ISSN 1991-3087

:   77-24978 05.07.2006 .

ISSN 1991-3087


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: 305008, ., , .7.

.: 8-910-740-44-28

E-mail: Rambler's Top100




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R.H. Ismailov


Candidate of medical sciences

Health centre No 1 for skin- venereal diseases,

Baku city, the Republic of Azerbaijan




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 Azerbaijan not only constitute the geographically risky regions for melasma but create a therapeutic problem for the dermatologists.


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 Azerbaijan this disease is often met and its treatment remains a problem for dermatologists.

Melasma is often met in dark skinned people. Mainly it locates in face, cheek, upper lip, nose, and chin. Its a disease without a symptom. It only causes cosmetic disorder and psychological stress.




Melasma is met in all races. Its 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).




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.




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.




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).




Melazma untreated doesnt 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).




As melazma is a chronic disease it resists the treatment (1, 5, 9). Most cases treatment must be conducted for a long time. One mustnt 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 mustnt 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.




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.


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