Introduction to gout. Epidemiology of gout. Pathology of gout. Risk factor for gout.

2. 
 Define
 Discuss the epidemiology
 Identify the age groups and gender differences
 Explain the pathology and pathogenesis
LEARNING OUTCOMES
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3. 
 Derived from the latin word gutta, meaning "a drop" (of liquid).
 Gout
 A rheumatic disease resulting from deposition of uric acid crystals (monosodium
urate) in the joints or soft tissues,
 caused by elevated level of serum uric acid (hyperuricemia).
 Hyperuricemia
 serum uric acid concentration > 7 mg per dL (420 μmol per L),
 caused by an imbalance in the production and excretion of urate
DEFINE GOUT
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4. 
 Gout has a worldwide distribution. The prevalence varies widely from country to country. Regional
differences may reflect environmental, dietary, and genetic influences.
EPIDEMIOLOGY
 The predominant age range  30-60 years.
 Men:
 uric acid levels rise at puberty
 peak age of onset  4th to 6th decade of life.
 Women:
 uric acid levels rise at menopause
 peak age of onset  6th to 8th decade of life.
 Male predominance
 Estimated prevalence  5.9% in men and 2% in women.
 Estrogenic hormones have a mild uricosuric effect gout unusual in premenopausal
women
Earlier onset of gout occurs in patients with renal insufficiency or a genetic abnormality of purine metabolism (eg, hypoxanthine-guanine
phosphoribosyltransferase deficiency or phosphoribosylpyrophosphate synthetase superactivity). Cyclosporine A can cause an accelerated
form of gout, even in premenopausal women, that can present after only a few years of hyperuricemia, particularly if the patient is also
receiving diuretics.
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5. 
 The prevalence of gout is higher in developed countries and in Oceanic populations compared with
other areas of the world despite no data being available for a large part of the developing world.
Global epidemiology of gout: prevalence, incidence and risk factors
•Chang-Fu Kuo,
•Matthew J. Grainge,
•Weiya Zhang
•& Michael Doherty
Nature Reviews Rheumatology
11,
649–662
(2015)
doi:10.1038/nrrheum.2015.91
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6. 
AGE GROUP & GENDER DIFFERENCES
Izatty Lim (0308188) 6

7. 
 Idiopathic
 Major determinant  Hyperuricemia
 Hyperuricemia
 ↑ production uric acid
 ↓ excretion uric acid
PATHOGENESIS
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8.  Hyperuricemia
PATHOGENESIS
 ↑ PRODUCTION URIC ACID
 Increased purine synthesis de novo due to:
- HGPRT reduction
- hosphoribosyl-pyrophosphate synthase
overactivity
- Glucose-6-phosphatase deficiency with
glycogen storage disease type 1
 ↓ EXCRETION URIC ACID
 Chronic renal disease
 Drug therapy
 Hypertension
 Lead toxicity
 Primary hyperthyroidism
 Hypothyroidism
 Glucose-6-phosphatase deficiency
 ↑ TURNOVER OF PURINES
 Myeloproliferative disorder
 Lymphoproliferative disorder
 Others; carcinoma
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9. 
Image taken from : Robbins Basic Pathology, 9th ed.
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10. Raised serum urate Increase risk of gout
Genetics Mutations in genes for urate transporter URAT1 & fructose transporter GLUT9
Age 2% of 45-64y/o men
6% men >75y/o have gout
Gender Men:women ratio is 3:1 respectively
Osteoarthritis Gout attacks more likely in joints affected by OA
RA is protective
Diet & alcohol
Hypertension
RISK FACTOR
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11. 
Thank You!
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