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Rudorfer, Matthew; Potter, William
doi: 10.2165/00003495-198937050-00006pmid: 2663417
Supplementing but not supplanting the original series of tricyclic and monoamine oxidase (MAO) inhibitor compounds, a new generation of antidepressant medications has been developed and marketed throughout the past decade. Constituting a more diverse group of drugs than the standard agents, the newer drugs in general have more selective acute biochemical actions (reuptake blockade of a single neurotransmitter, inhibition of 1 subtype of MAO), enabling more precise targeting of symptoms and avoiding common antidepressant-associated side effects, especially anticholinergic and cardiovascular effects. Moreover, a number of recent additions to this group, such as bupropion and ademetionine (S-adenosyl-methionine), incorporate novel mechanisms of action, challenging previous concepts of how antidepressants work, and offering opportunities for research into the pathophysiology of mood disorders. Caution in prescribing the newer antidepressants must be applied, however, as recent experience, e.g. with nomifensine, suggests that unforeseen toxicities may not appear until a medication has been in use for several years.
doi: 10.2165/00003495-198937050-00005pmid: 2663416
Current thinking on the general approaches to handling patients with Raynaud’s disease is briefly described, and the principles of management discussed. The various categories of drug treatment available — vasodilators, especially those active on the smallest blood vessels, drugs acting on endothelium and platelets and their products, rheologically active drugs and some whose action it is difficult to classify — are mentioned. By far the most widely tested drugs in this field are the dihydropyridine-like slow calcium channel antagonists, of which nifedipine is probably the best known. Side effects are common and the optimal dosage and drug formulation are yet to be achieved. Serotonin antagonists (naftidrofuryl, ketanserin) look promising, although ketanserin is not generally available yet. Drugs active in the sympathetic control of vascular tone may well be best reserved for the most severe forms of Raynaud’s, especially perhaps those associated with tissue loss in the secondary disease. Older vasodilators, such as glyceryl trinitrate (nitroglycerin) and some of the nicotinic acid derivatives, have not been studied of late but the transdermal applications of glyceryl trinitrate at least sound attractive. Drugs active in the cyclo-oxygenase systems, especially those with prostacyclin-like activity or thromboxane antagonists, are obviously promising; however, their unavailability in oral, sublingual or transdermal forms limits comment on them at present. Non-drug approaches such as biofeedback control of vascular responses may be interesting in a small number of patients, but the advice to ‘keep warm’ (and how to achieve this) is probably the most valuable suggestion that can be given to patients with Raynaud’s disease.
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