Melazma
Исмаилов
Рашад,
кандидат медицинских наук,
Азербайджанский государственный медицинский университет.
R.H.
Ismailov
Candidate of medical sciences
Health centre No 1 for
skin- venereal diseases,
Baku city, the Republic
of Azerbaijan
Abstract
Melazma is an acquired
disorder of macular hyperpigmentation limited to
face. It predominantly affects the female gender. Although the disease is
asymptomatic, it is a source of cosmetic misiance and
psychological stress for the patients. The countries with a high level of
actinic radiation, such as
Melazma is a macular hypepigmentational disease. Being an asymptomatic disease
it causes cosmetic disorder and psychological stress. In its etiology the main
factors are hereditary and ultraviolet rays. As there actinic radiation on a
big scale in
Melasma is often met in dark
skinned people. Mainly it locates in face, cheek, upper lip, nose, and chin.
It’s a disease without a symptom. It only causes cosmetic disorder and psychological
stress.
Epidemiology
Melasma is met in all races.
It’s often observed in Asians (1, 4); in countries underwent actinic radiation
and tropic countries.
Mainly
women at 30-55 have melasma. Mostly
in pregnant women. 90% of patients is women (7, 8, 12), 10% men (1,8). 50-70% pregnant women have this disease while using
oral contraceptives 5-34% (14-16).
Etiology
A
numourous factors have an important role in etiology
of melazma. (1, 3, 7). At
least 2 factors play a role in the etiology. 1. Hereditary factor. 2.
Ultraviolet rays. Besides these, it has been found that pregnancy, oral contraseptives, cosmetic fotosensitive
means, liver disfunctions, system diseases,
parasites, etc. play a role. (1, 5, 7, 9). In men melazma is mainly idiopatic. The
role of hormonal factors is not so big.
Pathogenesis
Hyperpigmentation in melazma can occur for 3 reasons:
1.
Increase of melanosm
synthesis
2.
Proliferation of melanocytes
3.
Increase of transfer of melanosom
to basal keratinocytes
In
melazma epidermal melanocytes
become active under the influence of UBS a bit changes in the level of estrogen
and progesterone and result in hyperpigmentation.
Clinics
Melazma rashes are the
disruption of polycyclic or shaped pigment. Pigmentation can be linear,
droplet, or big circled.(3, 5, 11). The rashes in face
are divided into 3 categories: central facial, molar and mandible. (1, 3, 5, 7, 8). Being melazma
histopathology pigment deposits are divided into 3 categories: epidermal,
dermal, mixed and endatermin (1, 3, 5, 7, 8).
Prediction
Melazma untreated doesn’t
remain and gets better itself. The disease slowly increases (3.4). In complete
remission is rare. After the treatment residives can
occur. Rarely after the influence of solar rays, spontaneous
remission can occur. A year after pregnancy rashes can disappear. (1, 3, 5, 11).
Treatment
As melazma is a
chronic disease it resists the treatment (1, 5, 9).
Most cases treatment must be conducted for a long time. One mustn’t accept sun
avoidance, cosmetic appliances, cleaning crème, oral contraceptives, photosensitive drugs. Protective crème must be
applied every morning, 4 seasons in order to protect from both UBA protective
factor >15 and UBB. Chlorine, indometasin, vitamin
C and E B corotin, codliver
oil and green tea can be used.
The
purpose in the treatment of melazma is to eliminate
blockade of melanocyte proliferation, slowing process
of melanocyte synthesis, concentration of melanosom. (3, 66, 7, 10).
Hydroxinon in 2-10% coagulation
in the treatment of melazma can be used 2 times a
day.
Influence
mechanism: it blockades to oxidize hidronin Arozin to DOFA and DOFA to melanin (3, 7, 13, 25).
Tretinsin 0.1% is used
approximately 10 months for a long time. (1, 5, 6, 11).
In autumn months it mustn’t be used.
Topical
steroids: dexametazon, hydrocortizon,
betamethazon, are used in the treatment of melasma. Topical steroids can give 80-90% effect in melazma within 8 weeks. But the treatment effect is short,
2-3 weeks later residive occurs. Within 4.6 months melazma returns its previous state.
Azel acid – being selective has a toxic impact on melonocytes which indicate hyperactive and abnormal
proliferation, it does not have toxic affect on normal melonocytes.
Besides the treatment of melazma, maligin
melanoma is used in hyperpigmentation after
inflammation, in lentilmaligna. The treatment mainly
lasts 5-8 months.
Chemical
peeling is effective in the treatment of melazma,
thus epidermis is removed with melanin pigment. Trixlorasetikacyte,
salicyte, fenol are done
with these preparations. Laser, criotherapy can also
an effective result.
References
1. Sarkar R, Bhalla M, Kanwarl A J. Acomparative study of 20% azelac
acid cream mono therapy versus a sequential therapy in the theatment
of melasmain darkskinned
patients. Dermatolqy: 2002: 205; 249 -54.
2. Verallo -
Rowell V.M Verallov. Graupe K, Lopez-Villafursted,
Carcia-Lopez M. Double - blind comparizon
of azelaic acid and hydroquinone in the treatment of melasma Acta Derm
Venerol 1989; 143; 58-61.
3. Kauh YC; Zachion T.F. Melasma, Adv Exp Med
Biol 1999, 455: 491-9.
4. Pathak M.A. Fitapatrick T.B, Kraus E.W/ Usefulness of retinoic acid in
the treatment of melasma. J. Am Acad Dermatol 1986, 15 894-99.
5. Pardya AG. Guean IL Disorders of hyperpiqmentation
Dermatol Clin 2000, 18, 91
- 8.
6. Grimes P.E. Melosma.
Etioloqic
and terapeutic considerations. Arch. Dermatol 1995: 131: 1453-7.
7. Kelly A.P. Aesthetic considerationsin patients of color. Dermatol
Clin 1997: 15: 687-93.
8. Kunacohak S, Leelan domlipi P, Wondwarisayawans Dermamabrasion:
a curafive treatment for melasma.
Aesthetic Plasf Surq
2001: 25 114-7.
9. Amer M. Metwolli M. Topical liquri: tin
improves melasma. Int. J.Dermatol
2000.39:299-301.
10. N.Z.Mu Y. Gulati O. Treatment of melasma
with Pucnoqenol. Phytother
Res 2002; 16: 567-71.
11. Goldberq DJ.
Lazer treatment of piqmentd lesions: Dermatol Clin 1997; 15; 397-407.
Поступила в редакцию 02.11.2009 г.