Drug therapy for individuals of any age is difficult but prescribing for older patients offers special challenges. Older people take about three times as many prescription medications as younger individuals do, mainly because of their increased prevalence of chronic medical conditions. However, taking several drugs together substantially increases the risk of drug interactions, unwanted effects, and adverse reactions. Many medications need to be used with special caution because of age-related changes in pharmacokinetics and pharmacodynamics. For some drugs, an increase in the volume of distribution (eg, diazepam) or a reduction in drug clearance (eg, digoxin) may lead to higher plasma concentrations in older than in younger patients. Pharmacodynamic changes with ageing may result in an increased sensitivity to the effects of certain drugs (eg, opioids) for any given plasma concentration. While a physician can usually do little to alter the characteristics of individual older patients to affect the kinetics or dynamics of drugs, the decision whether to prescribe anything at all, the choice of drug, and the manner in which it is to be used (eg, dose and duration of therapy) are all factors that are under control of the prescriber. Patient adherence to the regimen prescribed is important, and there should be a partnership between physician and patient in therapeutic decision making. We will discuss here ways of improving prescribing for older patients. Specifically, we will examine the scarcity of information to guide prescribing decisions, the general principles of prudent prescribing, and the opportunities to clarify and expand knowledge about drug therapy in the elderly.

Mycobacteria elicit two quite different immune responses. One is protective and is partly based on recognition and lysis of stressed, bacilli-laden cells expressing heat-shock proteins. The other suppresses this recognition and instead leads to indiscriminate necrosis of tissues containing mycobacteria (the Koch phenomenon). The type of response depends on the predominant T-cell maturation pathway, Th1 or Th2, which in turn is determined by priming by prior contact with environmental mycobacteria. Vaccination by BCG induces whichever response the recipient is primed to make, and this is a likely explanation of the variable efficacy of this vaccine in prevention of tuberculosis and therapy of cancer. Thus; BCG is a two-edged sword. We postulate that by using other mycobacterial preparations, such as killed Mycobacterium vaccae, it might be possible to suppress the indiscriminate necrosis and enhance Th1-regulated selective destruction of tumour cells.