In contrast, striking abnormalities were seen in CF patients when insulin was infused, since they did not experience normal suppression of the appearance rates of leucine, phenylalanine, or tyrosine (indexes of protein breakdown). At an insulin concentration of 45 ؎ 2 U/ml, normal control subjects suppressed the leucine appearance rate by 19 ؎ 5% (P < 0.01), ketoisocaproate appearance rate by 10 ؎ 3% (P ‫؍‬ 0.03), tyrosine appearance rate by 11 ؎ 2% (P ‫؍‬ 0.03), and phenylalanine appearance rate by 6 ؎ 3% (P ‫؍‬ 0.07). Phenylalanine conversion to tyrosine decreased by 22 ؎ 7% (P ‫؍‬ 0.03). At a similar insulin concentration of 44 ؎ 3 U/ml, normal suppression of amino acid appearance did not occur in CF. The leucine appearance rate decreased by 4 ؎ 2% (P ‫؍‬ 0.65), ketoisocaproate appearance rate by 1 ؎ 2% (P ‫؍‬ 0.94), tyrosine appearance rate by 0 ؎ 6% (P ‫؍‬ 0.56), phenylalanine appearance rate by 5 ؎ 6% (P ‫؍‬ 0.34), and phenylalanine conversion to tyrosine by 5 ؎ 6% (P ‫؍‬ 0.95). Poor suppression of the amino acid appearance rate in CF was not related to previously documented glucose tolerance status (IGT or CF-related diabetes without fasting hyperglycemia), fasting insulin levels, the acute insulin response, insulin sensitivity, cytokine or counterregulatory hormone levels, resting energy expenditure, caloric intake, pulmonary function, or clinical status. Protein synthesis was not significantly affected by insulin infusion in either normal control subjects or CF patients. In conclusion, clinically stable adult CF patients have normal indexes of protein breakdown and synthesis in the fasting state. In contrast, elevation of plasma insulin to physiological postprandial levels fails to normally suppress indexes of protein breakdown. It is therefore likely that inability to spare protein during the postprandial state is the cause of protein catabolism in these patients. Diabetes

Twelve delayed or recurrent intracranial hematomas were seen in 340 patients with head injuries. Eleven of these hematomas were associated with clotting abnormalities suggesting disseminated intravascular clotting and fibrinolysis (DICF). Seven of 8 delayed traumatic intracerebral hematomas were associated with clotting abnormalities. Two of these were at ventriculostomy sites, which suggests an increased risk of bleeding in association with the insertion of ventricular catheters in patients with DICF. There were 2 delayed epidural hematomas, 1 under a fracture and the other on the side opposite a craniotomy that had been made to treat an intracerebral hematoma, and there were 2 postoperative epidural hematomas. No postoperative hematomas occurred in the absence of DICF. DICF is a major factor in the development of delayed and recurrent intracranial hematomas in patients with head injuries.

Eighty patients with type I diabetes and end stage renal disease were prospectively evaluated for coronary artery disease with dipyridamole-thallium-201 scintigraphy and quantitative coronary angiography. Forty patients received dipyridamole orally, and 40 received it intravenously. The prevalence of coronary artery disease was 53%. There were no significant differences in the accuracy of the two dipyridamole tests (sensitivity = 85%, specificity = 85%, accuracy = 85% for the oral group; sensitivity = 86%, specificity = 72%, accuracy = 79% for the intravenous group). Combining the 80 patients into a single group gave a sensitivity of 86%, a specificity of 79%, and an accuracy of 83% for the detection of coronary disease. Although the accuracy of this test in this patient population was similar to that previously reported for other groups, the prevalence of disease was high and resulted in a low predictive value of a negative test (83%).

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