that the lesion may be the result of a hitherto unknown type of hypersensitivity response.Our results do not show that the adverse effects of practolol are due to a hypersensitivity reaction, but two pieces of evidence might tentatively support such a conclusion. The first is the low antibody concentrations found in the sera of patients with sclerosing peritonitis. This might have been due to a reduction in antigenic stimuli, since the patients had been taken off the drug some time before the clinical signs of intestinal obstruction appeared. Equally, however, the results could be explained by postulating that the antigenic metabolite is incorporated into connective tissue and the mass of antigenic determinants presented by the peritoneum is sufficient to fix most of the circulating antibody. The second piece of evidence is perhaps more pertinent and concerns the challenge study on one of the patients (case 4). This patient had high concentrations of circulating antibody before challenge with practolol, and when the drug was given, clinical signs of the tissue damage were produced. Other patients in the study might have shown an adverse response if the drug had been given for a longer period.Continued analysis of serum will probably provide only circumstantial evidence of a practolol-induced hypersensitivity reaction. An animal model is needed to study the tissue damage produced by the drug, and we are currently engaged in studies of this kind.
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