50 patients with mild to moderate essential hypertension underwent M-mode echocardiography and continuous intra-arterial ambulatory monitoring of blood pressure. Indices of left-ventricular (LV) mass were derived from echocardiographic data by standard formulae. 43 of the patients were followed up for 12+/-7 months with repeat M-mode echocardiography, and casual blood-pressure measurements. 25 of these patients received antihypertensive therapy and 18 were untreated. Mean 24 h systolic blood pressure was significantly correlated with echocardiographic LV mass; mean 24 h diastolic blood pressure was also correlated, but the relation was weaker. In the treated group there was a significantly greater fall in blood pressure and LV mass index than in the untreated group, and there was a significant correlation between the fall in systolic blood pressure and the fall in LV mass index in the treated group. Systolic blood pressure appears to be an important factor in the pathogenesis of LV hypertrophy, and in hypertensive patients changes in LV mass assessed by echocardiography correlate with changes in blood pressure.

Sensitivity of herpes simplex virus isolates to acyclovir became reduced in two bone-marrow transplant patients treated for established mucocutaneous infections. These isolates were thymidine-kinase-deficient mutants and were isolated within a week of discontinuation of a 1 week course of acyclovir therapy. The herpetic lesions in both patients continued to heal despite continued shedding of these viruses. Further studies and experience with this new class of antiviral agents are needed to determine the extent to which emergence of less sensitive virus will present clinical difficulties and to formulate treatment regimens that will minimise the emergence of such mutants.

The value of antibiotics was assessed in a randomised, double-blind study of amoxycillin and placebo in sixty adults admitted to hospital with acute exacerbations of asthma. 37 exacerbations were treated with amoxycillin and 34 were treated with placebo. Response to treatment was closely monitored but no significant difference in improvement was demonstrated between groups for length of hospital stay, time taken for 50% improvement in symptoms, patient's self assessment and respiratory function, and symptoms and respiratory function at time of discharge from hospital. Antibiotics should not be given routinely to patients admitted to hospital with acute exacerbations of asthma.

50 patients with actinic keratosis were studied over four months of treatment with either etretinate ('Tigason') or placebo. Each treatment was given for two months and the order of administration was randomised. The clinical response to treatment was assessed by direct measurement and photographs of the lesions at monthly intervals. Of the 44 patients who completed treatment with etretinate 37 had a complete or partial response. Of the 42 patients who completed treatment on placebo only 2 showed a complete or partial response. The response to treatment occurred within the first month of therapy and was maintained even when the dose was reduced because of toxicity.

A beta-blocker (pindolol) and a diuretic (clopamide) were given in different dosages, singly and in two different combinations, to 71 patients with mild to moderate essential hypertension. The trial design was such that patients took both drugs singly and in combination, and in different doses, according to a set plan. The best regimen for each patient was determined by taking into account not only blood pressure but also resting heart-rate, body-weight, serum potassium, and serum urate. For 19 patients (27%) monotherapy was best--pindolol for 16 and clopamide for 3. For the remaining patients, a combination of pindolol 10 mg and clopamide 5 mg was best for 39, and in 35 of these one tablet daily was sufficient. All patients reached the preset target blood-pressure. The differences in proportions responding best to the following pairs of regimens compared--monotherapy vs combination, and combination of clopamide 5 mg and pindolol 5 mg vs combination of clopamide 5 mg and pindolol 10 mg--were significant (2p less than 0.01). The process by which the best treatment is chosen according to this study design resembles much more closely that followed in general medical practice, than does the process in the conventional hypertension trial, in which only average effects are reported and compared.

Nineteen unselected patients with mild to moderate essential hypertension, whose average supine blood pressure after two months' observation on no treatment was 156/98 mm Hg, were advised not to add salt to food and to avoid sodium-laden foods. After 2 weeks of sodium restriction patients were entered into an 8-week double-blind randomised crossover study of 'Slow Sodium' (Ciba) versus slow sodium placebo. The mean supine blood pressure was 7.1 mm Hg (6.1%) lower in the fourth week of placebo than that in the fourth week of slow sodium (p less than 0.001). Urinary sodium excretion in the fourth week of slow sodium was 162 +/- 9 mmol/24 h and that in the fourth week of placebo was 86 mmol +/- 9 mmol/24 h (p less than 0.001). There was no difference in potassium excretion. These results suggest that moderate sodium restriction achieved by not adding salt and avoiding sodium-laden foods should, if not already, become part of the management of essential hypertension.

In about 80% of Bangladeshi volunteers a single oral or intramuscular immunisation with a new cholera toxoid immunogen (B subunit) gave rise to a local intestinal secretory immunoglobulin A (IgA) antitoxin response as measured in intestinal-lavage fluid by enzyme-linked immunosorbent assay methods. The rise in IgA antitoxin titre was similar for both immunisation routes and was comparable to that seen after clinical cholera; however, the response persisted longer after oral than intramuscular immunisation. A second immunisation by either route evoked an antitoxin response which usually closely resembled that seen after the first immunisation.

Twelve asthmatic patients with nocturnal wheezing were given a single nocturnal oral dose of slow-release aminophylline or matched placebo in a double-blind crossover trial. A dose of slow-release aminophylline (mean 683 mg; 10.4 mg/kg) gave a therapeutic plasma-theophylline concentration 10 h later (mean 10.9 mg/l). This was not associated with any adverse effects. Mean peak expiratory flow on waking was significantly greater with aminophylline (332 +/- 31 l/min) than placebo (283 +/- 32 l/min), whereas evening values did not differ. There was a significant difference between morning and evening peak flow on placebo (mean 22%) but not on aminophylline (5%), indicating abolition of the morning fall in peak flow. This was not at the expense of response to beta-agonists, since the response to inhaled salbutamol was the same for both treatments. The use of extra metered doses of inhaled beta-agonist during the night was significantly less with aminophylline, and there was a subjective improvement in nocturnal symptoms in all patients. Slow-release aminophylline in adequate dosage appears to be the most effective treatment yet demonstrated for nocturnal asthma.

In a multicentre double-blind randomised study comparing the effects of sulphinpyrazone 400 mg twice daily with those of placebo in patients after myocardial infarction 727 patients (365 on sulphinpyrazone, 362 on placebo) were enrolled and followed up for 12-48 months (mean 19.2). Treatment began 15-25 days after infarction. There were 49 reinfarctions (9 fatal, 40 nonfatal)-34 occurred in the placebo group and 15 in the sulphinpyrazone group, a reduction of 56%. In addition, a significant reduction of thromboembolic events was noted. It is concluded that sulphinpyrazone is effective in the prevention of reinfarction in patients surviving a recent myocardial infarction.