Neuropathic vds

5/22/2018 Neuropathic vds

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Neuropathic (Charcot) Arthropathy

Disturbance in sensation leads to multiple microfractures

o Pain sensation is intact from muscles and soft tissue Distribution and causes

o Shoulderssyrinx, spinal tumor

o Hipstertiary syphilis, diabetes

o Kneestertiary syphilis (more bone production), diabetes (less bone

production)

o Feetdiabetes

o Other causes

Amyloidosis

Congenital indifference to pain

Polio

Alcoholism

X-ray findings

o Sclerosis

o Destruction of joint

o Fragmentation

o Soft tissue swelling from synovitis

o Joint effusions

o Osteophytosis

o Disorganized and disrupted joint

o No osteoporosis

Marked sclerosis, fragmentation and joint destructionare the hallmarks of a neuropathic joint

here cause by tabes

DDX

o Degenerative joint disease

Eventually neuropathic joint shows more sclerosis More fragmentation in neuropathic


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More destruction of bone in neuropathic

o CPPD

Associated with chondrocalcinosis which a neuropathic joint is not

Neuropathic (Charcot) Arthropathy

General Considerations Most commonly caused by diabetes today

Bilaterally is rare in foot

Disturbance in sensation leads to multiple microfractures

o Pain sensation is intact from muscles and soft tissue

Distribution and causes

o Shoulderssyringomyelia, spinal tumor

o Elbows and wrists -- syringomyelia

o

Hips

tertiary syphilis, diabeteso Kneestertiary syphilis (more bone production), diabetes (less bone production)

o Feet diabetes, congenital insensitivity to pain, chronic alcoholism

o Other causes

Leprosy

Amyloidosisknee and ankle

Congenital indifference to pain

Polio

Alcoholism

Clinical Findings

Signs of inflammation in acute phase

Swelling is very common

Pain can occur in 75% of cases but is usually less severe than would be expected on the basis of

the radiologic findings

Instability

Loss of joint function

May produce a mass at the joint because of swelling

Imaging Findings

Conventional radiography is usually sufficient to make the diagnosis


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Findings include:

o Sclerosis from eburnation of subchondral bone

o Destruction of joint

o Fragmentation

o Subluxation and dislocation

o Soft tissue swelling from synovitis may be massive

o Joint effusions

o Osteophytosis

o Disorganized and disrupted joint

o No osteoporosis

Differential Diagnosis

Degenerative joint disease

o Especially in early stages

o Eventually neuropathic joint shows more sclerosis

o More fragmentation in neuropathic

o More destruction of bone in neuropathic

Calcium Pyrophosphate Deposition Disease

o Associated with chondrocalcinosis which a neuropathic joint is not

o Also more fragmentation in neuropathic joint

Osteomyelitis

o MRI and nuclear medicine scans, including FDG-PET scans, may help in differentiationTreatment

Usually non-operative

Surgery if unstable, nonreducible fractures or dislocations


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Neuropathic arthropathy (Charcot joint) can be defined as bone and joint changes that occursecondary to loss of sensation and that accompany a variety of disorders. Charcot first described therelationship between loss of sensation and arthropathy in 1868. The radiographic changes of thiscondition include destruction of articular surfaces, opaque subchondral bones, joint debris, deformity,and dislocation (see the images below). Neuropathic arthropathy (Charcot joint) poses a specialproblem in imaging when it is associated with a soft-tissue infection.[1, 2, 3, 4, 5, 6, 7]

Neuropathic arthropathy (Charcot joint). Neuropathic arthropathy of the shoulder in apatient with syringomyelia. Note the destruction of the articular surface, dislocation, and debris, which are
http://refimgshow%281%29/http://www.learningradiology.com/archives2011/COW%20467-Charcot%20Shoulder/charcotcorrect.htmhttp://refimgshow%281%29/http://www.learningradiology.com/archives2011/COW%20467-Charcot%20Shoulder/charcotcorrect.htmhttp://refimgshow%281%29/http://www.learningradiology.com/archives2011/COW%20467-Charcot%20Shoulder/charcotcorrect.htm


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pathognomonic for a neuropathic joint. Neuropathic arthropathy (Charcot joint).Osteolysis of the distal metatarsals and phalanges with tapering results in a pencil-like appearance in the late stage ofdiabetic neuropathy.Leprosyis one of many causes of neuropathic arthropathy (Charcot joint); joint manifestations of thisdisease include signs of Charcot disease, which advances despite treatment.[8] Neuropathicarthropathy related to diabetes,syphilis,leprosy, and connective tissue disorders is more common inthe elderly population. Neuroarthropathy related to asymbolia,spina bifida,and spinal trauma is morecommon in young individuals. Sensory impairment associated with spina bifidaandmyelomeningoceleis the most frequent cause of neuropathic arthropathy (Charcot joint) inchildhood.

Neuropathic arthropathy can be classified into hypertrophic and atrophic types. Hypertrophic changespredominate in the upper motor neuron lesions, and atrophic changes occur in peripheral nerve

injuries. The early stage ofosteoarthritissimulates neuropathic arthropathy (Charcot joint), bothradiologically and pathologically.

Progressive joint effusion, fracture, fragmentation, and subluxation should raise the suspicion ofneuroarthropathy. In the advanced stage, abnormal findings on radiographs include subchondralsclerosis, osteophytosis, subluxation, and soft-tissue swelling. Long-standing neuroarthropathy ischaracterized by disorganization of joints. The finding of considerable amounts of cartilaginous andosseous debris within the synovial membrane (termed detritic synovitis) should alert the pathologistthat the changes may represent a neuropathic joint. Other causes of detritic synovitis includeosteonecrosis,calcium pyrophosphate dihydrate crystal deposition disease,psoriatic arthritis,osteoarthritis, and osteolysis with detritic synovitis.

Preferred examination

Radiography may be the only imaging required for the diagnosis of neuropathic arthropathy (Charcotjoint). In the appropriate clinical setting, a fairly accurate diagnosis can be achieved. The roles ofultrasonography and computed tomography (CT) scanning are limited; however, these 2 modalitiescan be helpful in identifying any local collection, and they can be used to guide aspiration cytology.The role of magnetic resonance imaging (MRI) and radionuclide scanning is to differentiate soft-tissueinfection fromosteomyelitis.[9, 10]

Limitation of techniques

Radiographic findings in the early stages of neuropathic arthropathy (Charcot joint) may simulateosteoarthritis. Radiographs may not demonstrate findings that help in diagnosing osteomyelitis inneuropathic joints, which is a common problem.

The roles of ultrasonography and CT scanning are limited. Ultrasonography can be used to identifyany local collection when infection occurs and to guide aspiration for cytologic analysis; however, itprovides no further information regarding the integrity of underlying bone. Although CT scanning maybe helpful in evaluating cortical destruction, sequestra, and intraosseous gas, these changes are notspecific for neuropathic arthropathy.

The role of MRI and radionuclide scanning is to differentiate soft-tissue infection from osteomyelitis.Bone marrow edema is nonspecific and has several causes; therefore, differentiating bone marrowedema from neuropathic arthropathy (Charcot joint) may not be possible on the basis of MRI findingsalone. Similarly, enhanced bone activity on radionuclide scans is a nonspecific finding and may occurwith several neoplastic, inflammatory, and degenerative processes.

Differential diagnosis and other problems to be considered

Calcium pyrophosphate deposition diseaseandprimary osteoarthritisare in the differential diagnosis.In addition, in the early stage, neuropathic arthropathy (Charcot joint) can simulate osteoarthritis, and
http://emedicine.medscape.com/article/220455-overviewhttp://emedicine.medscape.com/article/220455-overviewhttp://emedicine.medscape.com/article/229461-overviewhttp://emedicine.medscape.com/article/229461-overviewhttp://emedicine.medscape.com/article/229461-overviewhttp://emedicine.medscape.com/article/311113-overviewhttp://emedicine.medscape.com/article/311113-overviewhttp://emedicine.medscape.com/article/311113-overviewhttp://emedicine.medscape.com/article/311113-overviewhttp://emedicine.medscape.com/article/311113-overviewhttp://emedicine.medscape.com/article/311113-overviewhttp://emedicine.medscape.com/article/330487-overviewhttp://emedicine.medscape.com/article/330487-overviewhttp://emedicine.medscape.com/article/330487-overviewhttp://emedicine.medscape.com/article/388348-overviewhttp://emedicine.medscape.com/article/388348-overviewhttp://emedicine.medscape.com/article/388348-overviewhttp://emedicine.medscape.com/article/394752-overviewhttp://emedicine.medscape.com/article/394752-overviewhttp://emedicine.medscape.com/article/394752-overviewhttp://emedicine.medscape.com/article/1348767-overviewhttp://emedicine.medscape.com/article/1348767-overviewhttp://emedicine.medscape.com/article/388348-overviewhttp://emedicine.medscape.com/article/388348-overviewhttp://emedicine.medscape.com/article/392096-overviewhttp://emedicine.medscape.com/article/392096-overviewhttp://emedicine.medscape.com/article/392096-overviewhttp://refimgshow%2813%29/http://emedicine.medscape.com/article/392096-overviewhttp://emedicine.medscape.com/article/388348-overviewhttp://emedicine.medscape.com/article/1348767-overviewhttp://emedicine.medscape.com/article/394752-overviewhttp://emedicine.medscape.com/article/388348-overviewhttp://emedicine.medscape.com/article/330487-overviewhttp://emedicine.medscape.com/article/311113-overviewhttp://emedicine.medscape.com/article/311113-overviewhttp://emedicine.medscape.com/article/229461-overviewhttp://emedicine.medscape.com/article/220455-overview


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bone fragmentation and collapse are seen in osteonecrosis, posttraumatic osteoarthritis, intra-articular steroid injection, infection, and alkaptonuria.

Baker et al reviewed neuropathic arthropathy in diabetics.[11] Neuropathic diabetic arthropathy,particularly in the feet, is the leading cause of morbidity in diabetic patients. It has many mimics.Ulcers, sinus tracts, or an abscess with an adjacent region of abnormal signal intensity in bone

marrow suggests osteomyelitis. Contrast-enhanced MRI allows differentiation of viable tissue fromnecrotic regions in diabetic foot infections, which require surgical debridement in addition to antibiotictherapy. Subtraction images are particularly useful for visualizing nonviable tissue.

Dialysis-associated spondyloarthropathy occurs in diabetic patients with a long history ofhemodialysis. Intervertebral disk space narrowing without T2 signal hyperintensity, extensive endplateerosions without endplate remodelling, and facet joint involvement are suggestive ofspondyloarthropathy instead of infectious diskitis or degenerative disk disease. The clinical features ofinfective diskitis and spondyloarthropathy overlap, but knowledge of the patient's medical history, andrecognition of imaging characteristics described above allows the radiologist to make a prompt andaccurate diagnosis, leading to prompt appropriate treatment.[11]

Special concerns

The incidence of osteomyelitis is increased in patients with neuropathic joints, particularly in the foot.Hence, careful follow-up imaging is essential.

CHARCOTS FOOT

Figure 1: X-ray of the feet showingCharcot's joint deformity.

Figure 2: Annotated x-ray of the feetshowing Charcot's joint deformity.
http://www.bimjonline.com/Imageoftheweek/Image17.12.2012/Charcot's%20Joint%20Annotated.jpghttp://www.bimjonline.com/Imageoftheweek/Image17.12.2012/Charcot's%20Joint.jpghttp://www.bimjonline.com/Imageoftheweek/Image17.12.2012/Charcot's%20Joint%20Annotated.jpghttp://www.bimjonline.com/Imageoftheweek/Image17.12.2012/Charcot's%20Joint.jpg


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(Click on image to enlarge) (Click on image to enlarge)

A Charcot joint(neuropathic joint) is due to a progressive destructive joint

disorder in patients with impaired pain sensation and proprioception. Incontemporary medicine, particularly when involving the foot/ankle, this is due to

longstanding diabetes.The 2 theories for the pathophysiology of this condition are the neuro-traumatic

theory in which repeated trauma with no sensory feedback occurs and theneurovascular theory in which the absence of neural stimuli results in vasodilatation

and hyperemia which promotes bone resorption.Other less common causes aside from diabetes include the D Ss:

SyphilisSteriods

Spinal Cord InjurySyringomyeliaSpina BifidaScleroderma

On plain film radiography it is characterised by multiple findings, remembered asthe6 Ds:

Dense bones (sub-chondral sclerosis)DegenerationDestructionDeformity

Debris (loose bodies)Dislocation
http://radiopaedia.org/articles/6-dshttp://radiopaedia.org/articles/6-dshttp://radiopaedia.org/articles/6-dshttp://radiopaedia.org/articles/6-ds


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Charcot

neuro-

osteoarthrop

athy

Charcot neuro-osteoarthropathy is a degenerative disease with progressive destruction of the

bones and joints.

It is seen in patients with neurological disorders with sensory loss of the feet, including tabes

dorsalis, leprosy, diabetic neuropathy, and other conditions involving injury to the spinal

cord.

In 1868 Jean-Martin Charcot gave the first detailed description of the neuropathic aspect of

this condition in a patient with syphilis.Today, diabetes mellitus is the most common etiology associated with Charcot

osteoarthropathy, with the joints of the foot and ankle being most commonly affected.

Here an illustration with the key MR-features of acute Charcot neuro-osteoarthropathy:

Subarticular marrow edema in the midfoot

Subcutaneous soft tissues are relatively uninvolved.
http://www.radiologyassistant.nl/data/bin/a5097979bb67f7_TEK-acute-Charcot.jpg


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The exact nature of Charcot arthropathy is unknown.

The neurotraumatic theorystates that Charcot arthropathy is caused by an unperceived

trauma to an insensate foot. The sensory neuropathy renders the patient unaware of the

osseous destruction that occurs with continuous ambulation.

The neurovascular theorysuggests that the underlying condition leads to the development of

autonomic neuropathy, causing the extremity to receive an increased blood flow, which in

turn results in a mismatch in bone destruction by increased osteoclastic activity and bone

synthesis (1).

The image shows a progressive neuro-osteoarthropathy of the tarsometatarsal joints (Lisfranc

dislocation) with subchondral cysts, erosions, joint distention and dislocation.


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Acute Charcot

Acute active Charcot neuro-osteoarthropathy is defined by clinical signs.

There should be neuropathy and a warm and swollen foot.

The skin temperature should be 2?C or more at the site of maximum deformity of the affected

foot compared with a similar site on the contralateral foot.

Osteomyelitis should be excluded and fever is not present.

Serum C-reactive protein level is normal or only a slightly elevated.

The differential diagnosis is infection (osteomyelitis, cellulitis, septic arthritis), inflammation

(gout, rheumatoid arthritis) and deep vein thrombosis.
http://www.radiologyassistant.nl/data/bin/a5097979bb8a5c_2beide.jpghttp://www.radiologyassistant.nl/data/bin/a5097979ba1d86_foot1.jpghttp://www.radiologyassistant.nl/data/bin/a5097979bb8a5c_2beide.jpghttp://www.radiologyassistant.nl/data/bin/a5097979ba1d86_foot1.jpg


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In this early stage, radiographic abnormalities are not present.

The acute stage of Charcot neuro-osteoarthropathy shows rapid and progressive bone and

joint destruction within days or weeks.

Immobility by total contact casting can prevent further bone and joint destruction.

Here a radiograph of a patient with diabetic neuropathy and a red hot foot.In the acute stage, the radiographs are normal and may not exclude the diagnosis of acute

Charcot neuro-osteoarthropathy.

Within 4 months there is progressive decrease of calcaneal inclination with equinus deformity

at the ankle.

There is destruction of the tarsometatarsal joint with the typical rocker-bottom deformity.

Bony debris is seen on the dorsal aspect of the foot.

In the acute stage, MRI shows only subchondral bone marrow edema.

Here MRI images of a patient with acute Charcot neuro-osteoarthropathy.

The bone marrow edema typically is not restricted to one or two bones, but is seen in the

entire midfoot.

Bone marrow edema and its enhancement are typically centered in the subchondral bone,

suggesting articular disease.

The subcutaneous tissues are relatively normal and there is no ulcer or other signs of

infection.
http://www.radiologyassistant.nl/data/bin/a5097979bc123d_TAB-Charcot.pnghttp://www.radiologyassistant.nl/data/bin/a5097979bba1c4_MR1.jpghttp://www.radiologyassistant.nl/data/bin/a5097979bc123d_TAB-Charcot.pnghttp://www.radiologyassistant.nl/data/bin/a5097979bba1c4_MR1.jpg


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Chronic Charcot

The chronic inactive stage no longer shows a warm and red foot.

The edema usually persists.

Crepitus, palpable loose bodies and large osteophytes are the result of extensive bone and

cartilage destruction.Joint deformity, subluxation and dislocation of the metatarsals lead to a rocker-bottom type

deformity in which the cuboid becomes a weight-bearing structure.

This results in excessive skin callus formation, blisters and foot ulceration.

At the stage of chronic inactive Charcot osteoarthropathy, bone healing and change of active

periosteal reaction will proceed into inactive periosteal reaction and sclerotic borders.

The classic radiographic description of neuro-osteoarthropathy is that of the five D' s.

Debris may be present and effusions may decompress along fascial planes, carrying bony

debris far from the joint.

Dislocation is the result of ligamentous laxity.
http://www.radiologyassistant.nl/data/bin/a5097979bc2309_lisfranc-1.jpghttp://www.radiologyassistant.nl/data/bin/a5097979bc1972_TAB-5D's.pnghttp://www.radiologyassistant.nl/data/bin/a5097979bc2309_lisfranc-1.jpghttp://www.radiologyassistant.nl/data/bin/a5097979bc1972_TAB-5D's.png


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On the far left, a normal radiograph in the acute stage of Charcot.

Subsequently progressive Charcot neuro-osteoarthropathy is seen with dislocation of the

Lisfranc joint.

CLASSIFICATION, EPIDEMIOLOGY, AND CLINICAL

PRESENTATION

Psoriatic arthritis (PsA) is a form of arthritis that occurs in patients with psoriasis. It has

the hallmarks of an "inflammatory" arthritis, including joint pain, erythema, and swelling,

often with prominent stiffness, not unlike the most well-characterized form of

inflammatory arthritis, rheumatoid arthritis (RA).[1-8]However, in terms of clinical, genetic,

histologic, and immunohistochemical patterns, PsA best fits with the

spondyloarthropathies,[1-5,7,9-13]which include ankylosing spondylitis, reactive arthritis, the

arthritis associated with inflammatory bowel disease, and undifferentiated

spondyloarthropathy. Distinct features of PsA, shared with other spondyloarthropathies,

include enthesopathy (inflammation of insertion sites of tendon, ligament, and joint

capsule), dactylitis (swelling of a digit), a tendency toward asymmetric, sometimesoligoarticular joint involvement, iritis, and a greater chance for male involvement than

what is seen in RA.[1,3-6,8,12,14]

Although sporadic case reports of an association between psoriasis and a unique form

of arthritis had appeared in the medical literature beginning in the late 1800s, it was not

until John Moll and Verna Wright,[1]in 1973, published a review of a large case series of

patients that PsA was definitively acknowledged in its own right. In their original case

series, 5 subtypes of PsA were characterized (Table 1). The oligoarticular form is the

most common. Subsequent case series, including patients with long duration of disease,

identify polyarticular presentation as most common, often with progressive joint

destruction and disability.[3,7,15,16]

Table 1. Uniqu e Clinical Features of PsA

DIP joint involvement

Nail changes


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Dactylitis

Enthesitis

Spondylitis

Lytic and periarticular new bone formation x-ray features

Iritis

What Is the Relat ionsh ip Between the Skin Lesion s o f Psoriasis and an

Inf lammatory Arthr i t is?

Psoriasis occurs in approximately 2% of the population of North America and Europe,

varying somewhat in other parts of the world, depending on genetic patterns.[17-

19]Studies report an occurrence rate of PsA of 6% to 39% in patients with

psoriasis.[20,21]The 6% figure is derived from a population-based case report series from

Olmstead County, Minnesota (the Mayo Clinic catchment).[21]The 39% figure is derived

from another Mayo Clinic study,[20]in which patients hospitalized with severe psoriasis

were carefully studied for manifestations of PsA. Recent large telephone surveys of

psoriasis patients have been conducted in Europe and the United States.[22]In the

EuroPSO survey, 30% were diagnosed with PsA, compared with 11% in the United

States.[23]A number of factors may contribute to this discrepancy, including inaccuracies

or lack of diagnosis; general lack of awareness about PsA; the possibility of

misdiagnosis with the more common form of arthritis, osteoarthritis; and lack of reporting

of joint symptoms to physicians and possibly the degree of psoriasis involvement.

Indeed, one study has suggested that patients with PsA experience less tenderness of

joints than do patients with RA, which may contribute to underreporting.[24]One bone

scan study of patients hospitalized for psoriasis showed evidence of periarticular light-up

despite absence of polyarticular symptoms.[25]The skin lesions of psoriasis usually

appear before the arthritis in up to 80% and typically by 5-10 years.[4,6,8,26]In

approximately 10% to 15%, the skin and joint symptoms arise simultaneously, and in

another 10% to 15%, the joint symptoms precede the development of psoriasis and

might be labeled undifferentiated spondyloarthropathy until the skin lesions develop. To

date, no specific marker, either clinical, immunohistochemical, or genetic, has been

identified which can definitively tell us which psoriasis patients are going to develop an

inflammatory arthritis. The only associated patterns identified are possibly a correlation


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with psoriasis severity, as previously stated, and nail involvement noted in up to 80% of

PsA patients.[26]

In addition to unique clinical features, see Table 1. Some characteristic x-ray changes

may aid in diagnosis. These include pencil-in-cup changes of digital joints, periostitis,

joint ankylosis, tuft osteolysis, asymmetric syndesmophytes, and sacroiliac

changes.[1,6,8,25,27,28](Figure) Laboratory features are otherwise not predictable, as acute-

phase reactants such as sedimentation rate and C-reactive protein may be variably

elevated, and rheumatoid factor and anti-CCP antibody are usually (but not always)

negative.[3,16,26]

Figure.Examples of unique radiographic features of PsA.

Chal lenges of Ass essing Disease Severi ty

Part of the difficulty in accurately assessing the prevalence of PsA prevalence stems

from not having an adequate set of criteria for disease classification. Most clinical

studies have relied on the original simple classification schema outlined by Moll and

Wright, ie, in a patient with psoriasis and inflammatory arthritis, presenting with 1 of the 5

subtypes identified in their original study.[1](Table 2) Various other criteria sets have

been proposed, as reviewed by Taylor and Helliwell, but none have become significantly

established.[3,11,29-32]Recently, a group of investigators led by Philip Helliwell have

conducted a patient-based exercise in which 588 patients diagnosed with PsA had

extensive history, physical examination, laboratory and x-ray evaluation, and were

compared with 536 "control" patients with other inflammatory arthritides. Using such

methodologic techniques as classification and regression tree (CART) and logistic


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regression analysis, a new criteria set is being developed which uses both clinical and x-

ray features.[11]

Table 2. Subtypes of PsA

Oligoarticular (< 5 joints), asymmetric

Polyarticular, often symmetric

Distal Interphalangeal (DIP) joint predominant

Spondylitis spine predominant

Arthritis mutilans (highly destructive/lytic)

The Spectrum of Disease Severi ty

The spectrum of severity of PsA is broad. Some patients will experience a mild degree of

pain and stiffness in a few joints with mild skin lesions, and at most will require therapy

with nonsteroidal anti-inflammatory drugs (NSAIDs), occasional intra-articular or

enthesial corticosteroid injections, and topical steroid creams.[26,33,34]Others will have

more severe joint and/or skin symptoms, with significant pain and stiffness and

embarrassing and uncomfortable skin lesions typically requiring moreimmunomodulatory therapy.[26,33,35,36]It is the latter group that is at risk for progressive

joint destruction and disability related to both physical as well as social/work-related

dysfunction, and that is also at higher risk for early mortality.[37,38]By observing a large

cohort of PsA patients over time, Gladman from Toronto found that in those patients

affected, PsA can result in joint deformity in 55%, lead to chronic disability in 20%, and

may result in early mortality.[7,38].Using data from the SF-36 measure of quality of life, it

has been noted that among the chronic diseases, psoriasis ranks second worst in

physical function and third worst in relation to mental function[39]as compared with

multiple other chronic disease states, including heart disease and cancer

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Neuropathic vds