Biomedical subjects

B Abila

Publications and source records attributed to B Abila.

10 recordsLinked to original sources

PubMed1994

Effects of two antihistamines on chloroquine and histamine induced weal and flare in healthy African volunteers.

This study investigated the effects of single doses of clemastine (2mg orally), mepyramine (2 micrograms intradermally) and placebo on weal and flare caused by intradermal chloroquine 2.5mg and histamine 2 micrograms in 11 healthy black subjects who experienced generalised pruritus with oral chloroquine. Compared with placebo, both antihistamines caused significant reductions in histamine-induced weal and flare. By contrast, chloroquine-induced weal and flare were not significantly altered by clemastine or mepyramine when compared with placebo. It is concluded that histamine is unlikely to be the main mediator of chloroquine-induced weal and flare. These findings are in consonance with the lack of significant effect of antihistamines on chloroquine-induced generalised pruritus.

Administration, Oral↗

PubMed1993

Anticonvulsant effects of extracts of the west African black pepper, Piper guineense.

A water extract of the West African black pepper Piper guineense L. was tested for activity against audiogenic seizures in DBA/2 mice, and against seizures induced in T.O. mice by N-methyl-DL-aspartate (NMDLA), pentylenetetrazole (PTZ) and maximal electroschock. Single intraperitoneal doses of the extract produced significant protection of DBA/2 mice against audiogenic seizures. The highest of three doses tested produced 100% and 58% protection at 6 h and 18 h after treatment, respectively. The extract also protected T.O. mice against convulsions induced by NMDLA and maximal electroshock but it had no significant effect on PTZ-induced convulsions. The doses of the extract tested did not cause significant impairment of performance of T.O. mice on a rotarod test. The results indicate that the extract of P. guineense has prolonged anticonvulsant activity at doses which do not cause significant CNS depression.

Acoustic Stimulation↗

PubMed1991

Halofantrine-induced pruritus amongst subjects who itch to chloroquine.

The incidence and nature of pruritus induced by chloroquine and halofantrine were studied in 82 patients with acute malaria and in 40 healthy subjects, using a visual analogue scale for quantitating pruritus. Results showed that the proportion of patients with acute malaria manifesting itch to halofantrine was significantly lower than the proportion manifesting itch to chloroquine. Furthermore, the intensity and duration of halofantrine-induced pruritus were significantly lower than those of chloroquine-induced pruritus. The few patients who itched to halofantrine all had a history of itching to chloroquine. The incidence and intensity of chloroquine-induced pruritus were significantly higher in patients with malaria than in healthy subjects. By contrast, there was no significant difference between malaria patients and healthy subjects as regards halofantrine-induced pruritus. These results suggest that itchers to halofantrine may constitute a small group within the population of itchers to chloroquine. Malaria infection appears to enhance chloroquine-induced pruritus but not halofantrine-induced pruritus and this may be of therapeutic importance.

Acute Disease↗

PubMed1990

Urine methylhistamine concentrations before and after chloroquine in healthy black subjects.

Urine concentrations of methylhistamine were measured in 11 subjects who experienced itching with chloroquine ('itchers') and in 14 who did not itch ('non-itchers'). In each group, urine methylhistamine concentrations were significantly greater at 12, 24 and 36 h after ingestion of 1 g chloroquine phosphate than before. There was no significant difference between itchers and non-itchers as regards urine methylhistamine concentrations at any time-point. Furthermore, there was no correlation between urine methylhistamine concentration and degree of pruritus in itchers. The findings suggest that histamine may be released by chloroquine, but it is unlikely to be the main cause of chloroquine-induced pruritus.

Adult↗

PubMed1989

Effects of clemastine, ketotifen and prednisolone on chloroquine-induced pruritus.

The effects of single doses of placebo, clemastine, ketotifen and prednisolone on chloroquine-induced pruritus were investigated in healthy black African volunteers using a visual analogue scale. There was no significant differences between the mean percentage degrees of pruritus recorded with placebo, clemastine and ketotifen. By contrast, the mean percentage degree of pruritus recorded with prednisolone was significantly lower than those with the other three treatments. If these results are confirmed in patients with malaria, it might be more rational to administer a single prophylactic dose of prednisolone in those who experience very disturbing pruritus with chloroquine.

Adult↗

PubMed1986

Exercise-induced hand tremor: a possible test for beta 2-adrenoceptor selectivity in man?

The effects of intravenous doses of propranolol, sotalol, timolol, atenolol and placebo on exercise-induced tachycardia and exercise-induced increases in hand tremor were assessed in four healthy volunteers. All active drugs produced significant reductions in exercise-induced tachycardia. Exercise caused consistent significant increases in hand tremor which were blocked by the three non-cardioselective drugs but not by atenolol or placebo. The blockade of exercise-induced hand tremor is suggested as a possible test for the assessment of the selectivity of beta-adrenoceptor blockade in man.

Adrenergic beta-Antagonists↗

PubMed1985

Tremor: an alternative approach for investigating adrenergic mechanisms in thyrotoxicosis?

The effects of nadolol (or placebo) and carbimazole on thyrotoxic tremor were investigated in 18 thyrotoxic patients. Both nadolol and carbimazole produced significant reductions in tremor power although nadolol did not cause any change in serum free tri-iodothyronine and free thyroxine concentrations. The results are discussed in terms of the pathogenesis of thyrotoxic tremor and the potential usefulness of tremor in the investigation of adrenergic mechanisms in thyrotoxicosis.

Adrenergic beta-Antagonists↗

PubMed1985

The tremorolytic action of beta-adrenoceptor blockers in essential, physiological and isoprenaline-induced tremor is mediated by beta-adrenoceptors located in a deep peripheral compartment.

The effects of intravenous propranolol 100 micrograms kg-1, sotalol 500 micrograms kg-1, timolol 7.8 micrograms kg-1, atenolol 125 micrograms kg-1 and placebo on essential, physiological and isoprenaline-induced tremor were studied. These beta-adrenoceptor blocker doses produced equal reduction of standing-induced tachycardia in essential tremor patients. Atenolol produced significantly less reduction of essential and isoprenaline-induced tremor than the non-selective drugs, confirming the importance of beta 2-adrenoceptor blockade in these effects. Propranolol and sotalol produced equal maximal inhibition of isoprenaline-induced tremor but propranolol was significantly more effective in reducing essential tremor. The rate of development of the tremorolytic effect was similar in essential, physiological and isoprenaline-induced tremors but all tremor responses developed significantly more slowly than the heart rate responses. It is proposed that these results indicate that the tremorolytic activity of beta-adrenoceptor blockers in essential, physiological and isoprenaline-induced tremor is exerted via the same beta 2-adrenoceptors located in a deep peripheral compartment which is thought to be in the muscle spindles.

Adrenergic beta-Antagonists↗

PubMed1985

Differential effects of alpha-adrenoceptor blockade on essential, physiological and isoprenaline-induced tremor: evidence for a central origin of essential tremor.

Intravenous thymoxamine reduced the power of essential tremor but increased that of physiological and isoprenaline-induced tremor. These findings indicate that essential and physiological tremor have dissimilar pathophysiological mechanisms. They also suggest that central adrenergic mechanisms are involved in the pathophysiology of essential tremor and that isoprenaline-induced tremor is not a good model of essential tremor. Furthermore, alpha-adrenoceptor blockers may be a useful therapy for essential tremor.

Adult↗

PubMedDate not supplied

Essential tremor: a review.

A review of current knowledge of essential tremor and its treatment is presented. Its prevalence in Africa is not known but it is quite common in those over 40 years in most communities of the world. The condition is characterised by slowly progressive postural tremor of the arms and head without an identifiable organic cause. It is often misdiagnosed as Parkinson's disease. Current treatment is with beta-adrenoceptor blocking drugs, but this treatment is not completely satisfactory. Further studies are required on its pathophysiological mechanisms and new therapeutic directions.

Diagnosis, Differential↗