RUINS IN POMPEI, ITALY

GOUT & PSEUDOGOUT By: Dr WAQAR MBBS, MRCP, ASST. PROFESSOR MAAREFA COLLEGE

GOUT 1) Definition: It is an inflammatory arthritis, due to deposition of uric acid crystals (in the form of sodium urate), in the joints. In “most” cases, it is associated with high uric acid in blood. Normal uric acid levels in the blood: *Males: upto 7mg/dl * Females: upto 6mg/dl Uric acid is produced from purines during daily cell breakdown, & then excreted in urine.

PATHOGENESIS * In gout, uric acid forms insoluble crystals ( sodium urate) which get deposited in the joint space & periarticular tissues. * These crystals then initiate inflammation which causes joint pain & swelling. *In the long run, crystals may also deposit under the skin, in tendons & in kidneys, causing “tophi” in the skin & tendons , & renal stones & renal insufficiency in the kidneys.

GENERAL POINTS ABOUT GOUT More common in males ( M:F 10:1) More in obese people Usually in adulthood ( older males) Family history often present 6) Hyperuricemia can be asymptomatic (no gout) 7) Gout can occur even with normal uric acid level * Male a classic * Obese case, but not * Above 40 “laazim”

CAUSES OF HYPERURICEMIA /GOUT Overproduction Decreased excretion of uric acid of uric acid ( much less common) ( most common) (CAN BE ASSESSED BY COLLECTING 24hrs. URINE) OVERPRODUCTION: * High purine synthesis ( due to some enzyme defect ( Lesh-Nyhan syndrome) * Leukemias conditions of high cell * Polycythemia production & so high * Psoriasis cell destruction

Causes of gout(contd.) * Tumor lysis syndrome ( destruction of cancer cells by chemo.) 2) DECREASED EXCRETION * Idiopathic ( primary gout): In these patients, cause of decreased excretion of uric acid is not known. 90% cases of gout are this ( prim. gout due to underexcretion) * Drugs ( thiazides, low dose Aspirin) * Alcohol * Renal failure * Dehydration

POSSIBILITIES WITH HYPERURICEMIA Acute gout Chronic gout Asymptomatic Renal stones ACUTE GOUT This is an acute attack of severe inflammation in the affected joint. Occurs suddenly & lasts for a few days. Most common joint is 1st metatarsophalyngeal joint of the foot( big toe) Severe pain, redness, swelling & hot Presentation can also be in other joints eg. ankle, knees, wrists, either singly or together

acute gout in big toe acute gout in ankle

Acute gout (contd) INVESTIGATIONS: Serum uric acid: * Usually high but 20% cases can have normal levels, so it is not 100% diagnostic 2) Joint fluid exam.: * Shows typical “needle shaped” crystals which are negatively birefringent under polarised light microscopy. This test is diagnostic, but not done frequently. If S/S are suggestive & uric acid is high, treatment is started for the acute attack without fluid test.

Synovial fluid under polarised light showing Needle shaped urate crystals

3) Leucocytosis & high ESR ( due to inflamm.) 4) X-Ray: a) May be normal in acute gout b) Chronic gout usually shows X-ray changes What Can Precipitate Acute Attack? Anything which worsens the hyperuricemia eg: Infections 2) Any surgery 3) Excess alcohol 4) Excess meat( red meat, liver, kidneys) 5) Sea- -food 6) Drugs ( which?)

TREATMENT OF ACUTE GOUT NSAIDs Steroids Colchicine Non-drug measures NSAIDs: Drugs of 1st choice. * Given in high doses initially * Indomethacin 50 mg tid, Diclofenac 50mg bd * Given for 1 -2 wks. 2) Corticosteroids: * Oral tabs ( prednisone) or intra-articular inj. * Used if NSAIDs can not be given or not helping * After few days, taper & stop * Before giving intra articular, exclude joint infec.

Rx of Acute gout (contd) 3) Colchicine: ( tablets) * Another alternative if NSAIDs can’t be given * Best effect if given in the first 12 -24 hrs. * Main side effects: Nausea, diarrhea, abd. pain * Not used too much these days 4) Non-drug measures: * Wt loss * Avoid purine rich foods(red meat, liver, shrimp, certain fish) 5) Avoid alcohol & certain drugs (thiazides, aspirin)

REMEMBER ! All the drugs used in the acute attack are analgesics & anti-inflammatory. They do not lower the uric acid levels. During the acute attack, do not lower the uric acid levels, coz it will worsen the attack.

D/D of acute gout 1) Septic artrhitis 2) Reactive arthritis 3) Psoriatic arthritis 4) Pseudogout ( reactive arthritis is a type of arthritis which occurs secondary to infections like urethritis, GI infections) CHRONIC GOUT Recurrent attacks of acute gout can cause chronic pain in the joints. This is called chronic gout & is chatacterised by: * Chronic pain * Joint deformity * Tophi: These are subcutaneous nodules made of uric acid. Found usually in the ear cartilage, fingers, olecranon process & Achilles tendon.

tophus in the ear tophus in the elbow

Tophus in Achille’s tendon tophi in fingers

X rays in Chronic gout Erosions wth overhanging edges

X-ray showing Tophi

X RAY FEATURES OF CHRONIC GOUT Joint destruction Bone erosion with overhanging edges Tophi

OTHER EFFECTS OF PERSISTENT HYPREURICEMIA Uric acid stones in the urinary tract Damage to the renal tubules, causing renal failure ( so check urea & creatinine in gout patients)

TREATMENT OF CHRONIC GOUT Uric acid Colchicine Non-drug Lowering drugs measures

Uric Acid Lowering Drugs Drugs which decrease Drugs which increase uric acid production uric acid excretion * Allopurinol * Probenecid * Febuxostat * Uricase Drugs are given lifelong. Aim is to keep uric acid less than 6mg/dl in blood

Drugs which decrease uric acid produc. * Allopurinol, Febuxostat, Uricase * Allop. & Febux. inhibit the enzyme “xanthine oxidase”( involved in uric acid synthesis). * Uricase: Changes uric acid to another substance 2) Drugs which increase uric acid excretion ( uricosuric drugs) * Probenecid *Not given if renal excretion of uric acid is already high, urate stones or urate nephropathy present * Less effective than Allopurinol

Indications of urate lowering therapy 1) If more than 2 acute attacks /yr. 2) Chronic gout (wth/wthout tophi) 3) Uric acid stones or urate nephropathy If the above criteria are not present, no need to lower uric acid, even if it is high. Very Imp. points about urate lowering Rx Never start during an acute attack. Start at least 2-3 wks after the attack. 2) Give NSAIDs or Colchicine alongwith these drugs, for a few weeks.

Non-Drug Measures for Chronic Gout Wt loss Avoid purine rich foods (red meat, liver, certain fish, shrimps, alcohol) 3) Stop drugs like thiazides, ASA Management of Asymptomatic Hyperuricemia No treatment needed Treatment is given only if there are renal stones or renal failure due to uric acid nephro- - pathy. ( give urate lowering drugs in case of no.2)

When chemotherapy is given for any cancer excess breakdown of cells excess uric acid is produced can cause acute gout. This is called “tumor lysis syndrome”. To prevent this, the following steps are taken: Give Allopurinol or Uricase( urate lowering drugs) 2) Good hydration (iv fluids) before starting chemo.)

PSEUDOGOUT (CPPD) Another crystal induced arthritis Crystals of Calcium Pyro Phosphate Dihydrate Can affect any joint but most commonly wrist, knees & symphysis pubis Mostly seen in old females( gout more in males) Can present as acute monoarthritis or oligoarthritis ( like gout) or chr. polyarthritis like R.A./O.A. Joint fluid shows CPP crystals which are positively birefringent (urate crystals are negatively birefringent) ( CPPD------Positive)

Crsytals of Pseudogout are positive bire- -fringent & are of various shapes BUT NOT NEEDLE SHAPED

Pseudogout (contd) 7) Often associated wth., hemochromatosis & hyperparathyroidism 8) X-Ray shows linear opacity in the joint cartilage. (X-ray of wrists, symphysis etc) 9) Treatment: * NSAIDs , steroids or colchicine * No role of Allopurinol or probenecid * Colchicine may be given for chronic cases 10) Treat any underlying cause

X-Rays in Pseudogout

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