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CME ARTICLE
Year : 2005  |  Volume : 50  |  Issue : 3  |  Page : 119-124
Hypertrichosis


Department of Dermatology or Venereology, LTM Medical College & General Hospital, Sion, Mumbai, India

Correspondence Address:
R G Valia
Department of Dermatology or Venereology, LTM Medical College & General Hospital, Sion, Mumbai
India
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Source of Support: None, Conflict of Interest: None


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Keywords: Hypertrichosis, Management


How to cite this article:
Valia R G. Hypertrichosis. Indian J Dermatol 2005;50:119-24

How to cite this URL:
Valia R G. Hypertrichosis. Indian J Dermatol [serial online] 2005 [cited 2017 Jun 22];50:119-24. Available from: http://www.e-ijd.org/text.asp?2005/50/3/119/18922


Significant racial and ethnic differences in hair growth are seen. If a person, particularly a female, looks upon her body hair growth to be excessive, that causes embarrassment and emotional upset. What is normal and excessive is shaped by social attitudes and now by the cosmetic industry.


   Definition: Top


Hypertrichosis is the term used for excessive hair growth on any part or whole body as compared to persons of the same age, sex and race.[1] Hypertrichosis must not be confused with hirsutism, which is defined as androgen-induced growth of terminal hair in women and children, in male pattern distribution. Hirsutism is androgen-dependent while hypertrichosis is not.


   Mechanism: Top


Hypertrichosis may be caused by (1) conversion of vellus hair into terminal hair in areas which usually do not have terminal hair, (2) increased duration of growing phase, anagen, of hair cycle, causing decrease in hair shedding, (3) increased hair density.


   Classification: Top


Hypertrichosis may involve lanugo, vellus or terminal hair. Hypertrichosis could be congenital or acquired. Both can be localized or generalized. [Table - 1] enumerates the classification of hypertrichosis. Due to lack of space, only a few illustrative examples will be discussed.

Examination and history: An examination of a patient with hypertrichosis should note.

(i) the type of hair involved - lanugo, vellus, terminal.

(ii) any distinctive, characteristic pattern.

(iii) age of the patient at onset.

(iv) history of present or past systemic disorder.

(v) history of drug administration.

(vi) any associated abnormalities.

(vii) family history.

(viii) ethnic and racial background of the patient.

It must be always kept in mind that hypertrichosis may be a manifestation of a more general medical problem.

Congenital generalized hypertrichosis:

(1) Congenital hypertrichosis lanuginosa (CHL): It is a rare inherited disorder considered autosomal dominant. Excess lanugo hair persists over the entire body after birth. Palms and soles are not involved. Much of hair on the trunk and limbs are shed in childhood.

(2) Universal congenital hypertrichosis: It has the same clinical picture as that of CHL. It is a congenital generalized terminal hair hypertrichosis and is X linked dominant.[2]

Acquired generalized hypertrichosis:

(1) Hypertrichosis lanuginosa associated with malignancy: It is a well-known cutaneus manifestation of internal malignancy. Normal hair follicles suddenly grow lanugo-type, white-yellow downy hair that covers a large area of the body, most prominent on the face, referred as malignant down. Most common associated malignancies are of the lung and colon[3],[4] but sometimes of other organs as well. Hypertrichosis may precede or follow malignancy by one to two years.

(2) Acquired generalized hypertrichosis not associated with malignancy: Some non-malignant systemic disease may cause hypertrichosis.

(3) Hypertrichosis associated with endocrine disorders: Thyroid disorders and disorders of diencephalon or pituitary can cause hypertrichosis.

(4) (a) Malnutrition:Hypertrichosis is seen in children with coeliac disease which causes malnutrition.[5]

(b) Anorexia nervosa: In other conditions of gross malnutrition hypertrichosis may occur. Hypertrichosis is reported in 20 to 77% of adults having anorexia nervosa.[6]

(c) AIDS: Besides trichomegaly of eyelashes, a more generalized form of hypertrichosis has been observed in patients with AIDS.[7]

(5) latrogenic: Drugs can cause hypertrichosis by various mechanisms. Drugs causing hypertrichosis are listed in [Table - 2].

Phenytoin may produce hypertrichosis after 2 to 3 months of use.[8] It may be associated with acne and gingival hyperplasia. Hair growth resolves within one year of discontinuation in most children. Acetazolamide used for treatment of glaucoma, causes hypertrichosis in children, mainly on the back and legs. Hypertrichosis develops in 60% of patients taking cyclosporin A within the first 6 months of therapy. Besides sebaceous hyperplasia in 10% and acne in 15% cases occur. Frequency of hypertrichosis in patients taking cyclosporin for organ transplantation varies from 24% to 94%. Vasodilator diazoxide causes hypertrichosis in 50% to 100% of children but only in 10% of adults.[11] Psoralens cause temporary hypertrichosis in light exposed areas. Oral and infrequently topical minoxidil causes hypertrichosis primarily on the face and extremities. Topical drug may cause generalized hypertrichosis resulting from absorption.[12] Penicillamine causes lengthening and coarsening of the hair on the trunk and the limbs. Streptomycin causes hypertrichosis in children being treated for tuberculosis. Cortisone may induce hypertrichosis, after prolonged administration. It is most marked on the forehead, the temples and sides of the cheeks but also on the back and extensors of the limbs.


   Congenital localized hypertrichosis: Top


(1) Nevoid

(a) Melanocytic nevi: They may be accompanied by a vigorous growth of coarse hair and become more pigmented in adolescence. In giant congenital melanocytic nevi, there is a significant risk of malignant change.

(b) Becker's nevus: It rarely presents congenitally. Usually it is an acquired lesion. It presents as a localized area of hyperpigmentation and hypertrichosis.

(c) Lumbosacral hypertrichosis: It is localized to the sacral midline. Often it indicates underlying spinal dysraphism such as a dermal cyst or a sinus, myelomeningocele, vertebral abnormalities and subdural or extradural lipoma.[13]

(2) Porphyria - Congenital erythropoietic porphyria manifests by extreme photosensitivity, causing vesiculobullous lesions on sun exposed areas, followed by hyperpigmentation, scarring and hypertrichosis. Same may occur in erythropoietic protoporphyria.


   Acquired localized hypertrichosis: Top


(a) Becker's nevus: Circumscribed hypertrichosis is seen more commonly at puberty or adolescence as irregular hypermelanotic patch. Increased hair growth, on the shoulder, anterior chest or scapular region. Coarse hairs appear within the lesion. There may be ipsilateral hypoplasia of the shoulder girdle, arm or breast and other vertebral abnormalities associated with Becker's nevus.[14]

(b) Porphyria cutanea tarda: Hypertrichosis is seen in approximately 60% of patients with porphyria cutanea tarda,[15] particularly in the temple areas. It may present on the face and upper trunk.

(c) Trauma: Circumscribed hypertrichosis has been observed following repeated friction as on the shoulders of sack bearers or sites of habitual biting in patients with mental retardation.

(d) Infection and inflammation: Areas overlying thrombophlebitis or chronic osteomyelitis, or vaccination sites may develop hypertrichosis.


   Management: Top


It is to be constantly remembered that overgrowth of hair may represent an underlying medical problem or may have an external cause, viz, trauma or a drug. Removal of that cause can resolve the condition.

When hypertrichosis is a cosmetic and psychological problem, it should be treated. Even if hairiness is considered within the range of normal, treatment must be offered if insisted upon. A wide variety of treatment modalities are available. They vary in permanence, convenience and expense. Individual patient's preference plays an important part in selecting the therapy.

Treatment modalities can be categorized as follows:

1) Cosmetic procedures

2) Physical methods

3) Electrosurgical procedures

4) Laser and light sources

5) Pharmacological treatment.

(1) Cosmetic procedures:

(a) Simplest approach is to hide cosmetically undesirable hypertrichosis with a suitable make up.

(b) Bleaching: A simple bleach is 6% hydrogen peroxide. Commercial bleaches are also available. It is a painless procedure. It makes the hair less visible by partially or wholly removing natural pigment imparting to hair a yellowish tinge. The effect lasts for about 4 weeks. Bleaching may cause irritation. Addition of ammonium persulphate may cause urticaria and even anaphylactic reaction.

(2) Physical:

Physical methods are the cheapest, easiest and expose the patients to the fewest side effects. They can be divided into two categories:

(a) Mechanical and (b) Chemical: Both the methods can be depilatory or epilatory. Depilation is the removal of hair at some point along the hair shaft. Epilation is the removal of entire hair from the skin surface. Results of epilation last longer than depilation because of any type of depilation requires hair to be 2-3 mm long.

Mechanical:

(i) Plucking: It is a temporary hair removal. It is painful and causes irritation. It is used for small localized hair growth. For more diffuse hypertrichosis, tweezers, mechanical devices with a rotating fine coiled spring that grasps the hair shaft and pulls it out, may be used. Electric, electronic or radiofrequency tweezers are not more effective than mechanical tweezers.[16] A twisted string, run rapidly over a hear-bearing area removing hair along with it, is used in the Middle-East. Adverse reactions to plucking are hyperpigmentation, folliculitis, scarring, ingrown hairs and distorted follicles.

(ii) Waxing: Wax epilation is essentially a plucking technique. It is carried out with cold, warm or hot wax. Usually the warm wax is applied over hairy area and allowed to harden. When it is abruptly stripped off, the embedded hairs are pulled out. It is an efficient method for vellus hair, is inexpensive and can be carried out at home. It does cause discomfort, irritation, folliculitis and poor removal of short hair.

Certain natural sugars are being widely used in place of waxes as they work as efficiently but with less trauma. All these methods require hair to be long enough to be embedded and pulled out.

(iii) Shaving: Shaving with a razor or an electric shaver should be popularized. It is fast, easy, effective and cheap. It is important to remove the fear that shaving leads to increased growth of coarse hair growth or pigmentation.[17] The disadvantage of shaving, particularly for the facial hair is the need to shave daily.

Chemical: Chemical depilatories remove hair by damaging it, so that the hair breaks at the skin surface. Chemical depilatories are available in two different forms; sulfides of strontium, barium and calcium and thioglycolates (thioglycolic acid and calcium thioglycolate). They dissolve the hair shaft by breaking disulfide keratin bonds. Thioglycolates are used in a concentration of 2-4% and act within 5-15 minutes. Sulfide preparations are more effective, but are more irritating to the skin and have a strong unpleasant odor.[18] Thioglycolates too have a high irritancy potential and may cause allergic contact dermatitis.

Chemical depilatories are more appropriate for weekly hair removal from small areas.

(3) Electrosurgical epilation: Unlike the previous methods of hair removal, the method is aimed at permanent hair removal. A fine wire needle is inserted into the hair follicle. An electric current, regulated and controlled, is transmitted through it. Electric hair destruction is by two actions: electrolysis and thermolysis. Electrolysis uses the galvanic current to destroy the hair growing cells in the dermal papilla, through the production of hydroxide ions, which destroys the follicle. Thermolysis is the destruction of the hair follicle by the heat produced by an alternating current. Galvanic electrolysis is slower but more follicles can be destroyed in one treatment. Thermolysis is quicker but the rate of regrowth of hair is more. Up to 50% of the follicles regrow the hair after these methods.[19] The success rate varies with the electrologist's skill and experience. They should be retreated. It is possible to blend the galvanic and alternating currents from a single apparatus,[20] a technique which has excellent efficacy and lower incidence of folliculitis. Both the methods destroy the hair follicle without scarring of the skin. Shaving 4-5 days prior to the procedure is important. Use of a topical anesthetic cream reduces the discomfort significantly.

Electrosurgical technique is a highly operator dependent. Success rate varies with the skill and experience of the operator. The complications are superficial scarring, hypopigmentation or hyperpigmentation and local infection. Electrosurgical epilation is most suitable for treatment of localized coarse hair, for example nevoid hypertrichosis.

(4) Lasers and light sources[21]: Lasers are very popular for long term hair removal. A variety of lasers is available. Physical parameters such as wavelength, pulse duration, fluence, spot size are important for choosing a proper laser for a patient. Ruby laser (694 nm, 2 msec), alexandrite laser (755 nm, 3-20 msec) and diode laser (810 nm, 50-250 msec) have wavelengths and pulse times which target the melanin in melanosomes of the hair bulb. The selective destructive effect on melanin is caused by the heat generated by laser burst, causing damage to the surrounding hair follicle.[22]

Intense pulse light (IPL) from a xenon flash lamp, which produces an incoherent multi-wavelength pulsed light (550-1200 nm) is also effective in the treatment of hypertrichosis.

The Q-switched Nd:YAG (neodynium yttrium-aluminium garnet) laser (1064 nm, 5-18 msec) works in conjunction with a suspension of carbon particles, that is rubbed into the skin prior to treatment. The carbon penetrates the follicle and absorbs the laser energy, causing local heat and damage to the surrounding follicle.[23] A Nd:YAG laser with a longer pulse duration (30 msec) is now available which does not require exogenous chromophore like carbon.

Lasers are noninvasive, rapid in action, less painful, less operator-dependent and are more effective than electrosurgical method. However, lasers cannot be targeted to a single hair or a small group of hair unlike electrosurgical treatment. However, irrespective of the laser or light source used, all these systems reduce hair growth only temporarily. An average of 20% hair is lost with each treatment. Hence, multiple treatments are required to achieve satisfactory results. After repeated treatments, hair clearance of 30% to 50% after 6 months of the last treatment is generally reported.[24] There is less optimism about the permanence of laser hair removal than in the past.

Adverse reactions: Erythema and perifollicular edema are common after hair removal by lasers or light sources. Vesiculation, crusting and pigmentary changes are less common. Most of these adverse reactions are temporary.[25] Laser treatments are administered as a course of a few visits, each separated by a several weeks. Hair follicle is most responsive to ablation in anagen phase.

(5) Pharmacological treatment:

(a) Systemic: There is no role for antiandrogen therapy in hypertrichosis as there is no androgen­-induced hair growth, unlike hirsutism.

(b) Topical: Eflornithine is a specific and irreversible inhibitor of the enzyme ornithine decarboxylase, present in the hair follicle, and is important for maintaining hair growth.

In a clinical study, in women with excessive hair, twice-daily application of eflornithine 15% cream was superior to a placebo in reducing hair growth. It was demonstrated by subjective and objective methods after 2-8 weeks treatment. After 24 weeks of treatment 58% of eflornithine and 34% of placebo recipients had some improvement in facial hirsutism and 32% vs 8% of patients showed marked improvement.[26] Hair growth returned to pretreatment level within 8 weeks of stopping treatment. Local irritation was the only adverse reaction to the treatment.



 
   References Top

1.Daniel S, Wendelin MD, David N. Hypertrichosis. Am J Acad Dermatol 2003;48:161-79.  Back to cited text no. 1    
2.Macias-Flores MA, Garcia Cruz D, Rivera H, et al. A new form of hypertrichosis inherited as an X-linked dominant trait. Human Genet 1984;66:66-70.  Back to cited text no. 2    
3.Fretzin DF. Malignant Down. Arch Dermatol I967;95:294-7.   Back to cited text no. 3    
4. Lyell A, Whittle CH. Hypertrichosis lanuginosa acquisita. Clin Exp Dermatol 1985; 10:255-7.  Back to cited text no. 4    
5.Wiseman CV, Harris W, Halmi K. Eating disorders. Med Clin North Am 1998;82:145-59.  Back to cited text no. 5    
6.Glorio R, Allevato M, De Pablo A, et al. Prevalence of cutaneous manifestations in 200 patients with eating disorders. Int J Dermatol 2000;39:348-53.  Back to cited text no. 6    
7.Prose NS, Abson KG, Scher RK. Disorders of the nails and hair associated with human immunodeficiency virus infection. Int J Dermatol l992;31:453-7.  Back to cited text no. 7    
8.Livingstone S, Peterson D, Bohs LL. Hypertrichosis occurring in association with dilantin therapy. J Pediatr 1955;47:351-2.  Back to cited text no. 8    
9.Wysocki GP, Daley TD. Hypertrichosis in patients receiving cyclosporine therapy. Clin Exp Dermatol 1987;12:191-6.   Back to cited text no. 9    
10. Bencini PL, Montagnino G, Grosti C, et al. Acne in a kidney transplant patient treated with cyclosporin A. Br J Dermatol 1986;l14:396-8.  Back to cited text no. 10    
11.Burton JL, Schutt WH, Delong ER, et al. Hypertrichosis due to diazoxide. Br J Dermatol 1975;93:707-11.  Back to cited text no. 11    
12.Peluso AM, Misciali C, Vincenzi C, et al. Diffuse hypertrichosis during treatment with 5% topical minoxidil. Br J Dermatol 1997;136:118-20.  Back to cited text no. 12    
13.Harris HW, Miller OF. Midline cutaneous and spinal defects. Arch Dermatol 1976;12:724-8.  Back to cited text no. 13    
14.Happle R, Koopman RJJ. Becker nevus syndrome. Am J Med Genet 1997;68:357-61.  Back to cited text no. 14    
15.Grossman ME, Bickers DR, Poh-Fitzpatrick MB, et al. Porphyria cutanea tarda: Clinical features and laboratory findings in 40 patients. Am J Med l979;67:277-86.  Back to cited text no. 15    
16.Verdick J. A critical evaluation of a method for treatment of facial hypertrichosis in women. Dermatologica 1984;168:87-9.  Back to cited text no. 16    
17.Lynfield YL, Mac Williams P. Shaving and hair growth. J Invest Dermatol 1970;55:170-2.  Back to cited text no. 17    
18.Natow AJ. Chemical removal of hair. Cutis 1986;38:91-2.  Back to cited text no. 18    
19.Wagner RF. Physical methods for the management of hirsutism. Cutis 1990;45:199-202.  Back to cited text no. 19    
20.Richards RN, Meharg GE. Elecrolysis: observations from 13 years and 140000 hours of experience. J Am Acad Dermatol 1995;66:2-6.  Back to cited text no. 20    
21.Dierickx C. Hair removal by lasers and intense pulse light source. Dermatol Clin 2002;20:135-40.  Back to cited text no. 21    
22.McCoy S, Evans A, James C. Histological study of hair follicles treated with a 3 msec pulsed ruby laser. Lasers Surg Med 1999;24: l42-50.  Back to cited text no. 22    
23.Wheeland RG. Laser assisted hair removal. Dermatol Clin 1997;15:469-72.  Back to cited text no. 23    
24.Lou WW, Quintana AT, Geronemus RG, et al. Prospective study of hair reduction with diode laser (800 nm) with long term follow-up. Dermatol Surg 2000;26:428-32.  Back to cited text no. 24    
25.Lanigan SW. Incidence of side effects of laser hair removal. J Am Acad Dermatol 2003;49:882-4.  Back to cited text no. 25    
26.Belfour JA, McClellan K. Topical eflornithine. Am J Clin Dermatol 2001;2:197- 201.  Back to cited text no. 26    


Tables

[Table - 1], [Table - 2]



 

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