Does acute non-traumatic pain increase the hepatic amino- to urea-N conversion in normal man?
Acute, severe atraumatic pain induces an increase in the ability of the liver to convert amino- to urea-N, and thus acts as a catabolic stimulus via regulation of liver function. The measurements of known endocrine regulators of urea synthesis do not explain the phenomenon. The present data, however, suggest the hypothesis that the effects of pain were attenuated by local analgesia. If this is confirmed by further experiments, it would indicate a signal transmission to the liver which has not been previously described.
There was no clear advantage of MRI with a limited field of view as compared with radiographic imaging of both hands in detecting progression of joint damage over 2 years in this group of patients with established RA. The conclusion drawn from this study is not that radiographs are better than MRI or vice versa, but that careful analysis is required to determine the optimal imaging method, or combination of imaging methods, for each study population, depending on the objective and duration of the study.