PMID- 27698552
OWN - NLM
STAT- MEDLINE
DCOM- 20170517
LR  - 20220409
IS  - 1177-8881 (Electronic)
IS  - 1177-8881 (Linking)
VI  - 10
DP  - 2016
TI  - Profile of adalimumab and its potential in the treatment of uveitis.
PG  - 2997-3003
AB  - Uveitis refers to the presence of intraocular inflammation, and as a strict 
      definition compromises the iris and ciliary body anteriorly and the choroid 
      posteriorly (the uvea). Untreated, uveitis can lead to visual loss or blindness. 
      The etiology of uveitis can include both infectious and noninfectious (usually 
      immune-mediated) causes, the latter of which are often mediated predominantly by 
      Th1 CD4(+) T-cells that secrete proinflammatory cytokines. Tumor necrosis 
      factor-alpha (TNF-alpha) is a proinflammatory cytokine involved in the pathogenesis 
      of uveitis, which at high concentrations can cause excess inflammation and tissue 
      damage. Adalimumab is a recombinant human IgG1 monoclonal antibody specific for 
      human TNF-alpha. Historically, corticosteroids and methotrexate were used to treat 
      uveitis; however, newer biologic agents such as adalimumab have revolutionized 
      therapy for noninfectious uveitis. Adalimumab has shown efficacy in treating 
      refractory uveitis in multiple settings, including idiopathic disease, juvenile 
      idiopathic arthritis, sarcoidosis, Behcets disease, and uveitis secondary to 
      spondyloarthropathies, among several other noninfectious uveitis conditions. In 
      this paper, we will review the profile of adalimumab, the role of TNF-alpha in 
      uveitis, discuss safety data, and summarize key articles evaluating the efficacy 
      of adalimumab in treating uveitis secondary to the most commonly associated 
      autoimmune diseases.
FAU - Balevic, Stephen J
AU  - Balevic SJ
AD  - Department of Pediatric Rheumatology, Duke University Medical Center, Durham, NC, 
      USA.
FAU - Rabinovich, C Egla
AU  - Rabinovich CE
AD  - Department of Pediatric Rheumatology, Duke University Medical Center, Durham, NC, 
      USA.
LA  - eng
GR  - T32 GM086330/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20160919
PL  - New Zealand
TA  - Drug Des Devel Ther
JT  - Drug design, development and therapy
JID - 101475745
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - FYS6T7F842 (Adalimumab)
RN  - YL5FZ2Y5U1 (Methotrexate)
SB  - IM
MH  - Adalimumab/*pharmacology/*therapeutic use
MH  - Antibodies, Monoclonal, Humanized/*therapeutic use
MH  - Arthritis, Juvenile/*complications/*drug therapy
MH  - Humans
MH  - Immunoglobulin G/*therapeutic use
MH  - Methotrexate/chemistry/*pharmacology
MH  - Sarcoidosis/*drug therapy
MH  - Tumor Necrosis Factor-alpha/chemistry/*immunology/metabolism
MH  - Uveitis/*drug therapy
PMC - PMC5034916
OTO - NOTNLM
OT  - TNF-alpha
OT  - adalimumab
OT  - autoimmune disease
OT  - uveitis
EDAT- 2016/10/05 06:00
MHDA- 2017/05/18 06:00
PMCR- 2016/09/19
CRDT- 2016/10/05 06:00
PHST- 2016/10/05 06:00 [entrez]
PHST- 2016/10/05 06:00 [pubmed]
PHST- 2017/05/18 06:00 [medline]
PHST- 2016/09/19 00:00 [pmc-release]
AID - dddt-10-2997 [pii]
AID - 10.2147/DDDT.S94188 [doi]
PST - epublish
SO  - Drug Des Devel Ther. 2016 Sep 19;10:2997-3003. doi: 10.2147/DDDT.S94188. 
      eCollection 2016.