disorders of hyperpigmentation

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  • 1. APPROACH TO A PATIENT WITHDISORDER OF PIGMENTATIONHistoryOnset : birth, infancy or laterCause: sun exposure, drugs, occupationSystemic complaintsFamily history: neurofibromatosis, tuberoussclerosis, vitiligo

2. Examination:Type of lesion: brown, blue, hypopigmented (checksensation), depigmented Shape: Ash leaf macules (tuberous slerosis)Koebner phenomenon (vitiligo) Distribution pattern : linear/segmental (nevusdepigmentosus), symmetric (vitiligo), specific sites(melasma, Addisons disease) 3. Examination aids:1. Hand lens2. Oblique lighting for elevation or depression3. Dermatoscopy4. Woods lamp - 365 nm. Epidermal pigmentaryanomalies made more prominent5. Histology:a) H and E for presence or absence of melaninb) Dopa reaction - melanocytes stain darkc) Silver stains - melanin stains black 4. CLASSIFICATION OFPIGMENTARY DISORDERSI. HYPOPIGMENTATIONII. HYPERPIGMENTATIONIII. DYSCHROMIA 5. HYPERPIGMENTATION 6. DISORDERS OF HYPERPIGMENTATIONMay be epidermal or dermalEpidermal hyperpigmentation due to- Increased melanin with normal number ofmelanocytes- Increased number of melanocytes Dermal hyperpigmentation- Melanin pigments appears blue-gray due toTyndall effect- Melanin from epidermis transferred to dermis- Melanin formed in dermal melanocytes 7. CLASSIFICATION EPIDERMAL 81. Physiologic:Pigmentary demarcation lines, sun tanning2. Genetic and Developmental:Lentigines, Freckles, Peutz-Jegherssyndrome, Melanocytic nevus, Caf-au-laitspots, Xeroderma pigmentosum, Beckersnevus, Nevus spilus, Acanthosis nigricans 8. 3. Post-inflammatory:Eczema, Psoriasis, Lichen planus, Lupuserythematosus, Scleroderma, Morphoea4. Infection:Tinea versicolor, Tinea nigra5. Nutritional:Kwashiorkor, Pellagra, Vit.B12, Vit.C, Folic aciddeficiency 9. 6. Physical:Trauma, Radiation dermatitis7. Endocrine:Melasma, Addisons disease, Cushingssyndrome, Phaeochromocytoma,Acromegaly, Hyperthyroidism8. Neoplastic:Malignant melanoma, Seborrhoeic keratosis,Pigmented basal cell carcinoma 10. DERMAL PIGMENTATIONGenetic and Developmental:Mongolian spots, Nevus of Ota/Ito, IncontinentiapigmentiInflammatory:Stasis dermatitis, Post inflammatory to eczemaand fixed drug eruptionChemicals and Drugs:Anti-malarials, OCP, Minocycline, Clofazimine,Topical hydroquinone, Amiodarone, zidovudine,psychotropic drugs, heavy metals andchemotherapeutic agents 11. Endocrine:MelasmaPhysical:Thermal burns, Post traumatic, TattoosInfection:Syphilis, Yaws, Pinta Neoplastic:Metastasis of melanoma 12. Nutritional:Chronic nutritional deficiencyMetabolic:Hemochromatosis, Alkaptonuria, Macular /Lichen amyloidosisMiscellaneous:Pigmented purpuric dermatosis, Purpura 13. KEY FEATURES Common acquired hypermelanosis At least 90% of patients are women. Increased prevalence in individuals who are Hispanic, or ofAsian, African or Middle Eastern descent (i.e. those with moredarkly pigmented skin). Most common location is the face, followed by the forearms. Symmetric patches of hyperpigmentation with irregularborders due to melanin within the epidermis &/or dermis. Exacerbating factors include pregnancy, use of oralcontraceptives and sun exposure. 14. PATHOGENESIS Exact pathogenesis of melasma is unknown. Genetic influences UV irradiation: following exposure, hyperfunctional melanocytes withininvolved skin produce increased amounts of melanin, The key role of UVirradiation is supported by;1. fading of lesions during winter months.2. distribution pattern demonstrating involvement of sun-exposedregions.3. sparing of relatively sun-protected sites such as the philtrum. Estrogens: predilection for women & association with pregnancy & OCP. Other medications: e.g. phenytoin, phototoxic drugs. Medical disorders: e.g. autoimmune thyroid disease. 15. CLINICAL FEATURES Light to dark brown or browngray patcheswith irregular borders Primarily on the face. The areas of hypermelanosis are distributedsymmetrically in three classic clinicalpatterns:(1) Centrofacial (most common), involvingthe forehead, cheeks, nose, upper lip(sparing the philtrum) and chin.(2) Malar, affecting the cheeks and nose.(3) Mandibular, along the jawline.Less common sites include the extensoraspect of the forearms& mid upper chest. 16. CLINICAL FEATURES Lesions often first appear or are accentuated followingexposure to UV irradiation or during pregnancy. In lightly pigmented individuals, this mask of pregnancyfrequently diminishes or disappears after parturition, but ittends to persist in women with more darkly pigmented skin. Melasma has also been subdivided into four types basedupon the primary location of the pigment: epidermal, dermalor mixed using Woods lamp examination. 17. CLINICAL FEATURESTYPE OF MELASMA CLINICAL FEATURESEpidermal Well-defined border Dark brown color Appears more obvious under black light Responds well to treatmentDermal The most common type Ill-defined border Light brown or bluish in color Unchanged under Woods light or become less obvious Responds poorly to treatmentMixed Combination of bluish, light and dark brown patches Mixed pattern seen under black light Partial improvement with treatmentIndeterminate in patients with very dark skin pigmentation inapparentunder Woods lamp. 18. HISTOPATHOLOGY Increased melanin deposition is observed in all layers of theepidermis. Epidermal melanocytes are normal to increased in number,and they are enlarged with prominent dendrites. An increased number of melanophages. While a Woods lamp has been used to localize melaninpigment to either the epidermis or dermis (i.e. epidermalversus dermal melasma), histopathologic studies andconfocal microscopy have shown that there is often a mixtureof the two forms in an individual patient. 19. HISTOPATHOLOGY(b) Perilesional normal skin, pigmented(c) Lesional: Epidermal hyperpigmentation. No inflammation, no dermal pigment 20. HISTOPATHOLOGY 21. HISTOPATHOLOGY(a) Photomicrograph showing epidermal melasma with increased concentration ofmelanin pigment in the epidermis (H and E, 200); (b) MassonFontana stain; 200) 22. HISTOPATHOLOGY(c) Increase in the number of melanocytes and underlying solar elastosis (H and E,200); (d) Melanin incontinence in the dermis (MassonFontana; 200) 23. TREATMENT Patient motivation are necessary for any treatment regimenfor melasma to be successful. For epidermal melasma, 2 months of therapy are typicallyrequired to initiate lightening and 6 months of treatment areoften needed to achieve satisfactory results. Cosmetic camouflage helps in case of recalcitrant melasma. Recurrence is the norm despite precautionary measures suchas strict sun protection. After achieving the desired bleaching, use as needed tomaintain results. 24. TREATMENT1. Avoid underlying cause:a) Discontinuation of OCP.b) Sun protection, including hats, clothing (if extrafacial), avoidancedaily application of a broad spectrum sunscreen SPF 30+, can helpto prevent accentuation of the pigmentation by UV exposure.2. Topical hydroquinone (24%) may lead to lightening over 36 monthsif the increase in pigmentation is limited to the epidermis.3. Topical tretinoin: as a monotherapy can be helpful, but the requiredtreatment period is often 24 weeks or longer. It thins the skin, penetration of other agents & have direct effect in melanisation.4. Triple combination: The most common topical regimen is acombination of hydroquinone (24%), tretinoin (0.050.1%) and acorticosteroid (class VVII). 25. TREATMENT5. Vitamin C (ascorbic acid).6. Azelaic acid 20%7. Kojic acid 1-4%8. Chemical peels: -hydroxy acids (Glycolic acid)& salicylic acid usedas adjunctive therapy.9. Dermabrasion: variable results and can cause scarring anddyspigmentation.10. Laser therapy & IPL: has limited benefits, especially for individualswith darkly pigmented skin, and it may lead to hypopigmentation.Q-switched ruby, alexandrite & Nd:YAG lasers are variablysuccessful in removing dermal pigment, especially epidermal PIH. 26. HYDROQUINONE (HQ) A skin-bleaching agent used fortreatment for melasma and otherdisorders of hyperpigmentation. It is topical tyrosinase inhibitor.INDICATIONS1. Melasma2. Ephelides3. Solar lentigens4. Postinflammatory hyperpigmentation5. Hyperpigmented scars e.g. post-acnescars.MECHANISMS OF ACTION1. Competitive inhibition with tyrosine: as a substrate for tyrosinase.2. Damage to melanosomes and melanocytes: selectively by production ofhighly reactive oxygen radicals. 27. HYDROQUINONEHOW TO USE HYDROQUINONE Test for skin sensitivity before using by applying the cream to a smallpatch of hyperpigmented skin. If no redness or itching occurs within24 hours, begin treatment. Clean and dry the skin before applying a thin film of cream once ortwice daily to the area(s) in need of bleaching. Rub into the skin well. Apply just enough to cover the affected areas and avoid applying tonormal skin, as this will lighten as well. Hence wash your hands afterapplying unless these are areas of treatment. Do not apply near the eyes, mouth, and other mucous membranes. If no bleaching effect is seen after 3 mo. of Tx, stop using it. 28. HYDROQUINONESIDE EFFECTS1. Irritant contact dermatitis: mild itching orstinging and reddening of the skin.2. Allergic contact dermatitis: less often-severeburning, itching, crusting, orswelling.3. Postinflammatory hyperpigmentation,4. Exogenous ochronosis5. Leukoderma. 29. OCHRONOSIS Ochronosis is the discoloration ofcertain tissues, such as the ear cartilage and theocular tissue, seen with alkaptonuria, ametabolic disorder. Additionally, ochronosis canoccasionally occur from exposure to varioussubstances such as:1. Hydroquinone.5. Mercury.2. Phenol.6. Benzene.3. Trinitrophenol.7. Antimalarials.4. Resorcinol. Irregular patches with characteristic pin-point,caviar-like papules affecting sun-exposed skin.Uncommon and is usually caused by prolongeduse of hydroquinone at a concentration >2%. 30. MONOBENZYL ETHER OFHYDROQUINONE (MBEH) 20% Is


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