URIC ACID

B
BY

M DR SHASHIDHAR

H
 Nucleic Acid Bases
Purines Pyrimidines
 Purine Synthesis
Purine synthesis is critical to fetal development,
therefore defects in enzymes will result in a nonviable
fetus.

PRPP synthetase defects are known and have severe

consequences

PRPP synthetase superactivity has been documented,

resulting in increased PRPP, elevated levels of
nucleotides, and increased excretion of uric acid.
Phosphoribosyl Pyrophosphate (PRPP)
Synthetase Defects
PRPP deficiency results in convulsions, autistic
behavior, anemia, and severe mental retardation.

Excessive PRPP activity causes gout (deposition of uric

acid crystals), along with various neurological
symptoms, such as deafness.
 Purine Degradation
Purine Nucleotides from ingested nucleic acids or
turnover of cellular nucleic acids is excreted by
humans as uric acid.
Humans excrete about 0.6 g uric acid every 24 hours.
Purine
Degradation
The enzyme
“nucleotidase” is also
known as purine
nucleotide
phosphorylase (PNP)
 Lesch-Nyhan Syndrome
Hypoxanthine Guanine Phosphoribosyltransferase (HGPRT)
deficiency

X-linked genetic condition

Severe neurologic disease, characterized by self-mutilating

behaviors such as lip and finger biting and/or head banging

Up to 20 times the uric acid in the urine than in normal

individuals. Uric acid crystals form in the urine.

Untreated condition results in death within the first year due to

kidney failure.

Treated with allopurinol, a competitive inhibitor of xanthine

oxidase.
Allopurinol and Hypoxanthine
Uric Acid
 Uric Acid
Is the final breakdown product of purine degradation
in humans

It is a weak acid with pKas of 5.75 and 10.3.

Urates, the ionized forms of uric acid, predominate in

plasma extracellular fluid and synovial fluid, with
~98% existing as monosodium urate at pH 7.4.
 Plasma is saturated with monosodium urate at a
B concentration of 415 mol/L (6.8 mg/dL) at 37°C.

At higher concentrations, plasma is therefore

supersaturated, creating the potential for urate
crystal precipitation.

M However, plasma urate concentrations can reach

4800 mol/L (80 mg/dL) without precipitation,
perhaps because of the presence of solubilizing
substances.

H
 urate is produced only in tissues that contain
B xanthine oxidase, primarily the liver and small
intestine.

Urate production varies with the purine content of

the diet and the rates of purine biosynthesis,
degradation, and salvage
M
Two-thirds to three-fourths of urate is excreted by
the kidneys, and most of the remainder is
eliminated through the intestines.

H
Uric acid is more soluble in urine than in water.

The pH of urine greatly influences its solubility.

pH 5 urine is saturated with uric acid at

concentrations ranging from 6 to 15 mg/dl.

At pH 7 saturation is reached at concentration

between 158 and 200mg/dl
Serum urate levels vary with age and sex.
Children: 3 to 4 mg/dl
Adult men: 6 to 6.8 mg/dl
Hyperuricemia
Defined as a plasma urate concentration > 7.0 mg/dl

Can result from:

Increased production of uric acid
Decreased excretion of uric acid
Combination of the two processes.
 Increased Urate Production
Diet provides an exogenous source of purines and,
accordingly, contributes to the serum urate in
proportion to its purine content.
Foods high in nucleic acid: liver, thymus and pancreas,
kidney and anchovy.
Endogenous sources:
De novo purine biosynthesis: 11 step
Increased PRPP synthetase activity and HPRT deficiency
are associated with overproduction of purine,
hyperuricemia and hyperuricaciduria.
 Decreased Uric Acid Excretion
Alterated uric acid excretion could result from
decreased glomerular filtration, decreased tubular
secretion or enhanced tubular reabsorption.

Decreased tubular secretion of urate causes the secondary

hyperuricemia of acidosis.

Diabetic ketoacidosis, starvation, ethanol intoxication,

lactic acidosis, and salicylate intoxication are accompanied
by accumulations of organic acids (B-hydroxybutyrate,
acetoacetate, lactate or salicylates) that compete with urate
for tubular secretion.
 Combined Mechanisms
Alcohol intake promotes hyperuricemia:

Fast hepatic breakdown of ATP and increases

urate production.
Can induce hyperlacticacidemia, and inhibition of
uric acid secretion.

The higher purine content in some alcoholic beverages

such as beer may also be a factor.
 Causes of hyperuricemia
Primary Secondary
No recognized cause Hereditary fructose
Hypoxanthine phosphoribosyltransferase deficiency
intolerance
Increased phosphoribosyl pyrophosphatase
Mieloproliferative
activity. disease
Linfoproliferative disease
Hemolitic anemia
Drugs: Low-doses salicylate,
diuretis, pyrazinamide, ethambutol,
nicotinamide, etanol
 Evaluation of Hyperuricemia
Hyperuricemia does not represent a disease.

Is not an specific indication for therapy.

The finding of hyperuricemia is an indication to

determine its cause.
The hyperuricemia of individuals who excrete uric
acid above this level while on a purine-free diet is due
to purine overproduction,

 whereas it is due to decreased excretion in those who

excrete lower amounts on the purine-free diet.
Complications of Hyperuricemia
The most recognized complication of hyperuricemia
is gouty arthritis

Nephrolithiasis
Urate Nephropathy
Uric Acid Nephropathy
 Nephrolithiasis
The prevalence of nephrolithiasis correlates with the
serum and urinary uric acid levels.

Serum urate levels 13 mg/dl

Urinary uric acid excretion > 1100 mg/d

 Urate Nephropathy
Deposits of monosodium urate crystals surrounded by
a giant cell inflammatory reaction in the medullary
intrerstitium and pyramids.

Clinically: silent or cause proteinuria, hypertension

and renal insufficiency.
Precipitation in renal tubules and collecting ducts
cause obstruction to urine flow.

Following sudden urate overproduction and

marked hyperuricaciduria:
 Dehydration and acidosis
 Lymphoma
 Cytolytic therapy
Treatment
 Asymptomatic Hyperuricemia
Treatment with anthyperuricemic agents entails
inconvenience, cost and potential toxicity.

“Routine” treatment of asymptomatic hyperuricemia

cannot be justified.
Treatment with anthyperuricemic agents in
asymptomatic hyperuricemia is not recommended.

“Treatment in special conditions” like patients during

cytolytic therapy for neoplastic disease.

 Justification:prevent uric acid nephropathy.

 Nephrolithiasis Prevention
Fluid ingestion (urine >2 L/d)

Alcalinization of the urine (sodium bicarbonate or

acetazolamide) to increase the solubility of uric acid.

Allopurinol (Decrease the serum urate concentration)

300 mg/d
 Uric Acid Nephropathy
Vigorous intravenous hydration and diuresis with
furosemide.

Acetazolamide and sodium bicarbonate (urine pH >7)

Allopurinol
B GOUT
Definition
Crystal arthropathies ,A group of disorders
characterized by the deposition of microcrystals in
joints resulting in acute or chronic arthritis or

M periarthritis

H
 Types of microcrystals deposited
B Monosodium urate (MSU) crystals
Classically termed gout

Calcium pyrophosphate dihydrate (CPPD) crystals

Also known as pseudogout
M
Calcium apatite (apatite) crystals

Calcium oxalate (CaOx) crystals

H
 GOUT
B Epidemiology: MSU gout

Prevalence
1.3–3.7% in the general population

Age/sex
M Middle-aged to elderly men
Postmenopausal women
More common in men than in women

H
 Epidemiology
Most common of microcrystalline arthropathy. Incidence
has increased significantly over the past few decades.

Affects about 2.1million worldwide

Peak incidence occurs in the fifth decade, but can occur at

any age

Gout is 5X more common in males than pre-menopausal

females; incidence in women increases after menopause.
After age 60, the incidence in women approaches the rate
in men.

People of South Pacific origin have an increased incidence.

 Risk Factors
Aging Precipitants of an acute
attack
Underlying disease (e.g., 1. Dietary excess
2. Trauma
renal, joint disease)
3. Surgery
4. Excessive ethanol
Diuretics
ingestion
5. Adrenocorticotropic
Hypertension hormone (ACTH)
6. Glucocorticoid
Obesity withdrawal
7. Hypouricemic therapy
Transplant recipients 8. Serious medical illnesses
 ETIOLOGY
B Hyperuricemia may arise from overproduction or
underexcretion of uric acid.
When hyperuricemia is present, plasma and
extracellular fluids become supersaturated with
uric acid; crystallization may occur and result in
clinical gout.
M 1 Microcrystals present in the joint are
phagocytosed by neutrophils.
2 Inflammatory mediators are released, and
lysosomal enzymes lead to synovial
inflammation.

H
 Pathogenesis of Gouty Inflammation

Urate crystals stimulate the release of numerous

inflammatory mediators in synovial cells and
phagocytes
The influx of neutrophils is an important event for
developing acute crystal induced synovitis
Chronic gouty inflammation associated with
cytokine driven synovial proliferation, cartilage
loss and bone erosion
 Pathophysiology
Primary gout is caused by inborn defects in purine
metabolism or inherited defects of the renal tubular
secretion of urate.

Secondary gout is caused by acquired disorders that

result in increased turnover of nucleic acids, by defects
in renal excretion of uric acid salts, and by the effects of
certain drugs
.
.
 Associated Conditions
Cardiovascular Disease
Paget’s disease
Arthritis- rheumatoid and osteoarthritis
Septic Arthritis
Metabolic syndrome
 Stages of Classic Gout
 Asymptomatic hyperuricemia
 Very common biochemical abnormality
 Defined as 2 SD above mean value
 Majority of people with hyperuricemia never develop symptoms of
uric acid excess
 Acute Intermittent Gout (Gouty Arthritis)
 Episodes of acute attacks. Symptoms may be confined to a single
joint or patient may have systemic symptoms.
 Intercritical Gout
 Symptom free period interval between attacks. May have
hyperuricemia and MSU crystals in synovial fluid
 Chronic Tophaceous Gout
 Results from established disease and refers to stage of deposition of
urate, inflammatory cells and foreign body giant cells in the tissues.
Deposits may be in tendons or ligaments.
 Usually develops after 10 or more years of acute intermittent gout.
 Symptoms & Signs
B General musculoskeletal manifestations
of crystal-induced arthritis

Acute mono- or polyarthritis

Bursitis
M Tendonitis
Enthesitis
Tophaceous deposits
Peculiar type of osteoarthritis

H
B
Synovial osteochondromatosis
Destructive arthropathies
Pseudo-rheumatoid arthritis
Pseudo-ankylosing spondylitis
M Spinal stenosis
Crown dens syndrome
Carpel tunnel syndrome
Tendon rupture

H
 MSU gout
B Acute arthritis

Most frequent early clinical manifestation

Usually monoarticular
M
Occasionally polyarticular

Metatarsophalangeal joint of the first toe is most

often involved (podagra).(Location of first attack
in 50% of cases)
H
 Other commonly affected joints
Finger
B Tarsal
Ankle
Knee

 First episode frequently begins at night with

dramatic joint pain and swelling.
M
 Joints rapidly become warm, red, and tender.

 Clinical appearance often mimics a cellulitis.

H
  Chronic nonsymmetric synovitis
 May be the presentation after many acute mono-

B or oligoarticular attacks

 Tenosynovitis

 Chronic tophaceous arthritis

Tophi are aggregates of MSU crystals surrounded
M by a giant cell inflammatory reaction.

 Extra-articular tophi
Common locations include in the olecranon bursa,
helix and antihelix of ears, ulnar

H surface of forearm, and Achilles tendon.

 RENAL DISEASE IN GOUT
 Chronic urate nephropathy
B  Results from deposition of MSU crystals in the renal
medulla and pyramids and is associated with mild
albuminuria
 Acute uric acid nephropathy
 Can be caused by hyperuricemia in the acute tumor lysis
syndrome seen in chemotherapy-treated patients with

M rapidly proliferating lymphomas and leukemias

 Uric acid precipitates in the distal tubules and collecting
ducts, resulting in acute renal failure.
 Uric acid nephrolithiasis
 Uric acid renal stones occur in 10–25% of people with gout.
 Correlates with serum uric acid level: Likelihood reaches 50% with
serum uratelevels > 13mg/dL.
H
 Differential Diagnosis
B Cellulitis

Acute septic arthritis

Palindromic rheumatism

M Psoriatic arthritis

Rheumatoid arthritis

Other crystalline arthropathies

H
B Diagnostic Approach
History, with particular attention to risk factors
Physical examination, with particular attention to
distribution of involved joints
Radiography may be helpful.
M Arthrocentesis with crystal analysis of synovial
fluid establishes diagnosis.

H
 Laboratory Tests
B
The definitive method of diagnosis
Effusions appear cloudy due to leukocytes, and
large amounts of crystals occasionally
produce a thick pasty or chalky joint fluid.

M Characteristic needle-shaped negatively

birefringent MSU crystals by polarizing
microscopy
Cell counts elevated from 2000–60,000/μL

H
 Diagnosis
Definitive diagnosis only
possible by aspirating and
inspecting synovial fluid or
tophaceous material and
demonstrating MSU
crystals
Polarized microscopy, the
crystals appear as bright
birefringent crystals that
are yellow (negatively
birefringent)
 Synovial Fluid Findings
Needle shaped crystals
of monosodium urate
monohydrate that have
been engulfed by
neutrophils
 Diagnostic Studies
 Uric Acid
 Limited value as majority of hyperuricemic patients will never develop gout
 Levels may be normal during acute attack

 CBC
 Mild leukocytosis in acute attacks, but may be higher than 25,000/mm

 ESR
 mild elevation or may be 2-3x normal

 Trial of colchicine
 Positive response may occur in other types of arthritis to include
pseudogout.
B
 Serum uric acid
Normal levels do not rule out MSU gout.
Almost always elevated at some time and can be
used to follow the course of hypouricemic therapy
M  Urine uric acid
A 24-hour urine collection for uric acid: Excretion
of > 800 mg/d on regular diet in the absence of
drugs suggests overproduction.

H
 Screening for risk factors or sequelae
B Urinalysis

Serum creatinine

Glucose
M
Lipids

Complete blood count

H Thyroid-stimulating hormone
 IMAGING
B  Early in the disease, radiographic studies may only
confirm clinically evident swelling.
 Chronic tophaceous gout
Cystic changes and well-defined erosions described as
punched-out lytic lesions with overhanging bony
edges (Martel’s sign, or G sign for gout), associated
with soft tissue calcified masses
M Similar radiographic signs observed in erosive
osteoarthritis, destructive apatite arthropathies, and
rheumatoid arthritis
 If renal stones are suspected
Abdominal flat plate (stones often radiolucent)
Consider noncontrast abdominal and pelvic CT scan or

H intravenous pyelography.
 DIAGNOSTIC PROCEDURES
B
Arthrocentesis for synovial joint fluid analysis

MSU crystals can often be demonstrated in the

first metatarsophalangeal joint and in knees not
M acutely involved with gout.

Arthrocentesis of these joints is a useful technique

to establish the diagnosis of gout between attacks.

H
 Differential Diagnosis Septic Arthritis

Septic and gouty arthritis present with many of the

same signs and symptoms
fever and monoarthritis
Beware: both septic and gouty arthritis may present in
the same joint
Differential Diagnosis synovial fluid analysis

gout septic
WBC > 50 k 15 k (5 to 80k)
PMNs > 90% ~70%
 Treatment Goals
Gout can be treated without complications.
Therapeutic goals include
terminating attacks
providing control of pain and inflammation
preventing future attacks
preventing complications such as renal stones, tophi,
and destructive arthropathy
 Treatment Approach
B Acute attacks
Treatment is given for symptomatic relief only as
attacks are self-limited and will resolve
spontaneously.

There are no good evidence-based treatment

M recommendations for gout. Toxicity of therapy
must be considered in each patient.
Short course of glucocorticoids may be the safest
treatment. Conservative treatment with rest, ice,
and elevation can be of benefit.

H
B
 Pharmacotherapy
NSAIDs
Colchicine
Glucocorticoids: local injection or systemic
M

H
 Acute treatment cont’d
Corticosteriods
 Patients who cannot tolerate NSAIDs, or failed NSAID/colchicine therapy
 Daily doses of prednisone 40-60mg a day for 3-5 days then taper 1-2 weeks
 Improvement seen in 12-24hr

ACTH
 Peripheral anti-inflammatory effects and induction of adrenal
glucocorticoid release
 40-80IU IM followed by second dose if necessary

Intra-articular injection with steroids

 Beneficial in patient with one or two large joints affected
 Good option for elderly patient with renal or PUD or other illness
 Triamcinolone 10-40mg or Dexamethasone 2-10mg alone or in
combination with Lidocaine
  Hypouricemic therapy has a goal of preventing
future attacks and eliminating tophaceous
B deposits.
 Lifestyle modifications
Control of body weight
Low-purine diet
Increase in liquid ingestion
Limitation of ethanol intake
M Avoidance of diuretics
 Pharmacotherapy
Probenecid
Allopurinol
Colchicine
H
 Factors to consider in decision to initiate
B pharmacotherapy

Number of acute attacks

Serum uric acid levels (progression is more rapid in

patients with serum uric acid >535 μmol/L [>9.0 mg/dL])

M Patient’s willingness to commit to lifelong therapy

Presence of uric acid stones

Urate-lowering therapy should be initiated in any patient

who already has tophi or chronic gouty arthritis.
H
 ACUTE ATTACK
Urate-lowering drugs (probenecid, allopurinol)
B should not be initiated during acute attacks.
NSAIDs
Effective in ~90% of patients for acute gouty
attacks
Resolution of signs and symptoms usually occurs
in 5–7 days.
M The most effective drugs are those with a short
half-life and include:
1.Indomethacin 25–50 mg tid
2.Ibuprofen 800 mg tid
3.Diclofenac 50 mg tid
H
 Colchicine(orally)
B Generally effective only within first 24 hours of attack
Contraindications
1.Renal insufficiency
2.Cytopenias
3.Liver function tests > 2× normal
4.Sepsis

M Effective in at least 85% of patients if used early in the attack

Dose: One to two 0.6 mg tablets every 6–8 hours over several
days with subsequent tapering
Must be stopped promptly at the first sign of loose stools
Elderly patients with gouty synovitis affecting small joints: Ice
pack applications together with lower oral doses of colchicine
H can be useful.
 Colchicine(intravenous)
B If used, never give any more than 2 mg over 24 hours and no
further drug for 7 days following.

Intravenous dose must never be given in a patient who has also

received an oral dose.

Can reduce, though not eliminate, the GI side effects seen with
oral colchicine
M Dose: 1–2 mg given slowly through an established venous line over
10 minutes in a soluset and no further drug for 7 days following

Life-threatening colchicine toxicity and sudden death have been

described with the administration of > 4 mg/d IV, or with less in
patients with renal insufficiency or whohave received prior oral
H colchicine.
 Glucocorticoids
Oral: prednisone 30–50 mg/d tapered over 5–7 days

B Given in combination with acetaminophen has similar efficacy for

pain and may be better tolerated than indomethacin

Intravenous: methylprednisolone 20–40 mg/d tapered over 5–7

days, primarily used in patients unable to take oral prednisone

M Intra-articular: 20–40 mg of triamcinolone acetonide or

methylprednisolone 25–50 mg

Septic arthritis must be ruled out prior to injection.

May be favored in patients with an attack involving only 1 or 2 joints

H Both NSAIDs and colchicine may be toxic in the elderly, particularly

those with renal insufficiency and GI disorders.
 Hypouricemic therapy
B Probenecid (Uricosuric agent)
Indications
Patients with good renal function who underexcrete
uric acid with < 600 mg in a 24-hour urine sample
Drug of choice to treat elderly patients with
hypertension and thiazide dependence
M Generally not effective in patients with serum
creatinine levels of >177 μmol/L (2.0mg/dL)
Dose: 250 mg twice daily, increase gradually as needed
up to 3 g in order to maintain a serum uric acid level <
300 μmol/L (5 mg/dL)
Urine volume must be maintained by ingestion of 1500

H mL of water every day.

 Allopurinol
Xanthine oxidase inhibitor
B Considered first-line therapy for uric acid–
lowering therapy
Indications
Drug of choice to treat overproducers, tophaceous
gout, stone formers, and patients with advanced
renal failure
M Can also be used in underexcretors when impaired
renal function prohibits use of probenecid
Dose: 100–300 mg q am, increasing up to 800 mg
qd if needed
Dose should be adjusted in patients with chronic

H kidney disease to minimize side effects.

 TOXICITY
B Patients with renal failure who use thiazide diuretics
and in patients allergic to penicillin and ampicillin
Drug interaction exists between allopurinol and
azathioprine; reduce azathioprine doseby one-fourth to
one-third of the normal dosage.

M Most serious side effects include:

1. Allopurinol hypersensitivity: skin rash with progression
to life-threatening toxic epidermal necrolysis
2. Systemic vasculitis
3. Bone marrow suppression
4. Granulomatous hepatitis
H 5. Renal failure
Non- Pharmacologic Treatments
Immobilization of Joint
Ice Packs
Abstinence of Alcohol
 Consumption can increase serum urate levels by increasing uric
acid production. When used in excess it can be converted to lactic
acid which inhibits uric acid excretion in the kidney
Dietary modification
 Low carbohydrates
 Increase in protein and unsaturated fats
 Decrease in dietary purine-meat and seafood. Dairy and vegetables
do not seem to affect uric acid
 Bing cherries and Vitamin C
 Prophylaxis
 Frequent attacks >3/year, tophi development or urate overproduction

 Avoid use of medications that contribute to hyperuricemia: Thiazide

and loop diuretics, low-dose salicylates, niacin, cyclosporine,
ethambutol
 Losartan promotes urate diuresis and may even normalize urate
levels. This action does not extend to other members of the ARB
class.
 Useful in elderly with HTN and gout

 Colchicine
 Colchicine 0.6mg qd-bid
 Use alone or in combination with urate lowering drugs
 Prophylaxis without urate lowering drugs may allow tophi to
develop
 Newer Therapies
 Uricase
 Enzyme that oxidizes uric acid to a more soluble form
 Natural Uricase from Aspergillus flavus and Candida utilis under
investigation
 Febuxostat
 New class of Xanthine Oxidase inhibitor
 More selective than allopurinol
 Little dependence on renal excretion
 Losartan
 ARB given as 50mg/dL can be urisuric. When given with HCTZ, it can blunt
the effect of the diuretic and potentiate its antihypertensive action
 Fenofibrate
 Studies note when used in combo with Allopurinol produced additional
lowering of the urate
 Complications
Renal Failure
ARF can be caused by
hyperuricemia, chronic
urate nephropathy
Nephrolithiasis
Joint deformity
Recurrent Gout
 COMPLICATIONS
B
Progressive articular destruction with joint
limitations
Recurrent attacks
Septic arthritis
M Acute uric acid nephropathy
Nephrolithiasis
Chronic renal insufficiency from deposition of
MSU crystals
Tophi

H
 PSEUDOGOUT
Calcium pyrophosphate Crystal Deposition Disease
(CPPD) is the syndrome secondary to the calcium
pyrophosphate in articular tissues.
This includes: Chondrocalcinosis, Chronic CPPD and
Pseudogout.
 Pseudogout
Etiology: It is unknown, but can be secondary to
changes in the cartilage matrix or secondary to
elevated levels of calcium or inorganic pyrophosphate.
Pathology: CPPD crystals are found in the joint
capsule and fibrocartilaginous structures. There is
neutrophil infiltration and erosions.
 Clinical Manifestations

Pseudogout: Usually presents with acute self-limited

attacks resembling acute gout. The knee is involved in
50% of the cases, followed by the wrist, shoulder,
ankle, and elbow.
It is predominantly a disease of the elderly, peak age
65 to 75 years old. It has female predominance (F:M,
2-7:1).
Prevalence of chondrocalcinosis is 5 to 8% in the
general population.
In 5% of patients gout can coexist with pseudogout.
The diagnosis is confirmed with the synovial fluid
analysis and/or the presence of chondrocalcinosis in
the radiographs.

Acute Pseudogout primarily affects men.

Disease Associations: hyperthyroidsm,

hypocalciuria, hypercalcemia, hemochromatosis,
hemosiderosis, hypophosphatasia, hypomagnesemia,
hypothyroidsm, gout, neuropathic joints, amyloidosis,
trauma and OA.
Chronic CPPD: predominately affects women; it is a
progressive, often symmetric, polyarthritis.
Usually affects the knees, wrists, 2nd and 3rd MCP’s,
hips, spine, shoulders, elbows and ankles.
Chronic CPPD differs from pseudogout in its
chronicity, involvement of the spine and MCP’s.

Chondrocalcinosis: Generally is an incidental

finding in XRays.

Diagnostic Tests: Inflammatory cell count in the

synovial fluid. Rhomboidal or rodlike intracellular
crystals. Imaging studies reveal chondrocalcinosis
usually in the knee, but can be seen in the radial joint,
symphisis pubis and intervertebral discs.
 Differential Diagnosis pseudogout

Gout
negative birefringent needle-shaped intraleukocytic
crystals
yellow when parallel
blue when perpendicular
Pseudogout
rod- or rhomboid-shaped crystals with opposite
refractive properties
Pseudogout
Differential Diagnosis: Includes septic arthritis, gout,
inflammatory OA, Rheumatoid Arthritis, neuropathic
arthritis and Hypertrofic Osteoarthropathy.
 Pseudogout
Therapy: It is similar to gout and includes
intrarticular corticosteroids. Colchicine can be used in
acute attacks and also in prophylaxis. There is no
specific treatment for chronic CPPD. It is important to
treat secondary causes and colchicine could be helpful.
THANK YOU
B