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Post Inflammation

Hyperpigmentation &
Hypopigmetation
DR. Dr. Yuli Kurniawati, SpKK(K), FINSDV, FAADV
Dept. Dermatology & Venereology
Faculty of Medicine Sriwijaya University/
Moh Hoesin General Hospital Palembang

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Postinflammatory
hyperpigmentation / PIH

 Sinonim : hipermelanosis pasca inflamasi

 PIH : Acquired excess of melanin pigment


following cutaneous inflammation or injury.

 Common , significant cosmetic and


psychosocial consequences

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Postinflammatory
hyperpigmentation / PIH

 Sinonim : post inflammation hypermelanosis

 PIH : Acquired excess of melanin pigment


following cutaneous inflammation or injury.

 Common , significant cosmetic and


psychosocial consequences

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Epidemiology
 >>> darkly pigmented skin
 Occur at any age , Male = Female

Pathogenesis :
 Epidermal type :
 increases melanin production and/or
transfer to keratinocytes
 role of inflammatory mediators (PG, LTs)

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Pathogenesis...

Dermal type
Melanin enter to dermis 
Damaged phagocytosed by and subsequently
basement resides within dermal macrophages
membane
( melanophages)

Macrophages Melanin
migrate into within dermal
epidermis,  melanophages Persisten
phagocytose  persist to PIH
melanosomes  long periods
Return to dermis

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Clinical features
 Asymptomatic hyperpigmented macules and
patches

 Tan to dark brown ( epidermal type)

 Gray blue to gray brown ( dermal type)

 Distribution and pattern provide clues to the


underlying etiology

 Exacerbated by continued inflammation, trauma


or exposure to UV iiradiation

 Dermal type  persist sometimes permanent

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Post inflammatory
hyperpigmentation
after varicella

PIH after acne

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Pathology
 Characterized :
increased pigment in keratinocytes 
epidermal type
Increased melanophages within dermis
dermal type

- Diferential Diagnosis

- Eryhtema dyschromicum persisten


- Melasma
- Pityriasis versicolor

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HIPOPIGMENTASI PASCA
INFLAMASI (HPI)

 Penyebab tersering kelainan


hipopigmentasi yg didapat
 Penyebab proses inflamasi kulit,
trauma, terapi dermatologi
 Stop Penyebab Sembuh spontan
 Destruksi total melanosit
Permanen HPI

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ETIOPATOGENESIS

 Unknown
 “kecenderungan kromatik
individual”  respon individu thdp
inflamasi/trauma  pengaruh
melanosit
 Autosomal dominan genetik

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inflamasi

Keratinosit & melanosit

Sitokin & mediator inflamasi


IFNγ, TNFα, TNFβ, IL-6, IL-7, ICAM-1

Destruksi melanosit

Reduksi melanosit, produksi


melanin, distribusi melanin
inadekuat
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Treatment

Hypo Disorders skin color Hyper


Pigmentation Pigmentation

Erythema,
etc
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Treatment post inflammation
hyperpigmentation
 Provided the underlying diseases
 Sun protection  daily board spectrum
sunblok
 Hidroquinon 2-4 % topical  3-6 month
 Azelaic acid , AHA ( alfa Hidroxy acid )
 Laser Th/  Q switched ruby,
alexandrite, ND-Yag  variably
successful in removing dermal pigment

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Treatment post inflammation
hypopigmentation
 Depend on causal  underlying
diseases
 Fototerapi
 Psoralen
 L-fenilalanin
 Levodopa
 Sunblock
 Antioxidant

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