Diabetic patients suspected of having osteomyelitis secondary to foot ulcers underwent scintigraphic imaging with Sulesomab, an anti-granulocyte antibody Fab' fragment labeled with technetium-99m. Among 122 patients who had osteomyelitis confirmed or excluded by histopathologic and/or microbiologic techniques, Sulesomab had a 91% sensitivity, a 56% specificity, and an accuracy of 80%. One planar imaging session was usually sufficient for diagnosis, typically requiring 20-30 minutes of camera time 1-2 hours after injection. Compared with ex vivo autologous white blood cell (WBC) scans, Sulesomab performed comparably but with significantly greater sensitivity (92% vs. 79%; P < .05). Sulesomab results were more sensitive than radiography (90% vs. 62%; P < .05) and more specific than bone scans (50% vs. 21%; P < .05) and would have altered management plans in most patients. No related adverse events occurred, and there was no induction of human anti-mouse antibody. Sulesomab is an effective and rapid imaging agent that is diagnostically comparable or superior to WBC scans in this setting, with significant advantages in safety and ease of use.

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PF4 has a half-life in plasma of less than 3 minutes, and its rapid clearance appears to be a function of binding to the vascular endothelium. Once bound to the endothelium, PF4 can be released by heparin in a time-dependent manner; recovery is greater the sooner heparin is administered following PF4 infusion. This heparin-induced release of PF4 can be abolished if the heparin is first complexed with hexadimethrine bromide. Likewise, this heparin-induced release of PF4 is dependent upon the type of heparin used; low molecular weight heparin fractions and fragments do not cause the PF4 rebound seen with intact heparin. Thus, it would appear that low molecular weight forms of heparin are advantageous in that their in vivo administration would not be mediated by such platelet modulators as PF4.

Serial technetium-99m radionuclide ventriculograms, indium-111 antimyosin antibody scans and tissue biodistribution studies were performed in C3H/He mice with experimentally induced viral encephalomyocarditis and the results were compared with pathologic assessments of myocardial necrosis. Postinfection ejection fraction decreased on days 10 (20.7 +/- 5.5%, n = 6), 20 (18.6 +/- 15.2%, n = 5), 30 (18.5 +/- 7.7%, n = 5) and 150 (30.0 +/- 18.7, n = 6) (p less than 0.001) in comparison with that in uninfected control mice (63.3 +/- 3.1%, n = 6). In the same group of animals, indium-111 antimyosin antibody scans showed intense positive myocardial accumulation on day 10 (in six of six mice) and only slight accumulation on day 20 (in one of five mice). In the chronic stage, two of five mice on day 30 and two of six mice on day 150 still showed positive uptake. The antimyosin scan myocardium to lung uptake ratio (expressed as mean count density [mean counts/pixel of the region] ratio) increased greatly on day 10 (p less than 0.001 versus values in uninfected control mice) but not subsequently. Biodistribution studies of the indium-111 antimyosin antibody showed that the heart to blood count ratio was significantly higher on day 10 (p less than 0.001 versus values in control mice) but not on days 20, 30 and 150. Pathologic examination showed active and ongoing severe myocardial necrosis with dilated ventricles on day 10. On day 20, there was less active necrosis and healing had appeared to begin. On days 30 and 150, myocardial fibrosis increased.(ABSTRACT TRUNCATED AT 250 WORDS)

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