Practolol-Induced Tissue Damage

In order to construct a hypothesis for the mechanism by which practolol produces such diverse pathological lesions, it is necessary to explore the two basic findings of auto-antibodies and drug-specific antibodies. An explanation for auto-antibody production was offered by Allison et al. (1971). They suggested that auto-anti-body production is due to a breakdown of a normal suppressor function mediated by T cells. Hadden et al. (1970) and Sherman et al. (1973) have shown that the function of lymphoid cells in vitro can be modified by drugs which react with adrenergic receptors. It is conceivable, therefore, that practolol could selectively interfere with lymphocyte subpopulations in vivo and alter their control function on antibody producing B cells. 

A possible clue to the role of practolol-specific antibodies was found when a retrospective analysis of sera was carried out in a group of patients who had taken part in a challenge study. The pre- and post-challenge antibody titers for the five patients in the study are shown in Table 4. The titer at the height of the adverse 

Test Group 1 Patients with the oculomucocutaneous syndrome 

Test Group 2 Patients receiving practolol but with no cHnical signs 

Test Group 3 Patients with drug-induced systemic lupus erythematosus 

---

Adverse effects associated with practolol have been collectively described as the oculomucocutaneous syndrome. The incidence of the syndrome is small but the seriousness of the tissue damage has tended to overshadow this incidence. Practolol was marketed in 1970, and by the end of 1975 the drug had been used for some 300,000 patient years in the UK, and around one million worldwide. By October 1974, 164 cases were known, and in November 1977, the total had reached 915 (Nicholls 1978). The drug was withdrawn in 1976. It is now reasonably certain that none of the other jS-blockers in clinical use has so far induced an oculomuco-cutaneous-type syndrome. 

The attendant publicity given to the tissue damage induced by practolol prompted a number of reports of similar reactions to propranolol and the so-called second generation jS-blockers. Most of the reports describe a particular feature of the syndrome, but no case has yet been described which convincingly demonstrates that any of the jS-blockers produce the same pattern of lesions as practolol. 

---