Rheumatology Labs Flashcards
acute phase reactants
*non-specific
*indicate that there is either an infectious, inflammatory, necrotic, hematologic, malignant, rheumatic problem potentially somewhere in the body
*manufactured in the liver
*some increase: ESR, CRP, fibrinogen, ferritin
*some decrease: albumin, transferrin
*2 most commonly tested to look for inflammation:
1. ESR
2. CRP
ESR (sedimentation rate, “sed rate”)
*rate that the RBCs fall over 1 hour; a measure of DISTANCE
*the more it falls, the higher the ESR
*“normal” depends on age & sex
underlying mechanism of ESR / sed rate
*RBCs are negatively charged, & charges repel each other
*cells stay high in the tube (i.e. do not fall) → low ESR
*in INFLAMMATION:
-RBC charges are overcome due to fibrinogen
-rouleaux form, which fall faster and further → higher ESR
formula for normal ESR in females
normal ESR = (age + 10) / 2
formula for normal ESR in males
normal ESR = age / 2
causes of increased ESR (sedimentation rate)
*old age
*female sex
*pregnancy
*anemia
*RBC abnormalities
*elevated fibrinogen:
-infection
-inflammation
-obesity
-malignancy
-diabetes
-ESRD
causes of decreased ESR (sedimentation rate)
*polycythemia
*RBC abnormalities
*protein abnormalities
C reactive protein (CRP)
*a protein produced by the liver that increases in response to inflammation or tissue damage in the body
*CRP rises quicker and returns to normal than ESR
*direct measurement
*cons:
-expensive
-variable reference range
-does not rise in certain conditions (i.e. lupus)
antinuclear antibody (ANA) - use
*a broad category of autoantibodies against the contents of the cell nucleus that are associated with a variety of autoimmune conditions
*used by many as a “screening test” for lupus
*appears in many rheumatic and non-rheumatic autoimmune diseases
*complicated test that needs clinical correlation
antinuclear antibody (ANA) - limitations
*present in the healthy population; makes it a horrible screening test
*only about 5% of patient with a positive ANA have lupus
*people with a relative with lupus have a 25% chance of being positive without evidence of a clinical disease
what to do with a positive ANA test
*take a detailed history & do a thorough exam
*if clinical symptoms exist, check more specific labs (anti-dsDNA, anti-Smith, anti-Scl-70)
anti-Smith antibody
*most specific antibody test for lupus (rules IN lupus)
*positive anti-Smith = prob has lupus
*not associated with disease prognosis or activity
anti-dsDNA
*specific test, not sensitive (rules IN lupus, does not rule out lupus)
*several different assays
*often rises with rising disease activity (can help with prognosis or progression of disease):
-may parallel renal activity
-follow trends in patients
anti-RO (SSA) / anti-La (SSB)
*not very specific or sensitive
*associated with multiple conditions: lupus, Sjogren’s syndrome, cutaneous lupus, neonatal lupus
*important in pregnancy (risk of congenital heart block in fetus)
*not helpful for disease activity
*if present in SLE, more likely to have severe cutaneous manifestations
anti-RO (SSA) / anti-La (SSB) in PREGNANCY
*can cause neonatal lupus:
-antibodies cross placenta at 16-18 weeks
-can cause RASH (clear within 6-8 months)
-can cause CONGENITAL HEART BLOCK:
~irreversible, may need pacer
~hydroxychloroquine may help prevent; steroids may prevent progression
*check SSA/SSB in females of child bearing age
anti-Scl-70 and anti-centromere
*most often associated with a nucleolar ANA
*antibodies associated with scleroderma
-anti-Scl70 = diffuse
-anti-centromere = limited
*has prognostic and diagnostic value
rheumatoid factor (RF)
*an IgM antibody that targets the IgG Fc region
*80% of patients with rheumatoid arthritis are positive (fairly specific and sensitive)
*can be positive in other conditions (lupus, Sjogren’s, HEPATITIS C, endocarditis, HIV, etc)
causes of “false positive” rheumatoid factor (RF)
*lupus
*Sjogren’s
*HEPATITIS , esp HEP C
*increased AGE
*endocarditis
*acute viral infection
*TB
*HIV
*interstitial lung disease
*cirrhosis
*sarcoidosis
*cryoglobulinemia
rheumatoid factor - limitations in ruling out rheumatoid arthritis
*can develop positive antibodies after symptoms start (about half of patients are negative at onset of disease)
*some never develop antibodies (seronegative rheumatoid arthritis)
anti-cyclic citrullinated peptide (anti-CCP)
*joints have high incidence of citrullinated antigens
*high SPECIFICITY (rule IN) for rheumatoid arthritis; may be present years before
*positive carries worse prognosis: worse disease, more radiographic damage
anti-neutrophil cytoplasmic antibody (ANCA)
*seen in many diseases, but most classically vasculitis
*3 types of ANCAs:
1. cytoplasmic (c-ANCA): against PR3
2. perinuclear (p-ANCA): against MPO
3. atypical: against many different antigens
c-ANCA - associations
*granulomatosis with polyangiitis (GPA)
*c-ANCA = anti-PR3
p-ANCA - associations
- microscopic polyangiitis
- eosinophilic granulomatosis with polyangiitis (EGPA)
- polyarteritis nodosa
*p-ANCA = anti-MPO
atypical ANCA - associations
*cocaine-induced vasculitis
*inflammatory bowel disease (also p-ANCA)