Common Rheomatological Problem.د-وفاء (1).pdf

Rheumatoid Arthritis
Osteoarthritis
Gout
Diagnosis and management

1. 5/19/2024 1
Common Rheumatologic problem
By dr wafa sheikh
Consultant Family Medicine

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Rheumatoid arthritis
Rheumatoid arthritis is a chronic inflammatory disorder
characterised by a chronic polyarthritis that primarily affects the
peripheral joints and related periarticular tissues.
It usually starts as an insidious symmetric polyarthritis, often with
non-specific systemic symptoms.
Diagnostic criteria include arthritis lasting longer than 6 weeks
(although evidence suggests that 12 wks is more specific), positive
rheumatoid factor, and radiological damage.

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Rheumatoid arthritis
INCIDENCE/PREVALENCE
Prevalence ranges from 0.5-1.5% of the population in industrialised
countries.
Rheumatoid arthritis occurs more frequently in women than men
(ratio 2.5 : 1).
The annual incidence in women was recently estimated at 36/100
000 and in men at 14/100 000.
AETIOLOGY/RISK FACTORS
The evidence suggests that the cause is multifactorial in people with
genetic susceptibility.

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American Rheumatism Association revised criteria for rheumatoid
arthritis classification 2008
Fourof the sevencriteria must be present, and at least one of the
first fourmust be present for at least 6 weeks.
Morning stiffness in and around joints, lasting more than 1 hour
Arthritis of three or more joint areas involved simultaneously
Arthritis of at least one area in a wrist, metacarpophalangeal (MCP), or
proximal interphalangeal (PIP) joint
Symmetric arthritis involving the same joint areas
Rheumatoid nodules
Positive serum rheumatoid factor
The symptoms cannot be accounted for by another illness such as
polyarteritis nodosa or lupus.

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Deforming arthritis characterized by ulnar deviation and swan neck
deformities & Swelling of the metacarpophalangeal joints .

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Initial investigation RA
AST, ALT, alkaline phosphatase.
CBC.
BUN, creatinine.
Hand x-rays.

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Radiological changes
Plain radiographsTo be detected by plain radiography, erosions
must have eroded through the cortex of the bone around the
margins of the MCP and PIP joint & can be identified by plain
radiography in 15 to 30 percent of patients in the first year of the
disease.
Magnetic resonance imaging (MRI)
a more sensitive technique than plain radiography .

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Tenosynovitis & synovitis
Synovial cysts
Displaced/ ruptured tendons
Bony erosions***Hallmark***
Lateral view of the elbow in a
patient with rheumatoid arthritis
(RA) reveals
soft tissue swelling and
osteopenia with destruction of the
elbow joint.

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Radiology
Marginal cortical
erosions
Subluxation/dislocation
lesser MPJ
Jointt space narrowing
Well marginated spur

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Laboratory markersRheumatoid arthritis (RA
Rheumatoid factor titers rarely change with disease activity, and
are not useful for following patients with RA, although whether or not
a patient's rheumatoid factor is positive is helpful in determining
prognosis
Anti-cyclic citrullinated peptide (CCP) Antibodies, a post-
translationally modified amino acid created by deimination of
arginine residues, may be as sensitive and more specific than
assays for RF for the diagnosis of RA. may be a better predictor of
progression to erosive joint disease than RF titers early in the
course of RA .

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Clinical evidence Rheumatoid arthritis
Beneficial
Antimalarials
Early intervention with disease modifying antirheumatic drugs
Methotrexate
Minocycline
Short term low dose oral corticosteroids
Sulfasalazine
Likely to be beneficial
Auranofin (less effective than other disease modifying antirheumatic drugs)
Leflunomide (long term safety unclear)
Treatment with several disease modifying antirheumatic drugs combined
Tumour necrosis factor antagonists (long term safety unclear)
Trade off between benefits and harms
Azathioprine
Ciclosporin
Cyclophosphamide
Long term low dose oral corticosteroids
Parenteral gold
Penicillamine

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Rheumatoid arthritis
Beneficial
AntimalarialsOne systematic review has found that
hydroxychloroquine reduces disease activity and joint inflammation
compared with placebo in people with rheumatoid arthritis.
MethotrexateOne systematic review has found that methotrexate
reduces joint inflammation and radiological progression and
improves functional status compared with placebo in people with
rheumatoid arthritis. One systematic review and subsequent RCTs
have found no consistent differences in efficacy between
methotrexate versus leflunomide, parenteral gold, or etanercept.
Minocycline
RCTs have found that minocycline improves control of disease
activity compared with placebo.

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Rheumatoid arthritis
Beneficial
One systematic review and one additional RCT found that Early
intervention with disease modifying antirheumatic drugs(oral
gold, intramuscular gold, hydroxychloroquine, methotrexate,
minocycline) significantly improved radiological progression, swollen
joint counts, and quality of life scores at 12-60 months compared
with delayed treatment.
One systematic review has found Short term low dose oral
corticosteroidsfor several weeks significantly reduces disease
activity and joint inflammation compared with placebo.

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Rheumatoid arthritis
Likely to be beneficial
One systematic review has found that Auranofin(oral gold) versus
placebo reduces disease activity and joint inflammation, but found
no evidence on radiological progression or long term functional
status.
One systematic review has found that leflunomideversus placebo
reduces disease activity and joint inflammation, improves functional
status and health related quality of life, and decreases radiological
progression.

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Trade off between benefits and harms
Azathioprine
Ciclosporin
Cyclophosphamide
Long term low dose oral corticosteroids
Parenteral gold
Penicillamine
systematic reviews & subsequent RCTS has found that these
drugs significantly reduces disease activity and joint inflammation,
improves functional status, and may decrease the rate of
radiological progression but Common and potentially serious
adverse effects limit the usefulness of these drugs.

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Rheumatoid arthritis
PROGNOSIS
The course of rheumatoid arthritis is variable and unpredictable.
Some people experience flares and remissions, and others a
progressive course. Over the years, structural damage occurs,
leading to articular deformities and functional impairment. About half
of people will be unable to work within 10 years.5 Rheumatoid
arthritis shortens life expectancy

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Osteoarthritis
Osteoarthritis is a heterogeneous condition for which the prevalence, risk
factors, clinical manifestations, and prognosis vary according to the joints
affected.
It most commonly affects knees, hips, hands, and spinal apophyseal joints.
It is characterised by focal areas of damage to the cartilage surfaces of
synovial joints, and is associated with remodelling of the underlying bone
and mild synovitis.
Risk factors for osteoarthritis include abnormalities in joint shape, injury,
and previous joint inflammation.
Obesityis a major risk factor for osteoarthritis of the knee.

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Osteoarthritis (OA)
The classic criteria method for OA of the kneeis based upon the presence
of knee pain plus at least three of the following six clinical characteristics :
Greater than 50 years of age
Morning stiffness for less than 30 minutes
Crepitus on active motion of the knee
Bony tenderness
Bony enlargement
No palpable warmth
These criteria result in a sensitivity and specificity for OA of 95 and 69
percent, respectively.

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Clinical manifestations of osteoarthritis
Age of onset Usually after age 40
Commonly
affected joints
Cervical and lumbar spine, first carpometacarpal joint, proximal interphalangeal
joint, distal interphalangeal joint, hip, knee, subtalar joint, first metarsophalangeal
joint
Uncommonly
affected joints
Shoulder, wrist, elbow, metacarpophalangeal joint
Symptoms Pain, stiffness, gelling
Findings on
physical
examination
Crepitus, bony enlargement, decreased range of motion, malalignment, tenderness
to palpation
Synovial fluid
analysis
Clear fluid, WBC <2000/mm3, normal viscosity
Radiographic
features
Joint space narrowing, subchondral sclerosis, marginal osteophytes, subchondral
cysts
Patterns of
presentation
Monoarticular in young adult; pauciarticular, large-joint in middle age; polyarticular
generalized; rapidly progressive; secondary to trauma, congenital abnormality, or
systemic disease
Prognosis Variable, generally slowly progressive

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Nodal osteoarthritis: ( osteophytes spurs )
•Characteristic bony enlargement of DIJ (Heberden's nodes)
•Occassionally PIJ (Bouchard's nodes) that resemble those of R.A.

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Osteoarthritis (OA)
NON-SURGICAL TREATMENTS
Beneficial
Exercise and physical therapy (pain relief and improved function)
Oral NSAIDS (short term pain relief only)
Likely to be beneficial
Acupuncture
Chondroitin
Corticosteroids (intra-articular short term pain relief)
Hyaluronan (intra-articular)
Joint bracing
Simple oral analgesics (short term pain relief only)
Taping
Topical NSAIDS (short term pain relief

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NON-SURGICAL TREATMENTS
Beneficial
Osteoarthritis (OA)
Systematic reviews and subsequent RCTs found that Exercise and
physical therapyreduced pain and disability in people with knee
osteoarthritis.
One systematic review and two subsequent RCTs found that oral
(NSAIDs) reduced short term pain compared with placebo
.Systematic reviews and subsequent RCTs found evidence that oral
NSAIDs are more effectivethan paracetamol (acetaminophen) in
reducing pain symptoms.

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Osteoarthritis (OA)
Likely to be beneficial
AcupunctureTwo systematic reviews and three subsequent RCTs
found limited evidence that acupuncture improved pain and function
compared with control.
ChondroitinOne systematic review and one subsequent RCT
found that oral or intramuscular chondroitin reduced pain and
improved function compared with placebo.

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Osteoarthritis (OA)
Likely to be beneficial
Hyaluronan (intra-articular)One large systematic review and one
subsequent RCT found that intra-articular hyaluronan and
hyaluronan derivatives improved pain and function compared with
placebo and had a longer lasting beneficialeffect than
corticosteroids for measures of pain and function at 5-13 weeks after
injection.
Joint bracingOne systematic review found limited evidence that a
brace or neoprene sleeve improved pain and function compared
with medical treatment alone. It also found that a brace improved
pain and function compared with neoprene sleeve at 6 months.

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Osteoarthritis (OA)
Likely to be beneficial
Simple oral analgesics (short term pain relief only)Systematic
reviews and subsequent RCTs provided limited evidencethat
paracetamol (acetaminophen) reduced pain compared with placebo
in the short term, but found that paracetamol was less effective than
oral non-steroidal anti-inflammatory drugs for reducing pain.
TapingOne RCT found limited evidence that taping may improve
symptoms compared with control treatment.
One systematic review and one subsequent RCT found that Topical
non-steroidal anti-inflammatory drugs reduced pain compared
with placebo at up to 2 weeks. However, two subsequent RCTs
found reduced pain and improved function at 4 and 12 weeks
compared with placebo.

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Osteoarthritis (OA)
Unknown effectiveness
CapsaicinWe found no systematic review or RCTs of capsaicin
Education (to aid self management) One cluster randomised RCT
found no significant difference between a primary care based
education programme for people with osteoarthritis of the knee and
waiting list control (routine care) in quality of life, pain, or disability.
GlucosamineTwo systematic reviews in people with osteoarthritis
of the knee found limited evidencethat glucosamine may be more
effective than placebo in improving pain and function.
Glucosamine was found to be as safe as placebo and less likely
than non-steroidal anti-inflammatory drugs to produce adverse
events.

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Osteoarthritis (OA)
Unknown effectiveness
Insoles One systematic review and subsequent RCTs provided
insufficient evidence to assess the effects of insoles in osteoarthritis
of the knee.
Opioid analgesicsTwo RCTs provided limited evidence that
tramadol improved some measures of pain and function but
increased adverse events compared with placebo.

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Gout
G outIs a syndrome caused by deposition of urate crystals.
It typically presents as an acute monoarthritis of rapid onset.
The first metatarsophalangeal joint is the most commonly affected
joint (podagra).
Gout also affects other joints: joints in the foot, ankle, knee, wrist,
finger, and elbow are the most frequently affected.
Crystal deposits (tophi) may develop around hands, feet, elbows,
and ears.

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Gout
Gout affects about 5% of men and 1% of women with up to 80% of
people experiencing a recurrent attack within 3 years.
Diagnosis is usually clinical, supported by signs of hyperuricaemia.
Risk factors are those which are associated with increased serum
urate concentrations, including older age, non-white ethnicity,
obesity, consumption of alcohol, meat and fish, and use of diuretics.
Hyperuricaemia may be associated with an increased risk of
cardiovascular events; we do not know if it is an independent risk
factor.

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Diagnosis: GOUT
This is usually made clinically.
TheAmerican College of Rheumatology (ACR) criteria for diagnosing
GOUT
(1) characteristic urate crystals in joint fluid;
(2) a tophus proved to contain urate crystals; or
(3) the presence of 6 or more defined clinical
laboratory and x ray phenomena .

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American College of Rheumatology criteria for acute gout
(people must fulfill 6 out of 12 criteria).
1.More than 1 attack of acute arthritis
2.Maximum inflammation developed within 1 day
3.Monoarthritis attack
4.Redness observed over joints
5.First metatarsophalangeal joint painful or swollen
6.Unilateral first metatarsophalangeal joint attack
7.Unilateral tarsal joint attack
8.Tophus (proved or suspected)
9.Hyperuricaemia
10.Asymmetric swelling within a joint on x ray film
11.Subcortical cysts without erosions on x ray film
12.Joint culture negative for organism during attack

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Gout
Plain radiograph of the hand demonstrating soft tissue calcifications
adjacent to interphalangeal joints and at the base of the thumb (arrows).
These findings represent calcification within gouty tophi

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Plain radiograph of the foot demonstrating features consistent with gout.
There is soft tissue swelling and extensive erosions involving the first
metatarsophalangeal joint, as well as calcifications within a tophus.
Gout

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Gout
Synovial fluid from a patient with acute gouty arthritis, when viewed
with compensated polarized microscopy,
reveals some needle shaped, birefringent crystals, one of which is
aligned with the axis of the compensator, and is bright yellow

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Clinincal evidence -GOUT
QUESTION: What are the effects of treatments for acute gout?
TREATMENT
Unknown effectiveness
Colchicine (oral)
Corticosteroids
Corticotropin (adrenocorticotrophic hormone)
Non-steroidal anti-inflammatory drugs
QUESTION: What are the effects of treatments to prevent gout in people
with prior acute episodes?
OPTION: ADVICE TO LOSE WEIGHT
ADVICE TO REDUCE ALCOHOL INTAKE
ADVICE TO REDUCE DIETARY INTAKE OF PURINES
COLCHICINE
SULFINPYRAZONE
XANTHINE OXIDASE INHIBITORS

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SUMMARY AND RECOMMENDATIONS
Acute Gout
The goal of therapy in an acute gout attack is prompt and safe
termination of pain and disability
We recommend NSAIDs such as (such as naproxen or indomethacinfirst
line therapy for most patients with acute gout who have no contraindications
to their use (Grade 1B).
Oral colchicineis effective for acute gout but frequently causes unpleasant
side effects. For patients intolerant of NSAIDs and for whom glucocorticoid
therapy is not appropriate, or for those who have used colchicine with
success in the past, we suggest its use (Grade 2B)
For patients who cannot take NSAIDs or colchicine and who are not
candidates for intraarticular corticosteroid injection because of polyarticular
disease, we suggest use of oral glucocorticoids(Grade 2B).

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SUMMARY AND RECOMMENDATIONS -
prevention of recurrent Gout
We recommend low dose prophylactic colchicine(0.6 mg twice daily
for patients with normal renal and hepatic function) during the
initiation of antihyperuricemic therapy (Grade 1A).
We suggest that colchicinebe continued for six months after normal
serum urate values have been obtained in patients without tophi
(Grade 2C).

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Ankylosing spondylitis (AS)
Ankylosing spondylitis (AS)is a chronic inflammatory disease
of the axial skeleton manifested by back pain and progressive
stiffness of the spine.
It characteristically affects young adults with a peak age of onset
between 20 and 30 years.
Although classically thought of as a spinal disease, radiographic
changes of the hips are present in approximately 10 percent of
patients when first evaluated by a rheumatologist .
In addition, other organs, such as the eyes, lungs, and heart, can be
affected.

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CLASSIFICATION CRITERIA FOR DIAGNOSIS OF ANKYLOSING
SPONDYLITIS
the 1984 Modified New York Criteria for ankylosing spondylitis.This
set of criteria consists of a subset of clinical parameters and a
subset of radiological parameters:
Clinical parameters
Low back pain and stiffness for more than three months that
improves with exercise, but is not relieved by rest.
Limitation of motion of the lumbar spine in both the sagittal and
frontal planes
Limitation of chest expansion relative to normal values correlated for
age and sex
Radiological parameters
Sacroiliitis grade >2 bilaterally
Sacroiliitis grade 3 to 4 unilaterally

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Flesche testThe severity of
cervical flexion deformity in
ankylosing spondylitis can be
assessed by measuring the
occiput to wall distance.
With the patient standing erect,
the heels and the buttocks are
placed against a wall, The patient
is then instructed to extend his or
her neck maximally in an attempt
to touch the wall with the occiput.
The distance between the occiput
and the wall is a measure of the
degree of flexion deformity of the
cervical spine.
Cervical flexion deformity in AS

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Schober testto measure the forward flexion of the lumbar spine in
a patient with suspected or proven ankylosing spondylitis.
With the patient standing erect, make a mark over the spinous
process of the 5th lumbar vertebra or on the imaginary line joining
the posterior superior iliac spine. Make another mark 10 cm above
it in the midline. When the patient bends maximally forward, the
distance between the two points normally exceeds 15 cm.

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Ankylosing spondylitis (AS)
An abnormal appearance of the sacroiliac (SI) joint using an
appropriate imaging technique is a hallmark of longstanding AS.
Plain spinal radiographs—An early sign of inflammatory and
destructive spinal involvement due to AS is squaring of the vertebral
bodies due to anterior and posterior spondylitis
Magnetic resonance imaging—Magnetic resonance imaging
(MRI) is more sensitive than plain radiographs in detecting the
changes of spondylitis .

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Bamboo spine in AS
Radiograph of the lumbar sacral
spine in a patient with advanced
ankylosing spondylitis showing a
"bamboo spine" with vertebral
fusion (arrows).

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Fusion of sacroiliac joints in AS
Ankylosis of the sacroiliac joint in advanced ankylosing
spondylitis with complete obliteration of the joint space.

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TREATMENT: SUMMARY AND RECOMMENDATIONS
recommend use of anNSAIDas initial therapy (Grade 1A).
The NSAIDcan be supplemented by use of an analgesic; occasionally, low potency
opiates may be used.
We recommend an exercise programfor all patients (Grade 1B).
We suggest NOT using systemic glucocorticoids (Grade 2C).
intraarticular glucocorticoidsfor persistent peripheral joint involvement, enthesitis
at sites other than the Achilles tendon, and for sacroiliitis (Grade 2B).
recommend traditional DMARD therapywith sulfasalazine for patients with
predominantly peripheral arthritis who do not respond adequately to NSAIDs, unless
there are contraindications (eg, allergy to sulfonamide antibiotics) to this drug (Grade
1A).
For patients with axial disease who do not respond to NSAIDs we recommend an
anti-TNF agent(Grade 1A).

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Osteoporosis
Definition—Osteoporosis is defined as low bone mass
with microarchitectural disruption, resulting in increased
skeletal fragility and fracture. Although bone strength is
comprised of many components, bone mineral density
(BMD) is measured most frequently in clinical practice.
Clinical manifestations—Osteoporosis is a silent
disease until fracture occurs. Complications of fractures
include pain, deformity, disability and loss of height.

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Osteoporosis

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Clinical risk factors for fracture
Advancing age
Previous fracture
Glucocorticoid therapy
Parental history of hip fracture
Low body weight
Current cigarette smoking
Excessive alcohol consumption
Rheumatoid arthritis
Secondary osteoporosis (eg, hypogonadism or premature menopause,
malabsorption, chronic liver disease, inflammatory bowel disease)

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WHO Diagnostic categories for osteopenia and
osteoporosis based upon bone mass measurements
Category Bone mass
Normal
A value for bone mineral density (BMD) within one standard deviation
of the young adult female reference mean (T-score greater than or
equal to -1 SD).
Low bone mass
(osteopenia)
A value for BMD more than one but less than 2.5 standard deviations
below the young adult female reference mean (T-score less than -1 and
greater than -2.5 SD).
Osteoporosis A value for BMD 2.5 or more standard deviations below the young adult
female reference mean (T-score less than or equal to -2.5).
Severe
(established)
osteoporosis
A value for BMD more than 2.5 standard deviations below the young
adult female reference mean in the presence of one or more fragility
fractures.

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WHO Diagnostic categories for osteopenia and
osteoporosis

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The Initial evaluation—typically begins with a history, physical
examination, and basic biochemical testing.
Lifestyle factorswhich contribute to bone loss, including smoking, excessive
alcohol, physical inactivity, and poor nutrition should be addressed.
Height and weightshould be measured.
postmenopausal women with low BMD (T-score below -2.5) and/or fragility
fracture have the following basic tests :
Biochemistry profile (especially calcium, phosphorous, albumin, total
protein, creatinine, liver enzymes including alkaline phosphates,
electrolytes)
25-hydroxyvitamin D
Complete blood count
Urinary calcium excretion

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DEXA SCAN OSTEOPROSIS

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vertebral fractures in osteoprosis

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Vertebral Fractures predict New Fragility Fractures
A woman with a vertebral fracture have a
5-fold increase in the risk of a new
vertebral fracture and a 2-fold increase in
the risk of a hip fracture
Black et al., J Bone Miner Res 1999
Melton et al, Osteoporos Int 1999
One woman in five will suffer from another
vertebral fracture within a year
Lindsay et al., JAMA, 2001

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SUMMARY AND RECOMMENDATIONS —
Prevention and treatment of osteoporosis
Nonpharmacologic therapy
Adequate calcium and vitamin D suggest for all postmenopausal
women with osteoporosis (Grade 2B).
In general, 1200 mg of elemental calcium daily, total diet plus
supplement, and 800 IU of vitamin D daily.
Important additional lifestyle measures include exercise, smoking
cessation, counseling on fall prevention, and avoidance of heavy
alcohol use for all postmenopausal women with osteoporosis.

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SUMMARY AND RECOMMENDATIONS —Prevention and treatment
of osteoporosis
Pharmacologic therapy
Postmenopausal women with established osteoporosis (T-score ≤-
2.5) or fragility fracture (hip or vertebral) be treated with a
pharmacologic agent (Grade 1A)
For the treatment of high risk postmenopausal women with T-scores
between -1.0 and -2.5, we also suggest pharmacologic therapy
(Grade 2B).
Bisphosphonates alendronateor risedronate, as first-line therapy for
the treatment of osteoporosis in postmenopausal women(Grade
2B).


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SUMMARY AND RECOMMENDATIONS —Prevention and treatment
of osteoporosis
Intravenous bisphosphonate Zoledronic acidformulation for
patients who cannot tolerate oral bisphosphonates, or who have
difficulty with dosing requirements, including an inability to sit upright
for 30 to 60 minutes (Grade 2B).
Raloxifenefor postmenopausal women with osteoporosis (low bone
mineral density [T score <-2.5] and no fragility fractures) who cannot
tolerate bisphosphonates (Grade 2B).
PTH therapyfor postmenopausal women with severe osteoporosis
(low bone mineral density [T score <-2.5] and at least one fragility
fracture) who are unable to tolerate any of the available
bisphosphonates (Grade 2B).

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