1. به نام خدا وند بخشنده و مهربان

2. Dr Gita Faghihi Dermatology ASSOc. Professor Isf.Univ.Med.Sci

3. Depends on: Amount of : Melanin, Chromophores such as :hemoglobin, carotenoids…

4.  Increase in amount of melanin or number of active melanocytes  deposition of exogenous pigments,…

5. CircumscribedReticularLineardiffuse

6.  Reticulate acropigmentation of Kitamura & Dohi  Naegeli–Franceschetti–Jadassohn syndrome  Dyskeratosis congenita,.…

7. Diffuse/Circumscribed  Lentigo/Lentiginosis  Melasma  Erythema dyschromicum perstans  Lichen planus pigmentosus  Café au lait spot  Poikiloderma (Poikiloderma of Civatte),,(Poikiloderma vasculare atrophicans)  Riehl melanosis  PIP  Acanthosis nigricans  Periorbital hyperpigmentation  Photoleukomelanodermatitis of Kobori  Transient neonatal pustular melanosis

8. Linear  Incontinentia pigmenti  Scratch dermatitis(flagellate bleomycin induced)  Shiitake mushroom dermatitis linearity of the lesions is probably related to Blaschko’s lines, which suggests that the predisposition to develop,,determined during embryogenesis

9. Others/unclassified(due to drugs,,exogenous..)  pigments iron: Hemochromatosis Iron metallic discoloration Pigmented purpuric dermatosis (Schamberg disease, Majocchi's disease, Gougerot– Blum syndrome, Doucas and Kapetanakis pigmented purpura/Eczematid-like purpura of Doucas and Kapetanakis, Lichen aureus, Angioma serpiginosum) Hemosiderin hyperpigmentation  other metals: Argyria Chrysiasis Arsenic poisoning Lead poisoning Titanium metallic discoloration  Carotenosis, Tattoo,Tar melanosis

12. acquired hypermelanosis …… after cutaneous inflammation or injury ….can arise in all skin types, But, more frequently affects darker patients, including : African Americans, Hispanics/Latinos, Asians

14.  Acne  Infect.(Dermatophytoses, viral exanthems bacterials..,  allergic reactions ( insect bites or a contact dermatitis, medication-induced PIH from(.. hypersensitivity reactions,  papulosquamous diseases (psoriasis or lichen planus, PR  cutaneous injury from irritants, burns, or cosmetic procedures

18.  LTC4,  prostaglandins E2 and D2, thromboxane-2, interleukin (IL)-1, IL-6,  tumor necrosis factor (TNF)-α,  epidermal growth factor, and  reactive oxygen species.

19. Photoprotection (a sunscreen) + topical depigmenting Topical tyrosinase inhibitors, such as:hydroquinone, azelaic acid, kojic acid, arbutin, and certain licorice extracts certain licorice extracts, can effectively lighten areas of hypermelanosis.

20.  topical 5% methimazole,  Topical 2% dioic acid can successfully treat hyperpigmentation secondary to a variety of etiologies../(PIH).

21. One of the most common…CIRCUMSCRIBED DISORDERS…

22. is an acquired symmetrical pigmentary disorder where confluent grey-brown patches typically appear on the face. %90 of individuals are women It is A disease with considerable psychological impacts The management of melasma is challenging and requires a long-term treatment plan.

23.  One of the most important factors in the development of melasma is ultraviolet exposure from sunlight or other sources  photosensitizing and anticonvulsant medication  mild ovarian or thyroid dysfunction  certain cosmetics.

24. is the most common and involves:  the cheeks,  nose,  forehead,  upper lip, and  chin.

25.  Wood's lamp examination is of benefit classifiying melasma(epidermal,dermal,mixed/..)

26. Kligman and Willis  Kligman and Willis : hydroquinone (5%) with tretinoin (0.1%) And dexamethasone (0.1%).

28. In 2006 In 2006, (FDA) released a statement proposing a ban on all OTC HQ agents based on rodent studies, which suggested that oral HQ may be a carcinogen s o,

30. azelaic acid inhibit the energy production and/or DNA synthesis of hyperactive melanocytes, azelaic acid antityrosinase activity. azelaic acid This may also account for the beneficial effect on postinflammatory hyperpigmentation. azelaic acid 20% cream twice daily over a period of 12 weeks

31.  Tranexamic acid tablets 250 mg twice daily 6 months  Tranexamic acid tablets were prescribed at a dosage of 250 mg twice daily for a therapeutic period of 6 months. 75% good to excellent response No side effects except hypomenorrhea and mild GI upset in <10%

32.  Arbutin,(3-5 %) a herbal agent,, higher concentrations of arbutin can lead to a paradoxical hyperpigmentation. Synthetic forms of arbutin, alpha-arbutin and deoxyarbutin, exhibit greater ability to inhibit tyrosinase Adding kojic acid, betulinic acid and niacinamide To arbutin gives better inhibition of Tyrosinase and higher efficacy

33. combination of  Tretinoin  Tretinoin, and  kojic acid, and  azelaic acid improve the melasma very effectively.

34. adapalene gel 0.1%  There is a lot of documented evidence about efficacy of adapalene gel 0.1% in melasma

35.  Dioic acid  Resveratrol

36.  chemical peel (such as glycolic acid,SA.. … etc..)  microdermabrasion  Laser (fractional,ruby,low fluence Q- switch nd:YAG …)  intense pulsed light (IPL)

39. Most common in individuals with skin phototypes III– IV(women are more commonly affected) Ashy, gray–brown to blue–gray macules and patches in a symmetric distribution Lesions favor the neck, trunk and proximal extremities Causes: ■ Genetic susceptibility ■Toxic effects of chemicals such as ammonium nitrate or barium sulphate ■ worm infestation ■ Viral infections ■ Adverse effect of drugs and medications

41.  is a skin condition with age of onset almost always before 40 years old  characterized by skin lesions that are usually symmetrical and generalized

42. A consistently effective treatment is not currently available But some case series responded to oral corticosteroids

43.  The use of narrow-band UVB phototherapy has shown success in a few patients  A low-potency topical steroid applied twice a day to the affected areas may be used, with or without a 4% hydroquinone cream for the hyperpigmentation  A patient from Turkey was described to have responded remarkably well to treatment with dapsone

44. Lichen planus pigmentosus

45. Lichen planus pigmentosus (LPP) is an uncommon variant of lichen planus that favors individuals with skin phototypes III–V, including those from India Latin America and the Middle East. LPP usually has its onset during the third or fourth decade of life; it presents as oval or round, brown, gray–brown or dark brown macules and patches in either sun-exposed areas (especially the forehead, temples and neck) or intertriginous zones. There may be no associated symptoms versus mild pruritus or burning, and, in contrast to some cases of EDP, early lesions do not have an erythematous border

47. Tacrolimus (protopic ) ointment is effective in LPP

49. a spectrum of disorders characterized by the deposition of amyloid within the skin and other tissues.  Primary (localized) cutaneous amyloidosis  Primary (localized) cutaneous amyloidosis is subdivided into three major forms– macular, lichenoid and nodular the first two are associated with hyperpigmentation. The most common locations are the upper back (macular amyloidosis) and the extensor surface of the lower extremities (lichen amyloidosis). Areas of involvement are often pruritic, and because rubbing plays a key role in the production of lesions, there is a characteristic rippled pattern with parallel bands or ridges of hyperpigmentation. Histologically, melanophages as well as amyloid deposits that stain positively with antikeratin antibodies are seen within the upper dermis.

52.  relief of pruritus. Sedating antihistamines have been found to be moderately effective.  Topical dimethyl sulfoxide (DMSO), a chemical solvent  intralesional steroids are beneficial if combined with other modalities.  Treatment with ultraviolet B (UV- B) light can provide symptomatic relief.

56. usually autosomal-dominant fashion punctate, irregular, atrophic, brown macules involving the dorsa of the hands and feet, the dorsa of the knees the extensor surface of the neck, both axillary regions, the abdominal skin and the inguinal region,

57. Most treatments attempted have been unsuccessful,  but an attempt to treat the disease with 20 % azelaic acid 20 % azelaic acid gave significant improvement  Er-YAG laser treatment

58. is characterized by the presence of hyperpigmented and hypopigmented pinpoint or pea-sized macules over the dorsa of the hands and feet and occasionally on the arms and legs

63.  Affected individuals often have fingernails and toenails that grow poorly or are abnormally shaped.  They also often have changes in skin coloring (pigmentation), especially on the neck and chest, in a pattern often described as "lacy."  White patches inside the mouth (oral leukoplakia

64. major consequence being:  bone marrow failure and/at increased risk of developing leukemia  People with dyskeratosis congenita are also In addition have a higher risk of other cancers, especially head, neck, anus, or genitals

65. is a cutaneous condition and refers to :  Reticulated red-brown patches with telangiectasias Poikiloderma of Civatte refers to erythema associated with a mottled pigmentation seen on the cheeks & sides of the neck

70.  Reticulate and zosteriform (“Zebra-like”) hyperpigmentation, in whorls and streaks  is a disorder of pigmentation that develops within a few weeks of birth and progresses for one to two years before stabilizing.

71.  chemical peel  Q-S laser A little help in some patients but, a proven treatment approach for LWNH does not exist.

74. and usually represent the presenting signs. They are divided into four overlapping stages:  (1) vesiculobullous, which favors the extremities during the first few months of life (but occasionally recurs during childhood in association with a febrile illness);  (2) verrucous, which favors the distal extremities in patients one to six months of age (and sometimes adolescents);  (3) hyperpigmented, which favors the trunk and intertriginous sites from three months of age through adolescence; and  (4) hypopigmented/atrophic, which affects the calves in adolescents and adults

76.  Hyperpigmented lines are fading in adolescence  linear, atrophic hairless lesions.  dental anomalies,  alopecia, wooly hair, and  abnormal nails  Seizure or MR  Retinal /ophthalmic disorders(blindness..)

79. is a rare acquired macular hyperpigmentation of oral mucosa and lips frequently associated with longitudinal pigmentation of the nails The pathogenesis is unknown, but no systemic involvement no family history of the disease or no intestinal polyposis, no systemic involvement no family history of the disease or no intestinal polyposis, or no malignant predisposition no malignant predisposition has been described

82. flat brown marks on the lips and inside the mouth, and frequently brown stripes on the nails.

86. usually affects the neck, arms, legs and trunk of children and young adults. The rash consists of reddish- brown spots

87.  The exact cause of this uncommon disease is unknown but recent research suggests genetic change in a protein (called c-kit) on the surface of mast cells may result in the abnormal proliferation of these cells.  Variety of factors can cause or worsen the symptoms of urticaria pigmentosa:  Physical stimuli such as heat, friction, and excessive exercise  Bacterial toxins  Venom  Eye drops containing dextran  Alcohol  Morphine  Emotional stress

88. Treatment of mastocytosis

91. Lentigines sun-exposed areas

92. is a cutaneous condition characterized by : light brown macules on mucosal surfaces

94. LEOPARD syndrome  L entigines,  e lectrocardiographic conduction defects,  o cular hypertelorism,  p ulmonary stenosis,  a bnormal genitalia,  r etardation of growth, and  d eafness syndrome) (ie, multiple lentigines syndrome) is a complex dysmorphogenetic disorder that is transmitted as an autosomal-dominant trait

95.  pigmented birthmarks  The name café au lait is French for "coffee with milk" and refers to their light-brown color

96. They can be treated with Q -Switch lasers

98. Nevus of Ota  Epidemiology is more common in Japanese, in women (9 times ) with onset either in the perinatal period or around puberty  Etiology genetic factors are thought to be important but familial cases are rare. Pathogenesis  represents aborted embryonic migration of melanocytes from neural crest to epidermis. Late pubertal onset is explained by pigmentation of the amelanotic nevoid cells present at birth by adolescent spurt of sex hormones. Clinical features  is characterized by speckled or mottled coalescing blue-grey pigmentation of the area supplied by ophthalmic and maxillary divisions of trigeminal nerve. It is usually unilateral (90%).

99.  The sclera is involved in two-thirds of cases (causing an increased risk of glaucoma).

100. Schamberg disease

101. Progressive pigmented Purpuric dermatoses. Schamberg”s

102. lasers Currently available lasers are not particularly helpful not particularly helpful for pigmented purpuric dermatoses

103.  (pentoxifylline) circulation,  Vitamins (Vitamin C 500mg twice daily ) Bioflavonoid (Complex with Rutin)

105.  skin hyperpigmentation,  vitiligo,  hair changes,  recurrent angular stomatitis Hyperpigmentation of the extremities especially over the dorsum of the hands and feet, with accentuation over the interphalangeal joints and terminal phalanges

108. Although several classes of drugs are known to induce ‘hyperpigmentation’, the most common are: minocycline,  minocycline,  phenothiazines  antimalarials,  chemotherapeutic agents  Zidovudine  Amiodarone mucosal pigmentations and Longitudinal or horizontal melanonychia may also be present

109. pigmentation usually resolves with discontinuation of the offending drug, but the course may be prolonged

110.  thiazides  tetracyclines followed by exposure to sunlight Edematous erythema with slight itching appeared on the sun-exposed areas,the cutaneous lesions almost disappeared after drug stop but pigmentations and depigmentations develop in spots in sun-exposed areas. Photopatch and oral challenge tests were positive.

111. Facial melanoses (FM) are a common presentation in dermatologic patients, causing cosmetic disfigurement with considerable psychological impact. Some of the well defined causes of FM include melasma, Riehl's melanosis, Lichen planus pigmentosus, and poikiloderma of Civatte. But there is considerable overlap in features amongst the clinical entities. Etiology in most of the causes is unknown, but some factors such as UV radiation in melasma, exposure to chemicals in EDP, exposure to allergens in Riehl's melanosis are implicated. Diagnosis is generally based on clinical features. The treatment of FM includes removal of aggravating factors, vigorous photoprotection, and some form of active pigment reduction either with topical agents or physical modes of treatment. Topical agents include hydroquinone (HQ), which is the most commonly used agent, often in combination with retinoic acid, corticosteroids, azelaic acid, kojic acid, and glycolic acid. Chemical peels are important modalities of physical therapy, other forms include lasers and dermabrasion. The end

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