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Facial Pigmentation Common Causes and How to Manage THOMAS STEWART Bbiomedsc(Hons), MB BS ROBERT ROSEN MB BS, Mmed, FACD

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Facial Pigmentation Common Causes and How to Manage THOMAS STEWART Bbiomedsc(Hons), MB BS ROBERT ROSEN MB BS, Mmed, FACD PEER REVIEWED FEATURE 2 CPD POINTS Facial pigmentation Common causes and how to manage THOMAS STEWART BBioMedSc(Hons), MB BS ROBERT ROSEN MB BS, MMed, FACD Facial pigmentation may be due to a generalised round 14% of GP consultations are for the management process but most often is localised to the face. of skin diseases.1 Pigmentary disorders represent a large Melasma and actinic damage pigmentation are proportion of diagnoses in dermatological populations.2 common and tend to be bilaterally distributed and Melasma, the most common facial pigmentation world- Awide, may account for up to 10% of new dermatology referrals,3 slowly progressive. Irregularly shaped isolated lesions should be viewed with more caution, and and GPs therefore need to be able to recognise it. biopsy may be required. Treatments include topical Skin pigmentation normally varies according to racial origin and oral medications, peels, intense pulsed light and the amount of sun exposure, and pigmentation disorders are often more troublesome in constitutionally darker skin (‘skin therapy and laser treatment. of colour’). Facial hyperpigmentation manifests as either localised to the face or part of diffuse disease. Pigmentation localised to KEY POINTS the face usually represents a benign condition, although it may be the cause of significant psychological distress because of its • Diagnosis of the type of facial pigmentation can be made high visibility and sociocultural implications (regardless of the on clinical grounds in most cases. nature of the problem, people generally desire uniformity of skin Facial pigmentation is a cause of considerable • colour). Increased facial pigment can, however, herald underlying psychosocial distress for many patients. systemic disease or malignancy. • Melasma, the most common facial hyperpigmentation worldwide, is most prevalent in women and people with Melanin contributes to racial and phenotypic appearance, but constitutionally darker skin. It occurs in approximately also has important roles in protecting from ultraviolet (UV) 25% of women who are pregnant. radiation damage and scavenging of toxins. Several pigment • Hydroquinone-based skin-bleaching preparations remain intensifiers have been identified, the most notable of which are the gold standard for the treatment of melasma. UV radiation and, in the setting of melasma, oestrogen and • Many patients with facial pigmentation can be managed progesterone. The process of pigment intensification is thought in the general practice setting but referral for specialist to involve an increase in pigment production and/or melanocyte management may be required for refractory cases. numbers, usually mediated, at least in part, by the enzyme tyrosinase. Several established treatments target this enzyme, although improved understanding of melanogenesis in recent times has MedicineToday 2016; 17(10): 30-38 seen the emergence of several novel treatment options. This article reviews the causes of hyperpigmentation and Dr Stewart is a Research Fellow, and Dr Rosen is a Dermatologic Surgeon and discusses treatment options for facial pigmentation that can be WHITESHOES911/DEPOSITPHOTOS. MODEL USED FOR ILLUSTRATIVE PURPOSES ONLY. PURPOSES ILLUSTRATIVE FOR USED MODEL WHITESHOES911/DEPOSITPHOTOS. Managing Director, Southern Suburbs Dermatology, Sydney, NSW. used in general practice. © 30 MedicineToday ❙ OCTOBER 2016, VOLUME 17, NUMBER 10 Downloaded for personal use only. No other uses permitted without permission. © MedicineToday 2016. Generalised versus localised disease (e.g. Crohn’s disease), and alcohol- 1. COMMON FACIAL PIGMENTATIONS hyperpigmentation ism is known to deplete folic acid stores. Generalised hyperpigmentation may be The endocrinopathies and metabolic • Melasma drug-induced, nutrition-related, have endo- disorders most commonly associated with crine or metabolic causes or occur after systemic hyperpigmentation are Addison’s • Postinflammatory inflammation. It can also occur with malig- disease, haemochromatosis and hyper- • Sun-damaged skin nancies or have genetic causes. Limited thyroidism; although patients may have • Photosensitivity facial pigmentation, the most common associated symptoms or a past medical – connective tissue disease presentation of localised hyperpigmenta- or family history suggestive of these – drugs tion, typically is part of several common conditions, pigment changes are often • Naevi and largely benign skin conditions. Solar among their first signs. Postinflammatory – Ota – Hori lentigines (freckles), melasma and post- hyperpigmentation is not a common cause inflammatory hyperpigmentation are some of ‘generalised’ hyperpigmentation. • Fixed macules – lentigines (solar and other) of the more common facial pigmentations Far less frequently, occult malignancy – seborrhoeic keratoses (Box 1). such as adreno corticotrophic hormone (ACTH)- producing lung carcinomas and Generalised hyperpigmentation metastatic melanomas may cause gener- disease are loss of androgen-stimulated hair, The causes of generalised hyperpigmen- alised hyper pigmentation. such as pubic and underarm hair. Patients tation are listed in Box 2. Drug-induced Symmetrical distribution is a hallmark with hyperthyroidism may display the Addi- hyperpigmentation may occur with use of of hyperpigmentation caused by systemic sonian pattern of pigmentation but involve- minocycline and hormonal contraceptives. disease. In patients with Addison’s disease, ment of mucous membranes is uncommon Nutrition-related hyperpigmentation may hyperpigmentation is most intense on and darkening of nipples and genital skin is be seen with deficiencies of vitamin B12 light-exposed areas, in skin creases and less striking; the eyelids are occasionally or folate associated with inadequate dietary flexures, at sites of friction and on mucous pigmented and some patients show localised intake or gastrointestinal malabsorptive membranes; other associated features of this ‘melasmal’ rather than diffuse pigmentation. 2. CAUSES OF GENERALISED HYPERPIGMENTATION* Drug and toxins • Inflammatory dermatoses such as • Carcinoid syndrome • Analgesics (NSAIDS) acne, psoriasis • Hyperthyroidism (one of the most • Antiarrhythmics (amiodarone) • Medication use (e.g. hydroquinone, frequent endocrine causes) • Antibiotics (tetracyclines [e.g. tretinoin) • Acanthosis nigricans minocycline], co-trimoxazole) • Postinfective (e.g. tuberculosis, Metabolic • Anticonvulsants (phenytoin) malaria, subacute bacterial endocarditis, HIV) • Chronic renal failure • Antidepressants (imipramine, desipramine) • Ultraviolet light (most frequent • Chronic liver disease • Antimalarial drugs (hydroxychloroquine, postinflammatory cause) • Haemochromatosis (most frequent chloroquine) metabolic cause) • Cytotoxics (bleomycin, busulfan, Nutritional • Porphyria cyclophosphamide, 5-fluorouracil) • Kwashiorkor • Heavy metals (arsenic, bismuth, gold, Malignancy • Pellagra mercury, silver) • Melanoma (rarely) • Scurvy • Hormones (oestrogen, progesterone, • Small cell lung carcinoma (rarely) adrenocorticotrophic hormone) • Vitamin B12/folate deficiency (most frequent nutritional cause) • Psychotropics (phenothiazines Genetic [e.g. chlorpromazine]) • Familial (e.g. periorbital Endocrine hyperpigmentation) Postinflammatory • Pregnancy • Chromosomal (e.g. xeroderma • Allergic dermatitis • Addison’s/Cushing’s disease (one of pigmentosum; dyskeratosis • Autoimmune disorders such as systemic the most frequent endocrine causes) congenital) lupus erythematosus/scleroderma • Phaeochromocytoma • Racial (e.g. naevi of Ota, Ito, Hori) * Causes listed in alphabetical order. MedicineToday ❙ OCTOBER 2016, VOLUME 17, NUMBER 10 31 Downloaded for personal use only. No other uses permitted without permission. © MedicineToday 2016. F ACIAL PIGmentation continued lentigines appear during childhood (Figure TABLE 1. FITZPATRICK SKIN TYPES 3). Melasma onset spans the reproductive Skin type Skin/hair/eye colour; example ethnicity Characteristics years from 20 to 40 years of age. Cutaneous systemic lupus erythematosus and naevus I White; very fair, red or blonde hair, blue Always burns, never tans of Hori (also known as acquired bilateral eyes, freckles; Celtic naevus of Ota) similarly have broad II White; fair, red or blond hair; blue, Usually burns, tans with spectrums of onset, appearing between hazel or green eyes difficulty the ages of 20 and 50 years, and 20 and III Cream white; fair with any eye or hair Sometimes mild burn, gradually 70 years, respectively. Actinic damage and colour (common) tans seborrhoeic keratoses become apparent during the fourth decade of life and usually IV Brown; typical Mediterranean Rarely burns, tans with ease Caucasian skin; Asian increase in number with age. V Dark brown; mid-eastern skin types, Very rarely burns, tans easily Comorbidities East Indian A specific history should be sought regard- VI Black; Aboriginal and Torres Strait Never burns, tans very easily ing endocrinological and metabolic Islander conditions associated with skin hyper- pigmentation (Table 1). Patients with haemochromatosis have slate • examination grey or brownish-bronze skin, mostly in – morphology Medication use sun-exposed areas and particularly on the – distribution. Hormonal contraceptive use commonly face; other associated features include skin triggers melasma in women. Minocycline and nail changes such as hair loss and Fitzpatrick skin type and phenytoin are other recognised causes koilonychia (twisted nail plate). Solar lentigines and other hyperpigmen- of facial
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