The objective was to study prevalence and underlying pathology of "swimmer's shoulder". Twenty-two competitive swimmers of national "D-Kader" (elite development swimmers) were evaluated by means of questionnaire, clinical examination and isokinetic testing of external rotation and internal rotation. At the examination current interfering pain necessitating a cessation or reduction of practice was found in 5 (23%) athletes. At isokinetic testing 8 (36%) athletes complained of shoulder pain. Any history of pain was seen in 14 (64%) swimmers. A positive impingement sign was noted in 11 (50%) athletes. Apprehension sign which is indicative of anterior instability was found in 11 (50%) swimmers. Clinical equivalents of dysfunction of scapulothoracic muscles such as scapular winging (5 athletes) and shoulder protraction (12 athletes) were noted. For comparison of results of isokinetic testing a control group of non-swimmers was selected matching the group of swimmers exactly in terms of age, sex and dominant side. External rotation/internal rotation ratio of peak torque and total work at 60 deg/sec and 180 deg/sec was significantly lower in swimmers than in controls. The ratio was independent of sex, dominant side, history of pain and pain at examination. During internal rotation competitive swimmers produced significantly higher peak torques and total work than controls. There was no significant difference in external rotation. In conclusion there are several different abnormalities of function contributing to the pathology of "swimmer's shoulder":--Laxity of anterior-inferior capsuloligamentous structures with atruamatic anterior instability due to repetitive overload.--Impingement with rotator cuff tendinitis.--Muscular imbalance of the rotator cuff muscles and scapulothoracic dysfunction.
The participation of the humoral immune system in rheumatoid arthritis (RA) is characterized by the production of rheumatoid factors (RF). RF are autoantibodies against the Fc part of IgG which are encoded by diverse germ-line genes. Most of the RF-encoding genes are unmutated, but in RA, a substantial quantity is encoded by somatically mutated genes. In addition, the synovial membranes (SM) of the diseased joints of RA patients are infiltrated by B lymphocytes which form germinal center-like aggregates. To analyze the local immune response, B cell foci from two RA SM were isolated by micromanipulation. From DNA of these foci, the rearranged kappa light chain variable region (V kappa) genes were amplified by polymerase chain reaction (PCR), cloned and sequenced. The amplification of different V kappa-J kappa combinations of different foci suggested oligoclonal expansion of B lymphocytes, which was confirmed by sequence analysis: each PCR product contained members of a single B cell clone. The sequence analysis of 29 different clones revealed rearrangements of diverse V kappa genes. Both frequent representatives of the V kappa 3 and the V kappa 1 family, as well as rarely used genes such as the L10 and B2 genes of the V kappa 2 and V kappa 5 families were found. Of the eleven potentially functional gene rearrangements, eight were significantly mutated, indicating their derivation from antigen-selected B cells. Intraclonal diversity in one of these clones may suggest ongoing mutation in the diseased synovial membrane of patients with RA.
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