Endgames Case Report

Recurrent episodes of hair loss in a 37 year old woman

BMJ 2012; 345 doi: http://dx.doi.org/10.1136/bmj.e6798 (Published 09 October 2012) Cite this as: BMJ 2012;345:e6798
  1. Carol Cunningham, specialist registrar in dermatology1,
  2. Ralf Paus, professor of cutaneous medicine2,
  3. Matthew Harries, dermatology consultant1
  1. 1Dermatology, Salford Royal Foundation Trust, Manchester M6 8HD, UK
  2. 2University of Manchester, Stopford Building, Manchester
  1. Correspondence to: C Cunningham car.cunningham{at}gmail.com

A 37 year old woman presented with recurrent episodes of hair shedding that led to reduced hair volume. The first episode of hair loss had occurred three months after the death of her father. Her scalp hair had become dry and of poor quality, and soon after her hair started “falling out by the roots.” After four months of serious hair shedding the hair loss slowed. Unfortunately, she then had a miscarriage, which resulted in a flare of the shedding. Investigations at this time identified low iron stores (ferritin 24.7 pmol/L, reference range 54-674 for men and 34-690 for women; 1 pmol/L=0.45 ng/mL). With increased iron consumption the shedding settled and was associated with improvements in hair quality and volume. A few months later she started a combined oral contraceptive (cyproterone acetate and ethinylestradiol), but within a month she developed side effects so stopped the treatment. Within six weeks she developed a further episode of increased hair shedding with loss of hair density.

On first attendance she reported a reduction in the rate of hair shedding, with evidence of hair regrowth. However, she thought that her hair volume was still subnormal and felt self conscious about it. She had no medical history of note, no allergies, and had been taking multivitamin and iron supplements for the past seven months. She had not used any topical treatments, had not changed the frequency of shampooing, and denied any traumatic hair care practices. On examination there was no evidence of scarring or inflammation of the scalp skin. Short regrowing hairs were seen, the vertex hair part width was normal compared with the occipital hair part width, and a pull test to assess for active hair shedding was negative.

Questions

  • 1 What is the most likely diagnosis?

  • 2 List four possible differential diagnoses

  • 3 How should this condition be evaluated clinically and with laboratory investigations?

  • 4 What is the prognosis?

  • 5 How should this condition be treated?

Answers

1 What is the most likely diagnosis?

Short answer

Telogen effluvium. Possible triggers in this patient include emotional stress, miscarriage, low iron stores, and discontinuation of the combined contraceptive pill.

Long answer

Telogen effluvium. This is a form of non-scarring diffuse alopecia that occurs when an increased number of scalp hairs move prematurely from the growth phase of the hair cycle (anagen) into the resting phase (telogen). It can occur in either sex and at any age. Patients present because they are shedding more scalp hairs than usual and may bring evidence of this with them (fig 1). Shed telogen hair shafts are recognised by their depigmented proximal tips, club shaped roots, and the absence of a root sheath (fig 2).

Figure2

Fig 2 Positive hair pull test. Telogen (club) hairs are identified by depigmented proximal tips

Increased shedding may be associated with reduced hair density, commonly noticed as slight recession of the temples. However, scalp skin looks normal and complete hair loss does not occur. Importantly, telogen effluvium is a diffuse process throughout the scalp and does not occur in sharply demarcated areas.

A triggering event for the hair loss usually occurs one to six months before the reported onset of hair loss. Increased numbers of telogen hairs are shed during the active phase, whereas recovery is suggested by regrowth of new short hairs and resolution of shedding. The box lists the recognised triggering factors.

Recognised triggers for telogen effluvium1

  • Hormonal changes, such as pregnancy, parturition, miscarriage, changes to or discontinuation of oral contraceptives

  • Acute illness, such as acute febrile disease, major surgery, and physical trauma

  • Chronic illness, such as hypothyroidism or hyperthyroidism, cancer, lymphoproliferative disorders, HIV, chronic renal or liver disease, and connective tissue diseases

  • Malnutrition—for example, “crash” dieting, low protein intake, chronic iron deficiency (with or without anaemia), vitamin D deficiency

  • Drugs—for example, oral retinoids, β blockers, anticoagulants, non-steroidal anti-inflammatory drugs, antidepressants, anti-arrhythmics, and antithyroid drugs,

  • Immunisations

  • Heavy metal poisoning—for example arsenic or thallium poisoning

  • Psychological or emotional stress

  • Seasonal hair moult (spring and autumn)

  • Inflammatory scalp disorders, such as seborrhoeic eczema and psoriasis

  • Early androgenetic alopecia

Possible triggers in our patient include emotional stress, miscarriage, low iron stores, and cessation of the combined contraceptive pill. In about a third of cases of acute disease, no trigger is clearly identified.

2 List four possible differential diagnoses

Short answer

Differential diagnoses include other non-scarring forms of diffuse alopecia, such as androgenetic alopecia, diffuse alopecia areata, anagen effluvium, and secondary syphilis.

Long answer

These include other diffuse non-scarring forms of alopecia, such as androgenetic alopecia, diffuse alopecia areata, anagen effluvium, and secondary syphilis.

The pattern of hair loss in androgenetic alopecia provides clues to the diagnosis. In women this condition manifests as diffuse hair thinning over the vertex of the scalp with preservation of the frontal hairline (female pattern hair loss; Ludwig pattern). A wider part width on the scalp vertex compared with the occipital scalp is typically seen, together with increased variation in the diameter of the hair shaft and visibly miniaturised hairs in the affected areas. By contrast, thinning occurs mainly over the crown and frontotemporal areas in men with this condition (male pattern hair loss; Hamilton-Norwood pattern). In most cases, hair loss progresses steadily over months to years and hair does not regrow without treatment, although increased shedding and episodic thinning may be seen in some patients. This pattern of hair loss is more common with increasing age but can occur at any time after puberty.

Diffuse alopecia areata is uncommon, with most cases presenting with patchy hair loss initially. Diffuse alopecia areata may be difficult to distinguish from telogen effluvium because acute hair shedding is a prominent feature in both conditions. Diagnostic clues include associated patchy scalp or loss of body hair, a family history of alopecia areata, nail changes (such as pitting), and the presence of “exclamation mark” hairs.2 The regrowth of depigmented hairs within an alopecia patch is diagnostic for alopecia areata. Histological evidence of lymphocytes surrounding the anagen hair follicle bulb may be needed to confirm the diagnosis in difficult cases.

Anagen effluvium occurs when growing (anagen) hair abruptly stops growing, resulting in severe hair loss. Because most scalp hairs are in anagen at any one time (85% hairs), when growth stops the hair loss is often dramatic and extensive, with much of the scalp coverage being lost. Anagen effluvium is the pattern of hair loss typically seen after chemotherapy. The time lag from the triggering event to hair loss is usually much shorter than in telogen effluvium (for example, one to three weeks after starting chemotherapy).

Hair loss in secondary syphilis classically has a patchy “moth eaten” appearance. However, diffuse hair shedding, particularly from the parietal region of the scalp, is occasionally seen in secondary syphilis; patients are unwell and risk factors for infection may be apparent.

Some patients with real (or perceived) hair loss alter their normal hair care practices—for example, they may reduce the frequency of shampooing (known to remove loose hairs). This will result in a relative increase in the observed numbers of hairs shed each time they wash or comb their hair and potentially provoke additional anxiety. Furthermore, patients may sometimes misinterpret normal levels of shedding (up to 100 hairs a day) as being abnormal. Objective tests for shedding (see below) are useful in these situations.

3 How should this condition be evaluated clinically and with laboratory investigations?

Short answer

Clinical assessment includes performing the hair pull test. Laboratory tests include a full blood count, ferritin and iron studies, erythrocyte sedimentation rate, thyroid function tests, urea and electrolytes, liver function tests, antinuclear antibody tests, measurement of zinc, and syphilis serology. Scalp biopsy may be needed in difficult cases.

Long answer

A hair pull test should be performed in all patients with hair loss. The clinician grasps 40-50 hairs between thumb and forefinger and pulls gently away from the scalp. In telogen effluvium an increased number of telogen hairs (>10% pulled hairs) are extracted from all areas of the scalp. Clinicians should standardise how they perform this test to make it reproducible, particularly as the number of hairs pulled and the time since the last shampooing (which removes loose hairs) will affect the findings.

Alternative methods of assessment include forced extraction (plucking) of hairs to allow total anagen and telogen hair numbers to be calculated (a “trichogram”). Non-invasive standardised hair count methods include the standardised 60 second hair count,3 and the loss of more than 100 hairs a day is generally regarded as abnormal. This last technique has been reported only in men.

Full blood count, ferritin and iron studies, erythrocyte sedimentation rate, thyroid function tests, renal and liver function tests, antinuclear antibody tests, and zinc measurements are commonly performed screening tests. If syphilis is suspected, a non-treponemal screening test (for example, the Venereal Disease Research Laboratory test or rapid plasma reagin test) should be performed.

A scalp biopsy may be needed to make a definitive diagnosis in clinically equivocal cases. Hair counts on horizontally cut punch biopsies will show the proportion of telogen hairs and help exclude other forms of non-scarring alopecia.4

4 What is the prognosis?

Short answer

Acute telogen effluvium is self limiting, with hair regrowth usually occurring within six months of initial hair loss.

Long answer

In acute telogen effluvium hair growth completely recovers within six months, often after resolution of the inciting event or treatment of the underlying cause. However, patients who have undergone a single episode of telogen effluvium are at greater risk of further episodes if exposed to similar triggering factors. The condition may also “unmask” other types of chronic hair loss, particularly androgenetic alopecia.

5 How should this condition be treated?

Short answer

Careful explanation of the nature of the hair loss is important. Underlying causes should be identified and treated.

Long answer

Careful explanation of the nature of the hair loss is important. Underlying causes (box) should be identified and treated. Studies have shown conflicting results in relation to iron supplementation. The decision to treat iron deficiency with or without anaemia should be made on an individual patient basis, and an underlying cause for the iron deficiency should be elicited.5

To accelerate hair regrowth or to slow down hair loss (or both), topical daily treatment with 2-5% minoxidil lotion for three to six months should be considered, although this is an off-label use of this lotion. Many patients are greatly distressed by their hair loss and may also benefit from cosmetic camouflage advice (such as scalp make-up, hair pieces) and psychological support.6

Patient outcome

This patient’s hair has fully regrown and she now has normal density hair.

Notes

Cite this as: BMJ 2012;345:e6798

Footnotes

  • Competing interests: All authors have completed the ICMJE uniform disclosure form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: no support from any organisation for the submitted work; no financial relationships with any organisations that might have an interest in the submitted work in the previous three years; no other relationships or activities that could appear to have influenced the submitted work.

  • Provenance and peer review: Commissioned; externally peer reviewed.

  • Patient consent obtained.

References