Dyschromia

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Introduction:

• Change in normal skin hue, not fading under mechanical action, most often due to a melanogenesis disorder (melanin overload or disappearance)

• Normal skin colour:

Depends on the phototype of the subject and the sun exposure, so we are talking about:

▪ Constituent Color: which is a reflection of genetically determined melanic pigmentation

▪ Inductive Color: by tanning after sun exposure

In the same subject, skin pigmentation varies according to anatomical regions: areas usually exposed to the sun as well as folds and external genitalia are naturally more pigmented

The colour of the skin is mainly the result of the presence of a pigment called melanin, whose essential role is to protect the basal layers of the epidermis from ultraviolet

Reminder:

• Dyschromic macules:

Pigmented macules: they are due to a build-up of pigment in the epidermis or

in the dermis

▪ Melanin: natural pigment of the epidermis

Localized: chloasma (pregnancy mask), coffee-to-milk stains

Generalized: Melanodermy of Addison's disease

▪ Non-melanic Pigment: most often metallic (tattoo, iron in hemochromatosis)

Achromic macules: they are due to a decrease (hypochromic macule) or an absence (achromic macule) of melanocytes of the epidermis and/or melanin secretion by them. They come in the form of light spots (e.g. vitiligo and achromic pityriasis versicolor

• Semiological analysis of a pigment disorder: it includes elements of interrogation that must be systematically sought, because they are not always mentioned spontaneously by the patient. He try to clarify: the acquired or congenital character, the date of appearance, the possible role of sunlight, the treatments undertaken and their results, the existence of an inflammatory phase preceding the pigment disorder, the different pre-dermatitis, systemic treatment of the patient

• Clinical review:

The colour of hyperchromy (brown, black, bluish grey, etc.) is an important semiological element:

▪ A brown to brown-black colour is, more often than not, an overload of melanin (hypermelanosis) in the epidermis

▪ A grey or bluish grey colour most often reflects dermal hypermelanosis or overload of exogenous pigments, normally not present in the skin

In the face of hypochromy, it must be specified whether it is total or partial and the existence of another elementary lesion (erythema, papule…)

Hyperpigmentations:

• Eliplions (freckles): maculating, localized, small (few millimetres), light brown incolour, common in blue-eyed red-eyed subjects, usually in childhood, are located on the face and the discovered parts, permanent but their number increases with age and their coloration increases after sun exposure, subjects carrying profuse sipelias generally exhibit a marked photosensitivity

The spelias correspond to hypermelanism (increased melanin synthesis)

• Lentigines: small hyperpigmented macules (1-3 mm), which is distinguished from the sphelides by their darker hue (brown or black) and by their lack of modification after sun exposure, generally regional, they can be spread over the entire surface of the coat and/or on the mucous membranes, may appear in childhood or later in life, sometimes integrated into complex multi-visceral expression syndromes.

Lentigines correspond to hypermelanocytosis (increase in the number of melanocytes)

• Coffee-to-milk stains: light brown macules, homogeneous in colour, rounded or oval, with regular or jagged contours, the size of which can vary from a few centimeters to several tens of centimeters, few in number, are readily located on the chest, dombes and sometimes limbs, their topography can be one-sided

• Mongolian stains: bluish-grey macules, ranging in size from a few millimetres to several tens of centimetres, common in Asians and blacks, present at birth, they disappear clinically during childhood, topography: lumps and buttocks

• Melasma (chloasma): hyperpigmentation on the upper part of the face, respecting the edge of the scalp, generally bilateral, non-symmetrical, inhomogeneous (variant from ochre yellow to black), increasing in summer, two factors etiological stimulation: hormonal stimulation (pregnancy, estrogen, progestin), ultraviolet stimulation. During pregnancy, hyperpigmentation also appears on the areola of the breasts, the abdominal white line, scars and genital mucous membranes

• Post-inflammatory hyperpigmentation: hyperpigmented residual spots that persist after healing of various dermatoses, in this case, the pigment disorder is not the result of a primitive damage to the melanocytic system

• Exogenous pigment: Exogenous dyschromies result from: accidental or voluntary transcutaneous penetration (tattoo, subcutaneous or intramuscular injection) of non-resorbable substances, absorption or intoxication by systemic pathway of certain metals or drugs

Argyria: silver absorbed per bone or injected for a long time can cause diffuse hyperpigmentation of the coat, an ardoized grey hue with metallic reflections, diffuse topography but above all discovered areas: oral mucous membranes, rhinopharyngeals, oculars or nails may be affected. Argyria has, more often than not, a professional origin (jewellers, photographs, manufacturers of silver nitrate), its therapeutic origin has become rare

• Metabolic hypermelanoses:

Hemochromatosis: diffuse skin hyperpigmentation, ardoized brown in colour with a greyish metallic reflection, sometimes intense, almost black, it gives the skin a dirty appearance badly washed, predominates to the discovered regions and folds, melancholy skin also occurs during secondary hemochromatosis by excessive iron intake (transfusion…)

Wilson's disease: hyperpigmentation of the lower limbs

Uremic melanodermy of kidney failure: diffuse, greyish, dull hyperpigmentation, more pronounced on the regions discovered and respecting the mucous membranes

• Endocrine hypermelanoses:

Addison's disease: A more pronounced melanodermy on the discovered and/or naturally pigmented parts, on areas subjected to repeated friction, trauma, oral mucosa (ardoized spots), damage to genital and conjunctivas is common

Visceral tumours with ectopic secretion of ACTH or MSH

Other endocrinopathies: Cushing syndrome, acromegaly, pheochromocytoma

Hypopigmentations:

• A leukodermy is a localized or diffuse thinning of the skin, all the easier to see as the skin is more pigmented, it can be the result of a lack of melanic pigment that results from:

Decrease in number of melanocytes or their complete disappearance

Failure to synthesize or transfer melanin

Localized Vasoconstriction

White substance deposit

• Oculocutaneous Albinisms: specifically refers to genetic diseases combining diffuse hypomelanosis and characteristic eye manifestations, they are due to a defect in melanin synthesis by melanocytes of the skin, dander and the eye. Diagnosis is clinical

In severe forms: the diagnosis is obvious: hair and hair are snowy white, blue eyes, pink is white skin, no tanning, skin is very sensitive to ultraviolet light with a major risk of skin cancer, absence of cut lesions pigmented ane

In less severe forms: hair is straw blond or light brown, blue eyes are light brown, skin is able to tan moderately, there may be pheliondes, lentigines and low pigmented nevus. Diagnosis of comparison with parents and siblings

• Vitiligo: white macules, scattered, whose confluence can lead, in the extreme, to widespread depigmentation, familial in more than a third of cases, the genes of susceptibility to vitiligo are unknown, global frequency of about 1%, both sexes are also affected, can appear at any age, but most often occurs in young adults during the second and third decades of life, role of psycho-affective or physical trauma

Clinical:

▪ Elemental injury: achromic macule, uniform in colour, milky white, devoid of melanin (Wood light examination), varying shape and size, always convex edges, normal surface, limited by often irregular contours but well sometimes highlighted by a hyperpigmented border, no functional signs or inflammatory signs but photosensitivity, hair, hair, eyelashes and eyebrows can be depigmented. Hair depigmentation in vitiligo lesions is also a predictor of poor therapeutic response

▪ Topography: often unilateral and bilateral, often symmetrical onset, certain parts of the body are more frequently affected: normally the most pigmented regions (axillary hollows, external genitalia), discovered regions, exposed to  light, peri-orificial regions, areas of bony protrusion (knees, tibial crests, malleolar regions, iliacious spines, sacred regions), regions exposed to repeated microtrauma (underwear, belt) Koebner

▪ Extension of lesions: there are generalized vitiligos (in extreme cases, can invade the entire tegument: vitiligo universalis), localized vitiligos, sometimes of segmental topography, unilateral

Association: with several diseases, especially autoimmune conditions (thyroiditis, Biermer anemia…)

Evolution: capricious and unpredictable, repigmentation is often done from hair follicles giving a speckled appearance

Diagnosis: exclusively clinical, Wood's light examination is very useful for detecting hypomelanottic lesions in light-skinned subjects, biopsy for anatomopathological examination is only performed for research purposes, it shows an absence melanocytes in the lesion skin

• Infectious hypomelanoses: pityriasis versicolor accounts for the bulk of fungal achromes

• Post-inflammatory hypomelanoses: secondary depigmentation associated with lupus erythematosus, psoriasis, eczema, eczema (this list is not limiting), the diagnosis is always easy because the lesions typical of the causal condition  are constantly found either through interrogation or clinical examination
• Leucodermies by physical and/or chemical agents: the anatomoclinic table is close to vitiligo, melanocytes are vulnerable to most physical aggressions (X-ray, UV, burns, cold) and various mechanical aggressions

Treatment:

• Hypermelanoses:

Eviction: Removal of the pathogen is the first therapeutic step to take: removing prolonged sun exposure or using UV sunscreens

Depigmenting agents: various products have been proposed in therapeutics in order to discolor the hyperpigmented skin, these are oxidizing agents (peroxides…) or reducing

Lasers: they have been proposed for the treatment of pigment lesions and tattoos

• Hypomelanoses: When an etiological factor can be identified, the removal of the pathogen is the first step: the removal of a depigmenting chemical, the treatment of a fungal agent…

Dermocorticoids: may be recommended for the treatment of highly localized vitiligos, however, very strict monitoring should be exercised

Local immunosuppressants (in France, Tacrolimus in ointment, at 0.03% and 0.1%): are used for the treatment of vitiligo often in combination with phototherapy

Cryotherapy: spared or superficial dermabrasion, may induce repigmentation of lenticular hypochromies of hypomelanosis in idiopathic drops

Surgical treatment: several trials of these methods of treating melanocytenic hypomelanoses, including vitiligo, have been attempted: autologous melanocyte transplant into depigmented skin

Antioxidants: in the context of the hypothesis that vitiligo results from a deficiency of free radical neutralization systems in the skin

Oral photo-chemotherapy: Combining psoralenes and UVA, currently remains the only treatment that can lead to the hope of rarely repigmentation of the lesion skin of vitiligo