally compromised shaft segment to reach the scalp surface. This rapid timeline is itself a diagnostic clue: telogen effluvium, by contrast, requires the follicle to transit through catagen and telogen before shedding, which takes 2 to 4 months.

Heavy metals such as thallium and arsenic cause anagen effluvium through a similar mechanism: direct inhibition of sulfhydryl-dependent enzymatic processes in the hair matrix, disrupting keratin synthesis. Radiation therapy to the scalp damages follicular stem cells; at low doses the effect is reversible, but at doses exceeding approximately 40 to 50 Gy the damage to the follicular bulge stem cell niche may be permanent, leading to irreversible cicatricial alopecia.

2. Classification and Clinical Manifestation

Type	Mechanism	Onset	Hair Loss Pattern	Reversibility	Classic Cause
Dystrophic anagen effluvium (most common, most tested)	Cytotoxic damage to matrix keratinocytes; shaft fractures at Pohl-Pinkus constriction	1 to 3 weeks after exposure	Diffuse, non-scarring; affects scalp, eyebrows, eyelashes, body hair	Reversible within 1 to 3 months of stopping the offending agent	Chemotherapy (doxorubicin, cyclophosphamide, taxanes)
Loose anagen syndrome	Defective anchoring of inner root sheath to hair shaft; anagen hairs easily extracted	Childhood onset (typically age 2 to 5)	Diffuse thin hair; painless, easy hair extraction	Tends to improve with age	Inherited structural defect; most common in fair-haired girls
Radiation-induced (low dose)	Sublethal damage to matrix cells	1 to 3 weeks post-radiation	Localized to radiation field	Reversible if dose < 40 Gy	Therapeutic cranial irradiation
Radiation-induced (high dose)	Permanent destruction of bulge stem cells	1 to 3 weeks post-radiation	Localized; progresses to scarring alopecia	Irreversible	Doses > 40 to 50 Gy
Heavy metal toxicity	Inhibition of sulfhydryl enzymes in matrix	Days to weeks after ingestion	Diffuse, non-scarring	Reversible after chelation and removal of exposure	Thallium (most classic), arsenic, mercury

Clinical pearl for exam purposes: when a vignette describes a child with easily pulled, painless hair and diffuse thinning (without chemotherapy exposure), the answer is loose anagen syndrome, not telogen effluvium or alopecia areata. The extracted hairs will have ruffled cuticles and absent root sheaths.

3. Diagnostic Workup

Test	Role	Expected Finding
Clinical history + timeline	Best initial step	Onset 1 to 3 weeks after chemotherapy, radiation, or toxic exposure
Hair pull test	Bedside screening	Positive; extracted hairs are dystrophic anagen hairs (not club hairs)
Trichoscopy (dermoscopy of scalp)	Non-invasive confirmatory	Black dots (broken/cadaverized hairs), Pohl-Pinkus constrictions, tapered fractures
Trichogram (microscopic hair analysis)	Most accurate diagnostic test	>80% dystrophic anagen hairs with tapered, pencil-point proximal ends
Scalp biopsy	Rarely needed; only for atypical cases	Normal follicle density (non-scarring), dystrophic anagen follicles, possible peribulbar pigment casts
Heavy metal panel (urine/blood)	When no chemotherapy history exists	Elevated thallium, arsenic, or mercury levels

The diagnostic approach to anagen effluvium is overwhelmingly clinical. In practice, the combination of a patient on chemotherapy who develops rapid diffuse hair loss within the first few weeks of treatment is essentially diagnostic. No further workup is typically needed.

When the diagnosis is uncertain (for example, in a patient without an obvious toxic exposure), the hair pull test is the best initial bedside maneuver. You gently grasp approximately 50 to 60 hairs between thumb and forefinger, apply steady traction from base to tip, and evaluate the extracted hairs. In anagen effluvium, the test is positive (more than 6 hairs extracted), and the hairs themselves are the key: they will have tapered, pencil-point proximal ends with pigmented, irregular shafts. This is in direct contrast to telogen effluvium, where the pulled hairs are club hairs with a rounded, depigmented bulb and no root sheath.

Trichoscopy (dermoscopy of the scalp) has become increasingly tested and is the non-invasive confirmatory step. The hallmark finding is black dots, which represent hairs that have fractured at the scalp surface and left behind a cadaverized remnant within the follicular ostium. You may also see broken hairs at different lengths and Pohl-Pinkus constrictions (focal thinning of the visible shaft).

The trichogram is the most accurate diagnostic test. This involves plucking 50 to 100 hairs and examining their roots under light microscopy. In anagen effluvium, you will see more than 80% of hairs as dystrophic anagen hairs. Normally, a trichogram from a healthy scalp would show approximately 85 to 90% normal anagen hairs and 10 to 15% telogen hairs. The difference is that the anagen hairs in anagen effluvium are dystrophic (malformed, tapered, lacking inner root sheaths), not the well-formed anagen hairs you see in health.

Scalp biopsy is reserved only for diagnostically ambiguous cases. The finding of normal follicle density differentiates this from scarring alopecias. You will see follicles arrested in a dystrophic anagen phase with possible melanin casts around damaged bulbs.

If the vignette describes diffuse hair loss without any chemotherapy or radiation history, strongly consider heavy metal poisoning. A 24-hour urine heavy metal panel or blood levels should be ordered. Thallium poisoning is the classic board-testable cause: the combination of acute gastrointestinal symptoms followed by diffuse alopecia 2 to 3 weeks later with painful neuropathy is the classic triad.

4. Management and Treatment

Clinical Scenario	Intervention	Details
Prevention during chemotherapy	Scalp hypothermia (cooling caps)	Applied 30 min before, during, and 30 min after infusion. Reduces local blood flow and drug delivery to follicles. Most evidence with taxanes and anthracyclines
Active hair loss	Supportive care	Psychosocial support, wig fitting, head coverings. No pharmacologic agent reliably halts ongoing loss
Post-exposure regrowth acceleration	Topical minoxidil 2% to 5%	Applied twice daily to the scalp. May accelerate regrowth by 1 to 2 months, though evidence is modest
Heavy metal poisoning	Chelation therapy + remove exposure	Prussian blue for thallium; dimercaprol (BAL) or succimer (DMSA) for arsenic. Hair regrows after toxin clearance
Radiation-induced (irreversible)	Surgical or cosmetic options	Hair transplantation, prosthetic hairpieces. Follicular stem cells are permanently destroyed at high doses
Psychological distress	Referral for counseling	Body image disturbance and depression are common, particularly in women and adolescents receiving chemotherapy

Acute management of anagen effluvium is fundamentally supportive. There is no medication that can rescue a hair follicle already damaged by a cytotoxic drug. The single most important management principle is that hair loss is reversible upon cessation of the offending agent. Regrowth typically begins within 1 to 3 months and produces visible coverage by 3 to 6 months. It is worth noting that regrown hair may initially differ in color or texture from the patient's baseline (this is commonly tested as a minor detail).

Scalp hypothermia using cooling cap systems is the main evidence-based preventive strategy. The cap is placed on the scalp approximately 30 minutes before chemotherapy infusion begins, kept throughout the infusion, and maintained for 30 to 90 minutes afterward. The mechanism is vasoconstriction of scalp blood vessels, which reduces the amount of cytotoxic drug delivered to the hair follicle. It also slows follicular metabolic rate, making the matrix cells less susceptible. Scalp cooling has the best evidence for taxane-based regimens (docetaxel, paclitaxel), with efficacy rates of approximately 50 to 80% in preserving hair. It is not recommended in patients with hematologic malignancies (leukemia, lymphoma) due to theoretical concern for the scalp acting as a sanctuary site for circulating malignant cells.

Topical minoxidil (2% or 5% solution) may be applied twice daily to the scalp to accelerate the regrowth phase after chemotherapy is completed. The evidence is modest but generally favorable: it does not prevent initial hair loss, but it may reduce the duration of visible alopecia by 1 to 2 months. There are no meaningful contraindications to topical minoxidil in this setting.

For patients with heavy metal-induced anagen effluvium, management is directed at the toxin. Thallium poisoning is treated with Prussian blue (potassium ferric hexacyanoferrate), which binds thallium in the gut and interrupts enterohepatic circulation. Arsenic poisoning is treated with chelation using dimercaprol (BAL) for acute symptomatic cases or succimer (DMSA) for less severe presentations. Hair regrows once the toxin is cleared.

For patients with permanent radiation-induced alopecia (doses exceeding 40 to 50 Gy), the follicular stem cells in the bulge region are irreversibly destroyed. No medical therapy can restore hair growth. Management options include hair transplantation from unaffected donor sites, scalp prostheses, or cosmetic camouflage.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Telogen effluvium	Also causes diffuse, non-scarring hair loss. Also triggered by systemic stressors	Onset is 2 to 4 months after the trigger (not 1 to 3 weeks). Pulled hairs are club hairs (rounded bulb), not dystrophic anagen hairs. Hair loss is less dramatic (usually 20 to 50%)
Alopecia areata	Can cause sudden, dramatic hair loss. Trichoscopy also shows black dots	Hair loss is patchy with well-demarcated oval/round patches. Pathognomonic finding is exclamation point hairs (short hairs that taper toward the scalp). May have nail pitting
Trichotillomania	Shows broken hairs on exam, can have black dots	Hair loss is in irregular, geometric patches, often frontotemporal. Hairs are broken at different lengths ("hair stubble field"). Patient may deny the behavior. Biopsy shows trichomalacia (pigment casts without peribulbar inflammation)
Alopecia totalis/universalis	Can cause total scalp or total body hair loss	This is a severe variant of alopecia areata, not a toxic insult. No temporal association with drugs. Biopsy shows peribulbar lymphocytic infiltrate ("swarm of bees" pattern)
Secondary syphilis	Can cause diffuse alopecia ("moth-eaten" appearance)	The alopecia is patchy and irregular ("moth-eaten"), not diffuse and total. Patient will have other signs: diffuse macular rash on palms/soles, condylomata lata, positive RPR/VDRL
Iron deficiency alopecia	Causes diffuse hair thinning in women	Onset is gradual over months, not acute. Low ferritin, low serum iron, elevated TIBC. Hair pull test shows telogen hairs, not dystrophic anagen hairs
Loose anagen syndrome	Easily pulled anagen hairs; seen in children	No toxic exposure. The pulled hairs have ruffled cuticles and misshapen bulbs. Predominantly affects young, fair-haired girls. Hair simply "doesn't grow long"

The highest-yield discriminator on any exam question is the timeline. If the vignette gives you diffuse hair loss within 1 to 3 weeks of starting chemotherapy, that is anagen effluvium until proven otherwise. If the same patient presents 3 months after completing chemotherapy with diffuse shedding, that is telogen effluvium (the physiologic recovery shedding that occurs as follicles re-enter telogen synchronously after resuming anagen).

6. Traps and High-Yield Pearls

The single most common way students get this topic wrong is by confusing anagen effluvium with telogen effluvium based on the clinical timeline. Both present with diffuse, non-scarring hair loss, and both can be triggered by chemotherapy. The trap is a vignette that describes a patient who completed chemotherapy 3 months ago and is now experiencing diffuse hair shedding. Students instinctively pick anagen effluvium because of the chemotherapy history, but the correct answer is telogen effluvium: the anagen effluvium already happened during treatment, and now the follicles that recovered are synchronously entering telogen and shedding their club hairs. The timeline is everything.

A second common trap involves thallium poisoning. The vignette will not hand you the diagnosis. Instead, it will describe a patient with acute gastroenteritis (nausea, vomiting, abdominal pain) followed by painful neuropathy and diffuse hair loss 2 to 3 weeks later. If you do not recognize thallium as a cause of anagen effluvium, you may anchor on a GI diagnosis or a neurologic diagnosis and miss the connection. The triad of GI symptoms, neuropathy, and alopecia should immediately trigger the thought of heavy metal toxicity. The treatment (Prussian blue) is frequently the tested answer.

A third pearl: when a vignette mentions that a patient's hair grew back with a different color or texture after chemotherapy, this is not a complication requiring workup. It is a normal phenomenon caused by altered melanocyte activity in the regenerating follicle and is tested as a "distractor" designed to make you order unnecessary labs.

The core competency being tested in anagen effluvium questions is pattern recognition based on onset timing, the ability to classify hair loss by the phase of the hair cycle affected, and the clinical reasoning required to distinguish it from telogen effluvium when the causative agent is the same.

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