This document discusses nonsteroidal anti-inflammatory drugs (NSAIDs), including their uses for pain, fever, and inflammation. It classifies NSAIDs based on their chemistry and half-lives. The mechanisms of NSAID action and their therapeutic effects such as analgesia, antipyresis, and anti-inflammation are described. Adverse effects involving the gastrointestinal tract and kidneys are also summarized. Specific NSAIDs like aspirin, diclofenac, ketorolac, and tolmetin are highlighted regarding their pharmacology, administration, and indications.

1. NONSTEROIDAL ANTI-INFLAMMATORY
DRUGS (NSAIDS)

3. PAIN: NSAIDs are mild analgesics effective in pain due to
inflammation.
FEVER:
Infection, tissue damage, inflammation, graft rejection,
malignancy or other disease
Cytokines (IL-1 , IL6, interferons
 & 
PGE2 (preoptic anterior hypothalamic (POAH) area)
Increases body temperature

4. INFLAMMATION
Acute transient phase (vasodilatation, ↑ vascular permeation)
Delayed subacute phase (infiltration of macrophages)
Chronic proliferative phase (degeneration & fibrosis).

6. CLASSIFICATION : (BASED ON CHEMICALLY)
A. NONSELECTIVE COX INHIBITORS (TRADITIONAL NSAIDs)
1. DRUGS WITH ANALGESIC & MARKED ANTIINFLAMMATORY ACTION
A. SALICYLATES
B. PYRAZOLONE DERIV.
ASPIRIN, BENORYLATE, DIFLUNISAL
PHENYLBUTAZONE, OXYPHENBUTAZONE
C. ACETIC ACID DERIV.
D. INDOLE DERIV.
E. ENOLIC ACIDS DERIV.
DICLOFENAC, ACELOFENAC, TOLMETIN, KETOROLAC,
INDOMETHACIN, SULINDAC
OXICAM: PIROXICAM, TENOXICAM,
BENZOTRIAZINE: AZAPROPAZONE
2. DRUGS WITH ANALGESIC & MODERATE ANTIINFLAMMATORY ACTION
A. PROPIONIC ACID DERIV.
B. ANTHRANILIC ACID DERIV. (FENAMATES)
IBUPROFEN, NAPROXEN, FENOPROFEN, FLURBIPROFEN
MEPHENAMIC ACID,
MECLOFENAMIC ACID
3. DRUGS WITH ANALGESIC & NEGLIGIBLE ANTIINFLAMMATORY ACTION
A. PARA-AMINOPHENOL DERIV. PARACETAMOL (ACETAMINOPHEN)

7. CLASSIFICATION : (BASED ON CHEMICALLY)
B. SELECTIVE COX-2 INHIBITORS
A. PREFERENTIAL COX-2
INHIBITORS
A. SULFONANILIDES : NIMESULIDE
B. PHENYL ACETIC ACID DERIV.
CONT…..
B. SELECTIVE COX-2 INHIBITORS
(COXIBS)
CELECOXIB
PARECOXIB
C. OXICAM : MELOXICAM
D. ALKANONES : NABUMETONE
E. INDOLE ACETIC ACID :
ETODOLAC
ETORICOXIB
LUMIRACOXIB
F. PROPIONIC ACID : ZALTOPROFEN

8. CLASSIFICATION : (BASED ON CHEMICALLY) CONT…..
C. MISCELLANEOUS
1. AMINOPYRIDINE DERIV. FLUPIRTINE
2. PYRAZOLONE DERIV.
3. ATYPICAL NSAIDs
METAMIZOL (DIPYRONE),
PROPYPHENAZONE
NEFOPAM, DIACEREIN

9. CLASSIFICATION : (BASED ON HALF LIFE)
SHORT – MEDIUM HALF LIFE
(< 6 HRS)
ASPIRIN
DICLOFENAC
LONG HALF LIFE
(>10 HRS)
DILFLUNISAL
NAPROXEN
IBUPROFEN
INDOMETHACIN
KETOPROFEN
PHENYLBUTAZONE
PIROXICAM
SULINDAC

10. NSAIDS
ANALGESIC
EFFECT
ANTIPYRETIC
EFFECT
THERAPEUTIC
EFFECTS OF
NSAIDs
ANTI-
INFLAMMATORY
EFFECT
RELIEF OF DYS-
MENORRHOEA

11. NSAIDS
HSR &
GIT – mucosal
ANAPHYLACTOID RN
irritation, damage
– asthma, rhinitis,
urticaria,
& bleeding
angioneurotic
oedema
TOXIC EFFECTS
OF NSAIDs
RENAL TOXICITY –
on prolonged use
HA

12. BOTH THERAPEUTIC EFFECT & SIDE EFFECT
DEPENDING UPON THE CONDITION
ACTION
1. Effect on platelet
(antiplatelet action)
2. Effect on ductus
arteriosus
TE
Useful in post MI &
post stroke patients
Helps in closure of
ductus arteriosus after
the birth
SE
Prolonged bleeding
time in other patients
Early closure of ductus
arteriosus if used
during labour
Prolongation of labour
3. Effect on labour Prevents premature
labour before term in full term

13. ASPIRIN
Acetyl salicylic acid
Rapidly converted in the body to salicylic acid
Acetylation of certain macromolecules including COX
Oldest analgesic - anti-inflammatory drugs

14. PHARMACOLOGICAL ACTION
1. Analgesic, antipyretic, anti-inflammatory actions:
Headache, myalgia, arthralgia, acts mainly by peripheral + CNS.
( high dose ↑ body temp)

2. Metabolic effects: High dose Convulsion, Depression, Confusion, Dizziness, Tinnitus,
Coma, Stupor, Vomiting …
3. Respiration: Stimulated by peripheral CO2 production ↓ sensitivity to CO
 2 at medulla..
4. Acid – base & electrolyte balance: ND Respiratory alkalosis
 renal excretion of
bicarbonate , K+, Na+..
HD Respiratory depression
 respiratory acidosis..

15. PHARMACOLOGICAL ACTION
5. CVS : ND no direct effect, HD Non-cardiogenic pulmonary oedema, TD central
  
vasomotor paralysis.
6. GIT: Epigastric distress, Nausea, Vomiting..
Hepatic : Restricted in hepatitis, In Children with influenza Reye’s syndrome.
7. Urate excretion: LD 1-2g/ days
 ↓ urate excretion,
HD > 5g/ day
 Uricosuria.
8. Blood: Prolongation of bleeding time (4-7 days)

16. PHARMACOKINETICS
Stomach/intestinal absorption & PB 80%
Conjugated with glycine or glucuronic acid
Excreted by glomerular filtration & tubular secretion
t1/2 15-20min, salicylic acid 8-12 hrs

18. ADR
Common:Nausea, vomiting,
epigastric distress, peptic ulcer.
Hypersensitivity:Urticaria,
rashes, angioedema, rhinorrhoea
etc.,,
Salicylism: Dizziness, tinnitus,
vertigo,mentalconfusion,
hyperventilation& electrolyte
imbalance

20. ACUTE POISONING
Dehydration, electrolyte imbalance, restlessness, delirium, hallucination,
convulsions, coma, death due to respiratory failure + CV collapse.
Treatment:
Respiration support
IV. electrolytes
Vitamin K
Hemodialysis
Alkaline diuresis
Blood transfusion

21. USES
1. As analgesic
2. As antipyretic
3. Acute rheumatic fever
4. RA
5. Osteoarthritis
6. Post myocardial infarction & post stroke
7. Others : Pregnancy – induced hypertension
Patent ductus arteriosus,
Familial colonic polyposis,
Prevention of colon cancer,
To prevent flushing attending nicotinic acid ingestion
& pre – eclampsia

22. PYRAZOLONE DERIVATIVES
Phenylbutazone:
Good anti-inflammatory action but week analgesic & antipyretics
Phenylbutazone is converted
ADME
to oxyphenbutazone (active metabolite)
Complete absorption & 98% PB
Hydroxylation & Glucuronidation & t½ = 60hrs
Dose: 100-200 mg

23. ADR: They are no more used because of serious
GIT toxicity
↑ in circulatory volume due to significant Na+ & H2O retention
Hypersensitivity reactions..
CNS side effects
Bone marrow depression
Steven Johnson's syndrome (SJS)
Hepatitis & Stomatitis
Goiter & Hypothyroidism (Prolonged use)
Interaction: Warfarin, Sulphonamides, Tolbutamide, Imipramine

24. Use: Rheumatoid arthritis (RA),
Osteoarthritis (OA) &
Ankylosing spondylitis (AS)

25. Oxyphenbutazone : Metabolite of Phenylbutazone
Metamizole (Analgin):
Analgesic & Antipyretic
Causes Agranulocytosis
Propyphenazone (Saridon):
Analgesic & Antipyretic Better tolerated
No Agranulocytosis

26. ACETIC ACID DERIVATIVES
Diclofenac Sodium:
Analgesic, Anti-inflammatory, Antipyretic = Naproxen
No antiplatelet action Does not block the Cardio Protective effect of Aspirin
(Low dose) May increase risk of
 HA & Stroke
Some selectivity for COX-2
ADME:
Oral, 99% PB,
Metabolized by CYP2C to hydroxyl derivative
Excreted in unchanged form in urine (< 1 % )
t1/2 = 1.1 hrs, Synovial conc. 3 fold longer than serum.

27. Adverse effects:
Mild epigastric distress, rashes, headache, dizziness
Its K+ salts is preferred to avoid volume overload
Diclofenac + Misoprostol ↓ upper GIT ulceration, may result in
diarrhoea
Diclofenac + Omeprazole Prevention of recurrent bleeding, renal
ADR common..
Dose 150 mg/d Impair renal blood flow & GF rate, elevation of serum
aminotransferases more common in diclo. than other NSAIDS..
Dose: 100-200 mg BD / TDS, 75 mg in IM

28. Preparation:
0.1% Ophthalmic prep. Prevention of postoperative ophthalmic
inflammation, after IOLs implantation & Strabismus surgery
3% Topical gel Solar keratosis
Rectal Suppository Pre-emptive analgesia & Post operative
nausea…
Oral mouthwash & IM injection

29. Uses:
RA, OA
AS (100-200 mg /day, Oral)
Short term management of Acute Musculoskeletal Injury 
Tendonitis, Bursitis
Toothache
Dysmenorrhea (To relieve discomfort & Pain)
Renal colic
Post operative inflammatory pain &
Inflammation after cataract surgery

30. Aceclofenac:
Similar properties as Diclofenac Uses & ADR
More selectivity for COX-2
Chondroprotective action Due to ↑ synthesis of glycosaminoglycan
Dose : 100 mg BD
Bromfenac:
Not used in Systemically due to severe irreversible hepatic damage
Used in only Topically for Ocular inflammation

31. Tolmetin:
It efficacy similar to Aspirin (A, AP & AI)
It well absorbed in orally, 99% bound with plasma protein
t1/2 = 1 hr
It accumulate in synovial fluid for few hours (6hrs)
Approximately 7 % Excreted in unchanged form in urine
Dose: 400-600mg TDS
ADR: GIT, Increase in bleeding time, Nervousness, Anxiety, Insomnia
Uses: RA, OA, AS Equally effective as compared to Aspirin /
Indomethacin, but better tolerated in equally effective doses
Reduced GI side effect Given with Food / Milk..

32. Ketorolac:
Potent Analgesic with moderate Anti-inflammatory
Inhibits platelet aggregation
Post operative pain = Morphine
ADME:
It well absorbed in oral, 80% PPB
Metabolized by Glucuronidation
Approximately 60% unchanged form of drug excreted in urine
t1/2 = 5-7hrs

33. Adverse effects:
Pain at the site of injection, Dyspepsia, Ulceration, Loose stools,
Drowsiness, Head ache, Dizziness, Nervousness, Pruritus,
Renal toxicity
More than 5 day orally / 2 days IM/ IV High incidence of GI
bleeding & Bleeding at surgical site
Drug interaction: Avoided with Anti-coagulants due to
hematological toxicity

34. Uses:
Post operative pain (Good analgesic action & Alternative drug to Opioids)
Musculoskeletal pain
Dental
Renal colic
Migraine
Pain due to bone metastasis
Not used in obstetric analgesia or Preanesthetic medication
Used in topically for non infective conditions Ocular inflammation, Allergic
(seasonal) conjunctivitis
Dose: 15-30mg oral, 30-60 mg IM, 15-30 mg IV Maximum 90 mg / day

35. INDOLE DERIVATIVES
Indomethacin:
Potent Anti-inflammatory & Antipyretic
Potent nonselective COX inhibitor, may also inhibit Phospholipase A & C,
Reduced neutrophil migration & Decrease T- cell & B-cell proliferation…
ADME:
Oral, 90% PB
t1/2 = 2-3hrs
Metabolized in liver
Excreted by kidney

36. ADR:
GIT: 50% GI irritation, Nausea, Vomiting, GI bleeding, Diarrhea,
CNS: Frontal head ache, Ataxia, Mental confusion, Hallucination, Depression,
Psychosis, including suicide have been reported
Kidney: Renal papillary necrosis
Hepatic: Acute pancreatitis, Jaundice
Blood: Occult blood loss, Neutropenia, Thrombocytopenia, Aplastic anaemia,
Inhibition of platelet aggregation
Lungs: Precipitation of bronchial asthma in sensitive individuals
Interactions: Probenecid, Diuretics, β-blockers, ACE inhibitors.
Dose: 25-50mg BD/ QID

38. Uses:
To accelerate closure of patent ductus arteriosus (PDA)
Sweet’s syndrome
Its AI action drug of choice for acute gout, RA, OA, AS, Psoriatic arthritis, Juvenile RA
(it relief from pain, ↓ joint swelling, tenderness, duration of morning stiffness & ↑ grip strength)
Pleurisy
Nephrotic syndrome
Diabetes insipidus, Urticarial vasculitis
Post episiotomy pain
Prophylaxis of heterotopic ossification in arthroplasty
& Reduce pain after traumatic corneal abrasion
Ophthalmic Conjunctival inflammation
Dental Gingival inflammation
Epidural injections produce a degree of pain relief
(Post laminectomy syndrome)
similar to Methyl Prednisolone

40. Sulindac:
Fluorinated derivative of indomethacin
Sulfoxide Prodrug Reversible metabolized to active sulphide metabolite
About 90% absorbed orally
Excreted in bile & then reabsorbed from the intestine
Enterohepatic cycling prolongs the duration of action 12-16 hrs
It suppress the Familial Intestinal Polyposis It may inhibit the development of Colon,
Breast, Prostate cancer in humans
GI ulceration & Bleeding is less common than indomethacin
Renal toxicity is less Due to regeneration of sulindac sulfoxide from active sulphide

metabolite
Stevens – Johnson epidermal necrolysis syndrome, thrombocytopenia, agranulocytosis
Sometimes associated with cholestatic liver damage
Dose: 100-200mg BD

41. ENOLIC ACID DERIVATIVES
Piroxicam:
(OXICAM)
Efficacy (A, AP & AI) similar to Aspirin/ Indomethacin / Naproxen
Better tolerated than Aspirin/ Indomethacin RA, OA
Inhibit COX, lowering PG level in synovial fluid, inhibits
activation of neutrophils,
proteoglycan & collagens in cartilage; reduces rheumatoid factor (IgM).
ADME:
Well absorbed in orally, 99% PPB
Undergoes enterohepatic circulation
Hydroxylation & Glucuronide conjugation, t1/2 = 57 hr
Accumulate in synovial fluid for 1-2 weeks
Approximately 4-10 % Excreted in unchanged form in urine
Dose: 20 mg/ d ( A single daily dose is sufficient because of the long half life)

42. ADR:
GIT less than Indomethacin but more than Ibuprofen
Faecal blood loss
Skin rashes
Pruritus
Reduces urinary excretion of Lithium which is clinically significant
Uses:
RA (pain relief, ↓ joint swelling, duration of morning stiffness) & equally effective as Aspirin
It better tolerated though aspirin & It very cheaper than aspirin
OA but Paracetamol is preferred (no inflammation in joint) & Acute gout (not preferred due
to slow onset) but Indomethacin is preferred,
AS, Acute musculoskeletal disorder
Dysmenorrhea
Injury as analgesic
Best tolerated is Naproxen > Ibuprofen > Piroxicam > Indomethacin / Aspirin

43. OTHER OXICAMS:
Tenoxicam: Similar to Piroxicam
Lornoxicams: Peculiar amongst other Oxicam that its onset is rapid,
but it has short half life (4h)
Dose : 20 mg /d
Prodrugs of Piroxicam Ampiroxicam, Droxicam, Pivoxicam
Adv: Less GIT side effects
Some other oxicams: Cinnoxicam & Sudoxicam

44. Ibuprofen:
PROPIONIC ACID DERIVATIVES
Alternative to Aspirin in 1969
Better tolerated than Aspirin / Indomethacin
Analgesic (low doses < 2400 mg/ d ) but
Very commonly used NSAID
Equally
ADME:
not AI effect
& Safe amongst the t-NSAIDs.
effective & safe antipyretic as Paracetamol & used as an alternative to
Paracetamol in children
Well absorbed in orally, 90-99% PPB
Concentration achieved in brain & synovial fluid is significant & it cross placenta
Hydroxylated & Carboxylated metabolite
Urine & Bile
Half life = 2 hrs

45. Dose: 400 -600 mg , TDS ( Maximum 3200 mg/ day)
Uses:









Closing patent ductus arteriosus (PDA) in preterm infants (Oral & IV)
Fascia & Muscle ( Topical cream)
Cream more effective than placebo cream in the treatment of primary knee OA
Post surgical dental pain (Liquid gel - Ibuprofen 400mg)
Contraindications:
Nasal polyps
Angioedema
Bronchospastic reaction
Aseptic meningitis ( Patient with SLE –systemic lupus erythematosus)
Fluid retention
Ibuprofen + Aspirin Antagonizes the irreversible platelet inhibition induced by Aspirin Increased the
 
risk of CV
Ibuprofen + Aspirin Decrease the total AI effect

Dexibuprofen Dextro enantiomer of ibuprofen

46. Naproxen:
A single enantiomer NSAID, more potent than Aspirin
It is good A, AI action & Reduces morning stiffness in RA
Also inhibit leukocyte function More suitable for acute gout

ADME:
Oral, 99 % bound with PP
Its free fraction is significantly higher in women than in men
Half life (14 hrs) is similar in both sexes
Dose should be reduced in elderly as t1/2 is doubled in elderly
Naproxen & Its metabolites (demethylated) excreted in urine
ADR:
Upper GIT bleeding
Rare cases of allergic pneumonitis, leukocytoclastic vasculitis & pseudo porphyria
Dose: 375 mg bid

47. Uses:
Usual rheumatological condition
Ophthalmic preparation
Oral suspension
Topical preparation
Fenoprofen:
(Slow release formulation)
It causes severe side effect of Interstitial Nephritis
Ischaemia due to inhibition of local release of vasodilator PGs.
Half life is 2.5 hrs
Approximately 30% excreted unchanged form in urine
Dose: 600mg QID

48. Flurbiprofen:
More complex mechanism of action than other NSAIDs
(S) (-) enantiomer Inhibits COX non selectively – in
affect TNF –α, NO synthesis
rat tissues, also
Hepatic metabolism is extensive Its (R) (+) & (S) (-) enantiomer
metabolized differently It does not undergoes chiral conversion
It undergoes enterohepatic circulation
Half life is 3.8 hrs
Approximately < 1% excreted unchanged form in urine
Uses:
Inhibition of intraoperative miosis (0.03% Topical ophthalmic)
Perioperative analgesia in minor ear, neck & nose surgery (IV)
Sore throat (lozenges)
Dose: 300mg TID

49. Ketoprofen:
Antagonist action of bradykinin & may stabilize lysosomes
Rapidly absorbed on oral, 99% bound with PP
t1/2=2 hrs
conjugation & Excreted in urine
It undergoes glucuronide
Dyspepsia, abdominal discomfort are reduced when taken with food, milk / antacid
Causes fluid retention & increase in creatinine concentration in plasma
Dexketoprofen:
Enantiomer of ketoprofen
More potent (2 times) than ketoprofen
Used in short term treatment of mild to moderate pain & dysmenorrhoea
Dose : 25 mg TDS

50. Oxaprozin:
Well absorbed in orally achieving peak conc. 3-6 hrs.
Half life = 50-60 hrs, once a day or alternate day
It has some uricosuric action Suitable for gout
Tiaprofen & Carprofen :
Reduces
serum uric acid
absorption of uric acid
concentration by inhibiting renal tubular
Tiaprofen is short acting (t1/2= 1-2hrs) but t11/2 is doubled in elderly
Tiaprofen is used in oral & parenteral route

51. FENAMATES DERIVATIVES
Mefanamic acid:
It is an A, AP & weak AI
Analgesic action is both due to central as well as peripheral mechanism
It antagonizes some action of PGs
Half life = 2- 4 hrs
Excreted in urine & bile
ADR:
Dyspepsia
Upper GIT discomfort, Diarrhoea
Skin rashes
Dizziness
Haemolytic anaemia is rare
Avoid in children & During pregnancy

52. Uses:
Mainly used as Analgesic & Dysmenorrhoea
Maintenance treatment of RA & OA but not in initiation of therapy
Dose : 250-500 mg TDS
Meclofenamic acid & Flufenamic acid

53. PARA-AMINOPHENOL DERIVATIVES
Paracetamol (Acetaminophen):
Acetanilide is parent compound
It was introduced as antifebrin
& Its antipyretic action was discovered by chance
for the treatment of fever Highly toxic

with less toxicity Phenacetin (1887)
 used in
Search was made for antipyretic compound
many years Causes nephrotoxicity & Banned

Later, Von Mering was introduced Paracetamol (1893)
Both metabolites Acetanilide & Phenacetin

It was more frequently used since 1949.

54. Pharmacological action:
It is effective in A & AP, but negligible AI effect
It is weak inhibitor of COX in presence of high concentration of cyclic endoperoxides at the
inflammatory site Poor inhibitor of COX at periphery, but in CNS cyclic endoperoxides

concentration is less so it is more effective
Produces A & AP action due to CNS action
It not inhibit the neutrophils migration
It does not produce CV effect
No respiratory stimulant effect
No alteration of acid-base balance
It does not cause GI irritation / erosion & bleeding
No effect on platelet aggregation, bleeding time & uric acid excretion

55. ADME:
Rapid & complete on oral absorption
20-50% bound with PP
Half life = 2 hrs
It undergoes glucuronide (60%) (lesser
In
in
children than in adults) and glutathione (20%)
conjugation
overdose due to N-hydroxylation there is

formation of N-acetyl – p – benzoquinone
imine (NAPQI) highly reactive undergoes

glutathione conjugation converted to
mercapturic acid
Alcohol
is an inducer of CYP2E1 that
facilitates conversion of paracetamol to NAPQI
 
↑ paracetamol toxicity & fatal dose is
reduced to 5-6g in chronic alcoholics
Excreted in urine

56. ADR:
Nausea & rashes
In large doses taken Acute paracetamol poisoning adults (>10g)
Usually 150 mg / kg leads to poisoning & 250 mg/kg or more is almost fatal
Children are more susceptible Because their ability to conjugate by glucuronidation is poor.
Symptoms:
Nausea, vomiting, anorexia & abdominal pain during first 24 hrs
Hepatotoxicity
Manifestations
Nephrotoxicity
are seen within 2 – 4 days Includes increased serum transaminases,
jaundice, liver tenderness, prolonged prothrombin time & hepatic lesions
may results in acute renal failure in some patient

57. Treatment :
Stomach wash is given
Activated charcoal prevent further absorption
Antidote N- acetyl cysteine (NAC) 150 mg/ kg IV infusion over 15 min repeated as required
Oral loading dose 140 mg / kg followed by 70 mg/kg every 4 hrs
NAC Partly replenishes the glutathione stores of the liver & Prevents binding of toxic metabolites
to the cellular constituents
Alternate drugs: Methionine is a essential AA, A repletor of glutathione..
Uses:
Analgesic in painful conditions like toothache, headache & myalgia
As an antipyretic More safe & used in all age gp, During pregnancy & Lactation..

58. PARTIALLY SELECTIVE COX-2 INHIBITORS
Nimusulide:
It has A, AP & AI effect similar to other NSAIDs
Weak PG inhibitor & AI action may be contributed by other mechanism such
as inhibition of release of TNFα, synthesis of PAF, metalloproteinase in
cartilage, reduced production of superoxide by neutrophils
ADME:
Well absorbed in orally, 99% bound with pp
Half life is 3-5 hrs
Mostly excreted after metabolism

59. ADR:
Less GIT side effect
Heart burn, Nausea
Diarrhoea
Rashes, Pruritus
Sedation & Dizziness
Hepatic damage & Agranulocytosis & even death (it banned in India for children
age less then 12 years)
Uses:
RA in adults not responding to other NSAIDs
Effective in pain conditions with / without inflammation low backache, sinusitis,
sports injury, dysmenorrhoea, OA & fever
It is suitable for intolerant to Aspirin & other NSAIDs & Asthmatic patients

60. COX-2 INHIBITORS
Celecoxib, Parecoxib & Etoricoxib (available in India) & Lumiracoxib
Advantage:
LessGIT side effects
No precipitation of bronchial asthma
No antiplatelet action (COX-1 inhibition)
Disadvantage:
Increase
COX-2
the incidence of CV thrombotic episodes (Rofecoxib & Valdecoxib banned in
many countries including India)
is continuously released in kidneys (juxtaglomerular cells) & thus COX-2 inhibitors
may cause renal toxicity comprised of sodium & water retention & oedema
Less effective in AI as PG formed due to COX-1 may also cause inflammation,
May delay healing of peptic ulcer as COX-2 facilitates production of gastro protective PGs.

61. Celecoxib:
10-20 times more potent
Well absorbed in orally, 97% bound with pp
Metabolized to carboxylic acid & glucuronide
Half life is 11hrs, It is excreted in urine & faeces
Plasma concentration
ADR :
increased in mild (40%) to moderate (180%) hepatic impairment
Less gastric mucosal irritant
May produce GI side effects such as abdominal discomfort, dyspepsia & diarrhoea (mild)
May cause CV side effects hypertension, thrombosis
Avoided with Fluconazole & lithium
Uses: Mainly used in RA & OA
& increased chances of artherogenesis
It is equally effective as Diclofenac / Naproxen in RA