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In a previous study, and in the present study, we have found that the baseline plasma samples of patients with asthma contain average levels of an endogenous heparin-like material (EHM) that is significantly higher than that noted in non-allergic, non-asthmatic controls. This material appears to have properties of both heparin and heparan sulfate. Three out of six patients responding to inhalational antigen challenge displayed an acute increment in EHM concentration that coincided with a fall in FEV values. The relation of EHM concentration to provoked asthma, or to asthma in general, remains to be determined.

Twenty-seven patients beyond the age of 50 were radiographically compared with age- and sex-matched controls for the degree of calcified atherosclerotic plaque formation in the aorta and its major pelvic branches. Significantly less calcification was present in the aorta, iliac and hypogastric arteries of the asthmatics (P = 0.01). Previous studies in other asthmatic patients have shown elevated endogenous heparin-like material to be present in their plasma. It is speculated that diminished atherosclerosis in asthmatic patients might be a consequence of elevated circulating endogenous heparin-like material.

Adverse reactions to intravascular administration of contrast media, while low in incidence, merit serious consideration in view of increased utilization of these substances all over the world. Evidence for involvement of soluble mediators, antibody-antigen reactions, psychogenic factors, and the acute activation systems, is reviewed. As a group, the pre-contrast challenge plasmas of reactors are characterized by slightly diminished concentrations of Cl-esterase inhibitor and total hemolytic complement, and by an accelerated rate of conversion of prekallikrein to kallikrein on exposure to contact activators. The role of intravenous pretesting and pretreatment is considered. A rationale for pretreatment with adrenocorticosteroids is presented.