TY  - CHAP
M1  - Book, Section
TI  - Drug-Induced Lupus
A1  - Yazdany, Jinoos
A1  - Manno, Rebecca L.
A2  - Papadakis, Maxine A.
A2  - McPhee, Stephen J.
A2  - Rabow, Michael W.
A2  - McQuaid, Kenneth R.
PY  - 2022
T2  - Current Medical Diagnosis & Treatment 2022
AB  - Drug-induced  lupus  shares  several  clinical  and  serologic  features  with  SLE  but  is  due  to  ongoing  exposure  to  a  drug  and  resolves  when  the  offending  drug  is  discontinued.  In  contrast  to  SLE,  the  sex  ratio  is  nearly  equal.  As  a  general  rule,  drug-induced  lupus  presents  with  fever,  arthralgia,  myalgia,  and  serositis  but  not  renal  involvement,  neurologic  symptoms,  or  other  features  of  SLE.  Serologic  testing  reveals  elevated  titers  of  antinuclear  antibodies  in  all  patients,  but  antibodies  to  DNA,  Sm,  RNP,  SS-A,  and  SS-B  are  rare.  Antibodies  to  histones  are  common  but  also  are  seen  in  SLE  and  thus  do  not  distinguish  drug-induced  lupus  from  SLE.  Complement  levels  are  usually  normal.  The  list  of  drugs  implicated  as  possible  causes  of  drug-induced  lupus  in  observational  studies  and  case  reports  is  extensive  (eTable  20–2).  There  are  definite  associations  between  the  development  of  drug-induced  lupus  and  the  use  of  hydralazine,  isoniazid,  and  minocycline  as  well  as  several  medications  no  longer  commonly  prescribed  (procainamide,  quinidine,  methyldopa,  chlorpromazine).  The  incidence  of  drug-induced  lupus  in  patients  taking  hydralazine  for  a  year  or  longer  is  as  high  as  5–8%;  for  most  other  medications,  the  risk  is  considerably  lower  (less  than  1%).  TNF  inhibitors  can  induce  antibodies  to  DNA,  but  the  incidence  of  lupus-like  syndromes  resulting  from  these  medications  is  low  (0.5–1%).  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/19
UR  - accessmedicine.mhmedical.com/content.aspx?aid=1184193104
ER  -