S1 Guideline for Diagnostic Evaluation in Androgenetic Alopecia in Men, Women and Adolescents

U. Blume-Peytavi; A. Blumeyer; A. Tosti; A. Finner; V. Marmol; M. Trakatelli; P. Reygagne; A. Messenger

Disclosures

The British Journal of Dermatology. 2011;164(1):5-15. 

In This Article

Steps in the Diagnostic Procedure

The European Consensus Group developed a diagnostic evaluation form (Table 1) for AGA, including history, clinical evaluation, diagnostic techniques and clinical documentation. This form can easily be implemented in daily clinical routine. Additionally, the information has been summarized in a clinical algorithm (Fig. 6).

Figure 6.

Clinical algorithm for the diagnosis of androgenetic alopecia (AGA). DD, differential diagnosis.

History

General The physician should record age, sex, age at first manifestation of hair loss and course of hair loss (chronic or intermittent) in the personal as well as in the family history. Patients with AGA usually complain about a long-standing, slowly progressing hair loss. The hair loss may be described as chronic, but the patients often report increased activity in autumn and winter. The patient should be asked about increased shedding or thinning or both. For thinning, the patient typically describes an accentuation of the frontal, parietal or vertex region, but complaints about diffuse thinning are possible as well. Initial signs of AGA can be itching and trichodynia. A family history for AGA is often positive, but a negative family history does not exclude the diagnosis. A positive family history of other hair disorders, such as alopecia areata or hirsutism may influence the extent of further diagnostic procedures. It is also important to determine if there are other concomitant hair disorders whose untreated presence could ultimately affect the efficacy of the treatments used for AGA (e.g. iron deficiency in diffuse hair loss in women).

A detailed history on systemic and newly diagnosed diseases within 1 year prior to first signs of hair loss should arouse suspicion that the hair loss is due to other causes or aggravating factors, such as diffuse effluvium as a result of severe infection, iron deficiency or thyroid dysfunction. Allergies are not important for the diagnosis of AGA, but they should be recorded for possible significance with regard to therapy (e.g. contact dermatitis due to propylene glycol in minoxidil solutions). The Consensus Group agreed to ask about eating behaviour, as chronic deficient diet or rapid significant weight loss can trigger diffuse effluvium. Concerning drug history there are a variety of drugs that can cause hair loss. Ask especially for chemotherapeutic agents (almost all of which can produce hair loss) and for hormones with pro androgenic or antithyroid action, and whether there is coincidence with hair loss. Particularly in men, the intake of anabolic steroids or supplemental androgens should be explored.

Moreover, consider lifestyle procedures such as special hairstyles (traction) and environmental factors like smoking and ultraviolet radiation (UVR) exposure in the history of the patient. Su and Chen[26] reported a dose-dependent association between smoking status and development of moderate to severe AGA in male patients. Additionally, UVR exposure as an aggravating factor should be taken into account, especially in Mediterranean countries.[27,28]

Women Although the majority of female patients with AGA have physiological hormonal function, an orienting gynaecological history should be done to exclude influencing hormonal dysregulations or associated underlying disorders (e.g. hormone-sensitive tumour). Careful evaluation of the gynaecological history should include menarche, menstrual cycle (regular/irregular), menopause, amenorrhoea, the use of oral or systemic hormonal contraception, hormone replacement therapy, fertility treatment, the number of pregnancies and births, time of last pregnancy/delivery, impaired fertility or problems in getting pregnant, miscarriages, gynaecological surgery, signs of hyperandrogenism (excessive body hair growth, skin changes like acne) or seborrhoea of scalp/skin. Irregular menstrual cycle, amenorrhoea, impaired fertility, problems in getting pregnant, miscarriages, signs of hyperandrogenism and seborrhoea may be indicative for hormonal dysregulation, such as polycystic ovary syndrome.[29–31] If the patient is taking hormonal contraception, ask for cycle duration and regularity before the intake of hormonal contraception.

Adolescents In adolescents it is first important to differentiate if the hair loss is congenital or acquired. Look for physical and mental development, particularly early onset of puberty. In childhood/adolescence, AGA is an acquired hair loss with a characteristic pattern distribution. The differential diagnosis includes diffuse effluvium (nutritional factors), artificially induced alopecia, hypotrichosis simplex (congenital) or ectodermal dysplasia (congenital, delayed physical/psychological development, sweating, dental or nail abnormalities). AGA without signs of premature puberty is not necessarily associated with endocrinological dysregulation, but referral to a paediatric endocrinologist is recommended.

Clinical Evaluation

Clinical examination should involve the scalp skin and hair, facial and body hair and skin as well as the nails.

Scalp Examination The scalp skin usually appears normal in AGA, but consider that seborrhoeic dermatitis of the scalp can be an associated and potentially aggravating factor.[6,32,33]

Look for signs of inflammation (erythema, scaling and hyperkeratosis), seborrhoea and signs of scarring (atrophy, loss of hair follicle ostia). Consider inflammatory or infectious diseases and tumours. Consider alopecia areata and scarring alopecias, which can mimic AGA, especially frontal fibrosing alopecia (Kossard[34]) in women. Look for signs of sun damage in balding areas, which may be an aggravating factor for AGA.[28] In long-standing AGA, discrete atrophy of scalp skin can be present.

Hair ExaminationScalp hair Part the hair to assess scalp hair density. Compare part width in the frontal, occipital and temporal regions to examine the distribution of alopecia. On close examination, focal atrichia of a few millimetres in diameter may be present in some women with AGA. Use a sheet of paper over a part to enhance contrast and look for short and fine miniaturized or broken hairs, variation of hair calibre, length and regrowth. Dermoscopy may be helpful.[35] A pull test, Sabouraud manoeuvre and a friction test are simple tests to get a first global impression of hair quality and hair growth activity.[36,37]

Evaluate and distinguish between diffuse decrease in hair density, a characteristic pattern distribution or localized alopecic patches. In males, AGA typically presents with a male pattern distribution including bitemporal recession and/or vertex thinning, and sometimes anterior recession. About 10% of men with AGA present a female pattern.

Women usually show a more diffuse distribution of hair loss with accentuation in the frontal and mid scalp and preservation of the frontal hairline, but the parietal and occipital scalp may also be involved. In cases of diffuse thinning, also think of diffuse telogen effluvium and diffuse alopecia areata as a differential diagnosis or concomitant condition.

The most frequently used scales in practice are the Hamilton–Norwood scale (Fig. 1) for male pattern distribution and the Ludwig scale (Fig. 2) or Olsen scale (Fig. 4) (frontal accentuation/Christmas tree pattern) for a female pattern. The experts agreed to use these scales in practice. The 5-point Sinclair scale (Fig. 3) is more complicated than the Ludwig scale but offers a broader range of categories. This could become important as more and more women consult their doctor in the early stages of hair loss.[36]

Figure 2.

Ludwig pattern of hair loss (3-point).19,20

Figure 3.

Sinclair scale (5-point) for grading of female pattern hair loss (drawing by Lucas Tosti based on the Sinclair scale published in Gan and Sinclair5).

Figure 4.

Olsen scale: Christmas tree pattern in female pattern hair loss.20,24

A recent publication described a new classification called BASP (basic and specific), which is based on the pattern of hair loss, including the shape of the frontal hair line and the hair density in the frontal and the vertex areas.[38]

Facial and Body Hair Look for abnormal facial and body hair density and/or distribution. Absent or reduced eyebrows/eyelashes and/or body hair may suggest alopecia areata. Think also of frontal fibrosing alopecia if eyebrows or eyelashes are absent or reduced. The experts stated that some women with AGA also complain of reduction of eyebrows or eyelashes.

If there is excessive terminal body hair growth, examine the distribution. Think of ethnic hypertrichosis, hypertrichosis due to medications or hirsutism. Look for signs of acne, seborrhoea and obesity, which are clues for hyperandrogenism.

Nail Examination Nail abnormalities are not typical for AGA, but occur in alopecia areata, certain deficiencies and lichen planus.

Laboratory

Measurement of ferritin level or thyroid-stimulating hormone may be considered depending on the individual history, especially in diffuse effluvium. The role of adequate serum ferritin levels during treatment of diffuse androgen-dependent alopecia in women has been suggested by Rushton and Ramsay[39] and Kantor et al.,[40] who reported a significantly lower mean ferritin level in women with AGA compared with controls. Since then, the relationship between iron deficiency and hair loss has been debated and reviewed recently by Trost et al.,[41] who found that it was still insufficient evidence to recommend supplementation in the absence of insufficient deficiency anaemia. More recently, Bregy and Trüeb[42] suggested no association between serum ferritin levels > 10 μg L−1 and hair loss in women.

Men In men, laboratory testing for the diagnosis of AGA is unnecessary, except if the history or examination provide clues for another underlying disorder or associated disease.

Note: Additional laboratory examinations may become necessary before starting specific treatments. Therefore, the Consensus Group agreed that for men above 45 years measuring the prostate-specific antigen (PSA) value should be recommended before starting finasteride therapy, albeit PSA is controversially discussed. Nevertheless, finasteride reduces PSA values and can delay diagnosis or mask detection of prostate cancer. The treating urologist should be informed on the patient's finasteride intake.

Women The experts agreed that an extensive endocrinological work-up is not necessary. An interdisciplinary approach involving gynaecologists, endocrinologists and dermatologists is recommended if the history and clinical examination are indicative of androgen excess [e.g. polycystic ovary syndrome (anovulatory cycle, elevated hormonal levels), cycle disturbances, androgen-secreting tumours]. The group agreed to perform a free androgen index test [FAI = total testosterone (nmol L−1) × 100/sex hormone-binding globulin (SHBG) (nmol L−1)] and prolactin as screening parameters.[30] Depending on the results, further endocrinological investigations may be required. Free testosterone and FAI seem to be sensitive for the detection of hyperandrogenaemia. In women, at least 80% of bound serum testosterone is bound to SHBG. Consequently, free serum testosterone levels are substantially influenced by SHBG levels, which limit the interpretation of free serum testosterone. The FAI takes this SHBG dependence into account. FAI levels of 5 and above are indicative for polycystic ovary syndrome.[43] Other disorders presenting with clinical and/or biochemical signs of hyperandrogenism such as congenital adrenal hyperplasia, androgen-secreting tumours or Cushing syndrome should be excluded. For this purpose further laboratory testing, e.g. 17-OH-progesterone, follicle-stimulating hormone, oestradiol, prolactin or cortisol may be necessary.

Note: It makes sense to take any hormonal level only on the condition that there is no hormonal intake. Oestrogens lead to elevated SHBG levels, whereas testosterone levels may be only slightly changed. Consequently, the FAI can be markedly improved by hormonal contraception.[44] Therefore, the minimum pause in hormonal contraception has to be 2 months. The measurements should be taken between 08.00 and 09.00 h, ideally between the second and fifth days of the menstrual cycle.

Children and Adolescents In children and adolescents with premature onset of AGA an interdisciplinary approach between the dermatologist and paediatric endocrinologist should be taken.

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