Gout

Dr. Müge Bıçakçıgil Kalaycı

GOUTGOUT

Common medical problem, Affects at least 1 percent of men in

Western countries, Male: female ratio 7:1 to 9:1.

Uric Acid OverproductionUric Acid Overproduction

Primary causesPrimary causes Idiopathic HGPRT deficiency Increased PRPP

activity

Secondary causesSecondary causes Excessive dietary purine

intake Increased nucleotide

turnover Myeloproliferative

disease Lymphoproliferative

disease Hemolytic anemia Psoriasis

Accelerated ATP degradation Hereditary fructose

intolerance Glycogen storage disease Severe muscle exertion Ethanol abuse

Uric Acid underexcretionUric Acid underexcretion

Renal insufficiency Inhibition of tubular

urate secretion: Keto- and

lactoacidosis

Enhanced tubular urate reabsorption: Diuretics, Insulin resistance, Dehydration

Undefined mechanism: Hypertension, Hyperparathyroi

dis Low-dose

salicylates, Pyrazinamide, Ethambutol Lead

nephropathy

GOUTGOUT

Clinical & Laboratory FeaturesClinical & Laboratory Features

StagesStages - Asymptomatic HyperuricemiaAsymptomatic Hyperuricemia

In physiological terms any level above 6.8 mg/dl is hyperuricemia, since it exceeds the soluble concentration of MSU in body fluids.

Vast majority of people with hyperuricemia will never develop symptoms.

Stages -Stages - Acute intermittent gout Acute intermittent gout

Characteristic gout attack: rapid development of warmth,

swelling, erythema and pain in the affected joint.

The initial attack is monoarticular and in 50% of cases involves the 1st

metatarsal joint, which will finally be affected in 90% of patients.

Acute PodagraAcute Podagra

StagesStages - Acute intermittent goutAcute intermittent gout

Other joints: MT, ankle, heels and knees.

Systemic symptoms: Fever, chills and malaise.

Early in the disease the episodes are infrequent

Between the attacks the previously affected joints are free of pain, despite this, MSU crystals can be

identified in the synovial fluid.

Stages – Chronic Tophaceous GoutStages – Chronic Tophaceous Gout

Usually develops after 10 years of acute intermittent gout.

In this stage the affected joints become persistently uncomfortable and swollen.

The intensity of these symptoms is much less than the acute attacks.

Stages – Chronic Tophaceous Stages – Chronic Tophaceous GoutGout

•Characterized by: •tophi formation and

•polyarticular involvement, including the small joints of the hands .

•Subcutaneous gouty tophi can be found in the fingers, wrists, ears, knees, olecranon bursa and pressure points

Tophi

Tophi

Provocative factorsProvocative factors

The degree of decrease or increasedecrease or increase in the concentration of synovial-fluid urate is more related to acute attack than the degree of hyperuricemia .

TraumaTrauma is frequently reported as an initiating event for an acute gouty attack: the attack occurs when the joint is allowed to

rest, there is arapid efflux of water from the joint

fluid and the result is sudden increase in urate concentration.

Provocative factorsProvocative factors

Alcohol ingestionAlcohol ingestion: By accelerating the breakdown of intracellular

ATP Alcohol contains large quantities of guanosine.

DrugsDrugs: thiazides, low dose aspirin.

Clinical association – Renal Clinical association – Renal

involvementinvolvement

Chronic urate nephropathyChronic urate nephropathy: Deposition of MSU in the renal medulla and

pyramids, Associated with mild microalbuminuria.

Acute uric acid nephropathyAcute uric acid nephropathy: ARF caused by hyperuricemia in tumor lysis syndrome or post chemotherapy.

Uric acid renal stonesUric acid renal stones: 10-25% of all people with gout, the incidence correlate with the serum urate

levels.

Radiological featuresRadiological features

In early stages :In early stages : Soft tissue swelling around the affected

joints Preserved joint space

Later:Later: Bony erosions that are both atrophic

and hypertrophic, Erosions with overhanging edges

Radiological featuresRadiological features

Laboratory Features and Laboratory Features and DiagnosisDiagnosis

Uric acid level in serum is of limited value in establishing the diagnosis:The majority of hyperuricemic

subjects will not develop gout.Normal level of uric acid

during gouty attack is frequent.

DiagnosisDiagnosis

Definitive diagnosis is possible only by aspiration and inspection of the synovial synovial fluidfluid or tophaceous materialtophaceous material.

Crystals are needle or rod-shaped. On compensated polarized microscopy,

they appear as a bright, birefringent birefringent crystalscrystals (usually intracellular) that are yellow when parallel to the axis of slow vibration.

Crystals

TreatmentTreatment

The management of gout involvestreating acute arthritic

inflammation and urolithiasis lowering urate levels with the goal

of preventing recurrent disease and progression.

Treatment of Acute Gouty ArthritisTreatment of Acute Gouty Arthritis

NSAIDsNSAIDs are considered first-line therapy. Selective Cox-2 inhibitors are an alternative

in patients with GI contraindications.

CorticosteroidsCorticosteroids or subcutaneous injections of corticotropin are additional alternatives.

Because colchicinecolchicine adverse effects can be serious, IV colchicine should not be used.

Long-Term or Prophylactic Long-Term or Prophylactic TherapyTherapy

NSAIDsNSAIDs and colchicinecolchicine are frequently used as prophylaxis against recurrent acute gout, since such episodes are common during the initiation of uric acid–lowering treatment.

AllopurinolAllopurinol and ProbenecidProbenecid - a potent uricosuric

agents equally acceptable as first-line drug.

PSEUDOGUT- CHONDROCALCİNOSİS

CPPD Crystals Deposition Disease(PSEUDOGUT-

CHONDROCALCİNOSİS)

Can cause monoarthritis clinically indistinguishable from gout – Pseudogout.

Rheumatic manifestation of calcium pyrophosphate crystal deposition in articular cartilage (chondrocalcinosis), synovium, and periarticular ligaments and tendons

Pseudogout is most common in the knee (50%) but often also the wrist, elbow, shoulder,ankle and hand.

Identification of crystals is the only means of positive diagnosis.

Increasing age is a predisposing factor; more than 80% of patients are over 60 years old.

Peak age 65-75.

Affects one or a few joints; typically those that are weight bearing or have suffered previous injury

Slowly progressive with occasional aexacerbations , which are usualy not associated with effusion, warmth, and redness

No rest pain (unless disease is end stage ) symptoms worse with or after sustained activity

Joints show bony swelling, crepitus, and restricted movement

Ca pyrophosphate (pseudogout)

Rod or rhomboid-shaped

Weakly positive birefringent