The urinary excretion of
3-methylhistidine (3 MEH) has been shown to be a reliable index of
muscle protein breakdown. It is decreased in
protein-calorie malnutrition and increased during the hypercatabolic phase of
sepsis and thermal
trauma. Losses of 3 MEH after moderate to severe skeletal
trauma in man and animals are reported as increased or unchanged. To clarify this response, 24 male and 6 female skeletal
trauma patients were evaluated for 24 hr urinary losses of 3 MEH,
nitrogen and
creatinine. Eight of the 24 males also received a catabolic
steroid for treatment of a
head injury. In addition, 3 male and 1 female septic patients were similarly evaluated. Controls consisted of 10 volunteers on a meat free diet for 4 days and of 8 volunteers who were given only intravenous 5%
dextrose in water for 3 days. The 3 MEH excretion for all control males was 3.6 mumole/Kg/day and for females was 2.8 Skeletal
trauma produced a 280% increase for the males and a 225% increase for the females.
Trauma with
steroids caused a 325% increase.
Sepsis induced a 227% increase in 3 MEH losses for males and 292% for females during the febrile episode.
Creatinine excretion also increased significantly in response to
trauma and
sepsis but the magnitude of the increase was less than for 3 MEH. This was reflected in the 3 MEH to
creatinine molar ratio increase from 0.018 for controls to 0.030-0.040 in
sepsis and
trauma. Patients with extensive
body weight loss showed decreases in 3 MEH and
creatinine excretion and a molar ratio similar to controls. The calculated contribution of
muscle protein to whole body
protein breakdown in the
trauma and septic groups showed a twofold increase compared to the control group. The data indicate that the increased
muscle protein catabolic response following stress of skeletal
trauma and
sepsis provides an insight on the origin of the large urinary
nitrogen losses following such insults.