These results, in addition to our other studies, show that detection of plasma DNA may be useful in the evaluation of certain patients for pulmonary em­bolism. In the present study, 82 percent of patients with pulmonary emboli were found to have measurable plasma DNA. Two of the four patients with pulmonary embolism who did not have measurable plasma DNA were symptomatic for three to four days before the first plasma was obtained, thus making a false-negative DNA assay more likely. There are also reasons to doubt the false-positive DNA results. Three of the four patients with a normal pulmonary angiogram but detectable plasma DNA showed low or decreasing titers of DNA; the fourth patient did not have enough plasma to titer. This contrasted with the three patients who had abnormal pulmonary angiograms whose plasma DNA levels increased when measured on subsequent days. Additionally, three of the four pa­tients with false-positive DNA results had a final diagnosis that did not unequivocally explain their pleuritic chest pain or dyspnea. Finally, it should also be noted that none of the 14 patients with a normal lung scan had detectable DNA, suggesting a higher specificity than the angiogram results imply.

Attempts by other investigators to confirm our findings have been inconsistent. Goldhaber et al studied 89 patients undergoing lung scanning for suspected pulmonary embolism. Only three of 16 patients with pulmonary embolism in their study (defined by high probability lung scan or abnormal pulmonary angiogram) had measurable plasma DNA; none of the 67 patients without pulmonary embolism (defined by normal or low probability lung scan, normal pulmonary angiogram, normal findings at au­topsy) had measurable DNA. However, relatively small differences between their assay technique and ours may have led to the large differences in results. For example, the group of Goldhaber et al used plasma rather than serum anti-DNA, and we found that CIE migration times vary between serum and plasma. Furthermore, because their plasma had antibody to both single- and double-stranded DNA, it is not clear whether their CIE technique was specific for pure dsDNA. Other differences in technique that may explain the discrepant results include overall electro­phoresis time, handling and reading of the CIE plates after migration, and effects of heat inactivation. levitra plus

Breitwiesser and others studied 40 consecutive patients undergoing pulmonary angiography for sus­pected pulmonary embolism, and of their 15 patients with abnormal angiograms, only two had detectable plasma DNA. None of the 25 patients with normal angiograms had detectable DNA. However, it is pos­sible that their anti-DNA serum was insensitive. A positive CIE result by this technique depends on how much precipitating antibody to dsDNA is present. Although Breitweiser and others reported an anti- DNA titer of 1:320 by Crithidia luciliae assay for their anti-serum, they did not test for precipitating DNA antibody using pure dsDNA in CIE.

One other group has reported encouraging results with this test. Riboldi et al measured plasma DNA in 49 selected patients and 13 normal controls. Fifteen of 16 patients with pulmonary embolism (defined by having multiple defects on perfusion lung scan) had detectable plasma DNA in a CIE assay system very similar to ours. None of the normal subjects had measurable DNA, but three of 33 control patients were positive (two with thrombophlebitis, one with chronic obstructive pulmonary disease). The DNA was detectable for six to ten days following the pulmonary embolism.