PMID- 15990071
OWN - NLM
STAT- MEDLINE
DCOM- 20051013
LR  - 20071114
IS  - 1568-9972 (Print)
IS  - 1568-9972 (Linking)
VI  - 4
IP  - 5
DP  - 2005 Jun
TI  - Subacute cutaneous lupus erythematosus: 25-year evolution of a prototypic subset 
      (subphenotype) of lupus erythematosus defined by characteristic cutaneous, 
      pathological, immunological, and genetic findings.
PG  - 253-63
AB  - Subacute cutaneous lupus erythematosus (SCLE) represents a widespread, 
      photosensitive, nonscarring, nonindurated form of lupus erythematosus 
      (LE)-specific skin disease. SCLE lesions are associated with a distinctive 
      immunogenetic background including the production of Ro/SS-A autoantibodies. 
      Individuals who have SCLE skin lesions as a component of their presenting 
      illnesses represent a distinctive subset (subphenotype) of LE that enjoys a good 
      prognosis with respect to life-threatening systemic manifestations of LE. SCLE 
      skin lesions can be triggered by a number of different drugs the majority of 
      which are capable of producing photosensitivity drug reactions in nonlupus 
      patients. Single agent or combination aminoquinoline antimalarial therapy will 
      suffice for 75% of SCLE patients. The remaining 25% will require other forms of 
      systemic antiinflammatory therapy (e.g., diaminodipenylsulfone (Dapsone), 
      thalidomide) or systemic immunosuppressive-immunomodulatory therapy. The 
      etiopathogenesis of SCLE skin lesions is thought to result from four sequential 
      stages: (1) inheritance of susceptibility genes (HLA 8.1 ancestral haplotype [C2, 
      C4 deficiency, TNF-alpha-308A polymorphism], C1q deficiency); (2) loss of 
      tolerance/induction of autoimmunity (ultraviolet light, photosensitizing 
      drugs/chemicals, cigarette smoking, infection, psychological stress); (3) 
      expansion/maturation of autoimmune responses (high levels of autoantibodies 
      (Ro/SS-A), immune complexes, autoreactive T-cells); and (4) tissue injury/disease 
      induction resulting from various autoimmune effector mechanisms (e.g., direct T 
      cell-mediated cytotoxicity, antibody-dependent cell-mediated cytotoxicity).
FAU - Sontheimer, Richard D
AU  - Sontheimer RD
AD  - Department of Dermatology, University of Iowa Carver College of Medicine, Iowa 
      City, IA 52242, United States. richard-sontheimer@uiowa.edu
LA  - eng
GR  - AR019101/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
DEP - 20041112
PL  - Netherlands
TA  - Autoimmun Rev
JT  - Autoimmunity reviews
JID - 101128967
SB  - IM
MH  - Humans
MH  - *Lupus Erythematosus, Cutaneous/genetics/immunology/pathology/physiopathology
MH  - Skin/immunology/*pathology
RF  - 40
EDAT- 2005/07/02 09:00
MHDA- 2005/10/14 09:00
CRDT- 2005/07/02 09:00
PHST- 2004/10/22 00:00 [accepted]
PHST- 2005/07/02 09:00 [pubmed]
PHST- 2005/10/14 09:00 [medline]
PHST- 2005/07/02 09:00 [entrez]
AID - S1568-9972(04)00214-9 [pii]
AID - 10.1016/j.autrev.2004.10.003 [doi]
PST - ppublish
SO  - Autoimmun Rev. 2005 Jun;4(5):253-63. doi: 10.1016/j.autrev.2004.10.003. Epub 2004 
      Nov 12.