|
Chemical
hypertrichosis
Irritating chemicals can promote hair growth.
This phenomenon has been known about since ancient times. Popular
hair loss treatment remedies from the ancient Greeks and Romans
often included irritant chemcials, particularly ammonia from urine
or even birds droppings (more concentrated ammonia) to be liberally
applied to the bald scalp. In the early part of the 20th Century
the approach was updated somewhat with doctors using rather nasty
chemical concotions including the likes of phenol to induce hair
growth (definately not recommended). Irritant chemicals cause
damage to the skin which, so long as the damage is not so severe
as to destroy the hair follicles, can cause increased hair growth.
Topical contact sensitizing agents such as Diphencypropenone
(DPCP), squaric acid dibutyl ester (SADBE), dinitrochlorobenzedine
(DNCB)
, psoralen
plus ultra violet A light (PUVA), and poison ivy can also promote
hypertrichosis in the area of skin exposed to the chemical. This
is used to advantage in treating alopecia areata where the agents
and irritants
have an affect on inflammation around hair follicles as well as
having a hair growth promoting effect on the hair follicles.
It is probable that any chemical that causes skin irritation has
the potential to promote hypertrichosis in a subset of individuals.
The chemicals described above cause irritation in almost everyone
who is exposed to them. Other chemicals commonly found in our environment
may not affect the majority, but they might affect a minority of
individuals. Those people who are allergic to particular chemical
products may be affected by hypertrichosis.
Chemical
hypertrichosis references
- Pestana
A, Olsen EA, Delong ER, Murray JC. Effect of ultraviolet light
on topical minoxidil-induced hair growth in advanced male pattern
baldness. J Am Acad Dermatol. 1987 May;16(5 Pt 1):971-6.
- Mitchell
AJ, Douglass MC. Topical photochemotherapy for alopecia areata.
J Am Acad Dermatol. 1985 Apr;12(4):644-9.
- Lassus
A, Kianto U, Johansson E, Juvakoski T. PUVA treatment for alopecia
areata. Dermatologica. 1980;161(5):298-304.
- Li LF,
Fiedler VC, Kumar R.The potential role of skin protein kinase
C isoforms alpha and delta in mouse hair growth induced by diphencyprone-allergic
contact dermatitis. J Dermatol. 1999 Feb;26(2):98-105.
- van der Steen PH, Boezeman JB, Happle R.
Topical immunotherapy for alopecia areata: re-evaluation of 139
cases after an additional follow-up period of 19 months. Dermatology.
1992;184(3):198-201.
- Rokhsar CK, Shupack JL, Vafai JJ, Washenik
K. Efficacy of topical sensitizers in the treatment of alopecia
areata. J Am Acad Dermatol. 1998 Nov;39(5 Pt 1):751-61.
- Shapiro J. Topical immunotherapy in the
treatment of chronic severe alopecia areata. Dermatol Clin. 1993
Jul;11(3):611-7.
- Happle R, Kalveram KJ, Buchner U, Echternacht-Happle
K, Goggelmann W, Summer KH. Contact allergy as a therapeutic tool
for alopecia areata: application of squaric acid dibutylester.
Dermatologica. 1980;161(5):289-97.
- Chase HB. Growth of the hair. Physiol Revs
1954; 34: 113-126.
- Rauch H. The effects of topical applications of chemical agents
on hair development. Physiol Zool. 1952; 25: 268-272.
- Chase HB, Montagna W. Relation of hair proliferation to damage
induced in the mouse skin. Proc Soc Exptl Biol Med 1951; 76:
35-37.
|
