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[Case Report]

Bilateral Shoulder Pain: Psoriatic Arthritis Masquerading as Overuse

Mario F. Ciocca, Jr, MD

Internal Medicine Series
Series Editor: Donald M. Christie, Jr, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 26 - NO. 9 - SEPTEMBER 98


In Brief: A 25-year-old man who played summer softball developed bilateral shoulder pain. The pain was not alleviated by decreased activity, and signs and symptoms, including previous bilateral foot pain that developed before the onset of a psoriatic scalp lesion, suggested psoriatic arthritis (PA). Bilateral pain is unusual with PA; more typically, patients have monarticular pain (see "Asymmetric Presentation of Psoriatic Arthritis," below). Discussed are differential diagnosis, etiology, clinical features, and treatment, including physical therapy, NSAIDs, and disease-modifying agents such as sulfasalazine.

One systemic disorder that initially can look very much like a sports-related overuse injury is psoriatic arthritis (PA). The following case report illustrates how the disorder can cause patients to delay seeking treatment and also how a careful evaluation can lead to the correct diagnosis and treatment.

Case Report

A 25-year-old man who played softball in a summer league had bilateral anterolateral shoulder pain of 1 year's duration. He had first noticed pain the previous summer while lifting weights. His pain was nonradiating and worse on the right side. Soon after the onset of pain, he noticed limited shoulder range of motion such that during the softball season he could throw only sidearm.

He decided to work out with lighter weights, concentrating on rotator cuff strengthening, but his symptoms did not improve. Six months after the pain began, he decided to completely rest his shoulders, but he continued to have pain and a further decrease in range of motion over the next 6 months.

He denied joint swelling, trauma, neck pain, instability, back pain, other arthralgias, morning stiffness, fever, eye symptoms, or cardiovascular, gastrointestinal, or genitourinary symptoms. He denied alcohol or other drug use and initially denied any other pertinent medical history.

On further questioning, however, he revealed that he had developed psoriasis of the scalp 1 year before the onset of his presenting illness and, shortly before that, onset of bilateral foot pain that was diagnosed elsewhere as posterior tibial tendinitis. He had treated his scalp lesion with prescription topical corticosteroids.

In addition, he noted that his father had psoriasis, but there was no family history of arthritis.

Physical exam. On physical examination, he was afebrile. He reluctantly removed his baseball cap to reveal a psoriatic plaque on the left frontal area. There were no other skin or nail changes.

Though inspection of his shoulders did not reveal any obvious atrophy, overall muscle mass appeared decreased in comparison with his lower-body development, and overall shoulder strength was decreased. Flexion and abduction of the right shoulder was limited to 45°. He had 90° of flexion and abduction of the left shoulder. There was no tenderness of the joint capsule, acromioclavicular joint, or shoulder girdle musculature. There were no impingement or apprehension signs.

Evaluation of his other joints revealed bilateral ankle effusions as well as bilateral swelling of the proximal second and third interphalangeal joints of the hands. Otherwise, his head, neck, chest, abdomen, and musculoskeletal examination results were normal.

Lab tests and imaging studies. Results of laboratory tests included a normal complete blood count, normal aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and total bilirubin levels; an erythrocyte sedimentation rate (ESR) of 22 mm/hr (normal range for men, 0 to 10 mm/hr); a negative rheumatoid factor, a negative antinuclear antibody, and a nonreactive rapid plasma reagin. Radiographs of the shoulders were normal.

Diagnosis and treatment. A working diagnosis of PA was made, and treatment was begun with naproxen (500 mg twice daily) and referral to an athletic trainer for physical therapy to improve range of motion. A rheumatology consultant also examined the patient, concurred with the sports medicine internist's diagnosis, and added sulfasalazine (1 g total per day) to the naproxen regimen, which had already given the patient some relief.

Within 2 months, the patient experienced a further reduction in shoulder symptoms, but his scalp lesion had progressed. The sulfasalazine dose was increased to 2 g daily, and within less than 2 months he reported an 80% improvement in his shoulder symptoms.

Look-Alikes and Possible Causes

Joint symptoms in active people are not always related to injury or overuse, and therefore a thorough approach to diagnosis is important.

Differential diagnosis. In this patient, the examination revealed symmetric polyarthritis, which could have had several possible causes (table 1). However, the combination of clinical and laboratory findings as well as the favorable response to treatment strongly supported the diagnosis of PA.


Table 1. Possible Causes of Symmetric Polyarthritis


Autoimmune diseases
Ankylosing spondylitis
Enteropathic arthritis
Lupus erythematosus
Reiter's syndrome
Rheumatic fever
Rheumatoid arthritis
Crystal-associated arthritis
Gout
Pseudogout
Infectious disease
Gonorrhea
Hepatitis
Human parvovirus B19 infection
Paraneoplastic phenomena
Sarcoidosis
Hemochromatosis

PA occurs in approximately 5% to 8% of those who have psoriasis (1). It usually develops after onset of the skin disease (15% develop arthritis symptoms within the first year), but in 10% of patients, arthritis may predate the skin disease by 1 to 33 years (1,2). Onychodystrophy, which the patient described here did not have, occurs in 90% of patients who have PA, and its appearance can coincide with or follow the onset of arthritis symptoms (3,4).

Etiology. The cause of PA is unknown, but a combination of genetic, immunologic, and environmental factors is thought to play a role.

Multiple human leukocyte antigen (HLA) subtypes are associated, particularly HLA-B27 (5). (HLA-B27 typing was not done for this patient. Though a positive test would have supported the diagnosis, a negative test would not have excluded the diagnosis.) HLA-B27 antigen is present in approximately 20% of those who have peripheral joint involvement, and its prevalence may increase to 70% in those with spine involvement (4). The development of PA appears to be driven by T lymphocytes, possibly by CD8 cells (4).

Environmental factors include trauma and infectious agents such as Streptococcus (6), which may cause immunologic cross-reactivity, and Chlamydia trachomatis (5). Additionally, human immunodeficiency virus (HIV) infection has been associated with the development of severe psoriasis and arthritis (6).

Signs and Symptoms

Clinical features. PA is one of the seronegative spondyloarthropathies, which include Reiter's syndrome, ankylosing spondylitis, and enteropathic arthritis.

PA commonly appears as asymmetric oligoarthritis involving one large joint and one or two interphalangeal joints (see "Asymmetric Presentation of Psoriatic Arthritis," below) (1). A distinctive feature of PA is arthritis of the distal interphalangeal joints of the hands, although the feet can also be involved (4). This may be the only clinical feature, but it is more commonly part of a generalized arthropathy (1). Less commonly, the pattern is symmetrical, as in my patient, and resembles rheumatoid arthritis (1).

About 20% to 40% of patients have involvement of the spine, occurring as sacroiliitis, syndesmophytes, or, rarely, cervical spine involvement (3). Fortunately, only a few patients develop severe destructive arthritis (arthritis mutilans).

Inflammation is not limited to the joints but may also occur at areas of tendon or ligament insertion into bone. This inflammation at insertion points (enthesopathy), which can be subtle, is peculiar to the spondyloarthropathies. My patient's bilateral posterior tibial tendinitis, diagnosed a year before the onset of his shoulder pain, was probably such an inflammation. This is especially likely given the bilateral symptoms and the absence of a history of substantial weight bearing or overuse before the onset of the tendinitis, about 2 months prior to the development of skin lesions.

Other features of psoriasis and PA include dactylitis ("sausage digits"), eye inflammation (conjunctivitis or iritis), and aortic insufficiency (3). Rarely, the syndrome of synovitis, acne, pustulosis, hyperostosis and osteomyelitis (SAPHO) or that of palmar-plantar pustulosis (PPP) may be found (1).

Lab abnormalities. Laboratory abnormalities are nonspecific and may include an ESR elevation (seen in 40% to 60% of patients) (3); mild normocytic, normochromic anemia (2); hypergammaglobulinemia (seen in 11%) (2); leukocytosis (2); and hyperuricemia (seen in 14% to 20% of women and 32% of men) (2). The antinuclear antibody is usually negative, and rheumatoid factor is found in only 9% of patients (2).

Imaging features. Radiographic features of PA are a mixture of bone remodeling and osteolysis. Typical radiographic changes are seen in the interphalangeal joints and the spine. Other radiographic findings include spurs, periosteal reaction, bony ankylosis, sacroiliitis, and syndesmophytes (3).

Conservative Treatment

The goals of PA treatment are reduced inflammation and improved range of motion. These may be achieved through nonsteroidal anti-inflammatory drugs (NSAIDs) and physical therapy (7). NSAIDs, however, can worsen the psoriasis in some patients (3).

Isolated episodes of joint, bursa, or tendon involvement can be managed with injectable long-acting corticosteroids (avoiding injection directly into a tendon) (7). Systemic corticosteroids are not effective and may cause a transition of skin lesions to pustular psoriasis, as well as provoke a rebound of the skin disease on medication withdrawal (4).

Most patients require disease-modifying agents. The standard treatment is sulfasalazine or low-dose methotrexate sodium (7). Recent studies support sulfasalazine use (8-11), and a meta-analysis of randomized, placebo-controlled trials also supports treatment with sulfasalazine over other agents (12). Other disease-modifying agents that have been used with varying degrees of effectiveness are antimalarials, gold, penicillamine, retinoids, azathioprine, cyclosporin A, and psoralen plus ultraviolet A (PUVA) (7).

Treatments of unproved efficacy are vitamin D3, somatostatin, bromocriptine mesylate, peptide T, and fish oil (3,7).

Keep an Open Mind

An active patient's joint symptoms are commonly from acute injury or overuse. However, this case presents unusual features of both the history and physical examination and demonstrates the need for a broad differential diagnosis followed by appropriate clinical and laboratory investigation. A careful history may bring to light medical conditions a patient considers insignificant, and a thorough physical examination may suggest an underlying medical condition. Physicians must keep an open mind in evaluating any patient so that prompt diagnosis, treatment, and return to an active lifestyle are not delayed.

References

  1. Helliwell PS, Wright V: Psoriatic arthritis: clinical features, in Klippel JH, Dieppe PA (eds): Rheumatology, ed 2. St Louis, CV Mosby Co, 1998, pp 6.21.1-6.21.8
  2. Rothschild BM: The myriad faces of psoriatic arthritis. Compr Therapy 1996;22(3):165-168
  3. Gladman DD: Psoriatic arthritis, in Kelley WN, Ruddy S, Harris ED Jr, et al (eds): Textbook of Rheumatology, ed 5. Philadelphia, WB Saunders Co, 1997, pp 999-1005
  4. Winchester R: Psoriatic arthritis. Dermatol Clin 1995;13(4):779-792
  5. Cuellar ML, Silveira LH, Espinoza LR: Recent developments in psoriatic arthritis. Curr Opin Rheumatol 1994;6(4):378-384
  6. Breathnach SM: Psoriatic arthritis: etiology and pathogenesis, in Klippel JH, Dieppe PA (eds): Rheumatology, ed 2. St Louis, CV Mosby Co, 1998, ch 22
  7. Espinoza LR, Cuellar ML: Psoriatic arthritis: management, in Klippel JH, Dieppe PA (eds): Rheumatology, ed 2. St Louis, CV Mosby Co, 1998, ch 23
  8. Clegg DO, Reda DJ, Mejias E, et al: Comparison of sulfasalazine and placebo in the treatment of psoriatic arthritis. Arthritis Rheum 1996;39(12):2013-2020
  9. Combe B, Goupille P, Kuntz JL, et al: Sulphasalazine in psoriatic arthritis: a randomized, multicentre, placebo-controlled study. Br J Rheumatol 1996;35(7):664-668
  10. Dougados M, vam der Linden S, Leirisalo-Repo M, et al: Sulfasalazine in the treatment of spondylarthropathy: a randomized, multicenter, double-blind, placebo-controlled study. Arthritis Rheum 1995;38(5):618-627
  11. Fraser SM, Hopkins R, Hunter JA, et al: Sulphasalazine in the management of psoriatic arthritis. Br J Rheumatol 1993;32(10):923-925
  12. Jones G, Crotty M, Brooks P: Psoriatic arthritis: a quantitative overview of therapeutic options: the Psoriatic Arthritis Meta-Analysis Study Group. Br J Rheumatol 1997;36(1):95-99


Asymmetric Presentation of Psoriatic Arthritis

Richard P. Sandor, MD

A 29-year-old man was referred to the orthopedic department for evaluation of right knee swelling that was thought to be a meniscal injury. He had been symptomatic for about 1 month.

He had relatively little pain, some stiffness, no locking, and no giving way. He had sustained no trauma and had no history of knee problems. In addition, there were no symptoms of inflammatory bowel disease, no family history of unusual arthritis, and no fever. He had received a vaccination for measles, mumps, and rubella (MMR) 3 weeks before the onset of symptoms. He had not lived or traveled in an area endemic for Lyme disease.

Examination showed a moderate effusion with somewhat limited motion. There was some warmth but no erythema. Mild, diffuse joint-line tenderness was the only meniscal sign. The patient had no abnormal ligamentous laxity. X-rays with standing views showed only the effusion. A joint aspirate showed a leukocyte count of 6,400, red blood cell of 1,100, no crystals, and no bacterial growth. Sedimentation rate was 19 mm/hr (normal 0 to 10 mm/hr), rheumatoid arthritis factor nonreactive, complete blood count within normal limits, and rapid plasma reagin nonreactive. Except for a slightly elevated alkaline phosphatase value, results of serum chemistry analyses were within normal limits.

The initial diagnosis was monarticular arthritis, possibly secondary to MMR vaccination. However, subsequent careful physical examination showed a patch of psoriasis on the patient's scalp. The patient's knee swelling did not improve with various anti-inflammatories and finally required an intra-articular corticosteroid injection, which resolved his symptoms completely.

At present, about 7 months following onset of symptoms, the patient's right knee remains asymptomatic. However, he recently developed atraumatic left knee swelling that was likewise successfully treated.

Discussion. Monarticular arthritis was the initial manifestation of the patient's psoriatic arthritis. One study (1) showed that this mode of onset can occur in up to 40% of patients and is the most common initial manifestation of the disease. However, it is more common for the monarthritis to begin in the small joints such as the distal interphalangeal joint of the finger (1). Ultimately, up to 40% to 50% of patients with psoriatic arthritis will have knee involvement (2).

The sports medicine practitioner must be aware that this and other (3) systemic diseases can cause monarticular symptoms that can be misdiagnosed as a local mechanical problem.

References

  1. Jones SM, Armas JB, Cohen MG, et al: Psoriatic arthritis: outcome of disease subsets and relationship of joint disease to nail and skin disease. Br J Rheumatol 1994;33(9):834-839
  2. Helliwell PS, Wright V: Psoriatic arthritis: clinical features, in Klippel JH, Dieppe P (eds): Rheumatology, ed 2. St Louis, CV Mosby Co, 1998, pp 6.21.1-6.21.8
  3. McCune WJ, Golbus J: Monarticular arthritis, in Kelley WN, Ruddy S, Harris ED Jr, et al (eds): Textbook of Rheumatology, ed 5. Philadelphia, WB Saunders Co, 1997, pp 371-380

Dr Sandor is an orthopedic and sports medicine physician with the Camino Medical Group in Sunnyvale, California, and an emergency room physician for Kaiser South in San Francisco.


Dr Ciocca is an internist and sports medicine physician at the University of North Carolina in Chapel Hill and a member of the American Medical Society for Sports Medicine (AMSSM). Dr Christie practices internal medicine and sports medicine at Community Health Plan in Poughkeepsie, New York, and is a fellow of the American College of Physicians and American College of Sports Medicine, a charter member of the AMSSM, and an editorial board member of The Physician and Sportsmedicine. Address correspondence to Mario F. Ciocca, Jr, MD, University of North Carolina Student Health, CB# 7470, Chapel Hill, NC 27599.


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