RT Book, Section
A1 Hilal-Dandan, Randa
A1 Brunton, Laurence L.
SR Print(0)
ID 1127551379
T1 Pharmacotherapy of Inflammation, Fever, Pain, and Gout
T2 Goodman and Gilman's Manual of Pharmacology and Therapeutics, 2e
YR 2016
FD 2016
PB McGraw-Hill Education
PP New York, NY
SN 9780071769174
LK accessbiomedicalscience.mhmedical.com/content.aspx?aid=1127551379
RD 2024/04/18
AB The  chapter  describes  the  nonsteroidal  anti-inflammatory  drugs  (NSAIDs)  used  to  treat  inflammation,  pain,  and  fever  and  the  drugs  used  for  hyperuricemia  and  gout.  The  NSAIDS  are  first  considered  by  class,  then  by  groups  of  chemically  similar  agents  described  in  more  detail.  Many  of  the  basic  properties  of  these  drugs  are  summarized  in  Tables  34–2,  34–3,  and  34–4.  Most  currently  available  traditional  NSAIDs  (tNSAIDs)  act  by  inhibiting  the  prostaglandin  (PG)  G/H  synthase  enzymes,  colloquially  known  as  the  cyclooxygenases  (COXs;  seeChapter  33).  The  inhibition  of  cyclooxygenase-2  (COX-2)  is  thought  to  mediate,  in  large  part,  the  antipyretic,  analgesic,  and  anti-inflammatory  actions  of  tNSAIDs,  while  the  simultaneous  inhibition  of  cyclooxygenase-1  (COX-1)  largely  but  not  exclusively  accounts  for  unwanted  adverse  effects  in  the  GI  tract.  Selective  inhibitors  of  COX-2  (celecoxib,  etoricoxib,  lumiracoxib)  are  a  subclass  of  NSAIDs.  Aspirin  irreversibly  acetylates  COX;  several  structural  subclasses  of  tNSAIDs,  including  propionic  acid  derivatives  (ibuprofen,  naproxen),  acetic  acid  derivatives  (indomethacin),  and  enolic  acids  (piroxicam)  compete  in  a  reversible  manner  with  arachidonic  acid  (AA)  at  the  active  site  of  COX-1  and  COX-2.  Acetaminophen  (paracetamol)  is  effective  as  an  antipyretic  and  analgesic  agent  at  typical  doses  that  partly  inhibit  COXs,  has  only  weak  anti-inflammatory  activity,  and  exhibits  fewer  GI  side  effects  than  the  tNSAIDs.