Pharmacotherapeutics of Gout Definition of gout Epidemiology in India Etiology Clinical Manifestations or signs and symptoms Pathophysiology: normal physiology, overproduction of uric acids, under-secretion of uric acid Diagnosis Therapy of acute gouty arthritis and chronic gouty arthritis

1. GOUT
Pharmacotherapy of GOUT JAYA SESHA SRAVANI VEDANTAM
19AB1T0007
III PHARM D
VIGNAN PHARMACY COLLEGE
VADLAMUDI

2. Definition of GOUT
The term gout describes a heterogeneous clinical spectrum of diseases
including elevated serum urate concentration (hyperuricemia),
recurrent attacks of acute arthritis associated with monosodium urate
crystals in synovial fluid leukocytes, deposits of monosodium urate
crystals (tophi) in tissues in and around joints, Interstitial renal disease,
and uric acid nephrolithiasis.
● The underlying metabolic disorder of gout is hyperuricemia,
defined physiochemically as serum that is supersaturated with
monosodium urate.
● Hyperuricemia means usually 7.0 mg/dL (416 μmol/L) for men
and 6.0 mg/dL (357 μmol/L) for women.

3. Epidemiology

4. Epidemiology of GOUT
In India, approximately 0.12-0.19% population being
affected by gout, and its prevalence has been more in men
aged above 50 y than premenopausal women as estrogen
hormone helps in urate clearance. Gout was described by
Hippocrates as "The disease of kings" owing to its
association with a rich diet.

5. ETIOLOGY

6. Etiology of GOUT
The conditions that are associated
with Hyperuricemia are:
Primary gout
Obesity
Diabetic ketoacidosis
Sarcoidosis
Congestive heart failure
Lactic acidosis
Renal dysfunction
Starvation
Lead toxicity
Hyperparathyroidism
Hypothyroidism
Renal transplantation
Drugs Capable of Inducing
Hyperuricemia and Gout
Diuretics
Ethanol
Ethambutol
Nicotinic acid
Pyrazinamide
Cytotoxic drugs
Salicylates (<2 g/day) L
Levodopa
Cyclosporine

7. PATHOPHYSIOLOGY

8. Normal
PURINE
METABOLISM

9. Over Production of uric
acid

10. ● Excess rates of cell
turnover,
● Increased breakdown
of tissue nucliec acids
● Due to enzymatic
derangements
● Cytotoxic medications
→
Overproduction of uric acid

11. Undersecretion of uric
acid

12. Undersecretion of uric acid

13. Due to direct trauma
Dehydration
Acidosis
Or
Rapid weight loss

14. Diagnostic
Evaluation

15. Diagnostic Evaluation
● Aspiration of synovialfluid - Identification of
intraoccular crystals and monosodium urate
monohydrate
● Radiographs - shows punched out marginal
erosions; secondary osteoarthritic changes
● MRI and computed tomography
● Elevated serum uric acid levels
● Response to Colchicine

16. Treatment

17. Goals
● Terminate acute attack
● Prevent recurrent
attacks
● Present complication
of chronic deposition of
urate crystals

18. Acute Gouty Arthritis

19. NSAIDs
● Indomethacin → 25-50mg QID - for 3 days then TID for 4-7 days
● Naproxen → 500mg TID for 3 days then 250-500mg OD for 4-7
days
● Sulindac → 200mg TID for 7-10 days
Any one drug at maximum dosage at onset of symptoms until 24
hours
Resolution in 5 to 8 days
ADRs :- Gastritis, bleeding, perforation, reduced creatinine clearance,
increased blood pressure, sodium and fluid retention, headache,
dizziness
● Give a Proton pump inhibitor to reduce ADRs

20. Corticosteroids
● Used when patient is found contraindicated to NSAIDs
● Can also be given in the form of systemic/intraarticular
injections
● Oral :- 30-60mg of Prednisone for 3 to 5 days; decrease to
5mg over 10 to 14 days (multiple joints)
● Intraarticular:- Triamcinolone acetonide - 20 to 40mg (one or
two joints)
ADRs :- Short term doses are well tolerated - increase in blood
sugar
Long term dose - Osteoporosis, hypothalamic pituitary axis
suppression, cataract muscle conditioning.

21. Colchicine
● Antimitotic drug
● Effective within 24 hours
● ADRs :-
○ GI effects:- nausea,
vomiting, diarrhoea
○ Neutropenia, axonal
neuromyopathy.
● 1.2mg initially, followed by
0.6mg (1 hour later).
● Low benefit-to-toxicity ratio.
● Decrease dietary intake of
purines.
● Increase fluid intake.
● Decrease salt consumption
● Rest the joint for 1 to 2
days
● Avoid application of heat
and joint exercises
● Weight loss
Non pharmacological

22. Chronic Gouty Arthritis

23. Xanthine oxidase inhibitors
Xan
↑
↑
↑
Xanthine oxidase
inhibitors
● Allopurinol - 100mg/day
○ ADRs :- skin rashes, leukopenia, GI
problems, headache, urticaria, rash,
hepatitis, eosinophilia
● Febuxostat - 80mg/day
○ Nausea, arthralgias,
minor ALT elevations

24. Uricosuric drugs
● Probenecid - 250mg BID for 1
to 2 weeks and 500mg BID for
2 weeks then daily dose
increase by 500mg every 1 to
2 weeks. Maximum dose is 2g.
● Sulfinpyrazone - 50mg TID for
3 to 4 days then 100mg BID.
Increased daily by 100mg each
week upto 800mg/day.
ADRs:- GI irritation, rash,
hypersensitivity, stone formation.

25. Miscellaneous agents
1. Fenofibrate :- Lipid lowering drug
a. Decreases dyslipidemia in gout patients
b. Increase clearance of hypoxanthine and xanthine
2. Losartan:- Angiotensin II receptor antagonist.
a. Also decrease serum urate concentration, and alkalinizes
urine by inhibiting renal tubular reabsorption of uric acid and
and increases urinary excretion.
3. Lenusirid:- 200mg/day
a. Administered in morning along with Xanthine Oxidase
inhibitors
4. Pegloticase:- Administered when no treatment works
a. 8mg IV/2hours for every 2 weeks.

26. References:-
1. Pharmacotherapy A Pathophysiologic Approach,
Eighth Edition, by Joseph T. DiPiro, Robert L.
Talbert, Gary C. Yee, Gary R. Matzke, Barbara G.
Wells, L. Michael Posey.
2. https://www.researchgate.net/publication/5121152
1_Epidemiology_of_gout_An_update