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Mun Andrey Vitalevich, assistant of the Dermatovenereology, children dermatovenereology and AIDS department Tashkent Pediatric Medical Institute Adilgereeva Madina Iskanderovna, assistant of the Dermatovenereology, children dermatovenereology and AIDS department Tashkent Pediatric Medical Institute Yusupova Shaxnoza Akramovna, Tashkent Medical Academy Islomova Feruza Komilovna, Tashkent Medical Academy E-mail: [email protected]
DIAGNOSTIC AND TREATMENT MANAGEMENT FOR SKIN HYPERPIGMENTATION. CONTEMPORARY OPPORTUNITIES
Abstract: The article presents results of the clinical study, which describes data on the clinic, classification, course ofhyperpigmentation in patients with III-IV skin phototype. Modern methods of treatment of melanoses - laser treatment on the device Spectra XT and phased comparative diagnostics on the JANUS platform II have been evaluated.
Keywords: hyperpigmentation, Otta nevi, melanin, JANUS II, Spectra XT, melasma, ephelids, lentigo, laser, melanosome.
The problem of pigment spots remains high for many years. In the practice of a dermatologist, at least 10 patients per month referring concerning hyperpigmentation of the skin [1; 2].
Despite that, such aesthetic problem does not affect the health, does not affect the performance and does not even attract the attention of others, for a person it is the cause of serious psychological discomfort [3; 4; 5].
Pigmentation is a complex biochemical process that occurs in the skin and depends on many factors. Synthesis of melanin pigment occurs from the amino acid tyrosine under the influence of the enzyme tyrosinase in the epidermal cells of melanocytes, which are located on the layer of basal kera-tinocytes [6]. Melanin synthesized from melanosomes along the processes of melanocytes is transmitted to keratinocytes, where it accumulates and distributed a certain colour of the skin. There are several types of melanin: eumelanin - brown and black, feomelanin - red and colorless - leukomelanin. The predominance of one of them in the skin and hair determines the color of human hair and skin [10; 19].
Endogenous and exogenous causes of hyperpigmentation are distinguished. Endogenous include genetic predisposition, hormonal disorders, somatic and skin diseases. Exogenous ones include: ultraviolet (UV) radiation, violation of the integrity of the skin (mechanical, chemical, thermal injury), cosmetic procedures. Almost all types of chemical peels and dermabrasion, as well as cosmetic procedures accompanied by skin trauma
(subcutaneous injections, implants, depilation, facial cleansing, plastic surgery) can cause hyperpigmentation [7; 8; 9].
There is most used classification of dyschromias in the scientific literature [11; 12; 13].
The following classification is considered to be the most complete and convenient. [9]: Hypermelanosis : 1. Primary hypermelanosis
1.1. Congenital Hypermelanosis: pigmented nevi, youth lentigo, incontinentia pigmenti.
1.2. Hereditary hypermelanosis: freckles, melanism, hereditary lentiginosis, lentiginosis periorificial.
1.3. Acquired hypermelanosis:
1.3.1. Limited hypermelanosis: chloasma, linear forehead pigmentation, melasma, pigmented perioral dermatitis, Brock's carotenedermitis, Otto nevus, Becker nevus.
1.3.2. Diffuse hyperpigmentation: Addison's disease, cachectic melanoderma.
1.3.3. Toxic hyperpigmentation: Rielh's melanosis, reticular pigmental poikiloderma of the face and neck, toxic melasma Hoffman-Haberman, drug melasma.
1.3.4. Artificial hypermelanosis: actinic melanoderma, Bushke- Eyhorn's marble skin pigmentation, parasitic melasma.
2. Secondary hypermelanosis
2.1. Post-infectious melasma: syphilitic melasma, tuberculous melasma.
2.2. Post-inflammatory melasma: lichen planus; limited neurodermatitis, nodular pruritus; scleroderma; hives; eczema; pyoderma; bullous dermatosis.
The most common types of hyperpigmentation are: Freckles, or ephelydes (translated from Greek - "solar blotches"), appear in spring in individuals with I-II phototypes. The reason of occurrence is the presence of a specific gene in melanocytes, in which an increased production of melanin occurs under the influence of UV radiation. Histologically, a normal amount of melanocytes is detected, in some of them, enlarged melanosomes that actively produce melanin are found. The brightest freckles appear at the age of 20-25 years. Up to 35 years, their number may increase, they fade with the age [20; 21].
Melasma, or chloasma - acquired uneven pigmentation, mainly on the face and neck. A significant role is played by hormonal imbalance. Melasma appears during pregnancy, during taking oral contraceptives, ovarian tumors, in perimenopause. The use of photosensitizing agents in the composition of external cosmetics or ingestion of certain photosensitizers is important in the development of dermatosis. Females suffer from melasma more frequently. The rash is characterized by uneven pigmentation of a brownish yellow colour in the central part of the forehead, above the upper lip, chin, cheeks and cheekbones. Depending on the location of the lesions, three clinical forms of melasma are distinguished: centrofacial (localization on the skin of the central part of the forehead, above the upper lip, back of the nose, chin), molar (localization in the cheeks, projections of the molars and the nose) and mandibular (pigmentation is localized in the area of the angles of lower jaw) [25; 26; 27]. In the diagnosis of melasma, an inspection using a Wood filter is extremely important. Based on the examination, one of the histological types of melasma can be diagnosed.
Epidermal melasma type. This type is characterized with foci becoming brighter and more contrast when viewed with Wood's fluorescent lamp. This phenomenon is associated with the predominant localization of melanin in the epidermis. This type of hyperpigmentation is most favorable in prognosis and the treatment.
Dermal type melasma. While viewing with a Wood's fluorescent lamp, the lesions do not contrast with the surrounding unaffected skin. This type indicates a deep migration of melanophages into the dermis, which indicates an unfavorable prognosis during treatment.
Mixed type of melasma. In this type, some areas become brighter and more contrast, while others - vice versa. Indicates
the localization of the pigment in the epidermis and in the dermis [28; 29].
Lentigo manifested in the form of oval, flat or convex spots on the skin of the face and other open areas of the body. Their color varies from light beige to dark brown. Lentigo can occur at any age, including in children (youthful lentigo) against the background of acute or chronic insolation. Senile lentigo appears, as a rule, after 40 years against the background of a violation of the lipid barrier and an increase in the permeability of the corneal layer of the epidermis. Less commonly, lentigo is triggered by PUVA therapy (PUVA-induced lentigo). The histological picture of lentigo is characterized by an increase in the number of melanocytes at the border of the epidermis and dermis without signs of atypism and pigment incontinence [14; 15].
Nevus Becker - nonmelanadangerous pigment formation. Debut of the disease occurs in adolescence. The center of light brown color with localization on the skin of the shoulder, chest, back has, as a rule, a linear or segmental arrangement. Subsequently, dark hair appears on the background of spots. It occurs in 0.5% of men and is associated with stigma of embryogenesis (breast hypoplasia, spina bifida and others). Histologically, an increase in the number of melanin in melanocytes, giant melanosomes, less often - an increase in the number of melanocytes. Traditional methods of treatment give a negative result. Recommend camouflage.
Nevus Ota is a pigment spot or a cluster of blue spots that occurs mainly on those areas of the face that innervate the 1st and 2nd branches of the trigeminal nerve. Other names: ocular skin melanosis or orbital-maxillary nevus. This formation appears due to the accumulation of melanocytes (skin cells that contain melanin pigment) in the lower layers of the skin. Spots or foci of spots with ocular skin melanosis have a confluent character and are located along the branches of the trigeminal nerve: on the cheekbones, temples, in the lower eyelid, on the cheek, on the skin above the upper jaw. Less commonly, pigmentation zones are found on the mucous membranes of the nose, mouth, sclera, conjunctiva, or iris. As a rule, the tumor appears only on one side of the face. The color of the hyperpigmented areas is blue, variations from gray to purple are possible. Color of the spots an explicit; their size can be different - from small to large. Sometimes in the area of increased pigmentation also appear small nodules [16; 17].
The management of patients with impaired pigmentation goes in several directions (depending on the pathology, etio-pathogenesis, and the wishes of the patient).
1) Clarification or elimination of foci of dyschromium, which are produced by surgical, physical and injection methods.
2) Masking with the use of external means, smoothing skin color, or the procedure of permanent makeup.
3) Prevention of hypermelanoses is primarily carried out by UV filters (SPF not less than 30), photo desensitization (for example, Vitamin B, provitamin A, sorbents, anti-malarial drugs) the elimination of provoking factors.
Modern aesthetic medicine and dermatology allow to get rid of almost any kind of hyperpigmentation by various methods.
Currently the greatest effect has a laser. The method is based on the photothermolysis phenomenon: the ability of pigment cells to absorb the energy of a laser beam, which subsequently leads to their destruction, which provides a good whitening effect. Lasers differ in wavelength, the longer the wave, the deeper the laser effect and the higher the efficiency of the procedure.
There is another way to affect the site of hypepigmenta-tion - this is photorejuvenation or selective photothermolysis. It stimulates skin rejuvenation processes to a greater extent. At the same time it leads to the destruction of melanin-containing structures.
The advantages of lasers to remove pigmentation:
- no restrictions on skin phototype;
- the possibility of treatment of deep-seated pigment neoplasms;
- control pulse parameters taking into account the characteristics of the patient's skin pigmentation;
- elimination of the risk of postprocedural hyperpigmentation;
- impossibility of mechanical or thermal damage to the skin;
- no risk of scarring of the skin;
- Anesthesia is not required before the procedure.
The most modern laser system for removing pigmented
tumors uses Q- Switched as a radiation source. Nd: YAG, capable of emitting two different wavelengths: 532 nm (green light) and 1064 nm(infrared light). Short pulse Neodymium laser generates an extremely powerful impulse in a compressed period of time (up to 6 nanoseconds), which allows you to focus the thermal effect exclusively on the target - the pigment melanin, maximally protecting the surrounding tissues from damage. Working with the QS system, the doctor can individually adjust the wavelength and pulse duration depending on the depth of the pigment.
Superficial accumulations of melanin with a light brown or yellowish color - freckles, lentigo, epidermal nevi,- well give in to removal by means of a wave of 532 nanometers. The green light of a laser is absorbed in a special way by melanin, causing destruction of the pigment in the surface layers of the skin. An intensive peeling of the pigment spot begins on the treated area, after which young cells form in its place, synthesizing and accumulating a normal amount of melanin.
Pigment spots of deep occurrence (dermal moles, nevus Otta, hyperpigmentation after injury) is removed using radiation with a wavelength of 1064 nm. The pulse of infrared light penetrates the basal layer ofthe epidermis and dermis, selectively destroying the cells, producing an excessive amount of pigment.
The use of laser technology allows to remove most types of pigmentation, including freckles, melasma, age-related len-tiginous spots, nevus Otta and Becker's. As the skin absorbs the fine laser radiation, it is heated at the site of hyperpig-mented spot location, resulting in the breakdown of clusters of melanosomes.
The laser treatment of hyperpigmentation performed on the Spectra XT - Lutronic, which is a platform and includes several procedures.
Spectra Toning is an innovative protocol for the treatment of hypermelanosis (melasma, lentiginosis and postinflammatory hyperpigmentation (PIH). In the past, attempts to treat such a skincondition with lasers and other light-based sources that affect melanin often led to irritation, post-inflammatory pigmentation and other complications, and sometimes increased the manifestations of melasma in patients ofAsian origin.
Spectra Toning uses a Q-switching mode with a ultrashort pulse and a flat beam profile. This provides effective treatment of dermal and epidermal hyperpigmentation in patients of all skin types. Spectra Toning is the new gold standard in the treatment of melasma.
"Spectra" - laser with Nd: YAG-crystal as an active medium with a flat profile and the beam mode with Spectral kvazilong pulses in 300 microseconds. It is the spectral mode, together with high peak power and a flat beam profile that has proven effective in treating melasma.
Current studies indicate that period of thermal relaxation (TRT) is approximately 0.2 microseconds. Therefore, the Spectra ultra-short laser pulse with a high peak power makes it possible to better affect the dermal and epidermal melanosomes [2; 27; 29].
We present the results of our own clinical observations of the treatment of hyperpigmentation on the Spectra machine. XT - Lutronic.
The study group included 16 patients with hyperpigment-ed spots. 4 of them had epidermal type of melasma. 3 had dermal, and 3 - mixed type. In 4 patients, procedures were made due to efelids, 2 patients about post-inflammatory hyperpigmentation. The total number of procedures varied from 2 to 10 depending on the depth of the pigment. The interval between treatments was 14 days. The effectiveness of the procedures was assessed on the JANUS diagnostic platform II before the start of the therapy and after the end of the procedures in three projections and in three emission (normal, polarized and ultraviolet light).
Based on test results with epidermal pigmentation intensity type melasma decreased by 80%, while dermal and mixed type at 33 and 42%, respectively, at Efelids efficiency was 97%, while the degree of regression postinflammatory hyperpig-mentation was 78% after 8 procedures. Thus, the diagnosis of
hyperpigmentation on the platform JANUS II allows to adjust the intensity of the laser exposure apparatus Spectra Xt to improve the efficiency of lightening pigment, which depends on the depth of its occurrence, the number of procedures and the intensity of the pigment.
References:
1. Guideline for dermatocosmetology. Araviyskaya E. A., Sokolovskiy E. V. SpB: "Foliant", 2008.- 631 p. (Russian).
2. Margolina A. A., Ernandes E. I., Zaykina O. E. New cosmetology. - M: "Cosmetics and medicine", 2000.- 204 p. (Russian).
3. Ferjtek O. et al. Cosmetology. Theory and practice: Lekarske a Kosmeticke Centrum s.r.o., 2002. (Russian).
4. Cho S. B., Kim J. S., Kim M. J. Melasma treatment in Korean women using a 1064-nm Q-switched Nd: YAG laser with low pulse energy // Clin Exp Dermatol. 2009.- 34.- P. e847-e850.
5. Pandya A. G. et al. Reliability assessment and validation of the Melasma Area and Severity Index (MASI) and a new modified MASI scoring method // JAAD. 2011.- 64.- P. 78-83.
6. Selivanova O. D. The use of highintensity laser emission in treatment of non-neoplastic pigmentation of the skin. Thesis Ph D. SPb, 2011.- 17 p. (Russian).
7. Guideline for dermatocosmetology. Araviyskaya E. A., Sokolovskiy E. V. SpB: "Foliant", 2008.- 632 p. (Russian).
8. Fitzpatrick T., Jonson R., Wolf K., Polano M., Surmond D. Dermatology.- M.: Practice, 2007. (Russian).
9. Skin pigmentation disorders Babayants R. S., Lanshakov Yu.I. M. Medicine 1987.- 144 p. (Russian).
10. Jang Y. H., Lee J. Y., Kang H. Y., Lee E. S., Kim Y. C. Oestrogen and progesterone receptor expression in melasma: an im-munohistochemical analysis // J Eur Acad Dermatol Venereol. Forthcoming. 2010.
11. Kang H. Y., Valerio L., Bahadoran P., Ortonne J. P. The role of topical retinoids in the treatment of pigmentary disorders: an evidence-based review // Am J Clin Dermatol. 2009.- 10 (4).- P. 251-260.
12. Jo H. Y., Kim C. K., Suh I. B., Ryu S. W., Ha K. S., Kwon Y. G. et al. Co-localization of inducible nitric oxide synthase and phosphorylated Akt in the lesional skins of patients with melasma // J Dermatol. 2009.- 36.- P. 10-16.
13. Imokawa G. Autocrine and paracrine regulation of melanocytes in human skin and in pigmentary disorders // Pigment Cell Res. 2004.- 17.- P. 96-110.
14. Margolina A. A., Ernandes E. I., Zaykina O. E. New cosmetology.- M: "Cosmetics and medicine", 2002. (Russian).
15. Ortonne J. P., Arellano I., Berneburg M., Cestari T., Chan H., Grimes P. et al. A global survey of the role of ultraviolet radiation and hormonal influences in the development of melasma // J Eur Acad Dermatol Venereol. 2009.- 23.- P. 1254-1262.
16. Dolzhnikova E. M. Pathogenetic aspects of skin aging // Expo Beauty Esthetic Forum.- M., 2003. (Russian).
17. Kim N. H., Lee C. H., Lee A. Y. H19 RNA downregulation stimulated melanogenesis in melasma // Pigment Cell Melanoma Res. 2010.- 23.- P. 84-92.
18. Goodman G. J., Baron J. A. The management of postacne scarring // Dermatol Surg. 2007.- 33.- P. 1175-1188.
19. Bedjanidze Z. Hormotal and immunological indicators in skin dyschromias. PhD., thesis.- Tbilisi,- 2006.- 17 p. (Russian).
20. Yokota T., Nishio H., Kubota Y., Mizoguchi M. The inhibitory effect of glabridin from licorice extracts on melanogenesis and inflammation // Pigment Cell Res. 1998.- 11.- P. 355-361.
21. Mirzoeva P. N. Correction of involutive changes in the skin with the associated use of substitutional hormone therapy and topical phytoestrogens. PhD., abstract.- M., 2008.- 19 p. (Russia).
22. Morgulis Yu. A. Hormonal substitutional therapy in seborheic dermatitis, rosacea and prematurehair loss treatment in women in menopause. Ph D., abstract.- M., 2010.- 24 p. (Russian).
23. Balkrishnan R., Kelly A. P., McMichael A., Torok H. Improved quality of life with effective treatment of facial melasma: the pigment trial // Drugs Dermatol. 2004,- Jul-Aug; 3 (4): 377-381.
24. Berlin A. L., Paller A. S., Chan L. S. Incontinentia pigmenti: A review and update on the molecular basis of pathophysiology // J Am Acad Dermatol. 2002. - Aug; 47 (2 Pt 1): 169-187.
25. Hwang S. W., Oh D.J., Lee D., Kim J. W., Park S. W. Clinical efficacy of 25% l-ascorbic acid (C'ensil) in treatment of melasma // J Cutan Med Surg. 2009; 13: 74-81.
26. Cook-Bolden F. E., Hamilton S. F. An open-label study of the efficacy and tolerability of microencapsulated hydroquinone 4% and retinol 0.15% with antioxidants for the treatment of hyperpigmentation // Cutis. 2008; 81 (4): 365-371.
27. Goldberg J. Laser and phototreatment.- T. 1.- M.: "Elsevier", 2010.- 187 p. (Russian).
28. Potekaev N. N., Kruglova L. S. Laser in dermatology and cosmetology.- M.: MVD, 2012.- 280 p. (Russian).
29. Todd M. M., Rallis T. M., Gerwels J. W., Hata T. R. A comparison of 3 lasers and liquid nitrogen in the treatment of solar lentigines // Arch Dermatol. 2000; 136: 841-846.
30. Graber E. M., Tanzi E. L., Alster T. S. Side effects and complications of fractional laser photothermolysis: experience with 961 treatments // Dermatol Surg. 2008; 34: 301-305.
