Crystal Deposition Arthritides

Gout Remedy Report

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• Urate crystal deposition in joints and other tissues — acute and chronic inflammation Epidemiology

• More common in men than in women; peak incidence 5th decade

• Most common cause of inflammatory arthritis in men over 30

• Rare in premenopausal women (estrogens promote renal urate excretion)

• Risk factors: metabolic syndrome. HTN. chronic kidney disease; t intake of meat.

seafood, and EtOH (lancet 2004:363:1277; NijM 2004:3S0.1093) Etiologies (A/mats 2005:143:499)

Uric acid (UA) is end product of purine catabolism and is renally excreted.

Serum level reflects balance between production and excretion.



Primary hyperuricemia


Rare inherited enzyme (HGPRT. PRPP) defic.


Secondary hyperuricemia

t meat, seafood, EtOH intake Myelo- & lymphoproliferative dis.

Chronic hemolytic anemia Cytotoxic drugs, psoriasis Severe muscle exertion


1 renal function Drugs: diuretics. PZA.

EMB. salicylates. CsA Keto- or lactic acidosis

Clinical manifestations

• Acute arthritis: sudden onset, painful monoarticular arthritis; flares episodic location: MTP of great toe ("podagra"), feet, ankles, knees; occasionally polyarticular overlying skin is warm, tense, dusky red; Pt may be febrile précipitants: rapid A UA Î purine or alcohol; surgery; infection; diuretics, dehydration recovery: subsides in 3-10 d; intercritical period • remission of joint pain between attacks

• Tophi: deposits of urate crystals foreign body rxn and deposition in SC tissue &

joints; commonly in joints of fingers, wrists, knees; also on pinna. Achilles tendon, and pressure areas, eg. ulnar aspect of forearm

• Bursitis: olecranon, patellar (must be differentiated from intra-articular effusion)

• Chronic tophaceous gout chronic arthritis from tophus formation pain, joint erosion

• Renal: uric acid stones; urate nephropathy (interstitial deposits)

• Asymptomatic hyperuricemia: serum UA > 6.8 mg/dl w/o disease manifestations Diagnostic studies

• t UA. but can be misleading and does not make the diagnosis of acute attack

• Arthrocentesis take care not to tap through an infected area thus introducing infection s into joint space polarized microscopy — needle-shaped, negatively birefringent crystals (yellow parallel and blue perpendicular to axis marked on polarizer), intra- or extracellular WBC 20.000-100,000/mm\ > 50% polys infection can coexist with ocute attacks. . always check Gram stain and culture

• Radiographs early — show soft tissue swelling, useful to exclude chondrocalcinosis or septic changes late -* bony erosions with overhanging edge, soft tissue calcifications within tophi

Acute Treatment for Gout




(PO or IV)

i inflammation Inhibits polymerization of microtubules prevention of Chemotaxis and phagocytosis

Gastritis; I dose in renal insufficiency Nausea, vomiting, and diarrhea IV and high PO doses — bone marrow suppression, myopathy, neuropathy 1 dose in renal insufficiency



(SC. IM. or IV)

J inflammation

Highly effective for recalcitrant cases Rule out joint infection first

Chronic treatment

• 4 urate production by I dietary intake of meat and seafood (note: vegetables high in purines are not associated with Î risk); * intake of lowfat dairy products; i alcohol (esp. beer); weight control

• Avoid dehydration and hyperuricemic drugs (eg. diuretics, low-dose ASA)

• Prophylaxis if frequent attacks or starting antihyperuricemic therapy:

daily low-dose colchicine (-50% . risk of acute flare; J Rheom 2004:31:2429) NSAIDs (less evidence of effectiveness; Ann Rhtum On 2006:65:1312)

• Antihyperuricemic therapy for tophi, frequent attacks, nephrolithiasis; goal UA <6 mg/dl however, do not start w/o prophylaxis and until 2-4 wks after acute attack as A in serum

UA concentration can precipitate an attack allopurinol (xanthine oxidase inhibitor); side effects: hypersensitivity, rash, diarrhea, dyspepsia, headache, renal failure. BM suppression, and hepatitis: CBC monitoring and dose adjustment necessary in Pis concurrendy taking AZA probenecid or sulfinpyrazone (uricosuric agents) for underexcreters (urine UA - 600 mg/24 h)

febuxostat (nonpurine xanthine oxidase inhib. N£JM 2005:353:2450) awaiting FDA approval

Calcium Pyrophosphate Dihydrate (CPPD) Deposition Disease


• Deposition of CPPD crystals w/in tendons, ligaments, articular capsules, synovium, cartilage

• Acute inflammation due to CPPD crystals in a joint is termed pseudogout

• Chondrocalcinosis calcification of cartilage visible on radiographs, resulting from CPPD

deposition in articular cartilage, fibrocartilage. or menisci


• î synovial & joint fluid levels of inorganic pyrophosphate produced by articular chondrocytes from ATP hydrolysis in response to a variety of insults or inherited defects favors CPPD crystallogenesis and deposition in the cartilage matrix


I • More common in elderly. 20% over age 60 have CPPD of knee joints in autopsy studies Etiologies

• Most cases idiopathic, but consider search for underlying cause, especially in the young

• Metabolic: hypomagnesemia. alkaline phosphatase deficiency, hyperparathyroidism.

hypothyroidism, familial hypocalciuric hypercalcemia, gout. Gitelman's syndrome. X-linked hypophosphatemic rickets, hemochromatosis

• joint injections with hyaluronate can precipitate attacks

• Familial chondrocalcinosis (autosomal dominant disorder)

Clinical manifestations

• Pseudogout: acute mono- or asymmetric oligoarticular arthritis, indistinguishable from gout except through synovial fluid exam for crystals location: knees, wrists, and MCP joints précipitants: surgery, trauma, or severe illness

• "PseudoRA": chronic polyarticular arthritis with morning stiffness; * RF

• Premature OA: destruction of articular cartilage and bony overgrowths — degen. of joints

Diagnostic studies

• Arthrocentesis take care not to tap through an infected area thus introducing infxn into joint space polarized microscopy — rhomboid-shaped, weakly positively birefringent crystals

(yellow perpendicular and blue parallel to axis marked on polarizer) WBC 2000-100,000/mm,i >50% polys infecvon con coexist with acute attacks, always check Gram stain and culture

• Screen for associated metabolic diseases when dx a new case: / Ca. Mg, TSH, Fe. glc. UA

• Radiographs: though not a prerequisite for the diagnosis of CPPD disease.

chondrocalcinosis appears as punctate and linear densities in articular cartilage, menisci, triangular fibrocartilage of the wrist, small joints of fingers, and symphysis pubis


• Acute therapy for pseudogout: same as for gout, though colchicine not as effective

• Chronic therapy treat predisposing disease

• Low-dose daily colchicine may be effective prophylaxis in some Pts



Definition (Aiwrfj 2002.136 896)

• A spectrum of systemic inflammatory arthritides w/ predilection for the spine, entheses, sacroiliac, and peripheral joints

• Notable for absence of rheumatoid factor or autoantibodies; * t ESR

• T prevalence of HLA-B27 (© in 50-90% vs. 6-8% of general pop.), but not used for dx

• Synovial fluid of affected joints shows an inflammatory, nonseptic picture

Ankylosing Spondylitis


• Onset in teens or mid-20s; onset after age 40 very unusual; male.female ratio 3:1;

Clinical manifestations

• Gradual onset of chronic, intermittent bouts of lower back pain and stiffness

• Morning stiffness that improves with hot shower and exercise

• Progressive limitation of motion in cervical, thoracic, and/or lumbar spine over time

© modified Wright-Schober test (<4 cm t in distance becween a point at lumbosacral jxn and one 10 cm above, when going from standing to maximum fonvard flexion)

• Enthesitis: inflammation at site of tendon/ligament insertion into bone. eg. Achilles tendinitis, plantar fasciitis, rigidity of spine (bamboo spine by x-ray)

• Arthritis in peripheral joints can occur, eg. hips, shoulders, knees

• Acute anterior uveitis (25-40% at some time during disease): presents with unilateral blurred vision, lacrimation. and photophobia

Cardiovascular disease (5%): ascending aortitis. Al. conduction system abnormalities

• Neurologic complications: spinal fractures. C1/2 subluxation, or cauda equina syndrome Imaging studies

• Radiographs of spine to assess progression of disease:

Sacroiliac joint disease with erosions and sclerosis

Calcification of spinal ligaments with bridging syndesmophytes ("bamboo spine") Squaring and generalized demineralization of vertebral bodies, "shiny corners"

• MRI spine to assess inflammation in sacroiliac joint

Treatment (Lancet 2007:369:1379)

• Supportive: physical therapy. NSAIDs. steroid injection

• Anti-TNF shown to improve symptoms and function (A™ Rheom Da 2006:65:423)

• Sulfasalazine and methotrexate: somewhat effective for peripheral arthritis, but little or no effect on spinal symptoms

Reactive Arthritis


• Ages 20-40; male.female ratio = 5:1; more common in Caucasians Pathogenesis

• Immune-mediated aseptic synovitis in a genetically susceptible host post-GU or CI i'n6cn

• Bacteria associated with disease

GU: Chlamydia and Ureoplasma urealyticum Gl: Shigella. Salmonella. Yersinia. Campylobacter. C. difficile Clinical presentation

• Originally described as a triad of seronegative arthritis, nongonococcal urethritis, and noninfectious conjunctivitis ("Reiter's syndrome")

• Arthritis: 10-30 d post-inciting infection mild constitutional sx. low back pain.

asymmetric, mono- or oligoarticular arthritis of primarily large joints (knees, ankles, feet), enthesopathy, and sacroiliitis. Can develop sausoge digits (dactylitis) of extremities.

• Urethritis/cervicitis: usually Chlamydia infection preceding arthritis, but also can see sterile urethritis in postdysenteric reactive arthritis

• Conjunctivitis: noninfectious, unilateral or bilateral and - uveitis, iritis, and keratitis

• Cutaneous manifestations (may go unnoticed by Pt)

circinate balantitis: shallow, painless ulcers of glans penis and urethral meatus keratoderma blenorrhagica: hyperkeratotic skin lesions on soles of feet, scrotum.

palms, trunk, scalp stomatitis and superficial oral ulcers

• Gl: diarrhea and abdominal pain either wI or w/o infectious agent

• CV: Al from inflammation and scarring of aorta and valve; conduction defects Radiographs

• Early; soft tissue swelling and effusions around affected joints

• Late: asymmetric proliferation of bone at site of inflammation

• Asymmetric sacroiliitis in 70% Pts Diagnostic studies

• PCR of urine or genital swab for Chlamydia, stool cultures. C. difficile toxin, etc.

but © studies do not rule out Treatment and prognosis

• NSAIDs. steroid injection for mono- or oligoarthritis, sulfasalazine if inflammation persists

• Antibiotics if evidence of active or antecedent infection, as cx may be ©

• Arthritis may persist for months to years and recurrences are common

Psoriatic Arthritis


• Seen in >10% of Pts w/ psoriasis (and not necessarily those with severe skin disease)

• Arthritis may precede onset of skin disease, even by years

• 20-40% of Pts with psoriatic arthritis have spinal or sacroiliac involvement

• Men and women are affected equally and most Pts in 30s and 40s Clinical manifestations

• Several clinical patterns of arthritis:

monoarticular/oligoarticular (eg. large joint. DIP joint, dactylitic digit): most common initial manifestation ■ polyarthritis (small joints of the hands and feet, wrists, ankles, knees, elbows): indistinguishable from RA arthritis mutilans: severe destructive arthritis with bone resorption axial disease: similar to ankylosing spondylitis - peripheral arthritis

• Enthesopathies. tendinitis

• Fingernails: pitting, transverse depressions, onycholysis, subungal hyperkeratosis

• Eye inflammation (30%): conjunctivitis, iritis, episcleritis and keratoconjunctivitis sicca

• Psoriatic skin lesions I Radiographs

• "Pencil-in-cup" deformity seen at DIP joints, erosive changes

• Spinal involvement, sacroiliitis Treatment

• Symptom control: NSAIDs; intra-articular glucocorticoid injections

• Anti-TNF (etanercept. infliximab, adalimumab) . progression of disease

• Sulfasalazine: only DMARD shown to Improve sx. but not progression of disease

• Other gold. MTX. CsA. AZA, leflunomide. PUVA, antimalarials, penicillamine

Enteropathy (IBD-Associated)


• Seen in 20% of Pts w/ IBD; more frequently seen in Crohn's than UC Clinical manifestations

• Peripheral, migratory, asymmetric, non-deforming oligoarthritis: abrupt onsec. large joints, course parallels Gl disease

• Spondylitis: associated more strongly with HLA-B27. course does no I parallel Gl disease

• Sacroiliitis

Erythema nodosum, pyoderma gangrenosum ( neutrophilic dermatosis -♦ painful ulcers w/ violaceous border. Ddx ind. idiopathic. IBD. RA. myelogenous leukemia), anterior uveitis


• 5-ASA compounds, etc for underlying IBD (see "IBD")

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