Arthritis in the
Elderly
“All the Pearls in 50 Minutes”
Gerald F. Falasca, M.D.
Johnson City, TN
March 2013
GOALS
• Practical advice
• Up to date on mgt
• Hone diagnostic skills
DISEASES
To Be Touched On
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Sjogren’s
PMR
DJD
RA
Gout
CASE 1
• A 70 year old woman presents
with widespread pain, stiffness
and fatigue. She recently started
keeping a water bottle at her
bedside. Physical exam is
remarkable for slight synovitis of
hands & wrists, and presence of
all fibromyalgia tender points.
CASE 1 – cont’d.
• Sed rate is 30 mm/hr but CRP is
normal CRP at 0.7 mg/dl (nl 0 - 1.0
mg/dl)
• C4 ↑ at 36 mg/dl.
• RF, CCP & ANA are negative.
CASE 1 – cont’d.
What is the most likely diagnosis?
A. Polymyalgia rheumatica
B. Rheumatoid arthritis
C. Fibromyalgia
D. Primary Sjogren syndrome
E. Paraneoplastic syndrome
Causes of Pain All Over in
the Elderly
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Polymyalgia rheumatica
Statins
Fibromyalgia
Depression
Sjogren’s
Rheumatoid
Lupus
Osteoarthritis
Primary Sjogren’s
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Dry eyes, dry mouth
Fatigue
Pain all over
No idea what is wrong with them
You probably have some in your
practice
Sjogren’s - History
• Use of eye drops?
• Can you eat crackers w/o water?
• Keep water on night table?
• Physical Exam: Nothing specific!
– Sometimes small joint puffiness
– Peripheral neuropathy
Sjogren’s - Lab
• SSA / SSB – insensitive
• ESR often up
• CRP high normal
Sjogren’s - TX
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Hydroxychloroquine
Low-dose prednisone
Methotrexate
Rituximab
• Fibromyalgia treatments (for
symptoms)
Polymyalgia Rheumatica
• 10-15% go on to GCA
• Respond well to treatment
• In other words, this is a
potentially serious disease that is
treatable.
PMR
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Pain all over; sudden onset.
Age > 50 (usually >70!)
Weight loss
Shoulder limitation of motion
(periarthritis)
• Proximal muscle tenderness
• Sed rate > 50 mm/hr
• Anemia
PREDNISONE in ELDERLY
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↓K+, ↑glucose
DEXA
Calcium + Vit D
T/C bisphosphonate
Eye exams: cataracts & pressure
Amer. College of Rheum.
• Recommendations for the
Prevention and Treatment of
Glucocorticoid-Induced
Osteoporosis 2010
• Arthritis Care & Research, Vol. 62,
No. 11, November 2010, pp 1515–
1526
• DOI 10.1002/acr.20295
GOUT
The risk factors
for gout were
known to the
ancients.
Risk Factors for Gout
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Obesity, metabolic syndrome
Ethanol
Diuretics
Fructose ingestion
Excessive purine ingestion
Ben Franklin (1706 -1790)
"Be temperate in wine, in
eating, girls, and sloth, or
the Gout will seize you and
plague you…"
-- Franklin
Drugs Associated with
Hyperuricemia
• Diuretics (loop and thiazide
types)
• Low-dose aspirin
• Ethanol
Hyperuricemia & Gout
Serum Uric Acid
(mg/dl)
< 7.0
Annual Incidence
of Gout (%)
0.1
7.0 – 8.9
0.5
> 9.0
4.9
This is chronic
refractory
gout!
Amer. College of Rheum.
• Guidelines for Management of
Gout. Part 1 & 2
• Arthritis Care & Research, Vol. 64,
No. 10, October 2012, pp 1431–
1461
• DOI 10.1002/acr.21773
The Three Phases of Gout
Treatment
• Treat acute attack
• Prevent new attacks
• Reduce uric acid level
(sometimes)
Phase 1 - Termination
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NSAID
Colchcine
Intra-articular steroids
Systemic steroids
IL-1 inhibitor (off-label use)
NSAIDs
• Treatment of choice in
otherwise healthy (elderly?)
patient.
• Avoid in renal insufficiency
and in peptic ulcer disease.
• Avoid salicylates (these cause
swings in serum uric acid).
Intra-Articular Steroids
• One or a few joints.
• Make sure infection not
present.
Oral Colchicine
• 1.2 mg followed by 0.6 mg 2 hrs
later.
• Loading dose same in renal
insufficiency.
• Maintenance (preventive) dose
0.6 mg qd or bid.
• 0.3 mg 2-3 times per week in
dialysis patients (preventive).
Systemic Steroids
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Polyarticular attacks or fever.
Longstanding attacks (>3-5 days).
Need divided doses.
Taper over 7-10 days.
Start prophylactic agent
(colchicine) as soon as possible.
Adjunctive Measures
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Rest
Ice
Elevation
Analgesics
Anti-motility agents (if using
colchicine or indomethacin)
• Continue hypouricemic agent if
patient has been taking it.
Phase 2 - Preventive
Therapy
• Colchicine or NSAID.
• Always use when beginning a
hypouricemic drug.
• Continue several weeks to years
(depending on tophi, serum uric
acid).
• Always use before surgery in
previously gouty patient.
Phase 3 - Hypouricemic
Therapy
• Not every patient needs it.
• May not need it in:
– Very elderly
– Non-compliant
– Infrequent attacks and no tophi
• May exacerbate attacks early on
Goals of Hypouricemic
Treatment
• Aim for serum uric acid under 6,
preferably near 5 for some
chronic gouty patients.
• But remember:
– allopurinol toxicity more likely with
higher dose.
– More likely with renal insufficiency.
Hypouricemic Agents
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Allopurinol
Febuxostat
Probenecid
Losartan (off-label)
Vitamin C (off-label)
Pegloticase
Major Toxicities of
Allopurinol
• Increased gout attacks early on (use
prophylaxis)
• Rash (may be severe)
• Stevens-Johnson syndrome
• Vasculitis
• Hepatitis
• Renal failure (interstitial nephritis)
• Bone marrow suppression
Allopurinol Hypersensitivity
Syndrome
• Fever
• Rash
• Renal Failure
• Hepatic injury
• Leukocytosis
• Eosinophilia (the
tipoff!)
• May be fatal. Hard to treat.
• Serious reactions to allopurinol reported
in 1 of 260 patients.
Arthritis Rheum 29:82, 1986
Febuxostat
• Non-xanthine inhibitor of XO and XD.
• Better tolerated than allopurinol.
• Lower uric acid levels than allopurinol
(53% vs. 21% met target of 6.0 mg/dl).
• Better dissolution of tophi.
Tophus Reduction
Mean Reduction in Tophus Area
Group
% Area Reduction
P Value
Feb 80 mg
83
P = .08 (NS)
Feb 120 mg
66
P = 0.16 (NS)
Allop 300mg
50
Becker MA. N Engl J Med. 2005 Dec 8;353(23):2450-61. Febuxostat
compared with allopurinol in patients with hyperuricemia and gout.
Febuxostat vs. Allopurinol
Percentage of Patients Achieving Serum
Uric Acid < 6 mg/dl
Study 1: Allopurinol dosed at 300 mg/d for ClCr ≥ 60 ml/min or
200 mg/d for 30 ≤ ClCr ≤ 59 ml/min.
Febuxostat: Best Use
• Allopurinol failures
• Renal insufficiency
• Tophaceous gout
Allopurinol & Febuxostat
Drug Interactions
• Life threatening interaction with
azathioprine, 6-mercaptopurine.
– Reduce dose of purine analogue by
approximately 2/3.
• Theophylline
• Other interactions also
Gout vs. Pseudogout
• Gout
– hallux, ankle, knee, hand
– younger, male
• Pseudogout
– knee, wrist, ankle
– older, female
• Almost any joint can be affected
by either disease!
CPPD Deposition
• Wrist: triangular ligament
• Pelvis: symphysis pubis
• Knee: menisci
• Also: annulus fibrosis, articular
capsules, bursae, ligaments,
tendons
Clinical Associations with
Psuedogout
• Aging
• Previous joint
surgery
• Previous joint
trauma
• Familial types
• Gout
• Amyloidosis
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Hyperpara
Hemochromatosis
Hypomagnesemia
Familial
hypocalciuric
hypercalcemia
• Hypophosphatasia
• Wilson’s disease
• Ochronosis
Pseudo-DJD Pattern of
CPPD
• 50% of CPPD patients.
• Wrists, MCPs, elbows, shoulders,
knees. Note difference from
usual DJD pattern.
• Heberden’s or Bouchard’s
frequently found.
• May be acute or chronic.
Treatment of Acute
Psuedogout
• Aspiration (more important
than in gout!)
• Rest
• Intra-articular steroids
• NSAIDs
• Systemic steroids
• Colchicine?
• IL-1 Inhibitors?
Pseudogout Prevention
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Colchicine
NSAID
Magnesium?
There’s no allopurinol for
pseudogout (unfortunately).
The Basic (Non-Acidic)
Calcium Phosphates
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Hydroxyapatite
Calcium carbonate
Octacalcium phosphate
Tricalcium phosphate
(whitlockite)
• Hydroxyapatite is nonbirefringent.
Syndromes Associated
with Hydroxyapatite
• Acute monoarthritis
(pseudopseudogout)
• Acute calcific tendinitis, bursitis
• Scleroderma, dermatomyositis
• Heterotopic calcification
• Milwaukee shoulder
• Crowned Dens Synd.
Acute Apatite
Monoarthritis
(Pseudopseudogout)
• Is usually a peri-arthritis.
• Intense inflammation (looks septic)
• Synovial fluid often noninflammatory.
• Often causes podagra (especially in
younger women).
• Look for the telltale calcifications on
radiographs.
CROWNED DENS SYNDROME
Crowned Dens Synd
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Headache
Pain with head rotation
Shoulder myalgias
Very elevated sed rate
RHEUMATOID
ARTHRITIS
In the Elderly
Rheumatoid
• Even in the elderly, completely
new paradigm of treatment.
• Dual goals:
– Symptom improvement
– Prevention of structural damage
Rheumatoid
• “Small joint polyarthritis with
morning stiffness”
• MCPs, wrists, MTPs
• ESR, CRP may or may not be up.
• RF or anti-CCP pos 70%
RA in the Elderly
• M:F ratio more nearly equal
• More shoulder involvement
• May overlap with polymyalgia
rheumatoica
Initial Tx of RA
• Low dose prednisone (actually a
good DMARD!)
• Methotrexate – safer than we
expected in 1987!
– Lung toxicity is possible
– Follow liver enzymes
– Added infection risk is relatively low
(2-3%).
What We Try to Prevent
The New Paradigm
• Is it likely that the patient will
have destructive or debilitating
disease in the long-term?
• If so, begin one or more DMARDs
(often MTX).
• If inadequate response after 3
months, add or switch DMARDs,
often includes a TNFI.
Anti-CCP
• CCP = cyclic citrullinated
peptides
• RA synovium overproduces CCP
• RA patients THEN make
ANTIBODIES to CCP
• 70% sensitive, 90% specific
• Anti-CCP is often present years
before RA manifests itself.
Goals of the New Criteria
• Identify persons with “early
arthritis” who are at high risk of
erosive or debilitating disease.
• Allow for earlier disease
modifying treatment.
• But…the criteria are not simple!
2010 ACR/EULAR CRITERIA FOR CLASSIFICATION OF
RHEUMATOID ARTHRITIS
Arthritis & Rheumatism 62(9): 2569–2581, 2010.
Lab Eval of Polyarthritis
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Rheum factor
Anti-CCP
ANA
C4
Lyme
CBC
Chem-12
• SSA, SSB
• Anti-RNP
Methotrexate
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Standard of care for RA.
dihydrofolate reductase inhibitor.
Best initial treatment for most patients.
Avoid in pre-existing liver disease, renal
disease and in drinkers.
• Main risk: pulmonary toxicity
• Higher doses being used, espec. Sub Q.
• 1/3 of patients will have little or no
radiographic progression on MTX alone.
Methotrexate (cont’d)
• Always give only once a week,
but dose may be split in two
parts, and given 12 hours apart.
• Most persons should receive
supplemental folate 1 mg/d.
• Follow liver enzymes (with
albumin), CBC, creatinine
monthly initially.
Methotrexate - Side
Effects
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Nausea, diarrhea
Stomatitis
Alopecia
Rash
Infections
MTX
pneumonitis
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Hepatitis
Cirrhosis
Pulm. fibrosis
Pancytopenia
Lymphoma?
• Don’t use if
creatinine > 2.0!
TNF Inhibitors
• Potent inhibitors of inflammation
• Have revolutionized the treatment
of RA since 1998.
• They retard erosions
• Act quickly
• Two approaches: monoclonal Ab
vs. soluble receptor
• $$$$
Side Effects of TNF Inhibitors
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Rashes, especially inject. site rxns.
Infections.
Reactivation of tuberculosis.
Demyelinating disease, optic neuritis,
seizures.
• Pancytopenia.
• Congestive heart failure (effect may
last for months).
• Malignancy (espec. lymphoma)
Prednisone
• Low dose prednisone: 7.5 mg/d
• Reduces number of erosions at
two years in early RA (22% vs.
46%).
• N Engl J Med 1995 Jul 20;333(3):142-6.
Remission: The New
Standard?
• Durable remissions are achievable
with combination therapy.
• Definition of remission important
however!
• Remission depends heavily on
treating early (first year of disease)
• New trials may report the remission
rate as the primary outcome measure
RA Take Home Messages
• The treatment paradigm has
changed in the past 10-15 years.
• Aggressive treatment changes
long-term outcome.
• The earlier treatment is started,
the better.
• There are new tools to help us
make an earlier diagnosis.
Osteoarthritis
• Everyone gets a little
• Minor degenerative changes on
xray often meaningless
• Knee, 1st CMC, DIPs, hip, back
• Usually localized
– Exception: Erosive or inflammatory
OA.
Nonpharmacologic Therapy for
Patients with OA
Amer. Coll. Of Rheumatology
• Patient education
Self-management programs (e.g., Arthritis Foundation
Self-Management Program)
Personalized social support through telephone
contact
Weight loss (if overweight)
Aerobic exercise programs
Physical therapy Range-of-motion exercises
Muscle-strengthening exercises
Assistive devices for ambulation
Patellar taping
Appropriate footwear
Lateral-wedged insoles (for genu varum) Bracing
Occupational therapy
Joint protection and energy conservation
Assistive devices for activities of daily living
http://www.rheumatology.org/practice/clinical/guidelines/oa-mgmt.asp
Pharmacologic Therapy for
Patients with OA
Amer. Coll. Of Rheumatology
• Acetaminophen
• COX-2-specific inhibitor
• Nonselective NSAID [plus misoprostol or a
proton pump inhibitor if at ↑GI risk]
• Non-acetylated salicylate
• Other pure analgesics: Tramadol
• Opioids
• Intraarticular glucocorticoids, hyaluronan
• Topical
Capsaicin
Methylsalicylate
http://www.rheumatology.org/practice/clinical/guidelines/oa-mgmt.asp
OA of the Knee
• Most sensitive and specific
finding on physical exam:
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CREPITUS!
• Sometimes knee pain is coming from
the hip
OA of Knee
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Glucosamine: mixed data
Corticosteroid injection
Viscosupplementation
Quadriceps exercises
Neoprene sleeve
Hinged brace
OA of the Hip Joint
• Mimicked by low back pain!
• Most common cause of
trochanteric bursitis is low back
pain too!
• Hip pain usually radiates to groin,
not to the “hip”.
Hip OA
• Injections don’t last long and are
not practical.
• Hip replacement is a good
operation.
1st CMC Osteoarthritis
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Brace off-the-shelf
Brace custom molded
Surgery
Liniment
NSAIDs
Toxicity in Elderly
• Peptic ulcer disease
• Hypertension
• Congestive heart failure
• CNS changes
• Intestinal ulceration
GI Less Toxic NSAIDs
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Celecoxib
Salsalate
Meloxicam
Nabumetone
Etodolac
Risk Factors for UGI Events
Amer. Coll. Of Rheumatology
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Age >=65
Comorbid medical conditions
Oral glucocorticoids
History of peptic ulcer disease
History of upper gastrointestinal
bleeding
• Anticoagulants
http://www.rheumatology.org/practice/clinical/guidelines/oa-mgmt.asp
RISK FACTORS FOR ULCERS
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NSAID Use
Age > 64
Prior event
CHF
Ethanol
Warfarin
Concomitant corticosteroid, low
dose aspirin, bisphosphonate,
SSRI
• H. pylori
PREVALENCE OF NSAID ULCERS BY AGE
Ann Rheum Dis. 2007 March; 66(3): 417–418.
PREVENTION OF NSAID
ULCERS
Arch Intern Med. 2002 Jan 8;162(2):169-75
NSAID ULCER PROPHYLAXIS
• H2 blockers NOT recommended
for prophylaxis
• PPI or misoprostol recommended
• PPI doesn’t seem to reduce
celecoxib ulcer complications
further.
• Low dose aspirin ELIMINATES
any benefit of celecoxib.
Amer. Coll. Of Gastro. 2009
• Patients with hx PUD should be
tested for H. pylori prior to NSAID
or ASA use.
Amer. Coll. Gastro. Guide. 2009
GI RISK
High
CV
RISK*
Mod
Low
High
No NSAID, no
COX-2
Naproxen + (PPI
or MIS)
Naproxen +
(PPI or MIS)
Low
COX-2 + (PPI or
MIS)
COX-2 or (NSAID NSAID alone
+ (PPI or MIS))
*High CV risk defined as those needing aspirin therapy.
Prophylactic Regimens
• Misoprostol 200 mcg QID
• Lansoprazole 15 or 30 mg/d
• Esomeprazole 20 or 40 mg/d
CV Risk - Celecoxib
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33 months
Placebo
200 mg BID
400 mg BID
Abs
6/676
18/683
23/669
%
0.9%
2.6%
3.4%
N Engl J Med. 2006;355(9):873.
RR
1.0
2.6
3.4