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Nucleic Acid Bases : 

Nucleic Acid Bases Purines Pyrimidines

Purine Synthesis : 

Purine Synthesis

Purine Nucleotide Synthesis : 

Purine Nucleotide Synthesis

Purine Synthesis : 

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 : 

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 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 : 

Purine Degradation The enzyme “nucleotidase” is also known as purine nucleotide phosphorylase (PNP)

Lesch-Nyhan Syndrome : 

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 : 

Allopurinol and Hypoxanthine

Uric Acid : 

Uric Acid

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.

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Plasma is saturated with monosodium urate at a 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. However, plasma urate concentrations can reach 4800 mol/L (80 mg/dL) without precipitation, perhaps because of the presence of solubilizing substances. B M H

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urate is produced only in tissues that contain 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 Two-thirds to three-fourths of urate is excreted by the kidneys, and most of the remainder is eliminated through the intestines. B M H

Renal handling : 

Renal handling Glomerular filtration Tubular reabsorption Secretion Postsecretory reabsorption

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

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Serum urate levels vary with age and sex. Children: 3 to 4 mg/dl Adult men: 6 to 6.8 mg/dl

Hyperuricemia : 


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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 : 

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 : 

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 : 

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 : 

Causes of hyperuricemia Primary No recognized cause Hypoxanthine phosphoribosyltransferase deficiency Increased phosphoribosyl pyrophosphatase activity. Secondary Hereditary fructose intolerance Mieloproliferative disease Linfoproliferative disease Hemolitic anemia Drugs: Low-doses salicylate, diuretis, pyrazinamide, ethambutol, nicotinamide, etanol

Evaluation of Hyperuricemia : 

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.

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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 : 

Complications of Hyperuricemia The most recognized complication of hyperuricemia is gouty arthritis Nephrolithiasis Urate Nephropathy Uric Acid Nephropathy

Nephrolithiasis : 

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 : 

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.

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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 : 

Asymptomatic Hyperuricemia Treatment with anthyperuricemic agents entails inconvenience, cost and potential toxicity. “Routine” treatment of asymptomatic hyperuricemia cannot be justified.

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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 : 

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 : 

Uric Acid Nephropathy Vigorous intravenous hydration and diuresis with furosemide. Acetazolamide and sodium bicarbonate (urine pH >7) Allopurinol


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

Types of microcrystals deposited : 

Types of microcrystals deposited Monosodium urate (MSU) crystals Classically termed gout Calcium pyrophosphate dihydrate (CPPD) crystals Also known as pseudogout Calcium apatite (apatite) crystals Calcium oxalate (CaOx) crystals B M H


GOUT Epidemiology: MSU gout Prevalence 1.3–3.7% in the general population Age/sex Middle-aged to elderly men Postmenopausal women More common in men than in women B M H

Epidemiology : 

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 : 

Risk Factors Aging Underlying disease (e.g., renal, joint disease) Diuretics Hypertension Obesity Transplant recipients Precipitants of an acute attack Dietary excess Trauma Surgery Excessive ethanol ingestion Adrenocorticotropic hormone (ACTH) Glucocorticoid withdrawal Hypouricemic therapy Serious medical illnesses


ETIOLOGY 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. 1 Microcrystals present in the joint are phagocytosed by neutrophils. 2 Inflammatory mediators are released, and lysosomal enzymes lead to synovial inflammation. B M H

Pathogenesis of Gouty Inflammation : 

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 : 

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

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Associated Conditions : 

Associated Conditions Cardiovascular Disease Paget’s disease Arthritis- rheumatoid and osteoarthritis Septic Arthritis Metabolic syndrome

Stages of Classic Gout : 

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 : 

Symptoms & Signs General musculoskeletal manifestations of crystal-induced arthritis Acute mono- or polyarthritis Bursitis Tendonitis Enthesitis Tophaceous deposits Peculiar type of osteoarthritis B M H

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

MSU gout : 

MSU gout Acute arthritis Most frequent early clinical manifestation Usually monoarticular Occasionally polyarticular Metatarsophalangeal joint of the first toe is most often involved (podagra).(Location of first attack in 50% of cases) B M H

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Other commonly affected joints Finger Tarsal Ankle Knee First episode frequently begins at night with dramatic joint pain and swelling. Joints rapidly become warm, red, and tender. Clinical appearance often mimics a cellulitis. B M H

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Chronic nonsymmetric synovitis May be the presentation after many acute mono- or oligoarticular attacks Tenosynovitis Chronic tophaceous arthritis Tophi are aggregates of MSU crystals surrounded by a giant cell inflammatory reaction. Extra-articular tophi Common locations include in the olecranon bursa, helix and antihelix of ears, ulnar surface of forearm, and Achilles tendon. B M H


RENAL DISEASE IN GOUT Chronic urate nephropathy 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 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. B M H

Differential Diagnosis : 

Differential Diagnosis Cellulitis Acute septic arthritis Palindromic rheumatism Psoriatic arthritis Rheumatoid arthritis Other crystalline arthropathies B M H

Diagnostic Approach : 

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

Laboratory Tests : 

Laboratory Tests 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. Characteristic needle-shaped negatively birefringent MSU crystals by polarizing microscopy Cell counts elevated from 2000–60,000/μL B M H

Diagnosis : 

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 : 

Synovial Fluid Findings Needle shaped crystals of monosodium urate monohydrate that have been engulfed by neutrophils

Diagnostic Studies : 

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.

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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 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. B M H

Screening for risk factors or sequelae : 

Screening for risk factors or sequelae Urinalysis Serum creatinine Glucose Lipids Complete blood count Thyroid-stimulating hormone B M H


IMAGING 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 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 intravenous pyelography. B M H


DIAGNOSTIC PROCEDURES Arthrocentesis for synovial joint fluid analysis MSU crystals can often be demonstrated in the first metatarsophalangeal joint and in knees not acutely involved with gout. Arthrocentesis of these joints is a useful technique to establish the diagnosis of gout between attacks. B M H

Differential Diagnosis Septic Arthritis : 

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 : 

Differential Diagnosis synovial fluid analysis gout septic WBC > 50 k 15 k (5 to 80k) PMNs > 90% ~70%

Treatment Goals : 

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 : 

Treatment Approach 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 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. B M H

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

Acute treatment cont’d : 

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

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Hypouricemic therapy has a goal of preventing future attacks and eliminating tophaceous deposits. Lifestyle modifications Control of body weight Low-purine diet Increase in liquid ingestion Limitation of ethanol intake Avoidance of diuretics Pharmacotherapy Probenecid Allopurinol Colchicine B M H

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Factors to consider in decision to initiate 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]) 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. B M H


ACUTE ATTACK Urate-lowering drugs (probenecid, allopurinol) 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. 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 B M H

Colchicine(orally) : 

Colchicine(orally) Generally effective only within first 24 hours of attack Contraindications 1.Renal insufficiency 2.Cytopenias 3.Liver function tests > 2× normal 4.Sepsis 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 can be useful. B M H

Colchicine(intravenous) : 

Colchicine(intravenous) 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 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 colchicine. B M H

Glucocorticoids : 

Glucocorticoids Oral: prednisone 30–50 mg/d tapered over 5–7 days 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 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 Both NSAIDs and colchicine may be toxic in the elderly, particularly those with renal insufficiency and GI disorders. B M H


ACTH Indications: patients with acute polyarticular refractory gout or with a contraindication for using colchicine or NSAID therapy Dose: intramuscular injection of 40–80 IU in a single dose or every 12 hours for 1–2 days B M H

Hypouricemic therapy : 

Hypouricemic therapy 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 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 mL of water every day. B M H

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Allopurinol Xanthine oxidase inhibitor 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 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 kidney disease to minimize side effects. B M H


TOXICITY 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. 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 5. Renal failure B M H

Non- Pharmacologic Treatments : 

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 : 

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

Prophylaxis : 

Prophylaxis Urate Lowering drugs Used for documented urate overproduction Goal is for serum urate concentration to 6mg/dL or less Start of therapy can precipitate acute attack; therefore, may need to use colchicine as a long as six months Xanthine oxidase inhibitors Allopurinol: blocks conversion of xanthine to uric acid. works for underexcretors and overproducers. Start typically 300mg/day and titrate weekly 100mg/day until optimal urate levels achieved. Start lower doses with renally impaired patients Uricosuric drugs Probenecid or Sulfinpyrazone: increase renal clearance of uric acid by inhibiting tubular absorption Side effects may prohibit use-GI and kidney stones Need measurement of 24hr urine in anyone for whom Probenecid therapy is initiated

Newer Therapies : 

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 : 

Complications Renal Failure ARF can be caused by hyperuricemia, chronic urate nephropathy Nephrolithiasis Joint deformity Recurrent Gout


COMPLICATIONS Progressive articular destruction with joint limitations Recurrent attacks Septic arthritis Acute uric acid nephropathy Nephrolithiasis Chronic renal insufficiency from deposition of MSU crystals Tophi B M 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 : 

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 : 

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.

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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.

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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 : 

Differential Diagnosis pseudogout Goutnegative birefringent needle-shaped intraleukocytic crystals yellow when parallel blue when perpendicular Pseudogoutrod- or rhomboid-shaped crystals with opposite refractive properties

Pseudogout : 

Pseudogout Differential Diagnosis: Includes septic arthritis, gout, inflammatory OA, Rheumatoid Arthritis, neuropathic arthritis and Hypertrofic Osteoarthropathy.

Pseudogout : 

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.

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