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GOUT
Dr. Mohanad
Purines
Purines are natural substances found in
all of the body's cells, and in virtually all
foods.
The reason for their widespread
occurrence is simple: purines provide part
of the chemical structure of our genes and
the genes of plants and animals
When cells die and get recycled, the
purines in their genetic material also get
broken down.
Uric acid is the chemical formed when
purines have been broken down
completely.
Hyperuricemia
 The condition when there are high
concentrations of uric acid in the blood.
 Serum levels of uric acid are >7mg/dL
(Normally, 2.4-6mg/dL in females; 3.4-
7mg/dL in males)
 At such a high level, uric acid tends to
aggregate and form crystals
 Primary Hyperuricemia: an innate
defect in purine metabolism and/or uric
acid excretion
 Secondary Hyperuricemia: high uric
acid levels due to medications/medical
conditions such as diabetic ketoacidosis,
psoriasis, chronic lead poisoning
Most uric acid dissolves in blood and
travels to the kidneys, where it passes out
in urine.
 If your body produces too much uric acid
or doesn't remove enough if it, you can get
sick.
High levels of uric acid in the body is
called Hyperuricemia.
Purine nucleotides
hypoxanthine
xanthine
Uric acid
Xanthine
oxidase
Alimentary
excretion
Urinary
excretion
Tissue deposition
in excess
Urate crystal microtophi
Phagocytosis
with acute
inflammation
and arthritis
uricosurics
colchicine NSAID
Allopurinol
Oxypurinol
Uric Acid
Uric acid is the end product in purine metabolism
Excretion of uric acid removes nitrogenous wastes from
body
2/3 of uric acid made is excreted via kidneys; 1/3 via GI
tract
Urate: protonated form of uric acid
 Uric acid can accumulate due to:
 Overproduction of purine nucleotides
 Enhanced cell turnover (purine degradation)
 Decreased in purine salvage pathway
 Underexcretion of uric acid
 Predisposition to many diseases
 People may live with elevated uric acid levels
without experiencing any symptoms
GOUT
Gout and gouty arthritis
Transient attacks of acute arthritis initiated by
crystallization of urates and neutrophils, followed
by chronic gouty arthritis with tophi in joints and
urate nephropathy
Sites: 50% have initial attack in first
metatarsophalangeal joint; also ankles, heels,
knees, wrists, fingers, elbows
Gout
Affects less than 0.5% of the population.
It is a common condition, presenting in 1-4%
of adult men.
Due to familial disposition, incidence may be
as high as 80% in families affected by
disorder.
Alcohol and Gout
alcohol metabolism contributes to urate retention
some red wines contain purines or oxypurines,
which lead to an increased purine load
alcohol may contribute to obesity which is
associated with under excretion of uric acid
Patients with a history of gout are advised to
drink plenty of fluid, approximately 2 litres per
day (nonalcoholic).
GOUT
Primary gout (90%): idiopathic with
overproduction of uric acid
Hyperuricemia in the absence of other
disease
Asymptomatic hyperuricemia can precede gout
Impaired secretion by kidneys
Secondary gout (10%): increased nucleic acid
turnover due to
chronic renal disease,
HGPRT deficiency( hypoxanthine-guanine
phosphoribosyl transferase deficiency)
Tumors
Leukemias
Lymphomas
After chemotherapy
Alcoholism
Accelerated ATP catabolism
"se co n da ry go u t"
H G P R T
E n zym a tic d e ficie n cy
"se co n d a ry g o u t"
L e u ke m ia
In crea se d n ucle ic a cid tu rn o ve r
"p rim a ry g o u t"
U n kn o w n d efe ct
ca u sin g d e cre a se d excre tion
H yp e ru rice m ia
GOUT
Arthritis: synovial fluid is poorer solvent for sodium
urate than plasma, so with hyperuricemia.
 Urates in joint fluid crystallize, particularly in ankle due
to lower temperature; crystals develop in synovial lining
cells, stimulate formation of antibodies, which
accelerates formation of new crystals.
Release of crystals attracts neutrophils and complement,
(generates c3a, c5a, attracts more neutrophils),
Releases free radicals, releases lysosomal enzymes
GOUT
 This will eventually causes acute arthritis that last days
to weeks without treatment; repeated attacks of acute
arthritis cause
 Renal failure, urate stones
 Risk factors for gout with Hyperuricemia are:
 Age > 30 years,
 Male, familial history of gout,
 Alcohol use,
 Obesity,
 Thiazide administration(reduce the clearance of uric
acid)
Pathogenesis
Enzymatic deficiencies and increased
nucleic acid turnover account for only 10%
of gout patients.
Remaining 90% are “primary gout” due to
an unknown defect limiting the ability to
excrete uric acid.
Pathogenesis
Uric acid normally dissolves in plasma
Poorly soluble in synovial fluid and
precipitates out as MSU crystals
(monosodium urate crystals )
Pathogenesis
Hyperuricaemia

May be asymptomatic

Deposition of monosodium urate crystals in synovial tissue
(contain various Ig’s, complement, fibrinogen, fibronectin)

Complement activated

Neutrophils phagocytose & lyse crystals

Release chemical mediators (e.g. TNF-α; IL-1)

ACUTE GOUTY ARTHRITIS

May resolve & become asymptomatic
(INTERCRITICAL GOUT)
May have recurrent episodes

Large deposits of chalky white urate  tophi

Chronic granulomatous inflammatory condition

Fibrosis of synovium

Erosion of articular cartilage

CHRONIC TOPHACEOUS ARTHRITIS

ankylosis

Tophi may be deposited in soft tissue

Can ulcerate if sub-cutaneous
Pathogenesis of Renal Involvement
Hyperuricaemia

Freely filtered by glomerulus, but reabsorbed in proximal
convulated tubules

Precipitation in renal tubules

Tubule obstruction

Crystal formation in interstitium

Renal stones

Recurrent pyelonephritis
Crystal Studies
Sodium urate crystals viewed under polarized
light with a red plate makes those in the plane of
the long axis of the red plate yellow, which
indicates that they are negatively birefringent.
Clinical features
Acute gouty arthritis
Painful
Involves one joint initially, then polyarticular
Podagra (painful, red metatarsophalangeal
joint)
Tophaceous gout
Development of tophi
Chalky, cheesy, yellow-white, pasty deposits of
monosodium urate crystals
Helix and antihelix of ear
Achilles tendon
Stages of Gout
Asymptomatic Hyperuricemia
Acute Attack
Intercritical Period
Chronic Gout
Acute gout
Sudden onset
Lasts 1-2w
May be triggered by – trauma, operation, alcohol,
exercise
Sites
1st MTP (75%)
Ankle
Finger
Olecranon
Chronic gout
 Polyarticular gout
 Tophi may form around joints and often also in the
pinna of the ear and with time may ulcerate and
discharge
 May cause joint stiffness and deformity as a result of
joint erosion
 May cause renal damage due to deposition of urate
crystals in the renal parenchyma
 Urate urolithiasis occurs in 10%; rarely chronic urate
nephropathy with renal failure may develop
Acute on chronic gout
Diagnosis
More than one attack
Maximum
inflammation in one
day
Monoarthritis
Redness
First MTP involved
Unilateral first MTP
Unilateral tarsal
attack
Tophus
Hyperuricemia
Asymmetric swelling
MSU crystals in joint
fluid
Joint fluid culture
negative
Diagnosis
Based on history and physical examination
Confirmed by arthrocentesis
Urate crystals: needle-shaped negatively birefringent
either free floating or within neutrophils & macrophages.
Uric acid level non specific.
30% may show normal level
Urine collection:
GOUT
Gross: chalky white appearance of gouty deposits
Micro: early - edematous synovium with acute and
chronic inflammatory infiltrate
 Late - tophi (large aggregates of urate crystals,
granulomatous inflammation, hyperplastic fibrotic
synovium);
Gout crystals are long, slender, needle shaped, but
difficult to visualize with routine staining because they
are dissolved during formalin processing (crystals are
water soluble); easier to identify on scrape or with
alcohol fixation
GOUT
With chronic disease, urate deposits may
be present in soft tissue, ligaments, skin
Gouty deposits may be surrounded by
fibrous tissue and be rimmed by
histiocytes and giant cells
Gout from sodium urate crystalsGout from sodium urate crystals
deposited in joints.deposited in joints.
This is gout. Gouty arthritis results from
deposition of sodium urate crystals in
joints.
The joint most often affected is the first
MP joint (big toe) as seen here.
Acute attacks are characterized by severe
pain, swelling, and erythema of the joint.
Gout or pseudogout?
Gout
>40
small joints esp 1st
MTP
Severe joint pain
swelling
Uric acid crystals neg
bifringent
Rest, nsiad prohylaxis
hyperuricaemia
Pseudogout
 Elderly
 Large joints esp knee
 Mod pain and swelling
 Calcium pyrophosphate
positively bifringent
 Rest, nsaid, joint aspiration
Treatment
Life style (food)
Colchicine
Prophylactic
Probenecid & sulfinpyrazone
Interfere with urate resorption
Allopurinol
Inhibitor of enzyme that converts the xanthine and
hypoxanthine to uric acid

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Gout

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  • 4. Purines Purines are natural substances found in all of the body's cells, and in virtually all foods. The reason for their widespread occurrence is simple: purines provide part of the chemical structure of our genes and the genes of plants and animals
  • 5. When cells die and get recycled, the purines in their genetic material also get broken down. Uric acid is the chemical formed when purines have been broken down completely.
  • 6. Hyperuricemia  The condition when there are high concentrations of uric acid in the blood.  Serum levels of uric acid are >7mg/dL (Normally, 2.4-6mg/dL in females; 3.4- 7mg/dL in males)  At such a high level, uric acid tends to aggregate and form crystals  Primary Hyperuricemia: an innate defect in purine metabolism and/or uric acid excretion  Secondary Hyperuricemia: high uric acid levels due to medications/medical conditions such as diabetic ketoacidosis, psoriasis, chronic lead poisoning
  • 7. Most uric acid dissolves in blood and travels to the kidneys, where it passes out in urine.  If your body produces too much uric acid or doesn't remove enough if it, you can get sick. High levels of uric acid in the body is called Hyperuricemia.
  • 8. Purine nucleotides hypoxanthine xanthine Uric acid Xanthine oxidase Alimentary excretion Urinary excretion Tissue deposition in excess Urate crystal microtophi Phagocytosis with acute inflammation and arthritis uricosurics colchicine NSAID Allopurinol Oxypurinol
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  • 10. Uric Acid Uric acid is the end product in purine metabolism Excretion of uric acid removes nitrogenous wastes from body 2/3 of uric acid made is excreted via kidneys; 1/3 via GI tract Urate: protonated form of uric acid
  • 11.  Uric acid can accumulate due to:  Overproduction of purine nucleotides  Enhanced cell turnover (purine degradation)  Decreased in purine salvage pathway  Underexcretion of uric acid  Predisposition to many diseases  People may live with elevated uric acid levels without experiencing any symptoms
  • 12. GOUT Gout and gouty arthritis Transient attacks of acute arthritis initiated by crystallization of urates and neutrophils, followed by chronic gouty arthritis with tophi in joints and urate nephropathy Sites: 50% have initial attack in first metatarsophalangeal joint; also ankles, heels, knees, wrists, fingers, elbows
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  • 14. Gout Affects less than 0.5% of the population. It is a common condition, presenting in 1-4% of adult men. Due to familial disposition, incidence may be as high as 80% in families affected by disorder.
  • 15. Alcohol and Gout alcohol metabolism contributes to urate retention some red wines contain purines or oxypurines, which lead to an increased purine load alcohol may contribute to obesity which is associated with under excretion of uric acid Patients with a history of gout are advised to drink plenty of fluid, approximately 2 litres per day (nonalcoholic).
  • 16. GOUT Primary gout (90%): idiopathic with overproduction of uric acid Hyperuricemia in the absence of other disease Asymptomatic hyperuricemia can precede gout Impaired secretion by kidneys
  • 17. Secondary gout (10%): increased nucleic acid turnover due to chronic renal disease, HGPRT deficiency( hypoxanthine-guanine phosphoribosyl transferase deficiency) Tumors Leukemias Lymphomas After chemotherapy Alcoholism Accelerated ATP catabolism
  • 18. "se co n da ry go u t" H G P R T E n zym a tic d e ficie n cy "se co n d a ry g o u t" L e u ke m ia In crea se d n ucle ic a cid tu rn o ve r "p rim a ry g o u t" U n kn o w n d efe ct ca u sin g d e cre a se d excre tion H yp e ru rice m ia
  • 19. GOUT Arthritis: synovial fluid is poorer solvent for sodium urate than plasma, so with hyperuricemia.  Urates in joint fluid crystallize, particularly in ankle due to lower temperature; crystals develop in synovial lining cells, stimulate formation of antibodies, which accelerates formation of new crystals. Release of crystals attracts neutrophils and complement, (generates c3a, c5a, attracts more neutrophils), Releases free radicals, releases lysosomal enzymes
  • 20. GOUT  This will eventually causes acute arthritis that last days to weeks without treatment; repeated attacks of acute arthritis cause  Renal failure, urate stones
  • 21.  Risk factors for gout with Hyperuricemia are:  Age > 30 years,  Male, familial history of gout,  Alcohol use,  Obesity,  Thiazide administration(reduce the clearance of uric acid)
  • 22. Pathogenesis Enzymatic deficiencies and increased nucleic acid turnover account for only 10% of gout patients. Remaining 90% are “primary gout” due to an unknown defect limiting the ability to excrete uric acid.
  • 23. Pathogenesis Uric acid normally dissolves in plasma Poorly soluble in synovial fluid and precipitates out as MSU crystals (monosodium urate crystals )
  • 24. Pathogenesis Hyperuricaemia  May be asymptomatic  Deposition of monosodium urate crystals in synovial tissue (contain various Ig’s, complement, fibrinogen, fibronectin)  Complement activated  Neutrophils phagocytose & lyse crystals  Release chemical mediators (e.g. TNF-α; IL-1)  ACUTE GOUTY ARTHRITIS  May resolve & become asymptomatic (INTERCRITICAL GOUT)
  • 25. May have recurrent episodes  Large deposits of chalky white urate  tophi  Chronic granulomatous inflammatory condition  Fibrosis of synovium  Erosion of articular cartilage  CHRONIC TOPHACEOUS ARTHRITIS  ankylosis  Tophi may be deposited in soft tissue  Can ulcerate if sub-cutaneous
  • 26. Pathogenesis of Renal Involvement Hyperuricaemia  Freely filtered by glomerulus, but reabsorbed in proximal convulated tubules  Precipitation in renal tubules  Tubule obstruction  Crystal formation in interstitium  Renal stones  Recurrent pyelonephritis
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  • 29. Crystal Studies Sodium urate crystals viewed under polarized light with a red plate makes those in the plane of the long axis of the red plate yellow, which indicates that they are negatively birefringent.
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  • 32. Clinical features Acute gouty arthritis Painful Involves one joint initially, then polyarticular Podagra (painful, red metatarsophalangeal joint) Tophaceous gout Development of tophi Chalky, cheesy, yellow-white, pasty deposits of monosodium urate crystals Helix and antihelix of ear Achilles tendon
  • 33. Stages of Gout Asymptomatic Hyperuricemia Acute Attack Intercritical Period Chronic Gout
  • 34. Acute gout Sudden onset Lasts 1-2w May be triggered by – trauma, operation, alcohol, exercise Sites 1st MTP (75%) Ankle Finger Olecranon
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  • 36. Chronic gout  Polyarticular gout  Tophi may form around joints and often also in the pinna of the ear and with time may ulcerate and discharge  May cause joint stiffness and deformity as a result of joint erosion  May cause renal damage due to deposition of urate crystals in the renal parenchyma  Urate urolithiasis occurs in 10%; rarely chronic urate nephropathy with renal failure may develop
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  • 41. Diagnosis More than one attack Maximum inflammation in one day Monoarthritis Redness First MTP involved Unilateral first MTP Unilateral tarsal attack Tophus Hyperuricemia Asymmetric swelling MSU crystals in joint fluid Joint fluid culture negative
  • 42. Diagnosis Based on history and physical examination Confirmed by arthrocentesis Urate crystals: needle-shaped negatively birefringent either free floating or within neutrophils & macrophages. Uric acid level non specific. 30% may show normal level Urine collection:
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  • 44. GOUT Gross: chalky white appearance of gouty deposits Micro: early - edematous synovium with acute and chronic inflammatory infiltrate  Late - tophi (large aggregates of urate crystals, granulomatous inflammation, hyperplastic fibrotic synovium); Gout crystals are long, slender, needle shaped, but difficult to visualize with routine staining because they are dissolved during formalin processing (crystals are water soluble); easier to identify on scrape or with alcohol fixation
  • 45. GOUT With chronic disease, urate deposits may be present in soft tissue, ligaments, skin Gouty deposits may be surrounded by fibrous tissue and be rimmed by histiocytes and giant cells
  • 46. Gout from sodium urate crystalsGout from sodium urate crystals deposited in joints.deposited in joints.
  • 47. This is gout. Gouty arthritis results from deposition of sodium urate crystals in joints. The joint most often affected is the first MP joint (big toe) as seen here. Acute attacks are characterized by severe pain, swelling, and erythema of the joint.
  • 48. Gout or pseudogout? Gout >40 small joints esp 1st MTP Severe joint pain swelling Uric acid crystals neg bifringent Rest, nsiad prohylaxis hyperuricaemia Pseudogout  Elderly  Large joints esp knee  Mod pain and swelling  Calcium pyrophosphate positively bifringent  Rest, nsaid, joint aspiration
  • 49. Treatment Life style (food) Colchicine Prophylactic Probenecid & sulfinpyrazone Interfere with urate resorption Allopurinol Inhibitor of enzyme that converts the xanthine and hypoxanthine to uric acid