Subcutaneous tendon rupture of extensor tendons on bilateral wrists associated with calcium pyrophosphate dihydrate crystal deposition disease.
ABSTRACT Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease is a well-recognized inflammatory joint disorder. Extensor tendon rupture associated with CPPD deposition has rarely been described. We report herein the case of a 58-year-old woman who underwent reconstruction for subcutaneous extensor tendon ruptures of the extensor tendons for the ring and little fingers on both wrists associated with CPPD deposition. The significance of this case is the occurrence at an earlier age compared to previous papers and the appearance on bilateral wrists.
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ABSTRACT: We report a case of closed rupture of the flexor tendons of the little finger caused by calcium pyrophosphate dihydrate crystal deposition disease of the pisotriquetrum joint. The patient could not flex the little finger and did not have wrist pain. Plain radiographs of the affected wrist joint showed severe arthritic changes of the pisotriquetrum joint and calcification around the joint. At operation, the pisotriquetrum joint capsule was ruptured and involved the flexor tendon of the little finger. The distal stump of the flexor tendon was transferred to the flexor tendon of the ring finger, and the pisiform was resected. Histological examination with polarized light microscopy revealed crystals showing weakly positive birefringence in the calcification.Hand Surgery 01/2013; 18(3):413-5.
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ABSTRACT: Most individuals seeking consultation at sports medicine clinics are young, healthy athletes with injuries related to a specific activity. However, these athletes may have other systemic pathologies, such as rheumatic diseases, that may initially mimic sports-related injuries. As rheumatic diseases often affect the musculoskeletal system, they may masquerade as traumatic or mechanical conditions. A systematic review of the literature found numerous case reports of athletes who presented with apparent mechanical low back pain, sciatica pain, hip pain, meniscal tear, ankle sprain, rotator cuff syndrome and stress fractures and who, on further investigation, were found to have manifestations of rheumatic diseases. Common systemic, inflammatory causes of these musculoskeletal complaints include ankylosing spondylitis (AS), gout, chondrocalcinosis, psoriatic enthesopathy and early rheumatoid arthritis (RA). Low back pain is often mechanical among athletes, but cases have been described where spondyloarthritis, especially AS, has been diagnosed. Neck pain, another common mechanical symptom in athletes, can be an atypical presentation of AS or early RA. Hip or groin pain is frequently related to injuries in the hip joint and its surrounding structures. However, differential diagnosis should be made with AS, RA, gout, psudeogout, and less often with haemochromatosis and synovial chondochromatosis. In athletes presenting with peripheral arthropathy, it is mandatory to investigate autoimmune arthritis (AS, RA, juvenile idiopathic arthritis and systemic lupus erythematosus), crystal-induced arthritis, Lyme disease and pigmented villonodular synovitis. Musculoskeletal soft tissue disorders (bursitis, tendinopathies, enthesitis and carpal tunnel syndrome) are a frequent cause of pain and disability in both competitive and recreational athletes, and are related to acute injuries or overuse. However, these disorders may occasionally be a manifestation of RA, spondyloarthritis, gout and pseudogout. Effective management of athletes presenting with musculoskeletal complaints requires a structured history, physical examination, and definitive diagnosis to distinguish soft tissue problems from joint problems and an inflammatory syndrome from a non-inflammatory syndrome. Clues to a systemic inflammatory aetiology may include constitutional symptoms, morning stiffness, elevated acute-phase reactants and progressive symptoms despite modification of physical activity. The mechanism of injury or lack thereof is also a clue to any underlying disease. In these circumstances, more complete workup is reasonable, including radiographs, magnetic resonance imaging and laboratory testing for autoantibodies.Sports Medicine 02/2008; 38(11):917-30. · 5.32 Impact Factor