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BACKGROUND: The biologically active form of vitamin D3, calcitriol, may offer a new therapeutic approach to psoriasis. Calcipotriol, a new vitamin D3 analogue, is at least 100 times less calcemic than calcitriol. OBJECTIVE: Our purpose was to study the efficacy and safety of calcipotriol in the treatment of psoriasis vulgaris. METHODS: In a right/left comparative, double-blind study, treatment with calcipotriol ointment (50 micrograms/gm) twice daily and placebo was given for 4 weeks. The preferred treatment was continued, without opening the code, for another 4 weeks. Efficacy, as measured by the Psoriasis Area and Severity Index and by the investigator's and patient's global assessment, and safety were assessed every 2 weeks. RESULTS: The mean Psoriasis Area and Severity Index fell in 4 weeks from 14.2 to 6.3 with calcipotriol and from 14.1 to 9.2 with placebo (p < 0.001; 95% confidence interval for difference: 1.78-->3.94). Local side effects were equally common with calcipotriol and placebo. The mean serum calcium remained unchanged. CONCLUSION: Topical application of up to 50 gm of calcipotriol ointment per week was found to be an effective and safe treatment of psoriasis vulgaris.

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Short-contact treatment with dithranol (anthralin) is a widely used treatment for chronic plaque psoriasis. Although effective, it causes staining and irritation, and is therefore inconvenient. Calcipotriol is a recently developed vitamin D analogue which is effective and easy to use. To evaluate the relative efficacy, safety and acceptability of these treatments a multicentre, open, randomized, parallel-group comparison was performed. Four hundred and seventy-eight patients with chronic plaque psoriasis were randomized to use one of the two treatments for 8 weeks. One group applied calcipotriol ointment (50 micrograms/g) twice daily. The other used a single application for 30 min each day of Dithrocream in the highest concentration tolerated. Severity of psoriasis was assessed by modified PASI score at baseline, and after 2, 4, and 8 weeks of treatment. A five-point scale was used by subjects and by investigators as an additional assessment of overall response, and a similar scale was used by subjects to grade acceptability. Total serum calcium was monitored at baseline and after 2 and 8 weeks on treatment. The mean PASI score fell from 9.1 to 4.7 after 8 weeks on dithranol (P < 0.001), and from 9.4 to 3.4 on calcipotriol (P < 0.001). The difference between the two treatments was significant in favour of calcipotriol at 2 weeks (P < 0.001), and remained so at subsequent assessments. At 8 weeks the difference between mean improvements in scores for the two groups was 1.6 (95% confidence interval 0.5-2.7). Efficacy grading by subjects and investigators, and acceptability grading by subjects, were all significantly better for calcipotriol.(ABSTRACT TRUNCATED AT 250 WORDS)

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The quality of life (QL) was evaluated in a 6 month double-blind trial in six European countries. Patients with a sustained supine diastolic blood pressure (SDBP), phase V, of 95 mm Hg or more on bendrofluazide, 5 mg daily (or an equivalent dose of a thiazide diuretic) were randomised to additional pinacidil (n = 127), 25 mg up to 100 mg daily, or nifedipine (n = 130), 20 mg up to 80 mg daily. The treatment groups were similar at entry for QL scores, average DBP of 103 +/- 6 (SD) mm Hg, and average age of 56 +/- 10 (SD) years. Eighteen patients on pinacidil and 12 on nifedipine withdrew due to side effects, such as oedema (both drugs) and flushing (nifedipine). The maximum antihypertensive effect was achieved within 6 weeks and maintained, resulting in a significant fall in SDBP of 13.7 mm Hg on pinacidil and 15.5 mm Hg on nifedipine at the end of the trial. There was no significant difference in the antihypertensive effect. The target SDBP was achieved in 57% of pinacidil-and 63% of nifedipine-treated patients. The average number of symptomatic complaints fell in both groups, with significant decreases in the reporting of blurred vision and headaches on nifedipine. Complaints of growth of body and facial hair increased on pinacidil but there were no significant between-drug comparisons with respect to side effects. In measures of psychological well being, patients on pinacidil showed a significant (p less than 0.05) improvement in total and cognitive function scores compared to nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)

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The concentration of lipids, lipoproteins and apolipoprotein A-I and B was measured in the plasma of 33 patients, enrolled in a double-blind, controlled trial of alprenolol in myocardial infarction, after one year on the study medication and again after 6 months off the medication. Sixteen patients received 200 mg alprenolol twice daily and 17 received placebo. There were no statistically significant differences between the parameters in the two groups after one year on medication. However, when medication was stopped, the ratio of apolipoprotein B to apolipoprotein A-I fell by 9% in the alprenolol group and increased by 2% in the placebo group. This difference was statistically significant. Our results suggest that alprenolol, a beta-blocker with weak intrinsic sympathomimetic effect, has slight effects on plasma lipoproteins. These effects were apparent only by measurements of apolipoproteins.

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In 40 patients with ischaemic heart disease the serum levels of magnesium, parathyroid hormone (PTH), phosphate, calcium, and ionized calcium remained unchanged and within normal limits following treatment for 12 months with alprenolol (n = 20) or placebo (n = 20). No changes occurred during a 2 week withdrawal period. The clinical implication is that the non-cardioselective betablocker alprenolol can be given to patients with ischaemic heart disease without the risk of inducing potentially cardiotoxic disturbances in serum magnesium and serum calcium levels. Whether this applies to cardioselective beta-blockers remains to be established.

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The histamine-releasing effect of human C5a was compared with that of concanavalin A in blood basophils and isolated adenoidal mast cells from the same donors. In basophils, C5a (10 ng/ml) induced a significant histamine release (7.5 +/- 2.1%, corrected value). In isolated adenoidal mast cells C5a had only a marginal effect (2% histamine release), although the cells responded markedly to concanavalin A stimulation (about 13% release). The results support the view that the heterogeneity of mast cells and basophils is also reflected in the expression of anaphylatoxin receptors on their surface.

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Of the complement peptides comprising anaphylatoxin activity, only C5a caused a very small (less than 1.5%) but statistically significant histamine release from isolated human adenoidal mast cells. C3a and the respective des-Arg-derivatives were found to be ineffective. In rat peritoneal mast cells, neither peptide caused histamine release.

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Mast cells from adenoid tissues of man do not form a homogeneous population but differ in size and ultrastructure. They degranulate on stimulation with specific antigen, ionophore A 23187, Concanavalin A and, under certain conditions, antihuman IgE or acetylcholine. Compound 48/80, dextran, purified C3a or C5a are ineffective. Adenosine exerts either an enhancing or inhibiting effect on the stimulated histamine release, depending on the actual conditions of the mast cells. The study of a range of known mast cell degranulation inhibitors revealed important differences between human adenoidal mast cells and human basophils or animal mast cell systems. The efficacies of the drugs or drug combinations so far tested correspond well with the established therapeutic effects in man.

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Methods of obtaining active nitrogen plasmas at both reduced and atmospheric pressures are described. The mechanism of energy transfer from the excited states of nitrogen to metal atoms and to organic molecules and the subsequent emission of characteristic radiation is outlined. The application of these processes to the detection and determination of traces of metals and organic compounds is discussed and recent work on gas chromatographic detectors, based on these systems, is reviewed.

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After treatment with alprenolol for 1 year, serum 3,3',5'-triiodothyronine (rT3) was significantly increased (P less than 0.01) in a group (n = 20) of euthyroid subjects compared to a control group (n = 20) given placebo. All subjects had definite or suspected myocardial infarction one year previously. Serum thyroxine (T4), free T3 index (FT4I), serum 3,5,3'-triiodothyronine, (T3) and free T3 index (FT3I) were not significantly different in the two groups. Alprenolol and placebo were gradually withdrawn over 14 days. On the first day after withdrawal a significant decrease in serum rT3 in the alprenolol treated group was the only change observed. Fourteen days after withdrawal a significant fall in serum T4, FT4I, rT3 and a rise in serum T3 and FT3I was found in the alprenolol treated group. Six months after withdrawal the only further change observed in the alprenolol treated group was an increase in T3 and FT3I. No changes occurred in the placebo treated group in any of the hormones studied. The results are consistent with a direct effect of long-term alprenolol treatment on the peripheral levels of serum T4, T3 and rT3 in euthyroid subjects. The changes in the thyroid hormones after withdrawal further indicate withdrawal of a permanent inhibition of 5'deiodinase during long-term treatment with alprenolol in euthyroid subjects.

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