Transcript Rheumatology

Rheumatology
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Immunologic Markers Found in
Rheumatic Diseases
Disease
Systemic lupus erythematosus (SLE)
Drug-induced lupus
Rheumatoid arthritis (RA)
Immunologic Markers
ANA (95% of patients)
Anti-dsDNA antibodies (60% of patients)
Anti-Sm antibodies
False–positive RPR (syphilis test)
Anti-histone antibodies
Ankylosing spondylitis
RF (75% of patients)
ANA (<50% of patients)
HLA-DR4 common
ANA
Anti-Jo-1 antibodies
HLA-B27 (90% of patients)
Psoriatic arthritis
Possible HLA-B27
Scleroderma
Anti-scl-70 ANA
CREST syndrome
Anti-centromere antibodies
Mixed connective tissue disease (MCTD)
Anti-RNP ANA
Sjögren's syndrome
Anti-Ro (anti-SSA) ANA
Anti-LA (anti-SSB) ANA
Polymyositis or dermatomyositis
Rheumatoid arthritis (RA)
• Chronic inflammatory disorder, with infiltration of synovial joints by
inflammatory cells and progressive erosion of cartilage and bone
• Synovial hypertrophy, with granulation tissue formation on articular
cartilage (i.e., pannus formation) caused by joint inflammation
• Most commonly seen in middle-aged women; increased frequency in
people with HLA-DR4 serotype
• PIP and metacarpophalangeal (MCP) joints usually first involved;
symmetric polyarthropathy develops, involving ankles, knees, shoulders,
hips, elbows, and spine
• H/P =
– Malaise, weight loss, insidious onset of morning stiffness with pain,
decreased mobility
– Warm joints, joint swelling, fevers, ulnar deviation of fingers; MCP
hypertrophy, swan neck deformities (i.e., flexed DIP plus hyperextended PIP),
boutonniere deformities (i.e., flexed PIP), subcutaneous nodules, pleuritis,
pericarditis, scleritis, chorea
Rheumatoid arthritis
• Labs =
– Rheumatoid factor (RF) positive in 75% of patients, but not specific for the
disease
– Positive antinuclear antibodies (ANA) in 40% of patients (see Table 9-5)
– Increased ESR, increased anticitrulline-containing protein IgM antibodies
– Joint aspiration shows 5,000–50,000 leukocytes
• Radiology = x-rays may demonstrate soft tissue swellings, joint space
narrowing, marginal bony erosions, or subluxation; MRI is more sensitive
than x-ray for detecting similar findings
• Treatment =
– Initially, NSAIDs and physical therapy, as needed
– Patients still mildly symptomatic following NSAID use may be started on
sulfasalazine or hydroxychloroquine and analgesics, as needed
– Moderate disease can be treated with methotrexate; anti-tumor necrosis
factor (TNF) drugs (e.g., infliximab) or corticosteroids may be considered
– Anti-TNF drugs and corticosteroids combined with other regimens in severe
disease
Rheumatoid arthritis
•
RA is a systemic disease, two-thirds of the patients present with constitutional
symptoms: fatigue, anorexia, weight loss, generalized weakness before onset of
the arthritis; diagnostic criteria (need four of the following):
–
–
–
–
–
–
–
•
•
•
•
Morning stiffness (>1hr) for 6wks
Swelling of wrists, MCPs, PIPs for 6wks
Swelling of three joints for 6weeks
Symmetric joint swelling for 6 wks
Joint erosions on x-rays
RF positive
Rheumatoid nodules
Joints never involved in RA: DIPs and joints of the lower back
The axial skeleton occurs less than peripheral, cervical spine is the most frequently
affected resulting in neck pain, stiffness and hyperreflexia.
RA has ↑risk of developing septic arthritis, particularly Staph. Aureu→red. swollen
joint and motion limited by pain.
RA @ ↑ risk of developing osteopenia and osteoporosis
Rheumatoid arthritis
• Once patient has erosive joint disease: a clear-cut indication for disease
modifying anti-rheumatic drugs (DMARD). Indomethacin or some other
NSAID may be used as an adjunct. These agents slow down the
progression of bony erosions and cartilage loss and therefore these agents
are now, recommended to be used earlier in the course of disease. Other
indications for their use are disease refractory to conservative treatment
and dependence on steroids. These agents include methotrexate,
hydroxychloroquine, sulfasalazine, leflunomide, etanercept, infliximab
and azathioprine.
– Methotrexate is the initial drug of choice and if not adequate, some other
DMARDs drug may be used. Its side-effects include stomatitis, nausea, anemia
and hepatotoxicity.
– Hydroxychloroquine is inferior to methotrexate even though very safe than
methotrexate.
– Leflunomide has a role in patients who have contraindications to
methotrexate such as significant pulmonary fibrosis.
– Etanercept and infliximab are the new generation TNF inhibitors, and highly
effective in patients who have refractory disease with methotrexate. They are
very expensive and are not indicated as first line of treatment.
Rheumatoid arthritis
Still’s disease
• Still’s disease (=systemic form of juvenile rheumatoid arthritis)
– Systemic features: high-grade fever, leukocytosis, fleeting maculopapular
rashes, hepatosplenomegaly, lymphadenopathy, pleuropericarditis and
myocarditis are characteristic
– Rheumatoid factor is rarely positive
– Treat: NSAIDs and monitor of the liver enzymes→if not respond to NSAIDs or
with myocarditis or anterior uveitis→corticosteroids
• Adult still’s disease is a variant of rheumatoid arthritis. It usually presents
in
– 20-30yr
– high spiking fevers
– evanescent salmon colored maculopapular or macular rash that involves
trunk and extremities.
– arthritis or arthralgias and significant leukocytosis.
– Rash typically develops along with fever. Temperature may show variation up
to 4C.
• To make the diagnosis of adult still’s disease, conditions like systemic lupus
erythematosus (SLE), rheumatoid arthritis, malignancy, infectious
mononucleosis and Parvovirus infection should not be present.
Rheumatoid factor and ANA are usually negative.
Systemic lupus erythematosus (SLE)
• Multisystem autoimmune disorder involving a variety of autoantibodies
affecting several body systems
• Antibody-mediated cellular attack occurs with deposition of antigenantibody complexes in affected tissues
• Risk factors = young women, blacks, Asians, Hispanics
• Hydralazine, procainamide, isoniazid, methyldopa, quinidine, and
chlorpromazine can cause similar symptoms that resolve when the drug is
discontinued
• H/P =
– Common findings include malar and discoid rashes, serositis, oral ulcers,
arthritis, photosensitivity, CNS symptoms, cardiac symptoms, and renal
symptoms
– Can also experience fevers, malaise, weight loss, abdominal pain, vomiting,
conjunctivitis, blindness
– Any combination of symptoms is possible and can change during the course of
the disease
SLE
• Labs =
– Positive ANA in 95% of patients (see Table 9-5)
– Anti-double-stranded DNA (dsDNA) antibodies in 60% of patients, but not
found in other rheumatologic disorders
– Presence of anti-Sm antibodies is very specific for disease
– Anti-histone antibodies may be seen for drug-induced, lupus-like symptoms
– Patients frequently have a false–positive test for syphilis
• Treatment = avoidance of sun, NSAIDs given for pain, hydroxychloroquine
improves skin and renal symptoms, corticosteroids given for
immunosuppression and to decrease exacerbations, other
immunosuppressant drugs given in cases resistant to corticosteroids,
anticoagulation required if patient considered hypercoagulable
• Complications = lupus anticoagulant and anticardiolipin antibodies
increase the risks of miscarriage and fetal death; disease follows variable
course, with some cases remaining benign and others progressing rapidly;
patient death results from progressive impairment of lung, heart, brain,
and kidney function
SLE
•
Systemic lupus erythematosus (SLE) is an autoimmune disorder involving multiple systems like
musculoskeletal, cardiovascular, hematological, skin, lungs, kidney and serous membranes. If four or more
of the diagnostic criteria set for SLE is met either serially or simultaneously diagnosis of SLE is made.
Myositis can be a feature present in cases of SLE but it is not included in the diagnostic criteria of SLE
– Systemic symptoms: Fatigue, fever, and weight loss.
– Cutaneomucous symptoms: Malar rash, discoid rash, alopecia, oral or nasopharyngeal ulcers, and
photosensitivity 3.Serositis: pericarditis, pleuritis
– 4.Nephritis: which can be
• -Mesangial, which is characterized by focal and segmental glomerular involvement with an
increase in mesangial cells;
• -Focal proliferative form;
• -Diffuse proliferative form, which is characterized by a "wire loop" pattern resulting from
immune complex deposition and subsequent thickening of the glomerular basement
membranes. It can result in irreversible changes and chronic renal failure
• -Membranous form, which is similar to primary membranous glomerulonephritis. 5.Neurologic
symptoms: Depression, psychosis, seizures, and neuropathy.
– 6.Non-erosive arthritis (>90% patients): like RA, mostly affects MCP and PIP, migratory and
asymmetrical but non- erosive.
– 7.Hematologic disease: Hemolytic anemia due to formation of autoantibodies against blood cells, a
form of type II hypersensitivity reaction→pancytopenis (↓RBC, WBC, PLT);
– 8. positive antinuclear antibodies; anti-dsDNA antibodies; anti-Sm antibodies;
6 subtypes of renal disorders in SLE
•
•
•
•
•
•
•
Type I: normal.
Type II: Mesangial is the earliest and the least severe form and is present in 10-20
percent of cases. Anti-DsDNA titers are not very high.
Type III: Focal proliferative is a severe form than Mesangial form and is present in
10-20 percent of cases. Urinalysis shows proteinuria and hematuria and serum
creatinine is elevated. Histopathology shows proliferative changes with some areas
of necrosis. Less than 50 percent of glomeruli are affected.
Type IV: Diffuse proliferative is the most frequent pattern of renal involvement
and unfortunately is the severest
form. Hematuria, proteinuria, renal insufficiency, hypertension, marked
hypocomplementemia and marked elevation of anti-DsDNA are all present.
Histopathology shows changes that are similar but more severe than in focal
proliferative type. More than 50 percent of glomeruli are affected. It has the worst
of all prognosis.
Type V: Membranous glomerulonephritis is present in 10-20% cases of SLE and
usually presents with nephrotic syndrome. Renal function is preserved. Basement
membrane is thickened and subepithelial deposits are present. It has better
prognosis than diffuse proliferative type.
Type VI: Sclerosing type represents healing of previous inflammatory damage and
presents with renal insufficiency and normal urinary sediment.
Immunosuppressive therapy is not effective in such patients as there is no active
inflammation.
Treatment of SLE renal problems
•
•
•
•
•
•
•
Type I (normal) and type II (mesangial proliferative) requires no treatment.
Extensive type III (focal segmental proliferative), and all type IV (diffuse
proliferative) require aggressive immunosuppression.
Type V (membranous glomerulopathy) requires treatment when proliferative
lesions are superimposed.
Drugs: corticosteroids→cyclophosphamide→hydroxychloroquine (safe)
Corticosteroids are the mainstay of treatment; usually IV methylprednisolone is
used. Immunosuppressive agents, like
Cyclophosphamide, may be needed when response to steroids is inadequate to
improve renal disease or the disease is aggressive.
Hydroxychloroquine is the safest drug for SLE.
– However, rarely, it may cause serious eye disease including retinopathy like macular
degeneration; corneal damage may also occur; so eye examinations at 6 months to 1 year
intervals should be performed in all such patients who are taking this drug. Visual field
defects, impaired color vision, bull’s eye pattern on funds and corneal whirls can all occur with
its use.
– The most common side effects of hydroxychloroquine are allergic skin reactions and nausea
but they are not serious ones. The incidence of nausea can be reduced if it is taken after
meals.
– Contraindications to its use include G6PD deficiency, porphyria cutanea tarda, liver failure and
hepatic failure. It is also need to be avoided in pregnancy.
– Though it may cause hepatic failure, deafness and blood dyscrasias they are very rare and can
be monitored by liver function tests (LFTs), hearing examination and CBC with differential
respectively. This monitoring is not recommended regularly.
MD SOAP CHAIR mnemonic for
symptoms of SLE
Malar rash of SLE
Polymyositis and dermatomyositis
• Progressive systemic diseases with skeletal muscle
inflammation; one third of patients with polymyositis also
have dermatomyositis (i.e., polymyositis with skin
manifestations)
• Risk factors = more common in women, blacks, elderly
• H/P =
– Symmetric progressive proximal muscle weakness (occurs in
legs first) and myalgias, muscle atrophy in later stages of disease
– Cutaneous manifestations of dermatomyositis are a red
heliotropic rash on the face, upper extremities, chest, or back;
violet discoloration of eyelids or scaly patches over hand joints
– Patients with lung involvement have dyspnea and poor
oxygenation saturation
Polymyositis and dermatomyositis
• Labs =
– Increased creatinine, aldolase, CK, aspartate aminotransferase (AST),
alanine aminotransferase (ALT), and lactate dehydrogenase (LDH)
– ANA frequently positive
– Anti-Jo-1 antibodies in patients with interstitial lung disease (see Table
9-5)
– Muscle biopsy shows inflammatory cells and muscle degeneration,
inflammatory cells within muscle fascicles in polymyositis and
surrounding muscle fascicles in dermatomyositis
• EMG = spontaneous fibrillations
• Treatment = high-dose corticosteroids, methotrexate, or
azathioprine for 4–6 wk followed by tapered dosing; IV immune
globulin or other immunosuppressants can be added to regimen in
resistant cases
• Complications = possible interstitial lung disease, increased risk of
several malignancies
Gottron’s sign = Scaly patches over the dorsum
of proximal interphalangeal and
metacarpophalangeal joints
Polymyalgia rheumatica (PMR)
• Rheumatic disease with multiple sites of muscle pain and
frequently associated with temporal arteritis; most common in
elderly women
• H/P = pain and stiffness in shoulder and pelvic girdle, difficulty
raising arms and getting out of bed because of pain, malaise,
unexplained weight loss; fever, minimal joint swelling, muscle
strength maintained, although movement limited by pain
• Labs = decreased Hct, markedly increased ESR, negative RF
• Radiology = MRI demonstrates increased signal at tendon sheaths
and synovial tissue outside of joints; positron emission tomographic
(PET) scan shows increased uptake in large vessels
• Treatment = low-dose corticosteroids, followed by tapered dosing
• Weakness is a symptom of polymyositis, but not of polymyalgia
rheumatica.
Fibromyalgia
• Disease causing chronic pain in muscles and tendons in
absence of apparent inflammation
• Unknown etiology, but frequently associated with
depression, anxiety, and irritable bowel disease
• Possible predisposition with hypothyroidism, RA, sleep
apnea; more common in women, 20–50 yr of age
• H/P = myalgias and weakness without inflammation;
“trigger points” on examination (i.e., specific locations that
when stimulated reproduce pain symptoms), fatigue;
possible depression, sleep disturbances, dizziness,
headaches, and mood disturbances
• Treatment = stretching, antidepressants (e.g., tricyclic
antidepressants [TCAs], selective serotonin reuptake
inhibitors [SSRIs]), patient education, physical therapy
modalities
Age
location
Fibromyalgia
Young adult
Polymyalgia rheumatica
>50 female
Polymyositis
40-60
Proximal muscles
ESR
Diffuse,
Pectoral and pelvic girdles,
multiple tender neck
points
musculoskeletal Stiffness (>1hr) and pain
pain,
↑↑↑↑↑↑
EMG/biopsy
-
Normal
Classic
findings
Anxiety, stress,
insomnia,
point
tenderness
over affected
muscle
Antidepressants
(amitrip
tyline),
NSAIDS,
rest
Temporal arteritis, great
response to steroids, very
high , elderly
T cell damage
myofibers→inflamm
↑, abnormal
EMG/biopsy, high risk
for cancer
complain
Treatment
Low-dose steroids; if with
giant cell arteritis→highdose prednisolone
Dermatomyositis
Muscle weakness
Muscle weakness
↑
↑
steroids
heliotrope rash;
Gottron’s sign; high
risk for cancer
(ovarian cancer)
prednisone→
methotrexate
Ankylosing spondylitis
•
•
•
Chronic inflammatory disease of the spine and pelvis that results in eventual bone
fusion
Risk factors = 20–40 yr of age, male > female, white > black
H/P =
– Hip and low back pain that is worse in the morning and following inactivity; pain improves
over course of day
– Possible limited range of motion in spine, hip, or chest
– Painful kyphosis that is relieved by bending forward
– Possible self-limited anterior uveitis
•
•
•
Labs = positive HLA-B27 in 90% of patients, increased or normal ESR, negative RF,
negative ANA
Radiology = x-ray shows bamboo spine (multiple vertebral fusions); MRI shows
increased signal in sacroiliac joints (sacroilitis) and vertebrae
Treatment = physical therapy, NSAIDs; exercise helps to prevent or delay
permanent deformities; sulfasalazine, methotrexate, or anti-TNF drugs may be
beneficial in more significant disease; joint replacement may be needed in
extremities
Sacroilitis seen in ankylosing
spondylitis
Reiter’s syndrome or Reactive arthritis
• Classic triad of urethritis, arthritis or arthralgias and
eye disease of conjunctivitis and the presence of
circinate balanitis (painless shallow ulcers present on
the glans penis or urethra).
• Onset of arthritis after infection with Chlamydia,
Salmonella, Shigella, Yersinia and Campylobacter. E.
Coli and Neisseria have not been implicated as possible
causes of reactive arthritis.
• Patients have negative rheumatoid factor. HLA-B27
positive
• NSAIDs are the mainstay of treatment of Reiter’s
syndrome/reactive arthritis.
Reiter’s syndrome or Reactive arthritis
• Typical skin lesion of Reiter’s syndrome is
– Keratoderma blennorrhagicum - It is found on palms
and soles. These lesions present as clear vesicles on
red bases and later on develop into macules or
papules. They resemble very closely to pustular
psoriasis.
Psoriatic arthritis
• Arthritis that develops in approximately 1% of patients with
psoriasis; DIP joints and spine most commonly affected
• H/P = asymmetric joint pain and stiffness, symptoms worse
in morning and improve with activity, symptoms usually
less severe than RA, possible anterior uveitis; joint line
pain, pain with stress on joints, pitting of nails
• Labs = negative RF and ANA, possible positive HLA-B27
• Radiology = x-rays show findings similar to RA and highly
destructive lesions of DIP and PIP joints (i.e., “pencil in cup”
deformities); MRI is more sensitive in finding marrow
edema
• Treatment = NSAIDs, methotrexate, sulfasalazine, or antiTNF drugs, depending on severity
Psoriatic arthritis
• Psoriatic arthritis: DIP joints; psoriatic nail disease (pitting)→sausageshaped digit; typically: skin→joint; 15% joint→skin
• It can present in 5 different forms.
–
–
–
–
–
Distal interphalangeal (DIP) joint involvement.
Asymmetric oligoarthritis.
Symmetric polyarthritis, similar to rheumatoid arthritis.
Arthritis mutilans, characterized by deforming and destructive arthritis.
Spondyloarthropathy, including both sacroiliitis and spondylitis.
• These patients often have nail changes (pitting nails and
onychodystrophy). Majority patients with psoriatic arthritis typically have
skin lesions for years before the joint involvement. However, 15% of
patients may develop joint disease prior to skin disease. DIP involvement
and the presence of nail changes may be the only clue in these patients. Xray of the joints shows both combination of erosion and bone growth.
Other changes include pencil cup deformity of fingers, fluffy periostitis,
and bilateral asymmetrical fusiform soft tissue swelling.
Psoriatic arthritis
Scleroderma
• Chronic multisystem sclerosis with accumulation of connective tissue, skin
thickening, and visceral involvement
• H/P = arthralgias, myalgias, hand swelling, Raynaud's phenomenon (i.e.,
blue distal extremities caused by arteriolar spasm), skin thickening,
esophageal dysmotility, intestinal hypomotility, dyspnea, possible
arrhythmias or heart failure
• Labs = positive anti-scl-70 ANA (see Table 9-5)
• CREST syndrome is a variant, with Calcinosis, Raynaud's phenomenon,
Esophageal dysmotility, Sclerodactyly, and Telangiectasias
– Skin thickening limited to distal extremities and face
– Labs show anticentromere antibodies
– Better prognosis than scleroderma
• Treatment = supportive care; angiotensin-converting inhibitors (ACE-I) for
malignant renal hypertension; calcium channel blockers and avoidance of
caffeine, nicotine, and decongestants to relieve Raynaud symptoms;
methotrexate or corticosteroids may improve skin thickening and
pulmonary symptoms
• Complications = pulmonary fibrosis, heart failure, acute renal failure
caused by malignant renal hypertension
Scleroderma
Scleroderma
• Diffuse scleroderma: diffuse fibrosis of skin and internal
organs.
– It usually occurs in women in their third to fifth decades.
– These patients have thickening of the skin begins in acral sites
(hands and feet) with loss of folds and wrinkles giving a mask
like appearance. Some areas may show both depigmentation
and hyper pigmentation.
– Raynaud’ s phenomena and calcinosis cutis are commonly seen.
– Polyarthralgia is an early symptom.
– Kidney: involvement→HT→scleroderma renal crisis
– Pulmonary arterial HT→RH failure
– Esophageal and gastric dysmotility→GERD
– Patients with scleroderma have positive ANA and anti Scl 70,
anti-topoisomerase-I Ab.
Mixed connective tissue disease
(MCTD)
• Overlapping features of SLE, scleroderma, and
polymyositis
• Can progress to a single diagnosis
• H/P = Raynaud's phenomenon, polyarthralgias,
arthritis, swollen hands, proximal muscle
weakness, esophageal hypomotility, pulmonary
symptoms; absence of renal and neurologic
symptoms
• Labs = positive anti-ribonucleoprotein (RNP) ANA
• Treatment = NSAIDs, corticosteroids, ACE-I,
supportive measures
Sjögren's syndrome
• Autoimmune disorder, with lymphocytic infiltration of
exocrine glands
• Can be seen in association with RA, SLE, or primary biliary
cirrhosis
• H/P = dry eyes, dry mouth, enlarged parotid glands,
purpura on legs, peripheral neuropathy, possible symmetric
arthritis associated with other autoimmune conditions
• Labs = positive anti-Ro (anti-SSA) and anti-La (anti-SSB)
antibodies
• Treatment = supportive care, corticosteroids for significant
symptoms
• Sicca syndrome is Sjögren's syndrome without a secondary
autoimmune association
Gout
•
•
•
Peripheral monoarthritis caused by deposition of sodium urate crystals in joints
Risk factors = renal disease, male gender, urate underexcretion, diuretic use,
cyclosporine use, cancer, hemoglobinopathies, excessive alcohol consumption
H/P =
– Sudden severe pain and swelling in one joint that frequently starts at night
– First metatarsophalangeal joint most commonly affected (i.e., podagra); ankle, knee, and foot
joints also common sites
– Possible concurrent fever, chills, or malaise
•
•
•
Labs = serum uric acid can be normal or increased; joint aspiration shows needleshaped, negatively birefringent crystals and several white blood cells (WBCs)
Radiology = x-ray may show punched-out bone lesions in chronic cases
Treatment =
– NSAIDs (especially indomethacin), colchicine, corticosteroids
– Decreasing alcohol and diuretic use and avoiding foods high in purines (e.g., red meats, fish)
help prevent exacerbations
– Probenecid (inhibits kidney uric acid resorption) or allopurinol (inhibits uric acid formation)
used in cases of chronic gout to prevent flare-ups
•
•
Complications = long-standing disease leads to chronic tophaceous gout with
formation of nodular tophi (large deposits of crystals in soft tissues), leading to
permanent deformity
Allopurinol should not be administered in acute attacks of gout.
Synovial aspirate from patient with
gout; under polarized light
Pseudogout (calcium pyrophosphate
dihydrate deposition disease, or CPPD)
• Calcium pyrophosphate dehydrate crystal deposition in
joints
• Familial condition associated with other endocrine diseases
(e.g., DM, hyperparathyroidism)
• H/P = similar presentation to gout, but less severe
symptoms; knee and wrist most commonly initially
affected joints
• Labs = joint aspiration shows positively birefringent,
rhomboid crystals
• Radiology = x-ray may show chondrocalcinosis (i.e.,
calcification of articular cartilage in joints)
• Treatment = NSAIDs, colchicine
• Podagra rules out CPPD and suggests a diagnosis of gout.
Synovial aspirate from patient with
pseudogout; under polarized light
Pseudogout
• Hemochromatosis is clearly associated (50%) with pseudogout.
Pseudogout also occurs more frequently in patients with
transfusion hemosiderosis, hyperparathyroidism,
hypomagnesemia, hypophosphatemia and hypothyroidism.
• Pseudogout: acute inflammatory changes of the large joints, most
commonly the knee joint. It is associated with fever, chills, and
leukocytosis. Synovial fluid analysis may show a leukocyte count as
high as 100,000/cmm. Do not confuse with septic arthritis. Gram
stain is usually negative in pseudogout. Episodes may be
precipitated by surgery or trauma and can last up to 10 days if not
treated. The diagnosis is confirmed by the finding of positively
birefringent calcium pyrophosphate crystals released from sites of
chondrocalcinosis (calcification of articular cartilage) into joint
space.