Psoriatic ArthritisLast Updated:
January 7, 2005 |
| Synonyms and related keywords: psoriasis,
arthritis, skin disease, bone disease, rheumatism, rheumatoid
arthritis, psoriatic arthropathy, arthritis mutilans, arthropathia
psoriatica, psoriatic spondylitis, asymmetrical seronegative
oligoarticular arthritis, dactylitis, sausage digits, pencil-in-cup
radiograph, opera-glass hand |
| Author: Anwar Al Hammadi, MD, Staff Physician,
Department of Dermatology, McGill University
Coauthor(s): Peter D Gorevic, MD, Professor and
Chief, Division of Rheumatology, Mount Sinai School of Medicine
|
| Anwar Al Hammadi, MD, is a member of the following medical
societies: American Academy of Dermatology
|
| Editor(s): Kristine M Lohr, MD, Associate
Chief, Program Director, Professor, Department of Internal Medicine,
Division of Rheumatology, University of Tennessee School of
Medicine; Francisco Talavera, PharmD, PhD, Senior
Pharmacy Editor, Pharmacy, eMedicine; Herbert S Diamond,
MD, Chairman, Department of Internal Medicine, Professor of
Medicine, Temple University School of Medicine, Department of
Internal Medicine, Western Pennsylvania Hospital; Alex J
Mechaber, MD, FACP, Director of Clinical Skills Program,
Assistant Professor, Department of Internal Medicine, Division of
General Internal Medicine, University of Miami School of Medicine;
and Arthur Weinstein, MD, Associate Chairman of
Medicine and Director, Professor of Medicine, Georgetown University
Medical Center, Section of Rheumatology, Washington Hospital Center
|
Background: In 1964,
the American Rheumatism Association listed psoriatic arthritis as a
clinical entity. However, diagnostic criteria have not been agreed upon,
and several proposed definitions have stressed separate features of this
multifaceted disease.
The high frequency of distal joint involvement in psoriatic arthritis
compared to rheumatoid arthritis and arthritis mutilans (as an unusual but
characteristic manifestation) have received special attention. The great
variety of clinical manifestations were framed in the definition suggested
by Moll and Wright in 1973, ie, "An inflammatory arthritis associated with
psoriasis, usually with a negative sheep cell agglutination (SCA) test,
ie, rheumatoid factor."
Other more detailed criteria have been suggested. Psoriatic arthritis,
a term used by the American Rheumatism Association, is widely accepted.
Pathophysiology:
Psoriatic arthritis is an autoimmune
disease with known human leukocyte antigen (HLA)–associated risk factors.
Psoriatic arthritis affects the ligaments, tendons, fascia, and joints. It
occasionally develops in the absence of detectable psoriasis, and it may
occur at higher frequencies when skin involvement is more severe,
especially when pustular psoriasis is present, although recent studies
suggest that this may not be valid.
Frequency:
- In the US: Psoriasis affects 2.5% of the white
population of North America, but it is less prevalent in the African
American and Native American populations. Psoriatic arthritis affects
5-8% of patients with psoriasis.
Recent survey results indicate approximately 1 million US adults have
psoriatic arthritis. This figure is significantly higher than
researchers had previously believed, and suggests many people with
psoriasis, a related skin disease, may not be aware they have psoriatic
arthritis. (This is according to a new study conducted by the National
Psoriasis Foundation [NPF].)
- Internationally:
Estimates of the frequency of
psoriatic arthritis in patients with all types of psoriasis vary widely
according to the nature of the diagnostic criteria and ascertainment
used, but most fall into the range of 5-8%. Considering the frequency of
psoriasis to be 1-3%, the prevalence of psoriatic arthritis in the
general white population ranges from 0.05-0.24%, a value approaching
half that of seropositive rheumatoid arthritis.
Mortality/Morbidity:
The course of psoriatic arthritis
usually is characterized by flares and remissions. Arthritis mutilans is
recognized as a typical but unusual form of psoriatic arthritis. Earlier
studies have reported that psoriatic arthritis results in joint
destruction and severe disability in a large proportion of patients. Of
patients observed in a large outpatient psoriatic arthritis clinic, 7%
required musculoskeletal surgery.
Race: Psoriatic arthritis is more common in white
persons than in persons of other races.
Sex: Men and women are affected equally; but, in the
subsets of psoriatic arthritis, male predominance occurs in the
spondylitic form, whereas female predominance occurs in the rheumatoid
form.
Age: Psoriatic arthritis characteristically develops
in persons aged 35-55 years, but it can occur in persons of almost any
age.
History: The following
list details the 5 patterns of psoriatic arthritis involvement:
- Asymmetrical oligoarticular arthritis
- Until recently, this was thought to be the most common
type.
- Usually, the digits of the hands and feet are affected first, with
inflammation of the flexor tendon and synovium occurring
simultaneously, leading to the typical "sausage" appearance
(dactylitis).
- Usually, fewer than 5 joints are affected at any one
time.
- Symmetrical polyarthritis
- Recently, this rheumatoidlike pattern has been recognized as one
of the most common types. The hands, wrists, ankles, and feet may be
involved.
- It is differentiated from rheumatoid arthritis by the presence of
distal interphalangeal (DIP) joint involvement, the relative
asymmetry, the absence of subcutaneous nodules, and a negative test
result for rheumatoid factor. This condition generally is milder than
rheumatoid arthritis, with less deformity.
- Distal interphalangeal arthropathy
- Although DIP joint involvement is considered classic and unique to
psoriatic arthritis, it occurs in only 5-10% of patients, primarily
men.
- Involvement of the nail with significant inflammation of the
paronychia and swelling of the digital tuft may be prominent,
occasionally making appreciation of the arthropathy more
difficult.
- Resorption of bone (osteolysis) with dissolution of the joint,
observed as the "pencil-in-cup" radiographic finding, leads to
redundant overlying skin with a telescoping motion of the digit.
- This "opera-glass hand" is more common in men than in women and is
more frequent in early-onset disease.
- Spondylitis with or without sacroiliitis
- This occurs in approximately 5% of patients with psoriatic
arthritis and has a male predominance.
- Clinical evidence of spondylitis, sacroiliitis, or both can occur
in conjunction with other subgroups of psoriatic arthritis.
- Spondylitis may occur without radiologic evidence of sacroiliitis,
which frequently tends to be asymmetric, or it may appear
radiologically without the classic symptoms of morning stiffness in
the lower back. Thus, poor correlation can exist between symptoms and
radiologic signs of sacroiliitis.
- Vertebral involvement differs from that observed in ankylosing
spondylitis. Vertebrae are affected asymmetrically, and the
atlantoaxial joint may be involved with erosion of the odontoid and
subluxation.
- Unusual radiologic features may be present, such as nonmarginal
asymmetric syndesmophytes (characteristic), paravertebral
ossification, and, less commonly, vertebral fusion with disk
calcification.
- Juvenile psoriatic arthritis
- Juvenile psoriatic arthritis accounts for 8-20% of childhood
arthritis and often is monoarticular at onset.
- The mean age of onset is 9-10 years, with a female predominance.
The disease usually is mild, although occasionally it may be severe
and destructive, progressing into adulthood.
- In 50% of children, the arthritis is monoarticular, and DIP
involvement occurs in a similar percentage.
- Tenosynovitis is present in 30% of children, and nail involvement
is present in 71%, with pitting being the most common but least
specific finding.
- In 47% of children, disordered bone growth with resultant
shortening may result from involvement of the unfused epiphyseal
growth plate by the inflammatory process.
- Sacroiliitis occurs in 28% of children and usually is associated
with HLA-B27 positivity.
- Although the presence of HLA-B8 may be a marker of more severe
disease, HLA-B17 usually is associated with a mild form of psoriatic
arthritis.
- Children have a higher frequency of simultaneous onset of
psoriasis and arthritis than adults, with arthritis preceding
psoriasis in 52% of children.
- Psoriatic arthritis may be present with or without obvious skin
lesions; with minimal skin involvement such as the scalp, umbilicus, or
intergluteal cleft; or with only nail malformations. Psoriasis usually
precedes arthritis (occasionally by as many as 20 y); however, in as
many as 15-20% of patients, arthritis appears before the psoriasis. If
the latter is the case, a family history of psoriasis may reveal a
hereditary pattern.
- Initial symptoms may be acute. When localized to the foot or toe,
symptoms may be mistaken for gout. Alternatively, patients may
experience only stiffness and pain with few objective findings.
Physical: Recognition of the patterns of joint
involvement as described in History is essential to the diagnosis of
psoriatic arthritis.
- Recently, the possibility that less joint tenderness occurs with
psoriatic arthritis than with rheumatoid arthritis has been
emphasized.
- The term enthesopathy or enthesitis, reflecting inflammation at
tendon or ligament insertions into bone, may be seen in psoriatic
arthritis as in other spondyloarthropathies. This is observed more often
at the attachment of the Achilles tendon and the plantar fascia to the
calcaneus with the development of insertional spurs.
- Dactylitis with sausage digits is seen in as many as 35% of
patients.
- Skin involvement includes the following:
- Arthritis generally is not considered to correlate strongly to any
particular type of psoriasis or to the severity of the skin disease.
However, in one study, arthritis was noted more frequently in patients
with severe skin disease, whereas in another, pustular psoriasis was
associated with more severe psoriatic arthritis.
- In patients presenting with an undefined seronegative
polyarthritis, looking for psoriasis in hidden sites such as the scalp
(where psoriasis frequently is mistaken for dandruff), perineum,
intergluteal cleft, and umbilicus is extremely important.
- A diagnosis of psoriatic arthritis may be missed because of an
inadequate physical examination.
- Nail involvement includes the following:
- Onycholysis, transverse ridging, and uniform nail pitting are 3
features of nail involvement that should be noted. A direct
correlation exists between the number of pits and the diagnostic
significance. When skin and joint disease begin simultaneously, nail
involvement frequently is present at onset.
- Involvement of DIP joints correlates moderately well with
psoriasis in adjacent nails, although this is not an invariable
association.
- Nails are involved in 80% of patients with psoriatic arthritis but
in only 20% of patients with uncomplicated psoriasis.
- Severe deforming arthritis of the hands and feet frequently is
associated with extensive nail involvement.
- Fungal infection of the nails is the main consideration in the
differential diagnosis in a patient with a seronegative
polyarthritis.
- Extraarticular features include the following:
- Extraarticular features are observed less frequently in patients
with psoriatic arthritis than in those with rheumatoid arthritis. In
psoriatic arthritis, a predilection exists for synovitis to affect
flexor tendon sheaths with sparing of the extensor tendon sheath; both
commonly are involved in rheumatoid arthritis. Subcutaneous nodules
are rare in patients with psoriatic arthritis. If nodules are present
in a patient who has psoriasis and arthritis, particularly if the
rheumatoid factor titer is positive, they suggest the coincidental
occurrence of psoriasis and rheumatoid arthritis.
- Ocular involvement may occur in 30% of patients with psoriatic
arthritis, including conjunctivitis in 20% and acute anterior uveitis
in 7%. In patients with uveitis, 43% have sacroiliitis and 40% are
HLA-B27–positive. Scleritis and keratoconjunctivitis sicca are
rare.
- Inflammation of the aortic valve root, which may lead to
insufficiency, has been described in 6 patients with psoriatic
arthritis and is similar to that observed more frequently in
ankylosing spondylitis and Reiter syndrome. Occasionally, patients may
develop secondary amyloidosis.
Causes: The pathogenesis of psoriatic arthritis
remains unknown, but much information has been gathered. In addition to
the genetic influences, environmental and immunological factors are
thought to be prominent in the development and perpetuation of the
disease. The de novo development or exacerbation of psoriasis and
psoriatic arthritis in patients with human immunodeficiency virus (HIV)
infection and CD4 deficiency remains controversial.
Psoriasis may remit following allogeneic bone marrow transplantation
and may exacerbate with interferon-alfa treatment for hepatitis C.
- Approximately 40% of patients with psoriasis or psoriatic
arthritis have a family history of these disorders in first-degree
relatives. The exact mechanism of the association between HLA and
psoriatic arthritis is not clear.
- HLA-B13, HLA-B17, HLA-B39, and Cw*0602 are found to occur with
increased frequency in both psoriasis and psoriatic arthritis when
compared to the general population.
- Psoriatic arthritis shows an increased frequency of HLA-B7 and
HLA-B27 and a lower frequency of HLA-DR7 and Cw7.
- HLA-B27 in the presence of HLA-DR7, HLA-DQ3 in the absence of
HLA-DR7, and HLA-B39 are predictors for disease progression, whereas
HLA-B22 is protective.
- Certain immunoglobulin genes also have been suggested to be
associated with psoriatic arthritis.
- Genome scan studies have demonstrated associations with genetic
markers.
- In psoriasis, linkages with loci on 17q, 4q, and 6p have been
reported in whole genome scans, with the strongest evidence for
linkage on 6p. Recent studies in psoriatic arthritis have demonstrated
associations with genetic markers. These include a tumor necrosis
factor-alpha (TNF-alpha) promoter polymorphism and class I major
histocompatibility complex (MHC) chain-related gene A.
- The pathologic process of skin and joint lesions in psoriatic
arthritis is an inflammatory reaction, and evidence also exists for
autoimmunity, perhaps mediated by complement activation. The
inflammatory nature of the skin and joint lesions in psoriatic
arthritis is demonstrated by synovial-lining cell hyperplasia and
mononuclear infiltration, resembling the histopathologic changes in
rheumatoid arthritis. However, synovial-lining hyperplasia is less,
macrophages are fewer, and vascularity is greater in psoriatic
arthritis compared with rheumatoid arthritis synovium.
- The cytokine profile in psoriatic arthritis reflects a complex
interplay between T cells and monocyte macrophages. Th1 cytokines (eg,
TNF-alpha, interleukin-1 beta, interleukin-10) are more prevalent in
psoriatic arthritis than in rheumatoid arthritis, suggesting that
these 2 disorders may result from a different underlying
mechanism.
- Antiepidermal keratin and anticytokeratin 18 antibodies have been
found in the sera of patients with psoriasis and psoriatic arthritis.
Several studies have shown a significant reduction in the number and
percentage of CD4+ T cells in the peripheral blood, whereas
they are found throughout the skin lesions and synovium.
- Dendritic cells have been found in the synovial fluid of patients
with psoriatic arthritis and are reactive in the mixed leukocyte
reaction; the inference is that the dendritic cells present an unknown
antigen to CD4+ cells within the joints and skin of
patients with psoriatic arthritis, leading to T-cell
activation.
- Fibroblasts from the skin and synovia of patients with psoriatic
arthritis have an increased proliferative activity and the capability
to secrete increased amounts of interleukin-1, interleukin-6, and
platelet-derived growth factors. Several studies suggest that
cytokines secreted from activated T cells and other mononuclear
proinflammatory cells induce proliferation and activation of synovial
and epidermal fibroblasts.
- Psoriatic plaques in skin have increased levels of leukotriene B4.
Injections of leukotriene B4 cause intraepidermal microabscesses,
suggesting a role for this compound in the development of
psoriasis.
- The temporal relationship between certain viral or bacterial
infections and the development or exacerbation of psoriasis or
psoriatic arthritis suggests a possible pathogenetic role for these
organisms.
- Pustular psoriasis is a well-described sequela of streptococcal
infections. However, the response to streptococcal antigens by cells
from patients with psoriatic arthritis is not different from that of
cells from patients with rheumatoid arthritis, making the role of
Streptococcus species in psoriatic arthritis
doubtful.
- Psoriasis and psoriatic arthritis have been reported to be
associated with HIV infection and to be prevalent in some HIV-endemic
areas. Although the prevalence of psoriasis in patients infected with
HIV is similar to that in the general population, patients with HIV
infection usually have more extensive erythrodermic psoriasis and
patients with psoriasis may present with exacerbation of their skin
disease after being infected with HIV.
- Trauma: A few studies have reported the occurrence of arthritis and
acroosteolysis after physical trauma in patients with psoriasis.
Gout Osteoarthritis
Reactive Arthritis and Reiter Syndrome Rheumatoid Arthritis
Septic Arthritis
Other Problems to be Considered:
Psoriasiform skin lesions may be observed in association with Reiter
disease, inflammatory bowel disease, and the syndrome of inappropriate
secretion of diuretic hormone.
|
Lab Studies:
- No specific diagnostic tests are available for psoriatic arthritis.
Diagnosis of the disease is made based on clinical and radiologic
criteria in a patient with psoriasis.
- Immunoglobulin M (IgM) rheumatoid factor in serum usually is
absent. However, in 33% of patients, immunoglobulin G (IgG)
antiglobulins have been detected in serum. When IgM rheumatoid factor
positivity is studied in a group of patients with psoriatic arthritis
and a similar comparison is undertaken in an age-matched and
sex-matched normal population, rheumatoid factor positivity generally
is found to be comparable in both groups.
- The erythrocyte sedimentation rate may be elevated in patients
with active psoriatic joint disease, but elevations higher than 100
mm/h (Westergren method) are uncommon. Severe skin and joint disease
may be associated with a mild normochromic normocytic anemia and
leukocytosis. Acute phase reactants, such as alpha2-macroglobulin, may
be increased.
- Antinuclear antibody titers in psoriatic arthritis do not differ
from those of age-matched and sex-matched control populations. In
10-20% of patients with generalized skin disease, the serum uric acid
concentration may be increased and, on occasion, may predispose to
acute gouty arthritis. Low levels of circulating immune complexes have
been detected in 56% of patients with psoriatic arthritis but do not
appear to parallel disease activity.
- The associations of psoriatic arthritis with HLA-B17, HLA-B13, and
HLA-B27 were described under Genetics. Serum immunoglobulin A levels
are increased in two thirds of patients with psoriatic arthritis and
in one third of patients with psoriasis. Levels of IgM tend to
increase with severe disease, but IgG levels usually are not
elevated.
- Synovial fluid is inflammatory, with cell counts ranging from
5,000-15,000/mm3 and with more than 50% of cells being
polymorphonuclear leukocytes. Within the synovium, the infiltrate
consists predominantly of T lymphocytes. Synovial fluid complement
levels are either within reference ranges or increased, and glucose
levels are within reference ranges.
Imaging Studies:
- Radiological features have helped to distinguish psoriatic arthritis
from other causes of polyarthritis. In general, the common subtypes of
psoriatic arthritis, such as asymmetric oligoarthritis and symmetric
polyarthritis, tend to result in only mild erosive disease. Early bony
erosions occur at the cartilaginous edge, and cartilage initially is
preserved with maintenance of a normal joint space.
- Juxtaarticular osteopenia, which is a hallmark of rheumatoid
arthritis, is minimal in psoriatic arthritis. Asymmetric erosive changes
in small joints of the hands and feet are typical of psoriatic arthritis
and have a predilection (in decreasing order) for DIP, proximal
interphalangeal (PIP), metatarsophalangeal, and metacarpophalangeal
(MCP) joints.
- Erosive disease frequently occurs in patients with either DIP
involvement or progressive deforming arthritis and may lead to
subluxation and, less commonly, bony ankylosis of the joint. Erosion of
the tuft of the distal phalanx, and even the metacarpals or metatarsals,
can progress to complete dissolution of the bone. Although this form of
acroosteolysis is not diagnostic, it is very suggestive of psoriatic
arthritis. The pencil-in-cup deformity observed in the hands and feet of
patients with severe joint disease usually affects the DIP joints but
also may involve the PIP joints.
- CT scan of the sacroiliac joint may be a sensitive method of
visualizing involvement in patients with spondylitis or
sacroiliitis.
- Recent studies have indicated that MRI may be a sensitive method for
demonstrating typical enthesopathic pathology of psoriatic arthritis,
particularly in the hands and feet.
Other Tests:
- Traditional methods of monitoring patients with rheumatic conditions
include clinical assessment for joint inflammation or damage and
radiographic evaluations. The radiologic scoring methods for evaluating
peripheral joints in psoriatic arthritis were developed for patients
with rheumatoid arthritis. A study validated the original Steinbrocker
method, a modified Steinbrocker method, and the Larsen method for
assessment of radiographs in patients with psoriatic arthritis. The
latter 2 methods now can be used to assess disease progression in
patients with psoriatic arthritis.
Histologic Findings:
The histopathology of psoriatic synovitis is similar to that
observed in other inflammatory arthritides, with a notable lack of
intrasynovial immunoglobulin and rheumatoid factor production and a
greater propensity for fibrous ankylosis, osseous resorption, and
heterotopic bone formation.
Medical Care: The
treatment of psoriatic arthritis is directed at controlling the
inflammatory process. Although no clear correlation exists between the
skin and joint inflammation in every patient, the skin and joint aspects
of the disease often must be treated simultaneously.
Initial treatment is composed of nonsteroidal anti-inflammatory drugs
(NSAIDs) for joint disease and topical therapies for the skin. In many
patients, this approach is sufficient to control disease manifestations,
although some patients have a worsening of psoriasis with NSAIDs. In these
patients, a drug belonging to a different family of NSAIDs should be used.
- Intraarticular injection of entheses or single inflamed joints with
corticosteroids may be particularly effective in some patients.
- Use disease-modifying drugs in individuals whose arthritis is
persistent. If the skin disease is well controlled with topical
medication, the joint disease can be treated with a variety of
second-line or cytotoxic drugs.
- Intramuscular administration of gold has been used in the past but
has been supplanted by newer disease-modifying antirheumatic
drugs.
- In patients with severe skin inflammation, medications such as
methotrexate (MTX), retinoic-acid derivatives, and psoralen plus
ultraviolet light (PUVA) should be considered. These medications have
been shown to work for both skin and joint manifestations.
- Sulfasalazine and cyclosporine are 2 second-line agents that have
received particular attention in the management of psoriatic arthritis.
Although these drugs may control the acute inflammation in psoriatic
arthritis, they have not been helpful in arresting the progression of
clinical and radiologic damage. Thus, the disease must be treated
earlier or better drugs are necessary to prevent the damage that may
ensue as a result of psoriatic arthritis.
- Cyclosporine appears to be an effective agent for the treatment of
psoriasis and psoriatic arthritis.
- The major concern with cyclosporine is its toxicity, especially
nephrotoxicity and hypertension. Combination therapy (eg,
MTX/sulfasalazine, MTX/cyclosporine) may be more efficacious in some
patients.
- Anti–TNF-alpha therapy, such as etanercept (Enbrel) and infliximab
(Remicade) has reportedly been used in treatment of psoriatic arthritis.
Etanercept was recently approved by the US Food and Drug Administration.
- Several other modalities have been tried in psoriatic arthritis,
including vitamin D-3, bromocriptine, peptide T, and fish oils, but
their efficacy remains to be proven.
- Antimalarials, particularly hydroxychloroquine (Plaquenil), usually
are avoided in patients with psoriasis for fear of precipitating
exfoliative dermatitis or exacerbating psoriasis. Two studies showed
that these reactions did not occur in patients treated with
hydroxychloroquine; therefore, it is used occasionally.
- Systemic corticosteroids usually are avoided because of possible
rebound of the skin disease upon withdrawal.
Surgical Care: Arthroscopic synovectomy has been
effective in treating severe chronic monoarticular synovitis. Because of
the enhanced tendency for fibrosis associated with this therapy,
anti-inflammatory and physical therapy measures aimed at improving range
of motion are important adjuncts to this intervention. Joint replacement
and forms of reconstructive therapy occasionally are necessary.
Diet: For people who have morning stiffness, the
optimal time for taking an NSAID might be after the evening meal and again
upon awakening. Taking NSAIDs with food can reduce stomach discomfort. All
NSAIDs are capable of damaging the mucous layer and causing ulcers and GI
bleeding when taken for long periods. Cyclooxygenase-2 (COX-2) selective
inhibitors are associated with a lower incidence of gastric ulcers.
Activity:
- Exercise is an important part of total treatment to limit the pain
and swelling of arthritis, which can make joints stiff and hard to
move.
- A directed exercise program can improve movement, strengthen
muscles to stabilize joints, improve sleep, strengthen the heart,
increase stamina, reduce weight, and improve physical
appearance.
- Generally, a normal amount of rest and sleep is sufficient to
decrease fatigue and reduce joint inflammation.
- In a very few people, psoriatic arthritis may cause extreme
fatigue.
The treatment of psoriatic arthritis
usually begins with NSAIDs. These include enteric-coated acetylsalicylic
acid (ECASA), naproxen, indomethacin, ibuprofen, diclofenac, tolmetin,
meloxicam, and other NSAIDs. ECASA and ibuprofen require frequent
administration, whereas meloxicam and slow-release indomethacin may be
administered in a once-daily routine, which may be preferred by some
patients.
Indomethacin is the strongest of the available traditional NSAIDs,
although it has significant adverse GI and CNS effects and a potential to
increase blood pressure. It is best used for short-term (eg, acute)
flares.
Several selective COX-2 inhibitors, such as celecoxib and rofecoxib,
have been developed and may be the optimal agents in patients at risk for
GI toxicity with NSAIDs. NSAIDs clearly control the mild inflammatory
features of psoriatic arthritis; however, some NSAIDs may aggravate the
skin psoriasis.
Drug Category: Nonsteroidal anti-inflammatories
-- Have analgesic, anti-inflammatory, and antipyretic activities.
Their mechanism of action may be inhibition of COX activity and
prostaglandin synthesis. Other mechanisms also may exist, such as
inhibition of leukotriene synthesis, lysosomal enzyme release,
lipoxygenase activity, neutrophil aggregation, and various cell membrane
functions.
Drug Name
|
Ibuprofen (Motrin, Ibuprin, Advil,
Excedrin IB) -- DOC for patients with mild to moderate pain.
Inhibits inflammatory reactions and pain by decreasing prostaglandin
synthesis.
|
| Adult Dose |
400 mg PO q4-6h, 600 mg q6h, or 800
mg q8h while symptoms persist; not to exceed 3.2 g/d
|
| Pediatric Dose |
20-70 mg/kg/d PO divided tid/qid;
start at lower end of dosing range and titrate; not to exceed 2.4
g/d
|
| Contraindications |
Documented hypersensitivity; peptic
ulcer disease, recent GI bleeding or perforation, renal
insufficiency, or high risk of bleeding
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effect of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of MTX
toxicity; phenytoin levels may be increased when administered
concurrently
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Category D in third trimester of
pregnancy; caution in congestive heart failure, hypertension, and
decreased renal and hepatic function; caution in coagulation
abnormalities or during anticoagulant therapy |
Drug Name
|
Diclofenac (Voltaren, Cataflam) --
Inhibits prostaglandin synthesis by decreasing activity of COX,
which, in turn, decreases formation of prostaglandin precursors.
|
| Adult Dose |
Persistent night pain or morning
stiffness: Up to 100 mg qhs may help to relieve pain; not to exceed
total daily dose of 200 mg
|
| Pediatric Dose |
>12 years: Administer as in
adults <12 years: Not established
|
| Contraindications |
Documented hypersensitivity; peptic
ulcer disease, recent GI bleeding or perforation, renal
insufficiency, and those at high risk of bleeding
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effect of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of MTX
toxicity; phenytoin levels may be increased when administered
concurrently
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Category D in third trimester of
pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia,
interstitial nephritis, and renal papillary necrosis may occur;
increases risk of acute renal failure in patients with preexisting
renal disease or compromised renal perfusion; low WBC counts occur
rarely and usually return to normal in ongoing therapy;
discontinuation of therapy may be necessary if persistent
leukopenia, granulocytopenia, or thrombocytopenia
develops |
Drug Name
|
Naproxen (Anaprox, Naprelan,
Naprosyn, Aleve) -- For relief of mild to moderate pain. Inhibits
inflammatory reactions and pain by decreasing activity of COX, which
is responsible for prostaglandin synthesis.
|
| Adult Dose |
250-500 mg PO bid; may increase to
1.5 g/d for limited periods
|
| Pediatric Dose |
<2 years: Not
established >2 years: 2.5 mg/kg/dose PO; not to exceed 10
mg/kg/d
|
| Contraindications |
Documented hypersensitivity; peptic
ulcer disease; recent GI bleeding or perforation; renal
insufficiency
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effect of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of MTX
toxicity; phenytoin levels may be increased when administered
concurrently
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Category D in third trimester of
pregnancy; acute renal insufficiency, interstitial nephritis,
hyperkalemia, hyponatremia, and renal papillary necrosis may occur;
patients with preexisting renal disease or compromised renal
perfusion risk acute renal failure; leukopenia occurs rarely, is
transient, and usually returns to normal during therapy; persistent
leukopenia, granulocytopenia, or thrombocytopenia warrants further
evaluation and may require discontinuation of
drug |
Drug Name
|
Indomethacin (Indocin) -- Rapidly
absorbed; metabolism occurs in liver by demethylation,
deacetylation, and glucuronide conjugation. Inhibits prostaglandin
synthesis.
|
| Adult Dose |
25-50 mg PO bid/tid 75 mg SR
bid; not to exceed 200 mg/d
|
| Pediatric Dose |
1-2 mg/kg/d divided PO bid/qid; not
to exceed 4 mg/kg/d or 150-200 mg/d
|
| Contraindications |
Documented hypersensitivity; GI
bleeding or renal insufficiency.
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effect of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of MTX
toxicity; phenytoin levels may be increased when administered
concurrently
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Category D in third trimester of
pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia,
interstitial nephritis, and renal papillary necrosis may occur;
increases risk of acute renal failure in patients with preexisting
renal disease or compromised renal perfusion; reversible leukopenia
may occur (discontinue if persistent leukopenia, granulocytopenia,
or thrombocytopenia develops) |
Drug Name
|
Sulindac (Clinoril) -- Decreases
activity of COX and, in turn, inhibits prostaglandin synthesis.
Results in a decreased formation of inflammatory mediators.
|
| Adult Dose |
150-200 mg PO bid or 300-400 qd;
not to exceed 400 mg/d
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity;
patients in whom aspirin, iodides, or other NSAIDs induce
hypersensitivity; GI bleed and renal insufficiency
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effect of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of MTX
toxicity; phenytoin levels may be increased when administered
concurrently
|
| Pregnancy |
C - Safety for use during pregnancy
has not been established.
|
| Precautions |
Category D in third trimester of
pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia,
interstitial nephritis, and renal papillary necrosis may occur;
increases risk of acute renal failure in preexisting renal disease
or compromised renal perfusion; low WBC counts occur rarely and
usually return to normal in ongoing therapy; discontinuation of
therapy may be necessary if persistent leukopenia, granulocytopenia,
or thrombocytopenia develops; caution in anticoagulation defects or
patients receiving anticoagulant therapy |
Drug Name
|
Celecoxib (Celebrex) -- For those
at risk of GI toxicity with NSAIDs. Inhibits primarily COX-2. COX-2
is considered an inducible isoenzyme, induced during inflammatory
stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At
therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus,
GI toxicity may be decreased. Seek lowest dose for each patient.
|
| Adult Dose |
200 mg/d PO qd; alternatively, 100
mg PO bid
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity
|
| Interactions |
Coadministration with fluconazole
may cause increase in celecoxib plasma concentrations because of
inhibition of celecoxib metabolism; coadministration with rifampin
may decrease celecoxib plasma concentrations
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Category D in third trimester of
pregnancy; may cause fluid retention and peripheral edema; caution
in compromised cardiac function, hypertension, and conditions
predisposing to fluid retention; caution in severe heart failure and
hyponatremia because may deteriorate circulatory hemodynamics;
NSAIDs may mask usual signs of infection; caution in the presence of
existing controlled infections; evaluate therapy when symptoms or
lab results suggest liver dysfunction |
Drug Name
|
Meloxicam (Mobic) -- Decreases
activity of COX, which, in turn, inhibits prostaglandin synthesis.
These effects decrease formation of inflammatory mediators.
|
| Adult Dose |
7.5 mg PO qd; may increase to 15 mg
PO qd
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity; active
GI bleeding
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effect of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of MTX
toxicity; phenytoin levels may be increased when administered
concurrently
|
| Pregnancy |
C - Safety for use during pregnancy
has not been established.
|
| Precautions |
Category D in third trimester of
pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia,
interstitial nephritis, and renal papillary necrosis may occur;
increases risk of acute renal failure in patients with preexisting
renal disease or compromised renal perfusion; reversible leukopenia
may occur (discontinue if persistent leukopenia, granulocytopenia,
or thrombocytopenia develops) |
Drug Name
|
Valdecoxib (Bextra) --
Second-generation COX-2 inhibitor that offers a very rapid onset and
prolonged efficacy. Inhibits primarily COX-2. COX-2 is considered an
inducible isoenzyme, induced during pain and inflammatory stimuli.
Inhibition of COX-1 may contribute to NSAID GI toxicity. At
therapeutic concentrations, valdecoxib does not inhibit COX-1
isoenzyme, decreasing GI toxicity.
|
| Adult Dose |
10 mg PO qd
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity
|
| Interactions |
Coadministration with fluconazole
may cause increase in valdecoxib plasma concentrations;
coadministration with rifampin may decrease valdecoxib plasma
concentrations
|
| Pregnancy |
C - Safety for use during pregnancy
has not been established.
|
| Precautions |
Category D in third trimester of
pregnancy; abdominal pain, nausea, and diarrhea may occur; caution
in compromised cardiac function, hypertension, and conditions
predisposing to fluid retention; caution in severe heart failure and
hyponatremia because may deteriorate circulatory hemodynamics;
NSAIDs may mask usual signs of infection; caution in the presence of
existing controlled infections; evaluate therapy when symptoms or
lab results suggest liver dysfunction |
Drug Category: Immunosuppressants -- Inhibit key
factors in the immune system responsible for inflammatory responses.
Drug Name
|
Methotrexate (Rheumatrex) --
Antimetabolite that inhibits dihydrofolate reductase, thereby
hindering DNA synthesis and cell reproduction. Adjust dose gradually
to attain satisfactory response.
|
| Adult Dose |
2.5 mg/wk PO/IM initially;
administer 3 doses over a 24-h period, then titrate to as high as 25
mg/wk depending on response
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity;
alcoholism; hepatic insufficiency; documented immunodeficiency
syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia,
leukopenia, thrombocytopenia, significant anemia); renal
insufficiency
|
| Interactions |
Oral aminoglycosides may decrease
absorption and blood levels of concurrent oral MTX; charcoal lowers
levels; coadministration with etretinate may increase
hepatotoxicity; folic acid or its derivatives contained in some
vitamins may decrease response; probenecid, NSAIDs, salicylates,
procarbazine, and sulfonamides (including TMP-SMZ) can increase
plasma levels; may decrease phenytoin plasma levels; may increase
plasma levels of thiopurines
|
| Pregnancy |
D - Unsafe in pregnancy
|
| Precautions |
Monitor CBCs monthly and liver and
renal function every 1-3 mo during therapy (monitor more frequently
during initial dosing, dose adjustments, or when risk of elevated
MTX levels, eg, dehydration); has toxic effects on hematologic,
renal, GI, pulmonary, and neurologic systems; discontinue if
significant drop in blood counts occur; fatal reactions reported
when administered concurrently with NSAIDs |
Drug Name
|
Cyclosporine (Sandimmune, Neoral)
-- Cyclic polypeptide that suppresses some humoral immunity and, to
a greater extent, cell-mediated immune reactions such as delayed
hypersensitivity, allograft rejection, experimental allergic
encephalomyelitis, and graft-versus-host disease for a variety of
organs. Demonstrated to be helpful in a variety of skin disorders,
especially psoriasis.
|
| Adult Dose |
2.5-5 mg/kg/d PO in divided doses
|
| Pediatric Dose |
Administer as in adults
|
| Contraindications |
Documented hypersensitivity;
uncontrolled hypertension or malignancies; do not administer
concomitantly with PUVA or UVB radiation in psoriasis because may
increase risk of cancer
|
| Interactions |
Carbamazepine, phenytoin,
isoniazid, rifampin, and phenobarbital may decrease concentrations;
azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole,
erythromycin, verapamil, grapefruit juice, diltiazem,
aminoglycosides, acyclovir, amphotericin B, and clarithromycin may
increase toxicity; acute renal failure, rhabdomyolysis, myositis,
and myalgias increase when taken concurrently with lovastatin
|
| Pregnancy |
C - Safety for use during pregnancy
has not been established.
|
| Precautions |
Evaluate renal and liver functions
often by measuring BUN, serum creatinine, serum bilirubin, and liver
enzymes; may increase risk of infection and lymphoma; reserve IV use
only for patients who cannot take PO |
Drug Category: Biologic therapies -- Postulated
mechanisms include free radical–mediated oxidative damage to DNA;
decreased secretion of IL-6, IL-1-beta, IL-10, and TNF-alpha; reduced
angiogenesis; induction of IFN-gamma; and IL-2 production by CD8 T cells.
Drug Name
|
Etanercept (Enbrel) -- Acts by
binding and inhibiting TNF, the cytokine that contributes to
inflammatory and immune responses.
|
| Adult Dose |
25 mg SC twice weekly
|
| Pediatric Dose |
0.4 mg/kg SC; maximum single dose
25 mg
|
| Contraindications |
Documented hypersensitivity,
sepsis, and concurrent live vaccination; reactivation of
tuberculosis; possible drug-induced lupus
|
| Interactions |
None reported
|
| Pregnancy |
C - Safety for use during pregnancy
has not been established.
|
| Precautions |
Caution in impaired renal function
and asthma; discontinue administration if a serious infection
develops; adverse effects may include pain at injection site,
localized erythema, rash, UTI symptomatology, GI upset, nausea,
vomiting, rhinitis, and cough |
Drug
Category: 5-Aminosalicylic acid derivatives -- Inhibit
inflammatory reactions and pain by decreasing activity of COX, which is
responsible for prostaglandin synthesis.
Drug Name
|
Sulfasalazine (Azulfidine, EN-Tabs)
-- Acts locally in colon to decrease the inflammatory response and
systemically inhibits prostaglandin synthesis. Loading dose is not
necessary.
|
| Adult Dose |
1 g PO tid/qid initially; titrate
to 2-4 g/d in divided doses depending on response
|
| Pediatric Dose |
<2 years: Not
established >2 years: 40-60 mg/kg/d PO in 3-6 divided
doses; follow by maintenance dose of 20-30 mg/kg/d divided qid
|
| Contraindications |
Documented hypersensitivity to
sulfa drugs or any component; GI or GU obstruction
|
| Interactions |
Decreases effects of iron, digoxin,
and folic acid; conversely, increases effect of oral anticoagulants,
oral hypoglycemic agents, and MTX
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Caution in patients with renal or
hepatic impairment, blood dyscrasias, urinary obstruction, or G-6-PD
deficiency |
Further Outpatient Care:
- Heat and cold treatments: Heat and cold treatments can temporarily
relieve pain and reduce joint swelling. Examples of treatments include
soaking in a warm tub or placing a warm compress or cold pack on the
painful joint.
Deterrence/Prevention:
- A number of medications cause an exacerbation of psoriasis;
therefore, avoidance of these medications may help prevent or minimize
flare-ups.
- Lithium and withdrawal from systemic corticosteroids are well
known to cause flares of disease.
- Beta-blockers, antimalarials, and NSAIDs also have been
implicated.
Complications:
- Until recently, psoriatic arthritis generally was believed to be a
mild disease, with severe joint deformity and destruction (called
arthritis mutilans) occurring in only approximately 5% of patients. This
severe condition usually occurs in the small joints of the hands and
feet. Some reports now suggest that arthritis mutilans may occur in as
many as 16% of patients and that it may be as severe as rheumatoid
arthritis.
- Atlantoaxial subluxation with attendant neurological complications
can occur. Rarely, patients with psoriatic arthritis may develop aortic
insufficiency.
Prognosis:
- Until recently, psoriatic arthritis generally had been considered a
milder disease than rheumatoid arthritis. The following factors
influence the degree of severity:
- Clinical subset (eg, arthritis mutilans, symmetric
polyarthritis)
- Severity of skin involvement
- Family history of arthritis
- New evidence suggests that psoriatic arthritis may be as disabling
and destructive as rheumatoid arthritis when the appropriate comparisons
are made; thus, treatment should be aggressive in those individuals with
progressive joint disease.
Patient Education:
- Patients may visit the Web sites of the Arthritis Foundation or the
National Psoriasis Foundation for more information on their
disease.
- For excellent patient education resources, visit eMedicine's
Psoriasis Center and Arthritis Center. Also, see eMedicine's patient
education articles Psoriatic Arthritis, Psoriasis, and Nail
Psoriasis.
Special Concerns:
- Children with juvenile psoriatic arthritis should be examined by an
ophthalmologist annually to check for several forms of eye inflammation
associated usually with various forms of juvenile arthritis.
| Caption: Picture 1. Psoriatic
arthritis. Severe fixed flexion deformity of the interphalangeal
joint. |
| |
| Picture Type:
Photo |
| Caption: Picture 2. Psoriatic
arthritis. Comparison between sites of involvements in both hands
and feet in psoriatic arthritis and rheumatoid arthritis. |
| |
| Picture Type:
Image |
| Caption: Picture 3. Psoriatic
arthritis involving the distal phalangeal joint. |
| |
| Picture Type:
X-RAY |
| Caption: Picture 4. Swelling and
deformity of the metacarpophalangeal and distal interphalangeal
joints in a patient with psoriatic arthritis. |
| |
| Picture Type:
Photo |
| Caption: Picture 5. Psoriatic
arthritis involving the distal phalangeal joint. |
| |
| Picture Type:
Photo |
| Caption: Picture 6. Severe
psoriatic arthritis involving the distal and proximal
interphalangeal joints. |
| |
| Picture Type:
Photo |
| Caption: Picture 7. Asymmetric
arthritis pattern of psoriatic arthritis (fixed flexion deformity).
|
| |
| Picture Type:
Photo |
| Caption: Picture 8. Psoriatic
arthritis. Arthritis mutilans, a typically psoriatic pattern of
arthritis, which is associated with a characteristic "pencil-in-cup"
radiographic appearance of digits. |
| |
| Picture Type:
Photo |
| Caption: Picture 9. Psoriatic
arthritis involving the distal phalangeal joint. |
| |
| Picture Type:
Photo |
| Caption: Picture 10. Psoriatic
arthritis. Arthritis mutilans (ie, "pencil-in-cup" deformities).
|
| |
| Picture Type:
X-RAY |
- Andrews BS, Lowe NJ: Therapy of psoriatic arthritis. In: Practical
Psoriasis Therapy. 2nd ed. St. Louis, Mo: Mosby-Year Book; 1993: 239-55.
- Bruce I, Gladman DD: Psoriatic Arthritis: Recognition and
Management. BioDrugs 1998; 9: 271.
- Calzavara-Pinton PG, Franceschini F, Manera C, et al:
Antiperinuclear factor in psoriatic arthropathy. J Am Acad Dermatol 1999
Jun; 40(6 Pt 1): 910-3.
- Cather JC, Abramovits W, Menter A: Cyclosporine and tacrolimus in
dermatology. Dermatol Clin 2001 Jan; 19(1): 119-37, ix.
- Clegg DO, Reda DJ, Mejias E, et al: Comparison of sulfasalazine and
placebo in the treatment of psoriatic arthritis. A Department of
Veterans Affairs Cooperative Study. Arthritis Rheum 1996 Dec; 39(12):
2013-20.
- Cuellar ML, Silveira LH, Espinoza LR: Recent developments in
psoriatic arthritis. Curr Opin Rheumatol 1994 Jul; 6(4): 378-84.
- Dougados M, Maetzel A, Mijiyawa M, Amor B: Evaluation of
sulphasalazine in the treatment of spondyloarthropathies. Ann Rheum Dis
1992 Aug;51(8):955-8.
- Eastmond CJ: Psoriatic arthritis. Genetics and HLA antigens.
Baillieres Clin Rheumatol 1994 May; 8(2): 263-76.
- Feldmann M, Brennan FM, Maini RN: Role of cytokines in rheumatoid
arthritis. Annu Rev Immunol 1996; 14: 397-440.
- Gladman DD, Shuckett R, Russell ML, et al: Psoriatic arthritis
(PSA)--an analysis of 220 patients. Q J Med 1987 Feb; 62(238): 127-41.
- Gladman DD, Anhorn KA, Schachter RK, Mervart H: HLA antigens in
psoriatic arthritis. J Rheumatol 1986 Jun; 13(3): 586-92.
- Gladman DD, Farewell VT: Progression in psoriatic arthritis: role of
time varying clinical indicators. J Rheumatol 1999 Nov; 26(11): 2409-13.
- Gonzalez S, Martinez-Borra J, Torre-Alonso JC, et al: The MICA-A9
triplet repeat polymorphism in the transmembrane region confers
additional susceptibility to the development of psoriatic arthritis and
is independent of the association of Cw*0602 in psoriasis. Arthritis
Rheum 1999 May; 42(5): 1010-6.
- Goodfield M: Skin lesions in psoriasis. Baillieres Clin Rheumatol
1994 May;8(2):295-316.
- Griffiths CE: Therapy for psoriatic arthritis: sometimes a conflict
for psoriasis. Br J Rheumatol 1997 Apr; 36(4): 409-10.
- Grundmann-Kollmann M, Mooser G, Schraeder P, et al: Treatment of
chronic plaque-stage psoriasis and psoriatic arthritis with
mycophenolate mofetil. J Am Acad Dermatol 2000 May; 42(5 Pt 1): 835-7.
- Gupta AK, Grober JS, Hamilton TA, et al: Sulfasalazine therapy for
psoriatic arthritis: a double blind, placebo controlled trial. J
Rheumatol 1995 May; 22(5): 894-8.
- Hohler T, Kruger A, Schneider PM, et al: A TNF-alpha promoter
polymorphism is associated with juvenile onset psoriasis and psoriatic
arthritis. J Invest Dermatol 1997 Oct; 109(4): 562-5.
- Kurschat P, Rubbert A, Poswig A, et al: Treatment of psoriatic
arthritis with etanercept. J Am Acad Dermatol 2001 Jun; 44(6): 1052.
- Mader R, Gladman DD, Long J, et al: Does injectable gold retard
radiologic evidence of joint damage in psoriatic arthritis? Clin Invest
Med 1995 Apr; 18(2): 139-43.
- Mease PJ, Goffe BS, Metz J, et al: Etanercept in the treatment of
psoriatic arthritis and psoriasis: a randomised trial. Lancet 2000 Jul
29; 356(9227): 385-90.
- Palit J, Hill J, Capell HA, et al: A multicentre double-blind
comparison of auranofin, intramuscular gold thiomalate and placebo in
patients with psoriatic arthritis. Br J Rheumatol 1990 Aug; 29(4):
280-3.
- Rahman P, Gladman DD, Cook RJ, et al: The use of sulfasalazine in
psoriatic arthritis: a clinic experience. J Rheumatol 1998 Oct; 25(10):
1957-61.
- Roenigk HH, Maibach HI: Psoriatic arthritis. In: Psoriasis. 2nd ed.
New York, NY: Marcel Dekkar; 1991: 171-87.
- Ruddy S, Harris ED Jr, Sledge CB, eds: Kelley's Textbook of
Rheumatology. 6th ed. Philadelphia, Pa: WB Saunders; 2000.
- Sakkas LI, Marchesoni A, Kerr LA, et al: Immunoglobulin heavy chain
gene polymorphisms in Italian patients with psoriasis and psoriatic
arthritis. Br J Rheumatol 1991 Dec; 30(6): 449-50.
- Sontheimer RD, Provost TT, eds: Cutaneous Manifestations of
Rheumatoid Diseases. 1st ed. Philadelphia, Pa: Lippincott Williams &
Wilkins; 1996: 233-6.
|