به دلیل کثرت فعالیتهای تحقیقی و کمبود وقت تا مدتی کوتاه از ارسال case report معذوریم!!!
History of Present Illness | |
The patient is a 40–year–old Hispanic gentleman and is a dedicated long distance runner. He had a 1–year history of right ankle arthralgias and a 2–month history of right knee arthralgias. Then, during a meeting he was attending in the U.S., he developed right thigh, calf & foot swelling, and a right knee effusion. | |
Presentation | |
He had persistent right leg swelling but the effusion in his right knee had resolved. He had a new effusion in his left knee and had developed arthalgias in the left ankle.
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Physical Examination | |
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Differential Diagnosis | |
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Additional Diagnostic Studies | |
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Subsequent Course | |
These pharmacologic interventions were initiated sequentially, in combination with physical therapy:
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Discussion | |
Five percent of patients with psoriasis are affected by an inflammatory arthritis in some form. Men and women are affected with equal frequency. Psoriatic skin disease may pre–date the onset of arthritis (70% of cases), present coincident with arthritis (15% of cases), or follow the onset of arthritis (15% of cases). Characteristic, but not necessarily pathognomonic, features of psoriatic arthritis include nail involvement (pitting, separation from the nail bed known as “onycholysis”, and yellow discoloration known as the “oil drop” sign); dactylitis (“sausage digits”); inflammation at the sites of ligamentous and tendonous insertion (“enthesopathy”); and absence of rheumatoid factor. There are five clinical patterns of psoriatic arthritis, which may evolve and are not necessarily mutually exclusive:
Radiographically, psoriatic arthritis is a unique blend of bone destruction & proliferation. Manifestations may include erosive arthritis giving rise to the classic “pencil–in–cup” deformity in the phalanges, osteolysis, sacro–iliitis, ankylosis, spondylitis, enthesopathy, and periostitis. Our understanding of the etiology and pathophysiology of psoriatic arthritis remains incomplete. However, what is known can be summarized as follows. Genetic factors play an important role as evidenced by the 70% concordance for psoriasis in monozygotic twins; 50–fold increased risk of developing psoriatic arthritis in 1st degree relatives of patients with the disease; and epidemiologic association with the expression of both class I and class II HLA alleles including –B13, –B17, –B27, –B38, –B39, –Cw6, –DR4, and –DR7. Environmental factors have also been implicated including infectious agents (streptococci & staphylococci) and trauma (“Koebner phenomenon”) that may precipitate the onset or a flare of disease activity. T–cells have been demonstrated to play a role in both initiation and perpetuation of disease activity. Interestingly, peripheral joint activity in psoriatic arthritis parallels cutaneous activity in 1/3 of cases. Treatment options include NSAIDs, intra–articular or low–dose systemic corticosteroids, and a variety of “disease–modifying” agents including anti–malarials, gold, methotrexate, sulfasalazine, azathioprine, and cyclosporin A. The TNF inhibitor, etanercept (Enbrel®) is also an approved therapy for patients with psoriatic arthritis. Factors which portend a worse prognosis include a strong family history of psoriasis, disease onset <20 years of age, expression of HLA–B27 or –DR4 alleles, polyarticular disease, erosive disease, and extensive skin involvement. | |
Summary of Teaching Points | |
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