Two regimens of steroid treatment for the initial attack of idiopathic nephrotic syndrome in children were compared in a controlled multicentre study. Short-course prednisone therapy consisted of 60 mg/m2 per 24 h until proteinuria had disappeared for 3 days, followed by 40 mg/m2 per 48 h until complete remission had occurred. The standard prednisone therapy was 60 mg/m2 per 24 h for 4 weeks, followed by 40 mg/m2 per 48 h for 4 weeks. 61 children with a first attack of idiopathic nephrotic syndrome were allocated at random to these groups. Urinary remission in the short-course group was achieved after 14 days of daily prednisone, and complete remission after an additional 16 days of alternate day prednisone. The cumulative rate of patients with sustained remissions after two years was significantly lower after the short course than after standard treatment (19% versus 41%, p = 0.001). The mean duration of remission in patients with a relapse was half as long after the short course (79 versus 169 days, p = 0.004). Complete initial remission of steroid responsive nephrotic syndrome can be obtained with half the standard prednisone dose, but the short course is followed by a higher rate of relapses, that require repeated prednisone administrations. In the long term, the standard regimen is preferable.

28 patients with stable chronic psoriasis completed a trial in which they were randomly allocated to receive either 10 fish-oil capsules ('MaxEPA') or 10 placebo capsules (olive oil) daily. Patients were specifically instructed not to change their normal diet. After 8 weeks' treatment there was a significant lessening of itching, erythema, and scaling in the active treatment group, with a trend towards an overall decrease in body surface area affected. No change occurred in the placebo group.

18 men with longstanding human immunodeficiency virus (HIV) antigenaemia but no symptoms received zidovudine in low-dose regimens (250 mg 6-hourly, 500 mg 6-hourly, or 500 mg 12-hourly) with or without acyclovir. Serum HIV antigen rose in only 1 patient and declined significantly in 13 (to below cut-off values in 9). In the 1 subject from whom HIV antigen positive cerebrospinal fluid was obtained, the fluid was antigen negative after 12 weeks of treatment. Acyclovir treatment alone or in addition did not seem to influence serum antigen levels. In 7 untreated men serum antigen levels rose or remained stable during follow-up. CD4+ cell counts increased in 14/18 treated subjects and 1/7 untreated subjects. No disease progression was observed in either group. Regression of enlarged lymph nodes was seen in the zidovudine-treated subjects. Adverse reactions to the study drugs were infrequent and mild. Anaemia caused symptoms in 2, but serious leucopenia or neutropenia was not observed.

In a multicentre clinical trial 1267 patients with hemispheric stroke of duration 12 h or less and haematocrit of 35% or more were prospectively randomised to either haemodilution (by venesection and replacement of the same volume of dextran 40 in saline solution) or control treatment groups. In the haemodiluted group mean haematocrit declined from 43% to 37% at 48 h and this fall was maintained for seven days. A plain computed tomographic scan was obtained in all but 37 patients. 87% of the strokes were infarcts and 13% were haemorrhages. After six months the numbers of dead or severely disabled patients were equally distributed in the two treatment groups, and this was true also within the ischaemic and haemorrhagic subgroups. Furthermore, haemodilution did not improve outcome either in the group with very recent ischaemic stroke (less than 6 h) or in the subgroup with highest haematocrit (greater than 45%). Thus, moderate haemodilution does not improve the outcome in acute stroke patients.

In a randomised, double-blind trial 60 patients with left ventricular dysfunction (ejection fraction less than 45%) but without clinical evidence of heart failure 1 week after Q wave myocardial infarction were given captopril 25 mg thrice a day, frusemide 40 mg daily, or placebo. Left ventricular volumes were measured at baseline and at 1, 3, 6, 9, and 12 months with cross-sectional echocardiography and Simpson's rule analysis of standardised apical views. The captopril group showed no significant change in left ventricular end-diastolic volume index but left ventricular end-systolic volume index was significantly reduced and stroke volume index and ejection fraction were significantly increased from 1 month on. In contrast, the frusemide and placebo groups showed significant increases in ventricular volumes, with stroke volume index unchanged and ejection fraction slightly reduced. The changes in the captopril group were significantly different from those in the other groups.

144 patients presenting within 4 h of onset of myocardial infarction were randomised to receive either 100 mg of single-strand recombinant tissue plasminogen activator (rTPA) in 3 h (n = 73) or placebo infused at the same rate (n = 71). All patients were given heparin 5000 units before the infusion and heparin was continued, initially at 1000 units per hour, after the infusion. Minor bleeding was more frequent in the rTPA recipients, and during subsequent anticoagulant therapy there were three clinically significant bleeding episodes in this group. Patency of the infarct-related coronary artery was determined by coronary angiography about one week post-infarction, 125 angiograms being assessable. The infarct-related artery was patent in 70% of patients who received rTPA and in 41% of those who did not (p = 0.0015). In the 103 patients who had assessable contrast ventriculograms, the global ejection fractions were 57.7% and 51.7%, respectively (p = 0.04). The difference in ventricular function was largest in patients with anterior infarction (52.7% versus 40.0%, p = 0.02). The magnitude of these changes suggests an improvement in ejection fraction of 12% overall and about 30% in patients with anterior infarction.

A randomised trial of 367 patients with acute myocardial infarction was performed to determine whether an invasive strategy combining thrombolysis with recombinant tissue-type plasminogen activator (rTPA), heparin, and acetylsalicylic acid, and immediate percutaneous transluminal coronary angioplasty (PTCA) would be superior to a noninvasive strategy with the same medical treatment but without immediate angiography and PTCA. Intravenous infusion of 100 mg rTPA was started within 5 h after onset of symptoms (median 156 min). Angiography was performed 6-165 min later in 180 out of 183 patients allocated to the invasive strategy; 184 patients were allocated to the non-invasive strategy. Immediate PTCA reduced the percentage stenosis of the infarct-related segment, but this was offset by a high rate of transient (16%) and sustained (7%) reocclusion during the procedure and recurrent ischaemia during the first 24 h (17%). The clinical course was more favourable after non-invasive therapy, with a lower incidence of recurrent ischaemia within 24 h (3%), bleeding complications, hypotension, and ventricular fibrillation. Mortality at 14 days was lower in patients allocated to non-invasive treatment (3%) than in the group allocated to invasive treatment (7%). No difference between the treatment groups was observed in infarct size estimated from myocardial release of alpha-hydroxybutyrate dehydrogenase or in left ventricular ejection fraction after 10-22 days. Since immediate PTCA does not provide additional benefit there seems to be no need for immediate angiography and PTCA in patients with acute myocardial infarction treated with rTPA.

In a prospective, randomised, placebo-controlled trial comparing the effect of (3-amino-1-hydroxypropylidene)-1,1-bisphosphonate (APD) (150 mg/day) plus calcium (1 g/day) with that of calcium alone on the bone mass of patients receiving long-term glucocorticoid therapy, the mean metacarpal cortical area in patients receiving APD increased by 1.2% between 0 and 6 months (p less than 0.06) and then remained stable between 6 and 12 months. In contrast, this index progressively declined in the placebo group (p less than 0.05 at 12 months). The two groups differed significantly in the changes at both 6 and 12 months (p less than 0.01). Mean vertebral mineral density, as measured by quantitative computed tomography, increased by 19.6% over 12 months in the APD group (p less than 0.02) but showed a non-significant decline of 8.8% in controls. The differences between the changes were again significant (p less than 0.005). Biochemical indices and bone histomorphometry indicated a reduction in bone resorption and bone formation but there was no evidence of osteomalacia. APD may thus prevent bone loss in glucocorticoid-treated patients over a year.

90 schoolchildren aged twelve and thirteen years kept a dietary diary for three days. In most cases the average intake of vitamins was close to the recommended daily allowance, although for a minority the intake was low; with minerals the recommended daily allowance was less commonly achieved. To examine the possibility that deficiency of dietary minerals and vitamins was preventing optimum psychological function, a multivitamin/mineral supplement or a placebo was administered double-blind for eight months to 60 of the children. The supplement group, but not the placebo group or the remaining 30 who took no tablets, showed a significant increase in non-verbal intelligence.

Sixteen of nineteen patients completed a randomised double-blind crossover trial to assess the effect of oral mexiletine (10 mg/kg bodyweight daily) on the symptoms and signs of chronic painful diabetic neuropathy. The median age of the sixteen patients was 50 years (range 30-64). Assessment with a five-item clinical symptom scale showed significant improvement during the mexiletine phase compared with the placebo phase. Pain was reduced during mexiletine but not during placebo, as assessed by a visual analogue rating scale. Mexiletine treatment had no effect on tendon reflexes, vibration threshold levels, beat-to-beat variation in heart rate during deep breathing, and postural blood pressure response. Mild side-effects were seen in three of the sixteen patients during mexiletine treatment.

24 infants consecutively treated with acyclovir or vidarabine for neonatal herpes simplex virus (HSV) encephalitis were followed up for 6 months to 3 years to assess neurological and developmental outcome. 15 patients had HSV-2 and 9 had HSV-1 encephalitis. Infants with HSV-2 encephalitis presented with a higher frequency of seizures, greater pleocytosis and protein concentrations in the cerebrospinal fluid, and more frequent evidence of structural damage on computerised tomographic scans of the brain than did those with HSV-1 encephalitis. 1 patient died. All 9 HSV-1 patients were normal at follow-up (mean 19.4 months) compared with only 4 (23%) of the 14 surviving HSV-2 infected infants (p = 0.003). Among infants with HSV-2 encephalitis, 50% became microcephalic; 57% had seizure disorders; 64% had ophthalmological defects; 64% had cerebral palsy; and 57% had mental retardation. Infants with neonatal HSV-1 encephalitis treated with systemic antiviral chemotherapy have excellent neurological outcomes; the neurological morbidity of those with HSV-2 encephalitis is still high.

79 women who had been menopausal for less than 36 months and who had not received any form of treatment to prevent bone loss were randomly assigned to a 12-month regimen of calcium 500 mg/day or calcium 500 mg plus intranasal salmon calcitonin 50 IU/day for 5 days per week. After 12 months of treatment bone mineral density had decreased in the calcium-only group by a mean of 3.16 (SEM 0.6)% (p less than 0.01) but had increased in the calcium plus calcitonin group by 1.38 (0.8)% (NS). The difference in response between the two treatment groups was also highly significant (p less than 0.01), as was the difference between values for hydroxyprolinuria/creatininuria (p less than 0.01). Endogenous calcitonin levels rose significantly in the calcium group but remained unchanged in calcitonin-treated patients. Treatment by calcitonin and calcium was not followed by increased secretion of parathyroid hormone. The findings suggest that intranasal calcitonin can counteract early postmenopausal bone loss.