RT Book, Section
A1 Crowson, A. Neil
A1 Magro, Cynthia M.
A1 Janin, Anne
A1 Barnhill, Raymond L.
A2 Barnhill, Raymond L.
A2 Crowson, A. Neil
A2 Magro, Cynthia M.
A2 Piepkorn, Michael W.
A2 Kutzner, Heinz
A2 Desman, Garrett T.
SR Print(0)
ID 1178392603
T1 Disorders of Pigmentation
T2 Barnhill's Dermatopathology, 4e
YR 2020
FD 2020
PB McGraw Hill Education
PP New York, NY
SN 9780071828222
LK dermatology.mhmedical.com/content.aspx?aid=1178392603
RD 2024/10/06
AB The  sources  of  pigment  that  cause  hyperpigmentation  of  the  skin  range  from  endogenous  products  such  as  melanin  and  hemosiderin  to  exogenous  agents  such  as  tattoo  dyes,  ingested  metals,  and  drugs.  In  some  instances,  these  agents  combine  to  produce  hyperpigmentation.  For  example,  in  argyria-  and  chlorpromazine-related  hyperpigmentation,  silver  particles  along  with  melanin  and  drug  metabolites  plus  melanin,  respectively,  contribute  to  dyschromasia.  Ultraviolet  (UV)  rays  often  enhance  pigmentation,  so  sun-exposed  skin  shows  more  intense  discoloration.  When  the  epidermis  is  heavily  melanized,  pigment  incontinence  may  result  in  upper  dermal  melanization  as  well.  Disorders  of  hypopigmentation  and  depigmentation  are  caused  mainly  by  damage  to  and  dysfunction  of  epidermal  melanocytes  (Figs.  15-1  and  15-2).  In  some  congenital  diseases  (eg,  piebaldism),  melanocytes  are  absent,  and  in  other  conditions  (eg,  idiopathic  guttate  hypomelanosis)  the  melanocytes  are  dysfunctional  with  rudimentary  dendritic  processes.  The  circulation  of  blood  through  the  superficial  capillary  plexus  may  influence  the  skin  color,  as  evidenced  by  nevus  anemicus.  Both  hyper-  and  hypopigmentations  may  be  congenital  or  hereditary,  postinflammatory,  or  induced  by  chemicals  and  foreign  materials.