PMID- 10499831
OWN - NLM
STAT- MEDLINE
DCOM- 19991109
LR  - 20131121
IS  - 0306-9877 (Print)
IS  - 0306-9877 (Linking)
VI  - 53
IP  - 1
DP  - 1999 Jul
TI  - Inhibition of TNF-alpha synthesis with thalidomide for prevention of acute 
      exacerbations and altering the natural history of multiple sclerosis.
PG  - 76-7
AB  - Multiple sclerosis (MS) is a common neurological disorder which has a 
      relapsing/remitting course and is presently incurable. A variety of agents have 
      been tried to prevent excerbations and alter the natural history of the disease. 
      Tumor necrosis factor-alpha (TNF-alpha) has been implicated as the most important 
      cytokine in the pathogenesis of MS. There is evidence that thalidomide is an 
      agent which blocks production of TNF-alpha by a mechanism different from other 
      agents. Hence it is hypothesized that using thalidomide as therapy would prevent 
      acute exacerbations of MS as well as alter its natural history.
FAU - Sastry, P S
AU  - Sastry PS
AD  - Leukaemia/Myeloma Unit, Royal Marsden Hospital, Sutton, Surrey, UK.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 4Z8R6ORS6L (Thalidomide)
SB  - IM
MH  - Disease Progression
MH  - Humans
MH  - Models, Neurological
MH  - Multiple Sclerosis/*drug therapy/physiopathology
MH  - Thalidomide/*therapeutic use
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
EDAT- 1999/09/28 00:00
MHDA- 1999/09/28 00:01
CRDT- 1999/09/28 00:00
PHST- 1999/09/28 00:00 [pubmed]
PHST- 1999/09/28 00:01 [medline]
PHST- 1999/09/28 00:00 [entrez]
AID - S0306-9877(97)90719-2 [pii]
AID - 10.1054/mehy.1997.0719 [doi]
PST - ppublish
SO  - Med Hypotheses. 1999 Jul;53(1):76-7. doi: 10.1054/mehy.1997.0719.