Twenty workers, consecutively attending the industrial health care centre for the first time with acute shoulder-neck pains, were subject to extensive rheumatological and ergonomic examinations. In seven patients congenital malformations or diseases causing musculoskeletal symptoms, or both, were probable aetiological factors. In the remaining 13 patients a significantly higher load was found on both shoulders (assessed by biomechanical film analysis) than in matched controls. The aim of the present investigation was to evaluate the influence of disease and to study the significance of measured individual and occupational factors in acute non-traumatic shoulder-neck pain among industrial workers. Material and methodsThe methods used for this investigation were approved by the ethical committee of the medical faculty, Umea University. PATIENTSThe first 20 workers (17 men, 3 women) at a manufacturing plant who attended the industrial health care centre with acute non-traumatic, shoulderneck pain were included in the study. The mean age of the patients was 35 years (SD 13-2). CONTROLSThe case-control method was used in this study to evaluate the role of ergonomic factors in acute non-traumatic shoulder-neck disorders. To eliminate confounding factors the controls were selected bypaired sampling and individual matching.6 Two controls were selected for each patient in whom causative disease or malformation was not found. The controls (n = 26) were obtained by paired sampling from employment records. The paired sampling was done with the additional requirements that the workers selected must match the corresponding case in the following criteria: age, sex, and place of work (the controls had to work in the factory halls). Furthermore, the workers selected as controls were not to have consulted the industrial health care centre for shoulder-neck disorders; this was verified by checking the patient records of the workers. From an age-class employment listing, the two workers who satisfied the above defined criteria closest to each patient were selected.
Serum creatine kinase (SCK) was measured in ten subjects in the laboratory before and after the performance of bicycle ergometry and a lifting task. SCK was significantly increased 24 h and 48 h after the lifting work but not after the bicycle ergometry, although the work performed on the latter was four-times as great as on the former. The lifting work resulted in muscle pain and tenderness and, for six subjects, in clinical signs of shoulder tendinitis. In a field study, an increase in SCK was noted among assemblers/welders and cash-register operators, but not among controllers and forklift-truck drivers. A health interview revealed that musculo-skeletal complaints were most often located in the upper extremity in the cases of the assemblers/welders and the cash-register operators. It is proposed that the SCK increase during work is a result of a high local muscular load due to fatigue and energy depletion of muscle cells producing a greater efflux of muscle enzymes. The evaluation of SCK changes during work may be an important tool in occupational health for early detection of work tasks producing local muscular strain.
Cystic puncture was performed percutaneously in 18 patients with solitary renal cysts and in 22 with multiple, congenital renal cysts. With the aid of tritiated water it was possible to estimate the fluid turnover in the cysts and compare it with their volume, pressure and potassium and creatinine levels. Fluid turnover was rapid in all the renal cysts. Two to five hours after i. v. injection of tritium, the tritium concentration in cystic fluid averaged 88% of the concentration in plasma fluid in patients with polycystic kidneys and 73% in patients with solitary cysts. Fluid turnover was more rapid in small than in large cysts, but there was no such difference between cysts with high and low pressure. It is possible that the fluid turnover was slightly faster in cysts with high potassium and creatinine levels than in those with low levels. The results show that the fluid turnover in a renal cyst of 10 ml is considerable— probably more than 100 ml/24 hours. This indicates that fluid inflow to the cyst comes mainly from cells in the cyst wall and not from a single glomerule. Fluid probably leaves the cyst actively via cells in the cyst wall, since the fluid turnover does not increase with high cyst pressure. The fluid turnover is probably secondary to the active solute transportation, which is performed by the cyst cells. This means that these cells have a tubular cell‐like function and should respond to pharmacotherapy.
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