Thinning hair at the frontal scalp and crown

Slideshow

  • CA0911DermChallenge_Alopecia

A woman aged 54 years presented with a complaint of hair loss. She stated that for the past year, she felt as though her hair was becoming very thin, especially on the frontal scalp and the crown of her head. There was no pain or pruritus associated with the hair loss. She had not tried any previous treatments.

The patient’s father started losing his hair in his late 20s, but there was no other family history of hair disorders. No fatigue, cold intolerance, weight gain, or dandruff were reported. A review of systems was positive for menstrual irregularities.


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Androgenetic alopecia is a disorder that is characterized by patterned and progressive hair loss caused by genetic factors, which in turn affect the hormones (androgens). Although the disorder has been known to start as early as age 11 years, it...

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Androgenetic alopecia is a disorder that is characterized by patterned and progressive hair loss caused by genetic factors, which in turn affect the hormones (androgens). Although the disorder has been known to start as early as age 11 years, it mainly affects adults in their 20s.

Approximately 80% of white men have a form of androgenetic alopecia by age 70 years.1 A smaller percentage of women express the trait. The inheritance is believed to be polygenic, meaning it can be inherited from one or both parents. Men with androgenetic alopecia are believed to have much stronger familial ties to the disease than women.2

Testosterone, the key hormone needed for puberty in men, is responsible for such secondary sex characteristics as growth of muscle mass, voice changes, sex drive, growth of the phallus and scrotum, and development of pubic and axillary hair. Dihydrotestosterone (DHT) is another hormone important during puberty. DHT is responsible for hair growth in the ears, nostrils, beard region, and limbs. It is also responsible for hair recession in the temporal region of the scalp, as well as for acne and growth of the prostate.

Testosterone is converted to DHT by 5-alpha-reductase, an enzyme that has two isoenzymes, known as type I and type II.3,4 Type I 5-alpha-reductase is primarily found in the liver and sebaceous glands. Type II 5-alpha-reductase, which is responsible for androgenetic alopecia, predominates in the liver, prostate gland, and hair follicles of the scalp, beard, and chest.3 When the body produces an increased amount of 5-alpha-reductase, it leads to an increase in DHT. An increase in DHT causes the production of miniaturized hair follicles and a reduction in the amount of hair fibers. The hairs are also associated with a shorter anagen phase (growing phase), which results in hairs that are in the telogen phase (resting phase) for a longer period of time.5 While the hairs are arrested in the telogen phase, they are much more susceptible to falling out during everyday grooming (i.e., washing and brushing the hair).

Women have a very similar pathogenesis for androgenetic alopecia. Because of alterations in androgen metabolism at the follicle, however, women are susceptible to the disorder during perimenopausal and menopause periods as well as during puberty.6 Systemic hormonal changes are also believed to contribute to the hair loss. Women who develop balding shortly after puberty are more likely to have a family history that is positive for pattern baldness in both male and female family members. Overall, androgenetic alopecia is less severe in women than in men.

Diagnosis of androgenetic alopecia in men is fairly easy. Patients will often present expressing a concern about thinning hair. The classical pattern of hair loss follows a symmetrical and progressive recession of the frontotemporal hairline, along with thinning of the vertex of the scalp. Hamilton developed a classification system based on the pattern and severity of hair loss. Norwood later reclassified the patterns into the major classification system now used to diagnose male pattern baldness.

The amount and pattern of hair loss may vary between individuals. Miniaturization of terminal anagen hairs to smaller vellus hairs is the hallmark of androgenetic alopecia.7 The small, fine, hypopigmented vellus hairs will be present in large amounts prior to permanent shedding. Initially, the scalp skin will be normal; as the disorder advances, however, the scalp will become smooth and shiny. Women with androgenetic alopecia will have diffuse thinning of hair on the crown and frontal scalp, with sparing of the frontal hairline. Ludwig developed the classification system for hair loss in women.2

A sufficient biopsy is needed to properly diagnose androgenetic alopecia. A punch biopsy >4 mm in diameter with transverse sectioning is needed for quantitative evaluation. A horizontal section at the level of the lower infundibulum will allow for appreciation of the increased amounts of miniaturized hair follicles. For women, there should also be a hormonal evaluation, especially if there are menstrual irregularities.8

Although the diagnosis of androgenetic alopecia is fairly straightforward, a few hair diseases are commonly mistaken for the disorder. Any nonscarring alopecia, such as alopecia areata and telogen effluvium, may be mistaken for androgenetic alopecia.4 Others include iron deficiency, hyperthyroidism, systemic lupus, trichotillomania, and seborrheic dermatitis.2,9

Obtain a good history and diagram the patient’s family tree to determine whether the parents or grandparents had androgenetic alopecia. Early-onset or severe alopecia in women should suggest the possibility of pathologic hyperandrogenism, and appropriate laboratory tests should be performed.

Patients with androgenetic alopecia may suffer from low self-esteem, anxiety, and depression, especially if the onset of the disorder occurs during the teenage years. For this reason, it is important to diagnose androgenetic alopecia at an early stage and initiate treatment in the hopes of halting the progression of the disease. At this time, only topical minoxidil (Rogaine) (2% and 5%) and oral finasteride (Propecia, Proscar) are approved by the FDA to treat androgenetic alopecia.4

Minoxidil is approved for use in men and women, and those using the product should expect to halt hair loss and produce longer, larger-caliber hairs. Unwanted facial hair (if the medication comes in contact with facial skin) and contact dermatitis are major side effects of minoxidil.

Oral finasteride is approved for use in men older than age 18 years and works by inhibiting Type II 5-alpha-reductase. Those using this medication should expect a halt of their hair loss and an increased amount of hair counts. Major side effects, which are seen in less than 2% of individuals, include such changes in sexual function as decreased libido, ejaculatory dysfunction, and erectile dysfunction. Gynecomastia and decreased levels of prostate-specific antigen may also be seen.

In women of childbearing age, finasteride and spironolactone (Aldactone) can lead to feminization of a male fetus and should only be used in postmenopausal women. For advanced progression of androgenetic alopecia, such hair prostheses or surgical procedures as scalp flaps, hair transplant, and scalp reduction may be considered.2

The prognosis for androgenetic alopecia is fair. Progression is usually very gradual and can last for decades. It is very important to stop the progression of hair loss early, because most hair loss is permanent. Current treatments are successful, and surgical procedures can be performed to transplant hair in sites of alopecia.

The patient in this case was diagnosed with androgenetic alopecia and was treated with topical 5% minoxidil. On follow-up, she stated that her hair loss had halted and that she felt as though her hair was thicker. She has had no significant progression of her disease.

Kerri Robbins, MD, is a resident in the department of dermatology at Baylor College of Medicine in Houston. The author has no relationships to disclose relating to the content of this article.


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References

1. Olsen EA, Messenger AG, Shapiro J, et al. Evaluation and treatment of male and female pattern hair loss. J Am Acad Dermatol. 2005;52:301-311.

2. Fitzpatrick TB, Johnson RA, Wolff K, Suurmond R, eds. Color Atlas and Synopsis of Clinical Dermatology, 5th ed. New York, N.Y.: McGraw-Hill; 2005:959-962.

3. Paller AS, Mancini AJ. Hurwitz Clinical Pediatric Dermatology, 3rd ed. Philadelphia, Pa.: Elsevier Saunders; 2006.160-161.

4. JL Bolognia, JL Jorizzo, RP Rapini, eds. Dermatology, 2nd ed., St. Louis, Mo.: Elsevier-Mosby; 2008:987-988.

5. Simpson N, Barth J. Hair patterns: hirsuties and baldness. In: Dawber RPR, ed. Disease of the Hair and Scalp, 3rd ed. Malden, Mass.: Blackwell Science, Inc.; 1997:67-122.

6. Knochenhauer E, Azziz R. Ovarian hormones and adrenal androgens during a woman’s life span. J Am Acad Dermatol. 2001;45:S105-S115.

7. TP Habif. Skin Disease: Diagnosis and Treatment, 2nd ed., Philadelphia, Pa.: Elsevier Mosby; 2005:516-519.

8. DE Elder, R Elenitsas, BL Johnson, GF Murphy, X Xu, eds. Lever’s Histopathology of the Skin. 10th ed., Philadelphia, Pa.: Lippincott Williams & Wilkins; 2009:479-481.

9. RP Rapini. Practical Dermatopathology. Philadelphia, Pa.: Elsevier Mosby; 2005:99-145.

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