X-ray Follow-up after Open Reduction Internal Fixation of Distal Forearm Fracture.

Background Following surgery, the standard regimen for fractures of the distal forearm includes radiographs taken 2-weeks postoperatively. However, it is unclear whether these radiographs have any therapeutic risks or benefits for patients. Objective The purpose of this study is to determine the importance of radiographs taken 2-weeks after surgery on distal forearm fractures, especially if it leads to further operations, and to establish whether this practice should be continued. Materials and Methods This is a retrospective cohort study of patients with a distal forearm fracture treated surgically with a volar locking plate at two university hospitals in Denmark. Standard aftercare at both departments is 2 weeks in a cast. Patients attend a 2-week follow-up, at which the cast is replaced with a removable orthosis and radiographs are taken. It was recorded whether these radiographs had resulted in any change of treatment in terms of further operations, prolonged immobilization, additional clinical follow-up, or additional diagnostic imaging. Results A total of 613 patients were included in the study. The radiographs led to a change of standard treatment for 3.1% of the patients. A second operation was required by 1.0%; 0.5% were treated with prolonged immobilization, and 1.6% had additional outpatient follow-up due to the findings on the radiographs. Additional diagnostic imaging was performed on 1.9% of the patients. Conclusion The radiographs taken at the 2-weeks follow-up resulted in a change of treatment in 3.1% of the cases. Given the low cost and minimal risk of radiographs of an extremity, we concluded that the benefits outweigh the costs of routine radiographs taken 2 weeks after surgical treatment of distal forearm fractures.

Low Recurrence Rate and Risk of Distant Metastases following Marginal Surgery of Intramuscular Lipoma and Atypical Lipomatous Tumors of the Extremities and Trunk Wall.

OBJECTIVE: The purpose of the present study was to determine the local recurrence rate, risk of dedifferentiation, and distant metastasis after surgical excision of intramuscular lipomas (IML) and atypical lipomatous tumors (ALT). SUBJECTS AND METHODS: We retrospectively assessed all IML and ALT surgically removed from the extremities or trunk wall in our clinic between 1997 and 2006. Data from 141 patients with IML and 35 patients with ALT were extracted from the National Pathology Registry and patient files. RESULTS: IML and ALT recurred in 10 and 6 tumors, respectively. No metastases were observed in either group. The 5- and 10-year local recurrence-free survival rates were 97.1% (94.3-99.9) and 94.8% (CI: 91.1-98.6) for IML and 84.6% (CI: 72.1-97.1) and 81.1% (CI: 67.6-94.8) for ALT, respectively. ALT were found to dedifferentiate in 2/35 cases. CONCLUSION: Both IML and ALT showed a low recurrence rate when removed surgically from the extremities or trunk wall with intended marginal resection. No distant metastases were observed in any of the groups. It, therefore, seems safe to treat these tumors with marginal resection.

Effect of hyperglycemia and hyperinsulinemia on the response of IL-6, TNF-alpha, and FFAs to low-dose endotoxemia in humans.

Insulin therapy to maintain euglycemia increases survival in critically ill patients. To explore possible mechanisms of action, we investigated the effect of endotoxin on circulating cytokines, free fatty acids (FFA), and leukocytes during manipulated plasma glucose and insulin concentrations. Ten volunteers underwent three trials each, receiving an intravenous bolus of endotoxin (0.2 ng/kg) during normoglycemia (trial A, control), during a hyperglycemic clamp at 15 mM (trial B), and during a hyperinsulinemic euglycemic clamp (trial C). Endotoxin induced an increase in neutrophil count, a decrease in lymphocyte count, and an increase in serum levels of TNF-alpha, IL-6, and FFA. There was no difference in the TNF response between the three trials; the IL-6 levels were increased during the late phase of trials B and C compared with trial A. The endotoxin-induced elevation in FFA in trial A was suppressed during trials B and C. Clamping (trials B and C) caused a reduction in lymphocyte count that persisted after endotoxin injection. We conclude that low-dose endotoxemia triggers a subclinical inflammatory response and an elevation in FFA. The finding that high insulin serum concentrations induce a more prolonged increase in the anti-inflammatory cytokine IL-6 and suppress the levels of FFA suggests that insulin treatment of patients with sepsis may exert beneficial effects by inducing anti-inflammation and protection against FFA toxicity, and thereby inhibit FFA-induced insulin resistance.

Interleukin-6 production by contracting human skeletal muscle: autocrine regulation by IL-6.

Interleukin-6 (IL-6) is a cytokine with immuno-regulatory functions. However, contracting skeletal muscle expresses and subsequently releases IL-6 in high amounts, and recent evidence in IL-6 deficient mice suggests a role of IL-6 in metabolism. Since IL-6 mRNA levels also increase in abdominal adipose tissue in response to exercise, we wanted to examine the possible existence of a positive feedback mechanism between muscle and adipose tissue. We obtained biopsies from human skeletal muscle and abdominal subcutaneous adipose tissue in relation to either 3h of bicycle exercise or recombinant human IL-6 infusion (rhIL-6) or saline infusion. In muscle, IL-6 mRNA increased (p<0.05) immediately after exercise, peaking at this time-point, whereas IL-6 mRNA in adipose tissue increased 1.5-h post exercise (p<0.05) displaying a different kinetic of induction. During rhIL-6 infusion, IL-6 mRNA increased 120-fold in muscle (p<0.05). In conclusion, the present study demonstrates that muscle IL-6 is regulated by an autocrine mechanism at the transcriptional level.

Immunohistochemical detection of interleukin-6 in human skeletal muscle fibers following exercise.

Interleukin-6 (IL-6) is produced by many different cell types. Human skeletal muscles produce and release high amounts of IL-6 during exercise; however, the cell source of origin in the muscle is not known. Therefore, we studied the protein expression of IL-6 by immunohistochemistry in human muscle tissue from biopsies obtained at time points 0, 3, 4.5, 6, 9, and 24 h in relation to 3 h of bicycle exercise performed by healthy young males (n=12) and in resting controls (n=6). The IL-6 expression was clearly increased after exercise and remained high even by 24 h, relative to pre-exercise or resting individuals. The IL-6 immunostainings of skeletal muscle cells were homogeneous and without difference between muscle fiber types. The IL-6 mRNA peaked immediately after the exercise, and, in accordance, the IL-6 protein expression within muscle cells was most pronounced around 3 h post-exercise. However, the finding that plasma IL-6 concentration peaked in the end of exercise indicates a high turnover of muscle-derived IL-6. In conclusion, the finding of marked IL-6 protein expression exclusively within skeletal muscle fibers following exercise demonstrates that skeletal muscle fibers of all types are the dominant cell source of exercise-induced release of IL-6 from working muscle.

Exercise and IL-6 infusion inhibit endotoxin-induced TNF-alpha production in humans.

During "nondamaging" exercise, skeletal muscle markedly releases interleukin (IL)-6, and it has been suggested that one biological role of this phenomenon is to inhibit the production of tumor necrosis factor (TNF)- alpha, which is known to cause pathogenesis such as insulin resistance and atherosclerosis. To test this hypothesis, we performed three experiments in which eight healthy males either rested (CON), rode a bicycle for 3 h (EX), or were infused with recombinant human IL-6 (rhIL-6) for 3 h while they rested. After 2.5 h, the volunteers received a bolus of Escherichia coli lipopolysaccharide endotoxin (0.06 ng/kg) i.v. to induce low-grade inflammation. In CON, plasma TNF-alpha increased significantly in response to endotoxin. In contrast, during EX, which resulted in elevated IL-6, and rhIL-6, the endotoxin-induced increase in TNF-alpha was totally attenuated. In conclusion, physical exercise and rhIL-6 infusion at physiological concentrations inhibit endotoxin-induced TNF-alpha production in humans. Hence, these data provide the first experimental evidence that physical activity mediates antiinflammatory activity and suggest that the mechanism include IL-6, which is produced by and released from exercising muscles.