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L6                                                Dermatology                                       D. Alaa  

Disorders of Pigmentation 

Causes of hypopigmentation 

  Infection:  pityriasis versicolor  
  Postinflammmatory hypopigmentation: psoroiasis, diaper rash  
  Pityriasis alba: mild type of atopic dermatitis 
  Hereditary diseases: piebaldism and oculocutaneous albinism(OCA)  
  Chemical : rubber 
  Pharmacological: topical and intralesional steroids 
  Idiopathic: vitiligo 

Vitiligo 

It affect 0.5-2% of general population worldwide 

Average age of onset is 20 years but any age can be inflicted by this disease 

Characterized by absence or decrease of melanocytes reflected by absence or decreased DOPA-
positive melanocytes 

Pathogenesis   

Genetic:

 

Environmental:

 

Autoimmune theory:

 

 

Humoral immunity

association with other auto-immune diseases in particular hypo and 

hyper thyroidism in addition to Addison’s , DM etc… 

 

Cellular immunity:

 T cells that infiltrate perilesional epidermis are predominantly CD8 T 

cells  

Intrinsic defects of melanocytes theory:

 They found there is a dilatation in rough endoplasmic 

reticulum of melanocyes in perilesional skin 

Defective free radical defense:

 H2O2 overproduction in lesional skin leads to   oxidative damage 

of melanocytes  

Neural theory:

 especially in segmental vitiligo. They  believe  that  neuropeptides released from 

nerve endings cause decreased melanin production  

Viral theory: 

cytomegalovirus DNA has been identified in skin biopsy specimen of some patients 

with vitiligo, causing damage to melanocytes  


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Clinical Presentation 

  Present as asymptomatic, non-scaly depigmented macules and patches 
  Affect mostly face (periorificial), hands, knees, elbows, ankle, nipple, anogenial  
  Can  present  as  isolated  localized  patch  of  grey  or  white  hair  (poliosis)  or  as  premature 

diffuse graying of hair ( canities) 

Classification 

  Localized 
  Unilateral (segmental): stop abruptly at the medline 
  Acrofacial: affect extremities and face  
  Generalized 

Treatment 

If less than 20% of BSA is affected by vitiligo: 

  Topical corticosteroids: first option  
  Topical immunosuppressant e.g. tacrolimus and topical pseudocatalase  
  Surgery: punch graft and cultured melanocytes for vitiligo unresponsive to topical Rx 

If more than 20% of BSA is affected by vitiligo:  

  Narrowband UVB(311 nm): first choice  
  Psoralen  plus  phototherapy(PUVA):  psoralen  can  be  applied  topically(topical  PUVA)  or 

oral (oral PUVA) followed by exposure to artificial UV light or natural sunlight. 

  Excimer laser 
  Permanent depigmentation: e.g. monobenzyl ether of hydroquinone is used when vitiligo 

involve more than 50% of BSA and unresponsive to phototherapy 

  Others:  systemic anti-oxidant  

Piebaldism 

Autosomal  dominant,  cc  by    stable  depigmented  patches  on  anterior  trunk,  mid  extremities,  
forehead and frontal scalp(white forelock), sparing the back 

Present at birth 

The involved skin has no melanocytes  

Treatment:  topical  steroid  and  phototherapy  is  not  effective.  Auto  graft  from  normal  skin    is 
successful 

 

 

 


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Oculocutaneous albinism(OCA) 

Autosomal recessive group of diseases characterized by diffuse pigmentary dilution due to partial 
or  total  absence  of  melanin  in  skin,  hair  follicles  and  eyes  despite  the  normal  number  of 
melanocytes in skin 

Eyes may be affected by decreased visual acuity, nystagmus and photophobia 

Those patient are at increased risk for skin cancer 

Treatment is photoprotection, photoprotection and photoprotection 

Causes of hyperpigmentation 

  Infection: Pityriasis versicolor 
  Drug-induced : amiodarone, minocycline  
  Postinflammatory hyperpigmentation: lichen planus and fixed drug eruption 
  Erythema ab igne: net-like hyperpigmentation due to long-term exposure to heat e.g. laptop 

on the thighs 

  Idiopathic: melasma 

Melasma 

Synonyms: chloasma, mask of pregnancy 

It is most prevalent among young to middle aged women 

Hispanic, Asian, African or middle eastern descent are inflicted by this disease 

Pathogenesis 

  Exposure to UV : improvement or disappearance  of lesion in winter, involvement of sun-

exposed areas and sparing of philtrum  

  Genetic/ethnic  predisposition : Mostly it is related to darker skin type 
  Hormones: OCP, pregnancy (appearnace or exacerbation) 
  Autoimmune thyroid diseases 

Clinical features 

  Brown patches on the face, but may affect extensor forearm and central upper chest 
  May lighten or disappear after delivery in light skinned women  

Treatment 

  Sun protection, sun protection and sun protection 
  Hydroquinone  (tyrosinase inhibitor).  Side  effects: allergic and irritant contact dermatitis, 

ochronosis  

  Others: Chemical peels: using salicylic acid and glycolic acid and laser  

 


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Ochronosis 

There are two types; 

1)  Exogenous:  due  to  prolonged  application  of  hydroquinone,  and  products  containing 

mercury, resorcinol  

2)  Endogenous: Autosomal recessive due to mutation  in homogentisic acid oxidase.  

Macular amyloidosis 

  Pruritic confluent or rippled hyperpigmented macules and patches 
  Mostly involve upper back and forearms 
  Women affected more than men 
  local  friction  from  nylon  brushes,  towels  and  other  rough  materials  contributes  to  the 

production of this disease 

 

Treatment

: breaking itch-scratch cycle , stopping friction e.g. brush  use addition to use  of 

topical steroids plus keratolytics 

 

Drug Reactions 

Epidemiology 

  The skin is one of the most common targets for adverse drug reactions 
  Women are more susceptible than men 
  Paradoxically, the incidence of most immunologically mediated drug eruptions is increased 

in the setting of immunosuppression; for example, in patients with AIDS  

  The incidence of adverse reactions also increases with the age of the patient 
  Time interval between drug introduction and skin eruption because most of drug eruption 

occurs within 1-3 weeks after initiation of new   

Treatment 

1.  Withdrawal of suspect drug as soon as possible 
2.  If many drugs are incriminated, stop all non-essential drugs 
3.  If the suspect drug is essential, substitute with another that does not cross-react 
4.  For mild drug eruption, start topical steroid  and for severe drug eruption such as  SJS/TEN 

and DRESS, start systemic steroids 

Clinical type 


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Note

:  

  Stevens-Johnson syndrome: if less than 10% of body surface area is involved 
  Toxic epidermal necrolysis when more than 30% of body surface area is involved 

 

 

 

Mubark A. Wilkins 




رفعت المحاضرة من قبل: Mubark Wilkins
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