1 Family Nurse Practitioner III 475 Musculoskeletal Problems Gout Definitions • Primary gout : disturbance in purine metabolism causes under- excretion or overproduction of uric acid, leading to sodium urate crystals; inherited disease • Secondary gout : increased uric acid from myeloproliferative disease or its treatment (hemolytic anemia, renal disease, psoriasis, use of diuretics, etc.) Risk Factors • Hyperuricemia – under-excretion by the kidneys – metabolic overproduction – combination • Male • Alcohol abuse • Obesity • Age: middle-aged men and postmenopausal women • Family history of gout • Drugs (diuretics, low-dose salicylates, cyclosporine) • Other: renal insufficiency, HTN, hematologic malignancy Provocative factors that can trigger an acute gout attack • Repetitive joint trauma • Surgical stress • Drugs – diuretics in the elderly – initiation of antihyperuricemics • Binge on alcohol or “rich” foods
Transcript
1
Family Nurse Practitioner III 475Musculoskeletal Problems
Gout
Definitions• Primary gout: disturbance in purine metabolism causes under-excretion or overproduction of
uric acid, leading to sodium urate crystals; inherited disease• Secondary gout: increased uric acid from myeloproliferative disease or its treatment (hemolytic
anemia, renal disease, psoriasis, use of diuretics, etc.)
Risk Factors• Hyperuricemia
– under-excretion by the kidneys– metabolic overproduction– combination
• Male • Alcohol abuse• Obesity• Age: middle-aged men and postmenopausal women• Family history of gout• Drugs (diuretics, low-dose salicylates, cyclosporine)• Other: renal insufficiency, HTN, hematologic malignancy
Provocative factors that can trigger an acute gout attack• Repetitive joint trauma• Surgical stress• Drugs
– diuretics in the elderly– initiation of antihyperuricemics
• Binge on alcohol or “rich” foods
Four stages in the history of gout• Stage I: Asymptomatic hyperuricemia• Stage II: Acute gouty arthritis• Stage III: Intercritical gout (the asymptomatic intervals between attacks)• Stage IV: Chronic tophaceous gout
Uricosuric drugs Inhibit urate reabsorption in the proximal tubule
ProbenecidSulphinpyrazone (no longer available in the U.S.)LosartanFenofibrate
Uricolytic drugs Degrade uric acid UricaseSource: Schlesinger, N. (Sept. 2009) Management of gout in seniors: Addressing barriers and setting goals for optimal control. Supplement to Clinical Geriatrics, 8-14.
Normalizing the Hyperuricemia (Goal < 6 mg/dL)• First treat risk factors and attempt to correct the underlying cause• If does not work, consider pharm treatment for either:
For “Underexcreter”• Uricosuric agent is drug of choice in patients < 60 years old, with good renal function*, and no
history of kidney stones** Uricosuric drugs require a creatinine clearance of > 50 ml to be effective.
• Uricosuric of choice: probenecid– safe drug– SE: skin rash and GI upset
For “Overproducer” & “Underexcreter”Allopurinol - decreases uric acid production• Used in those who do not meet requirements for probenecid• No need to check 24-hour uric acid excretion• SE can be severe: GI upset, HA, rash, marrow suppression, fever, liver or kidney failure,
vasculitis, alopecia, lymphadenopathy
4
Typical Stepwise Therapy: Single agent XOI (xanthine oxidase inhibitor) titrated to maximum appropriate dose. If serum urate target not achieved and there is continuing disease activity, add uricosuric
to XOI with both agents titrated to maximum appropriate dose If serum urate target not achieved, and there is continuing disease activity, add
pegloticase (Uricase)
Diet/Activity/Education• Diet
– modify dietary and alcohol-use patterns– purine restriction difficult to follow/uncertain benefit
• Activity: limit stress on the joints• Patient Education:
– Gout is a “symptom” of the disease hyperuricemia
Follow-Up• F/U in 1-2 weeks after acute attack to:
– review therapy, lab results, and medication side effects; to plan antihyperuricemic therapy• See again in 4-6 weeks
– to adjust meds and review treatment goals• If well-managed, follow yearly• * Start preventive therapy 1 month after resolution of acute attack, if appropriate.
See: American College of Rheumatology website for clinical practice guidelineshttp://www.rheumatology.org/Practice/Clinical/Guidelines/Clinical_Practice_Guidelines/
*** The next 3 pages are from the ACR clinical practice guidelines for gout.
Workup• Laboratory: only needed to rule out other causes• Radiology: Plain films of affected joint(s):
– narrowed joint space, bone cysts, osteophytes
See: American College of Rheumatology website for clinical practice guidelineshttp://www.rheumatology.org/Practice/Clinical/Guidelines/Clinical_Practice_Guidelines/for use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and knee.
• Weight loss• Exercise program• Warm, moist heat may be beneficial• Pain control (biofeedback, relaxation, meditation)• Meds: acetaminophen, ASA, oral NSAIDs, capsaicin analgesic lotion (for hands), topical
NSAIDs, tramadol• Recommend that persons age 75+ years should use topical rather than oral NSAIDs.
Follow-Up• Every 2 weeks X 2• If stable, every 3-6 months
– monitor for medication side effects, such as peptic ulcer• May need joint replacements in future
Rheumatoid Arthritis (RA)
DefinitionA chronic inflammatory disease that predominantly affects the peripheral joints
Etiology of RA• Unknown• Genetic predisposition appears to be important• Most commonly believed etiology: autoimmunity• Cellular and immune mechanisms result in destructive inflammatory process, primarily
involving the synovium.
Course of RA• Affects women 3X more commonly than men• Most common age: 25-45 years• Begins insidiously in most cases• Usually progressive but often with exacerbations and remissions
Signs & Symptoms of RA• Insidious onset: fatigue, anorexia, weight loss, generalized stiffness• Proceeds to symmetric joint swelling and warmth of hands, feet, wrists, knees, hips • PIPs, MCP, and wrist joints typically involved• Also MTP, ankle, knee, elbow jts., C-spine• DIPs, thoracic/lumbar spine typically spared• Joint stiffness after waking and after periods of inactivity• Deformities due to inflammation and fibrosis of joint capsule (ulnar drift, swan neck,
Work-Up• CBC: mild anemia (of chronic disease)• ESR: usually elevated• Rheumatoid Factor > 1:80 titer (80% of pts)• Positive ANA in 30% of RA patients• Synovial fluid: decreased viscosity, and increased WBC count
Morning stiffness in and around the joints, lasting at least 1 hour before maximal improvement. (1 point )
Arthritis of 3 or more joint areasAt least 3 joint areas simultaneously have had soft tissue swelling or fluid (not bony overgrowth alone) observed by a physician; the 14 possible joint areas are right or left proximal interphalangeal (PIP) joints, metacarpophalangeal (MCP)joints, wrist, elbow, knee, ankle, and metatarsophalangeal (MTP) joints. (1 point )
Arthritis of hand joints At least one area swollen (as defined above) in a wrist, MCP or PIP joint. (1 point)
Symmetric arthritisSimultaneous involvement of the same joint areas (see 2 above) on both sides of the body (bilateral involvement of PIPs, MCPs, or MTPs is acceptable without absolute symmetry). (1 point )
Rheumatoid nodules Subcutaneous nodules, over bony prominences, or extensor surfaces, or in juxta-articular regions, observed by a physician. (1 point )
Serum rheumatoid factor Demonstration of abnormal amounts of serum rheumatoid factor by any method for which the result has been positive in < 5% of normal control subjects. (1 point)
Radiographic changesRadiographic changes typical of RA on posteroanterior hand and wrist radiographs, which must include erosions or unequivocal bony decalcification localized to or most marked adjacent to the involved joints (osteoarthritis changes alone do not qualify). (1 point )
* For classification purposes, a patient shall be said to have rheumatoid arthritis if he/she has satisfied at least 4 of these 7 criteria. Criteria 1 through 4 must have been present for at least 6 weeks.
Total Criteria Point Count: ____________
RA Score: 4-7 points = Diagnostic of Rheumatoid Arthritis2-3 points = Cannot exclude RA0-2 points = Unlikely RA
12
Management See: American College of Rheumatology website for clinical practice guidelines
http://www.rheumatology.org/Practice/Clinical/Guidelines/Clinical_Practice_Guidelines/ See “Diagnosis and Management of Rheumatoid Arthritis” at
http://www.aafp.org/afp/2011/1201/p1245.pdf
Interventions: Patient Education• Importance of good nutrition• Moderate exercise program• Avoid heavy work and vigorous exercise • Living with a chronic illness• Splints to help avoid deformity• Warm, moist heat for relief of stiffness• Ice packs during active periods
Referrals and Follow-Up• F/U in 2 weeks X2, then monthly X 2, then every 3 months• Referrals to:
– rheumatologist, if available– physical therapist– occupational therapist
RA can be a devastating disease.The patient needs a great deal of psychologic support and encouragement.
Osteoporosis
Review National Osteoporosis Foundation’s Clinical Guide to Prevention and Treatment of Osteoporosis at https://my.nof.org/file/bonesource/Clinicians-Guide.pdf(and also available as an app for a small fee)
DefinitionA loss of bone mass that increases susceptibility to fracture. Bone loss occurs when the rate of reabsorption is greater than the rate of formation.
Demographics Although osteoporosis has been considered a disease of women, its existence in men has
been well documented by epidemiological studies.o Of the 10 million Americans who have osteoporosis, 2 million are men and an
additional 3.5 million men are at risk for the disease Medical cost of fractures in US = $13.8 billion
o Hospitalizations $8.6 billiono Nursing Home care $3.9 billiono Outpatient Services $1.3 billion
300,000 hip fractures/year in US (90% have osteoporosis)o 24% excess mortality in first year
o 50% never fully recovero 25% require LTC/Nursing Home care
Although hip fracture incidence is lower in men than in women, 36% of men die the year following a fracture, nearly twice the percentage of women.
Once person has 1 vertebral fracture, very high risk of more fractures (vertebral, hip) For 50 year old female, there is a 40% risk of having an osteoporotic fracture in her
remaining lifetime The age of men with primary osteoporosis varies from 23 to 86 years although the average
age is in the mid-60s. Osteoporosis occurring in either sex after age 70 is classified as senile.
Causes of Bone Loss in Women Estrogen deficiency—causes 15% of bone loss (first phase—postmenopause)
o Note: Effect of hormone therapy is erased after being off estrogen for 7 years Disuse—causes 6% of bone loss Calcium and Vitamin D deficiency—causes 16% of bone loss (occurs mainly 15-20 years
after menopause)
Primary Osteoporosis in Women• Type I: postmenopausal endocrine changes; imbalance between bone formation and resorption
(due to decreased estrogen)– usually affects women 15-20 years after menopause– rate of trabecular bone loss is markedly increased– predisposes vertebral bodies and radius to fractures
• Type II: age-related reduction in vitamin D– affects men and women 70 + years old– usually hip and vertebral fractures– proportionate loss of trabecular and cortical bone
Risk Factors Associated with Osteoporosis in Women• Age older than 65• Female gender• Caucasian or Asian race• Thin body frame• Family history (ask if patient mother ever broke her hip…increases risk!)• Longstanding Ca def.• Underweight (obesity is protective)• Sedentary lifestyle• Use of thyroid replacement therapy, steroids, or heparin• Alcohol abuse (alcohol can be toxic to cells in bone marrow)• Cigarette smoking (reduces ambient estrogen level)• Renal/liver disease• Secondary amenorrhea• Multiple myeloma• Endocrine disease
Classifications of Osteoporosis in Men Primary: unknown cause Secondary: caused by alcoholism, anticonvulsants, GI disorders, glucocorticoid excess,
hypercalciuria, hypogonadism, immobilization, long-term heparin or warfarin therapy, neoplastic diseases, organ transplantation, rheumatoid arthritis, smoking, and thyrotoxicosis
Senile: caused by alteration in calcium homeostasis, inadequate calcium and vitamin D intake, and physical inactivity
Risk Factors for Osteoporosis in Men Hereditary: Family history of osteoporosis, advanced age, thin build, Caucasian or Asian
hormone deficiency; overactive thyroid, parathyroid, or adrenal glands; chronic intestinal diseases; organ transplantation
o Testosterone has a major impact on the attainment of peak BMD and the maintenance of BMD in men. Although an abrupt cessation of testicular function does not occur, total and free testosterone levels may decline with age or remain in the normal range into the ninth decade. Elderly men with low testosterone levels are more than twice as likely to have hip fractures than men of similar age with normal testosterone levels.
Pharmacologic: Vitamin D overdose, vitamin A overdose, corticosteroids (oral, inhaled, nasal), chemotherapy drugs, long-term heparin or warfarin therapy, aluminum-containing antacids
Symptoms• Result from fractures of vertebrae, wrist, hip, humerus
15
• Generalized skeletal pain is uncommon• Pain usually results from collapse of the vertebrae, often with minimal trauma• Hip fractures from moderate trauma
– impaired ability to walk• Distal forearm fx: tries to break a fall
Work-Up Tests to R/O secondary osteoporosis:
o CBC, ESRo Liver function testso Thyroid function testso Serum levels of albumin, phosphorous, alkaline phosphate, creatinine, and calcium
Alkaline phosphatase will be increased if there is a healing fractureo Serum levels of testosterone and luteinizing hormone (LH) should be included
because of the clear association of hypogonadism and osteoporosis in men The total testosterone level, which measures bound and free testosterone in the
serum, is the preferred test. Testosterone levels normally undergo rapid diurnal changes; they are highest
in the morning and drop by 30-50% in mid-afternoon
Differential Diagnosis of Osteoporosis [From: Lawson, M.J. (2001). Evaluating and managing osteoporosis in men. In CE Connection: Advanced Pharmacology, 44-55.]
Laboratory Test
Osteoporosis Osteomalacia Hyperparathyroidism Tumors (such as multiple myeloma)
Serum calcium Normal Decreased Increased Normal or highSerum phosphate
Normal Decreased Decreased Normal
Serum alkaline phosphate
Normal Increased Increased Normal
Other Creatinine, thyroid profile, testosterone, leutinizing hormone
25 hydroxy vitamin D
Parathyroid hormone CBC, ESR, urinary and serum protein electrophoresis
Bone mineral density measurements (BMD)• Helpful in diagnosis and prevention of osteoporosis• Measurements are different at various skeletal sites due to differing amounts of cortical and
trabecular bone• Several techniques for measurement of bone mass: SPA, DPA, QCT, DEXA Test if:
o < age 65, postmenopausal and one or more additional risk factorso All females age 65 and over regardless of risk factorso Postmenopausal women who present with fracture
16
o Women on HRT for prolonged periodo Women considering therapy for osteoporosis if BMD testing would facilitate the
decision (to get baseline – F/U DEXA in 2-3 years)
DEXA• = dual energy x-ray absorptiometry• “Gold standard” • Can measure density at spine, hip, wrist, total skeleton• Accurate and precise• Exam time low: 10 minutes• Radiation low: 1-3 mrems
SPA• = Single-photon absorptiometry• Measures density of appendicular bone (radius, calcaneus)• Exam time short: 10-20 minutes• Radiation exposure = 5 mrem
QCT• = quantitative computed tomography• Used mostly for spinal area, but also hip and radius Allows assessmento f trabecular bone alone• Exam time short: 10-20 minutes• Significantly more radiation exposure
– (> 200 mrem)• Less accurate than other techniques, expensive
Ultrasonometry Site: heel, fingers, tibia Inexpensive, portable, no radiation Less precise
17
Bone Density Interpretation T-score (compares patient to standard/ideal) and is expressed in standard deviation
o Normal BMD is within 1 standard deviation below the young-adult meano In osteopenia (low bone mass), BMD is between 1 and 2.5 standard deviations of the
young-adult meano Osteoporosis is defined as a BMD of 2.5 or greater standard deviations below the
young-adult mean Z-score (compares to own age group)
Use of FRAX (Fracture Risk Assessment Tool
Prevention of Osteoporosis• Maximization of peak bone mass
– adequate calcium and vitamin d intake– avoidance of smoking and heavy alcohol use– regular exercise
• Minimizing bone loss from menopause– Estrogen replacement therapy– 1000-1500 mg of calcium; adequate vitamin D– encourage weight-bearing exercise
Treatment of Established Osteoporosis• 1200-1500 mg calcium (carbonate or citrate)/400-800 IU vitamin D3 (*** calcium
supplementation of 500 mg or more per day without Vitamin D increases the risk of MI by 30%)
• Calcium Metabolism Modifiers• Calcitonin [Miacalcin] (50 U/day) if unwilling or unable to take estrogen or for men
[used for treatment only]• Bisphosphonate: inhibit osteoclast bone resorption [used for prevention and treatment]
• Alendronate (Fosamax)• Risedronate (Actonel)• Ibandronate (Boniva)• Reclast (zoledronic acid) also a bisphosphonate; 5 mg IV q 12 months. Hydrate patient
prior to administration. Cost: (Epocrates): $1137.
• Parathyroid Hormone Analogues Forteo (teriparatide) regulates bone metabolism, intestinal calcium absorption, and renal
tubular calcium and phosphate reabsorption; given 20 mcg subcu q day
receptors, inhibiting bone resorption and turnover [used for prevention]
18
Monoclonal Antibodies, EndocrineProlia (denosumab) first of a new class of agent; should be considered a second-line
treatment; a fully human monoclonal antibody to RANKLo Denosumab binds to the receptor activator of nuclear factor-kappa B ligand
(RANKL), a soluble protein/cytokine essential for the formation, function, and survival of osteoclasts, which are the cells responsible for bone resorption.
o Given 60 mg subcu every 6 months• NSAIDs or other analgesics for pain
QUESTION: Are there any concerns/problems with using bisphosphanates?
QUESTION: How long do you treat osteoporosis with pharmacologic agents?
Treatment Algorithm for Osteoporosis If known to have vertebral fracture: treat with bisphosphonate, calcitonin, Forteo (depending
on severity and patient) If no known vertebral fracture:
o If not willing to consider pharmacological treatment, treat with OTC calcium with vitamin D, exercise, and no smoking
o If willing to consider treatment: If > 65 years old, get BMD measurement If < 65 years old
If no risk factors, treat with OTC calcium, exercise, no smoking. Offer BMD measurement
If risk factors present, get BMD measurement
Vitamin D Deficiency (Source: Medscape app) In adult, can cause chronic muscle aches and pains Diagnosis: measurement of serum 25-hydroxyvitamin D (25[OH]D)
o ≥ 30 ng/mL = Normalo 21-29 ng/mL = Vitamin D insufficiencyo < 20 ng/mL = Vitamin D deficiency
Screening is recommended only in those individuals who are at high risk for vitamin D deficiency, including:
o Patients with osteoporosiso Patients with a malabsorption syndromeo Black and Hispanic individualso Obese persons (BMI > 30)o Patients with disorders that affect the metabolism of vitamin D and phosphate
(e.g., chronic kidney disease) Recommended treatment for vitamin d-deficient adults:
o 50,000 IU of vitamin D2 or D3 once weekly for 8 weeks ORo 6,000 IU/day of vitamin D2 or D3 for 8 weeks
19
o When the serum 25(OH)D level exceeds 30 ng/mL, provide maintenance treatment of 1500-2000 IU/day
Recommended treatment for vitamin-D deficient patients who are obese, have a malabsorption syndrome, or ae taking medication that affects vitamin D metabolism:
o At least 6,000-10,000 IU of vitamin D dailyo When the serum 25(OH)D level exceeds 30 ng/mL, provide maintenance
treatment of 3,000-6,000 IU/day If the 25(OH)D concentration remains persistently low despite several attempts at
correction with oral vitamin D, a trial of ultraviolet B light therapy (ie, by tanning lamps) may be considered to improve vitamin D status.
Falls in the Older AdultSource: Moncada, LVV. (Dec. 1, 2011) Management of falls in older persons: A prescription for prevention. American Family Physician, 84 (11), 1267-1276.
Nonmodifiable Risk Factors for Falls in Older Adults Age older than 80 years Arthritis Cognitive impairment/dementia Female sex History of CVA or TIA History of falls History of fractures Recently discharged from hospital (within 1 month) White race
Potentially Modifiable Risk Factors for Falls in Older Adults Environmental hazards Medications
o Antidepressants (tricyclics, SSRIs)o Antihypertensiveso Antipsychoticso Benzidiazepineso Diureticso NSAIDso Sedatives and hypnoticso Polypharmacy (4+ prescription medications)
Metabolic factorso Dehydrationo Diabeteso Low BMIo Vitamin D deficiency
Review: 2010 AGS/BGS Clinical Guidelines at http://www.guideline.gov/content.aspx?id=37707
Note: You can download the AGS app for a small fee!
Fibromyalgia Syndrome (FMS)
Source: Buttaro, TM, Trybulski, J, Bailey, PP, & Sandberg-Cook, J. (2008) Primary care: A collaborative practice (3rd ed.). St. Louis: Mosby Elsevier.
Definition A disorder characterized by symptoms of widespread musculoskeletal pain, fatigue, non-
restorative sleep, depression, headaches, and GI complaints such as IBS Defined as > 3 months of musculoskeletal pain present above and below the wait
bilaterally, associated with pain on palpation of tender points, with no other source of pain identified. The pain is usually accompanied by profound fatigue and sleep disturbance
May occur in presence of other rheumatologic disorders such as SLE and RA Most patients with chronic fatigue syndrome also meet the diagnostic criteria for FMS
Demographics 8-9 X more prevalent in women than men Onset generally at 40-50 years of age; rarely begins after age 55 Approx. 2% of total population is affected, with incidence increasing with age to 8% in
women 60-69 years old Affects 3-6 million Americans FM undiagnosed in as many as 3 out of 4 people
Pathophysiology New research has implicated CNS dysfunction, rather than muscle, autoimmune, or viral
disease. Normally pain beginning in the periphery is processed in the spinal cord and transmitted
to the brain In FMS, some pain becomes heard "louder" at the level of the spinal cord and brain (=
central sensitization) The brain responds with pain recognition at a lower threshold and over a wider area than
that originally involved. The cause of the CNS dysfunction is unknown at this time.
Clinical PresentationTriad of core symptoms of FM:
Note: There is controversy as to whether chronic fatigue syndrome (CFS) and fibromyalgia are the same or different conditions. It is suggested that they are similar with pain being the predominant problem in people with FM, whereas fatigue is the major complaint in people with CFS.
American College of Rheumatology 1990 Criteria for Classification of Fibromyalgia[Patient is considered to have FM if both criteria are satisfied. The widespread pain must have been present for >3 months]
History of widespread pain
22
Pain considered widespread when all of the following are present: pain on the left side of the body pain on the right side of the body pain above the waist pain lower the waist axial skeletal pain (cervical spine or anterior chest or thoracic spine or low back)
Pain in 11 of 18 tender point sites on digital palpationPerform digital palpation with an approximately force of 4 kg. (8.8 pounds) of pressure (achieved with the thumb, using enough pressure to blanch the thumbnail)
Occiput: bilateral, at the suboccipital muscle insertions Low cervical: bilateral, at the anterior aspects of the intertransverse spaces at C5-C7 Trapezius: bilateral, at the midpoint of the upper border Supraspinatus: bilateral, at origins, above the scapula spine near the medial border Second rib: bilateral, at the second costochondral junctions, just lateral to the junctions
on upper surfaces Lateral epicondyle: bilateral, 2 cm distal to the epicondyles Gluteal: bilateral, in upper outer quadrants of buttocks in anterior folds of muscle Greater trochanter: bilateral, posterior to the trochanteric prominence Knee: bilateral, at the medial fat pad proximal to the joint line
23
Diagnostics In-depth H & P Exclude underlying autoimmune disorders such as RA and lupus thru normal labs
including CBC, ESR, RF, ANA, and TSH Vitamin D-25-hydroxalase: low levels may worsen muscle pain and balance; treat with
high dose oral vitamin D Hepatitis C: symptoms of hepatitis C mimic those of FM Sleep studies may be done for those with obstructive sleep apnea/daytime sleepiness
(falling asleep during daytime activities such as driving)
ManagementGoals of therapy: patient empowerment to control pain, enhance sleep, maintain mobility
Pharmacology amitriptyline (Elavil) 10-20 mg, taken 2-3 hours before bedtime cyclobenzaprine (Flexeril) 5-10 mg at hs SSRIs (such as Prozac) alone or in combination with amitriptyline dufloxatine (Cymbalta), a dual serotonin-norepinephrine reuptake inhibitor gabapentin (Neurontin) 300 mg tid pregabalin (Lyrica) Trazodone (Desyrel) and zolpidem (Ambien) may help sleep
Demographics Average age of onset: 65-70 (rare in people under 55) Occurs 1:200 people > age 65 Women affected twice as often as men Whites affected much more frequently than African-Americans
Cause Underlying cause of PMR has not been discovered (no infectious agents, no environmental
factors) Possible genetic factors (due to commonality in whites Since it is seen almost exclusively in the elderly suggests mechanisms involving senescence
of the immune system
Signs/Symptoms New or increased pain and stiffness of the shoulders and hips (limb-girdle muscle pain and
stiffness)o Since more than half of the aged have documented MSK disease, it is easy to assume
that an existing process has flared upo May be unilateral early on, but quickly become symmetrical o Typically, low neck and proximal shoulder muscles are affected before the hip,
buttock, and thigh muscles Patients often restrict activity because of pain and so suffer secondary muscle atrophy,
weakness, and growing dependence, often becoming depressed Associated symptoms are often revealed only by specific inquiry:
o Intermittent mild fevero Night sweatso Modest loss of appetite and weighto Fatigueo Malaiseo Depression
PMR unrecognized in the majority of its victims Symptoms may emerge rapidly, but more typically the presentation is insidious, with
graduate progression of proximal muscle pain and stiffness over several weeks
25
The course of the disease, if not treated, is chronic and steady over months to years, after which symptoms may remit. However, flare-ups may occur years after the original episode.
Diagnosis Based on the clinical picture ESR > 40, and often > 100, is typical and may be used to monitor the response to therapy Normochromic anemia, as seen in other chronic inflammatory diseases, is typical WBC and differential typically normal ANA and RF tests and CPK normal
Treatment Oral low-dose steroids, starting with 15-20 mg of prednisone daily If the symptoms resolve and the ESR returns to essentially normal within a month, the dose
may be tapered slowly The daily maintenance dose may be as low as 5 mg, but if symptoms or elevated ESR return,
higher doses must be given Prednisone is usually maintained for at least a year and may be needed must longer before
being successfully tapered and stopped.
Disease Progression/Remission/Complication More than 2/3 of patients achieve full remission or long symptom-free periods without
prednisone. However, relapses are common and can be seen as late as 8 years after successful treatment Giant cell arteritis may be seen at some time in as many as 1/3 of patients with PMR (to be
