Gout Treatment Megan Chan, PGY-2 UHCMC 2015. Gout Acute gouty arthritis = monosodium urate crystals in synovial fluid leukocytes – Serum urate ≥ 6.8 =

Slides:



Advertisements
Similar presentations
GOUT Disease caused by tissue deposition of Monosodium urate crystals as a result of supersatuaration of extra cellular fluid with MSU.
Advertisements

Team Meeting Presentations
1 Oxypurinol for Gout Arthritis Drugs Advisory Committee June 2, 2004 Cardiome Pharma Corp Vancouver, BC Canada.
FREEDOM FROM RHEUMATOLOGICAL DISORDERS
Gout Update 2014 Bernadette C. Siaton, MD
SUA
TXF Caveat on urate levels Serum uric acid level may be normal at the time of an acute attack. Normal level does not rule out gout. May be better.
Purine degradation & Gout (Musculoskeletal Block) Purine degradation pathway Fate of uric acid in humans Gout and hyperuricemia: Biochemistry Types Treatment.
Purine Degradation & Gout (Musculoskeletal Block)
Prepared by : Tamara Odeh Diana Jawhari Supervised by : Dr. Ola Ayesh.
Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. Chapter 74 Drug Therapy of Gout.
Gout.
Gout : Clinical review and trial design issues Joel Schiffenbauer FDA/DAAODP AAC/June 3, 2004.
 Gout is characterized by elevated uric acid concentrations in blood and urine due to variety of metabolic abnormalities that include overproduction.
Gout & hyperuricemia.
Gout: Its not all crystal clear Robert L. Wortmann, M.D. Department of Internal Medicine The University of Oklahoma College of Medicine, Tulsa.
1 Uric acid and Gout James Witter MD, PhD Arthritis Advisory Meeting June 2, 2004.
Gout Dr. Wael H.Mansy, MD Assistant Professor College of Pharmacy King Saud University.
Familial metabolic disease Characterized by : Acute arthritis Uric stones in the kidneys Hyperuricemia.
Gout By Shravya & Helen. Gout is… An inflammatory arthritis associated with hyperuricaemia and intra-articular sodium urate crystals.
GOUT. Definition Heterogeneous group of diseases involving : An elevated serum urate concentration (hyperuricemia) Recurrent attacks of acute arthritis.
Gout extra Q’s. After giving Marilyn analgesia you arrange an ultrasound and guided aspiration of Marilyn's first metatarsophalangeal joint. The initial.
GOUT TREATMENT. Gout prevalence doubled over the last 20 yrs. Factors? - longevity - diuretic use - low dose ASA - obesity - end stage renal disease -
Clinical Case #6 By Chen, chun-Yu (Kim) Chen, I -chun (Afra) Chen, I -chun (Afra)
Four Stages of Gout  Asymptomatic hyperuricemia Elevated levels of uric acid in the blood but no other symptoms Does not require treatment  Acute gout/Acute.
Gout Familial metabolic disease characterized by : Acute arthritis Uric acid stones in the kidneys Hyperuricemia.
GOUT. Demographics Affects middle-aged to elderly men postmenopausal and elderly women (usually have OA and HPN causing mild renal insufficiency, and.
Agents Used to Treat Hyperuricemia and Gout
GOUT: DIAGNOSIS AND MANAGEMENT. Gout Metabolic disorder due to excessive accumulation of uric acid in tissues leading to acute and chronic arthritis and.
Drug Therapy of Gout. Drug therapy of gout What Is Gout?
Gout. The most common cause of inflammatory arthritis in US adults (3.9% of Americans; approx. 8.3 million people; ) Prevalence is greater in.
Angelo L Gaffo Kenneth G Saag Core Evidence 2009:4 25–36
Dr. Müge Bıçakçıgil Kalaycı
StagesClinical Features (1)Asymptomatic hyperuricemiahigh uric acid level is present but without symptoms (2) Acute Gouty Arthritishigh uric acid level.
Velyn Wu, MD FAAFP CAQSM 2/17/2016 Musculoskeletal Medicine
Gout -revisited Shrenik Shah. definition Monosodium urate (MSU) crystal deposition  episodic and later persistent joint inflammation and tophi All MSU.
Gout Pharmacotherapy Ryan L. Crass, PharmD PGY1 Pharmacy Resident
Gout and Pseudogout dr. MUH. ARDI MUNIR, M.Kes., Sp.OT., M.H., FICS.
Colchicine: Colchicine: Effective & specific gout Rx, but less favored than NSAIDs because of slow onset of action & high incidence of side effects. Effective.
ANTI-GOUT DRUGS. GOUT A familial metabolic disease characterized by recurrent episodes of acute arthritis due to deposits of monosodium urate in joints.
Gouty Arthritis Dr.noori rheumatologist Gout: Definitions  Gout is a disease characterized by hyperuricemia and monosodium urate deposition in the body.
© Copyright Annals of Internal Medicine, 2016 Ann Int Med. 165 (1): ITC1-1. In the Clinic Gout.
Drugs in gout epidemiology Male to female ration 10:1 Prevalence of hyperuricemia 5% Prevalence of gout 0.2%
Purine Degradation & Gout (Musculoskeletal Block) Purine degradation pathway Fate of uric acid in humans Gout and hyperuricemia: Biochemistry Types Treatment.
GOUT Katie Margelot NURS 870. Definition Gout is an acute, sudden inflammatory disease of the joint, caused by high concentrations of uric acid in the.
Gout Ashley Guzman Primary Care I: Acute and Chronic Health Problems
Crystalopathies Joanna Zalewska.
Gout Asad Khan Consultant Rheumatologist
Gout.
Drugs in gout epidemiology Prevalence of hyperuricemia 5%
Introduction to pathology
Treatment algorithm for hyperuricemia in gout
History Salient Features Physical Exam
GOUTY ARHTRITIS.
Drug Therapy of Gout 1.
GOUT.
Gout and Hyperuricaemia
Antiuricaemic drugs Dr A.W Olusanya.
GOUT By: Sunit tolia, PGY III.
Lecture 9 Musculoskeletal Disorders Gout
Scott Vogelgesang, M.D. Division of Immunology: Rheumatology & Allergy
Gout and Hyperuricaemia
Gout Scott Smith PGY-1 1/11/2018.
TREATMENT OF THE ACUTE GOUT ATTACK:
Drugs in gout epidemiology Prevalence of hyperuricemia 5%
Consultant Rheumatologist Imperial College Healthcare
Presentation transcript:

Gout Treatment Megan Chan, PGY-2 UHCMC 2015

Gout Acute gouty arthritis = monosodium urate crystals in synovial fluid leukocytes – Serum urate ≥ 6.8 = insoluble in extracellular fluids Tophi = painless nodular deposits of monosodium urate crystals in tissues Chronic urate nephropathy – Crystals deposit in renal medullary interstitium Uric acid nephrolithiasis content/uploads/image/2012_2/12%20Tophus/2aj.jpg mages/corporate/X- ray-Toe-Joint-with- Tophus-with- Calcification-Gout.jpg

Risk Factors Obesity HTN HLD HF Insulin resistance Hyperglycemia Renal disease Older age Genetics High purine/fructose diet Alcohol Meds: loop & thiazide diuretics, acetylsalicylic acid, ASA

Usually Monoarticular In order of frequency: – 1 st metatarsophalangeal joint = Podagra – Ankle – Heel – Knee – Fingers – Elbows

Lifestyle Modifications Diet Weight loss Alcohol cessation Mead T, Arabindoo K, Smith B. Managing gout: there's more we can do. J Fam Pract. 2014;63(12):

Diagnosing gout How good is joint aspiration to look for negatively birefringent crystals? – 85% sensitive, 100% specific Is imaging necessary to diagnose gout? – No, but if you got it you may see subcortical bone cysts, tophi, erosions /AA00BB07-78FF-45BD-90119D22B17E6D32.jpg

Acute Gout How useful is a uric acid level during an acute flare? – Helpful if elevated but may be falsely normal/low (25-40% of pts) 2/2 cytokine effect So when is the most accurate time to check serum uric acid levels? – ≥ 2 weeks after complete resolution of a flare

Acute Attacks Initiating treatment within 24 hours has been associated with decrease pain and shorter duration of symptoms. For mild-moderate pain involving a few small joints or 1-2 large joints  Monotherapy: – NSAIDS Naproxen 500mg BID, Indomethacin 50mg TID – Colchicine (unless >36 hrs after symptom onset due to diminished benefit) – Corticosteroids Prednisone 30-50mg daily  taper over 7-10 days post flare to prevent rebound attacks

Acute Attacks For severe pain (>6 out of 10) and/or polyarticular (≥4 joints in more than 1 region of the body)  Combination therapy: – Colchicine + NSAID – Colchicine + corticosteroids For NPO pts, can give intraarticular/IV/IM steroids or SQ ACTH Continue acute treatment until attack resolves (~5-14 days)

Mead T, Arabindoo K, Smith B. Managing gout: there's more we can do. J Fam Pract. 2014;63(12):

Chronic Gout Tx Criteria for Urate Lowering Therapy (ULT): – Presence of tophi – ≥ 2 acute attacks per year (some tx after 1 flare) – CKD stage 2-5 – Hx of urolithiasis Start ULT + anti-inflammatory prophylaxis AFTER an acute gout attack resolves. If on ULT prior to a gout attack, continue regimen. If gout symptoms persist despite serum urate level < 6.0, increase ULT to obtain a target of <5.0. When do you start ULT therapy? What do you do with ULT therapy if pt is on it and has an acute attack? What do you do if your pt still has symptoms when their serum urate is <6.0?

Urate Lowering Therapy Allopurinol = first line – xanthine oxidase inhibitor – Consider Rheum involvement if GFR <50 Febuxostat—reports of hepatic failure but not commonly seen clinically – xanthine oxidase inhibitor – Use in renal insufficiency Probenecid = alterative to those with xanthine oxidase allergy or intolerance – Increases urinary uric acid secretion – Hardly used because it’s difficult to tolerate and increases risk of nephrolithiasis

Allopurinol Hypersensitivity 1 in every 1000 patients SJS/TEN, eosinophilia, leukocytosis, fever, hepatitis, renal failure High mortality (20-25%) and no cure! Screen for HLA-B*5801 allele in high risk groups: – Koreans with CKD stage 3 or worse – All Han Chinese & Thai patients

Mead T, Arabindoo K, Smith B. Managing gout: there's more we can do. J Fam Pract. 2014;63(12):

Anti-inflammatory Prophylaxis Should be started with ULT to prevent flares: – Low-dose Colchicine (0.6 daily or BID) – Low-dose NSAIDS (Indomethacin 25mg BID) – Oral steroids (<10mg/day) = second line Should continue for whichever is greater: – 3 months after target serum urate level is achieved in those with no tophi – 6 months after target serum urate level is achieved and tophi have resolved Sometimes can take 1-2 years to wean people off without flares occurring

How long should ULT be continued? Indefinitely! How often should you monitor serum uric acid levels? – Every 2-5 weeks until target is achieved – Then every 6 months

Refractory Gout If urate does not reach goal <6mg/dL (or <5mg/dL) at max doses of first-line xanthine oxidase inhibitors. Add uricosuric agent: – Probenecid, Fenofibrate, Losartan Last resort: Pegloticase = IV pegylated q2 wks recombinant form of urate oxidase enzyme that converts uric acid to allantoin (water soluble) – Can develop Ab over time that cause infusion reactions Investigational: Anakinra = IL-1 inhibitor Note: Low adherence rate to gout therapy (<50% will take tx as prescribed in their first year). Check for this first!

Work.jpg

Summary Practice Recommendations Prescribe an anti-inflammatory drug when initiating ULT (grade A). Increase the dose of ULT to achieve a lower target of <5mg/dL if gout symptoms persist despite a serum urate level <6mg/dL (grade B). Do not initiate ULT during an acute gout flare. However, if already on ULT regimen when a flare occurs, do no stop it (grade C). Asymptomatic hyperuricemia does not equal gout and should not be treated with ULT. – However some rheumatologist will treat urate levels >13 in young pt to prevent consequences of deposition.

References Mead T, Arabindoo K, Smith B. Managing gout: there's more we can do. J Fam Pract. 2014;63(12): UptoDate Special thanks to Dr. Pioro for the special Rheum insights!