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At least 19 recordsLinked to original sources
PubMed2004

A randomized open label clinical trial to compare the efficacy and safety of intravenous quinine followed by oral malarone vs. intravenous quinine followed by oral quinine in the treatment of severe malaria.

The treatment of patients with severe malaria in sub-Saharan Africa has become a challenge to clinicians due to poor compliance to quinine and the increasing multidrug resistance to antimalarials by the P. falciparum parasite. The aim of this study was to compare the efficacy and safety profile of two truncated antimalarial regimens of intravenous quinine followed by oral Malarone (Malarone arm) with intravenous quinine followed by oral quinine (quinine arm) in the treatment of severe P. falciparum malaria. The outcome measures were parasite clearance time, fever clearance time, efficacy, and adverse events profile. Consecutive patients aged 1-60 years, with a diagnosis of severe malaria with positive blood smears for P. falciparum parasites and admitted to the Moi Teaching and Referral Hospital were randomized into the two study arms. Of the 360 patients studied 167 and 193 cases were randomized into the Malarone and quinine arms, respectively. Of the five (1.4 per cent) patients who died, three came from the quinine arm. The frequency of adverse reactions was higher in the oral quinine group (31.6 per cent) than in the Malarone group (25.7 per cent). The mean parasite clearance time was 120 h and 108 h for the quinine and Malarone arms of the study, respectively, and the mean fever clearance times were 84 h and 72 h for the quinine and Malarone arms, respectively (p=0.1). Truncated therapeutic regimen using malarone after intravenous quinine is safer and as effective as conventional intravenous quinine followed by oral quinine in the treatment of severe malaria. The P. falciparum recrudescence rate was lower with the use of Malarone than for quinine.

Administration, Oral↗
PubMed1991

Red cell and plasma concentrations of combined quinine-quinidine and quinine in falciparum malaria.

Red cell and plasma quinine-quinidine, and quinine concentrations in children with uncomplicated falciparum malaria who were treated with a combination of quinine/quinidine/cinchonine (combined drug) and quinine alone, respectively, were measured, using the extraction fluorescence method. The cure rates obtained with the high dose regimen of the combined drug (100%) were significantly higher than in the low dose regimen group (37.5%) (p less than 0.05), and the quinine regimen produced a 50% cure rate. Similar mild and transient ECG effects were noted in both the combined drug group and the quinine group. In patients treated with the combined drug, quinine-quinidine concentrations in both red cell and plasma of the high dose regimen group were significantly higher than those in the low dose regimen group (p less than 0.001, p less than 0.001). In quinine-treated patients, red cell quinine concentration in those with RII failure was significantly lower than that in patients with cure or RI failure (p less than 0.05). Both red cell and plasma levels of quinine-quinidine were higher than quinine levels. The red cell:plasma quinine-quinidine concentration ratios rose steadily to the high level from day 3 to day 6, while the ratio of quinine alone fluctuated around the low level and then gradually fell. The evidence suggests that red cell drug concentrations are more closely related to the outcome of treatment than to plasma concentrations and that the combined drug may be very useful for treatment of multi-drug-resistant P. falciparum infections. Further study is needed.

Antimalarials↗
PubMed1996

c-Fos induction in the rat nucleus of the solitary tract by intraoral quinine infusion depends on prior contingent pairing of quinine and lithium chloride.

Intraoral infusions of sucrose or saccharin induce c-Fos-like immunoreactivity (c-FLI) in the intermediate nucleus of the solitary tract (iNTS) of rats after acquisition of a conditioned taste aversion (CTA). The induction of c-FLI in the iNTS may be a consequence of the shift in behavioral response from ingestive to aversive behaviors that characterize acquisition and expression of a CTA. To test this hypothesis, rats were intraorally infused with 0.3 mM quinine sulfate, an aversive taste, 1. prior to conditioning, 2. after 3 noncontingent (unpaired) infusions of quinine and toxic lithium chloride (LiCl) injections, 3. after conditioning with 3 contingent pairings of quinine and LiCl, and 4. after extinction with repeated unpaired infusions of quinine. Intraoral infusions of quinine induced c-FLI in the iNTS only after acquisition of a CTA against quinine; quinine failed to induce c-FLI in the iNTS of unconditioned, noncontingently treated, or extinguished rats. The pattern of c-FLI in the iNTS induced by expression of a CTA against quinine was quantitatively and anatomically similar to that elicited by sucrose in rats expressing a CTA against sucrose. We conclude that aversive responses per se are not sufficient to induce c-FLI in the iNTS. Furthermore, contingent pairing of quinine and LiCl does not cause a shift in behavioral response from palatable, ingestive behaviors to aversive behaviors as in acquisition of a CTA against sucrose. Thus, we also conclude that a shift in behavior from ingestive to aversive responses is not required for increased c-FLI expression in the iNTS during CTA expression. Therefore, the induction of c-FLI in the iNTS during expression of a CTA may be correlated with neuronal processes specific to acquisition and expression of a CTA.

Animals↗
PubMed1992

The effects of rubidium, caesium and quinine on 5-HT-mediated behaviour in rat and mouse--3. Quinine.

It has been shown that caesium, which shares properties with quinine as a K(+)-channel blocker, enhanced 5-HT-mediated behaviour in both rats and mice. It was therefore of interest to investigate the effects of quinine on 5-HT-mediated behaviour in the rat and mouse. Quinine, dose-dependently (ED50 = 5 mg/kg), produced the 5-HT behavioural syndrome in rats pre-treated with tranylcypromine (TCP) (15 mg/kg, i.p.). p-Chlorophenylalanine (i.p., 300 mg/kg x2) or (-)-propranolol (20 mg/kg, i.p.), pindolol (4 mg/kg, i.p.) and ritanserin (0.4 mg/kg, s.c.), all prevented the behavioural syndrome induced by quinine (72 mg/kg, i.p.) plus TCP. The administration of quinine (72 mg/kg, i.p.) enhanced the 5-HT syndrome elicited by p-chloramphetamine (4 mg/kg, i.p.) and the 5-HT agonists, 8-OH-DPAT (0.5 mg/kg, s.c.), 5-MeODMT (2 mg/kg, i.p.), DOI (8 mg/kg, s.c.) and quipazine (25 mg/kg, i.p.) in rats. Pretreatment with quinine also potentiated the 5-HT2-mediated head-twitch in the mouse but had no effect on the hypothermia in the mouse, induced by 8-OH-DPAT (0.5 mg/kg, s.c.). Quinine also enhanced the rate of synthesis of 5-HT in the brain of the rat. On the basis of these findings, together with those in the preceding two papers, it is suggested that the effects of rubidium, caesium and quinine, to enhance differentially various aspects of 5-HT function are mediated by actions on 5-HT-modulated K(+)-channels. This conclusion is also discussed in relation to the actions of lithium and electroconvulsive shock on 5-HT function in brain and the treatment of manic-depressive disease.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMedDate not supplied

Towards optimal regimens of parenteral quinine for young African children with cerebral malaria: the importance of unbound quinine concentration.

Young African children with severe malaria are given quinine using a regimen designed for Thai adults. We measured quinine in the blood, plasma and plasma water of young children in Kenya after rapid intravenous and intramuscular dosing, and calculated the therapeutic range of unbound quinine. The peak plasma quinine concentration after rapid intravenous dosing was 12.3 +/- 3.7 mg/L (mean +/- SD), 43% higher than in adults given the same regimen previously; this was due to a smaller apparent volume of distribution in the children. The therapeutic range of unbound quinine was calculated as 0.2-2.0 mg/L. Simulations of unbound quinine were made for the standard quinine regimen: unbound drug concentrations rose above the therapeutic range after each dose. The possible risks of quinine-induced visual impairment are discussed. Alternative, lower dose regimens for young African children with severe malaria are described.

Child↗
PubMed2006

Effect of delta9-tetrahydrocannabinol on quinine palatability and AM251 on sucrose and quinine palatability using the taste reactivity test.

Here we provide evidence that the cannabinoid agonist, Delta9-tetrahydrocannabinol (Delta9-THC) enhances quinine palatability and the CB1 antagonist/inverse agonist, AM251, reduces sucrose and quinine palatability using the taste reactivity test, which provides a direct measure of palatability independently of appetitive behavior. In Experiment 1, rats were treated with a low dose of Delta9-THC (0.5 mg/kg) or Vehicle 30 min, 60 min, 120 min or 240 min prior to a 5-min intraoral infusion of a highly unpalatable 0.05% quinine solution. Regardless of the post-injection interval, Delta9-THC reduced rejection of quinine. The Delta9-THC-induced palatability shift was reversed by AM251. In Experiment 2, rats were injected with either AM251 (1 mg/kg) or Vehicle prior to receiving a 5-min intraoral infusion of either 32% sucrose or 0.05% quinine solution. AM251 significantly decreased sucrose-elicited hedonic reactions across both time intervals; however, AM251 did not significantly modify the rejection of 0.05% quinine solution. When the concentration of the quinine solution was reduced to 0.01% in Experiment 3, AM251 enhanced quinine aversion. Although the range of concentrations of the solutions tested in the present data is limited, our results suggest that the cannabinoid system may modulate the palatability of ingested substances regardless of the palatability of the ingested substance.

Animals↗
PubMed1991

Changes in platelet function and reactivity induced by quinine in relation to quinine (drug) induced immune thrombocytopenia.

Quinine, a drug known to induce immune mediated thrombocytopenia, has been postulated to mediate binding of drug dependent antibodies to a range of platelet membrane glycoproteins. Quinine may not act solely as a hapten however, as we have shown that it inhibits platelet aggregation (ex vivo and in vitro) and release and modifies the ability of activated platelets to bind the adhesive proteins fibrinogen and fibronectin in a dose dependent fashion. Studies on the effect of quinine on the binding of monoclonal antibodies HuPlml (GpIIIa) FMC25 (GpIX) and AN51 (GpIb) to platelets shows a selective reduction in AN51 binding. In addition quinine induced platelet antibodies from thrombocytopenic patients, in the presence of quinine, have been shown to inhibit binding of these monoclonal antibodies to platelets to varying degrees. These observations suggest that quinine causes widespread but specific conformational changes in platelet membrane antigens which may expose neoantigens resulting in the production of quinine induced antibodies.

Antibodies, Monoclonal↗
PubMed1987

The effects of quinine on the calcium and magnesium content of the sarcoplasmic reticulum and the temperature-dependence of quinine contractures.

A significant decrease in the Ca2+ and increase in the Mg2+ content of the terminal cisternae (TC) of the sarcoplasmic reticulum (SR) during quinine contraction was demonstrated by electron probe analysis of rapidly frozen frog muscles. The extent of Ca2+ release (71% of total) from the TC and the absence of an increase in total cell Ca2+ support the conclusion that quinine contractures are caused by passive efflux of Ca2+ from the SR when the latter is uncompensated due to inhibition of the SR Ca2+ pump by quinine. A rapid warming contraction (RWC) was observed, in the presence of quinine, when the temperature of intact and skinned muscles was increased from about 5 degrees C to 18-23 degrees C. The duration of the latency of quinine contracture, in intact muscle bundles, was approximately 31 s at 3 degrees C and 2 s at 23 degrees C. The results suggest a significant temperature sensitivity of the passive Ca2+ channels of the SR membrane, although an effect of temperature on the lipid partition coefficient of quinine into the SR has not been ruled out.

Animals↗
PubMedDate not supplied

Morphine-induced modification of quinine palatability: effects of multiple morphine-quinine trials.

Morphine pretreatment attenuates aversive taste reactions elicited by quinine solution when assessed by the taste reactivity test. To determine whether this effect changes across trials, rats were administered morphine (2 mg/kg, subcutaneously) 30 min before a 5-min intraoral infusion of quinine solution (0.05%) on each of eight trials. Neither tolerance nor sensitization developed to morphine-induced attenuation of quinine aversiveness; morphine suppressed quinine-elicited aversive reactions on each trial. In addition, when tested in the absence of morphine, rats displayed a reduced aversion to quinine, suggesting that quinine became conditionally less aversive following previous pairings with morphine.

Animals↗
PubMed1991

Susceptibility of Plasmodium falciparum to different doses of quinine in vivo and to quinine and quinidine in vitro in relation to chloroquine in Liberia.

Chloroquine-resistant Plasmodium falciparum has been spreading rapidly after its emergence in 1988 in Yekepa. The in vivo and in vitro susceptibilities to quinine and quinidine, compared to chloroquine, were studied by investigating the number of treatment days required for radical cure and estimating the quinine concentrations concomitantly. The minimal inhibitory concentrations (MIC) for schizont maturation in all successful in vitro tests were 5.12 x 10(-6) mol/l for quinine and 1.28 x 10(-6) mol/l for quinidine, indicating that all 50 isolates were sensitive to the two drugs. The IC50 and IC90 values were 0.22 and 0.78 x 10(-6) mol/l for quinine and 0.07 and 0.26 x 10(-6) mol/l for quinidine, respectively. In vitro inhibition of parasites by 1.6 x 10(-6) mol/l of chloroquine was obtained in 31 out of 47 isolates, 16 (34%) being resistant. The IC50, IC90 and geometrical mean MIC for quinine were all about two times higher for the chloroquine-resistant than for the chloroquine-sensitive isolates (P = 0.006). P. falciparum infected children (n = 64) were randomly allocated to four groups and treated with quinine (10 mg/kg body weight twice daily) for 1 day (3 doses), 2, 4 and 7 days, respectively. All cleared their parasitaemias by day 4 but 5 out of 15 of those treated with only three doses showed a recurrence of parasitaemia between days 7 and 14; these were considered to be recrudescences. In the other groups, recurrent parasitaemias only occurred between days 17 and 28 and were considered to be reinfections.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Response of Kampuchean strains of Plasmodium falciparum to antimalarials: in-vivo assessment of quinine and quinine plus tetracycline; multiple drug resistance in vitro.

Forty-three patients were enlisted in the in-vivo test for sensitivity of Kampuchean strains of Plasmodium falciparum to quinine. The mean parasite density count on day 0 was 32,398 asexual parasites per microliter of blood. With a dosage of 1.5 g quinine base daily for 10 days the average parasite clearance time was 5.6 days, and the average duration of fever 3.4 days. The in-vivo test was evaluated at 7 and 10 days after the start of therapy. After 7 days only 16 patients were parasite negative by microscopic examination (S); 20 patients had an RI recrudescence, four patients responded at the RII level and three at the RIII level. Evaluating the in-vivo test at 10 days, the number of patients parasite negative increased to 18, the number of those with an RI level of resistance increased to 21, two patients gave an RII response and two had an RIII level of resistance. Twenty-two adult males were included in an in-vivo test of the sensitivity of P. falciparum to quinine plus tetracycline. The course of treatment was: quinine 3 x 500 mg daily for 10 days, tetracycline 3 x 500 mg for 7 days. Parasite density counts on day 0 averaged 11,393 asexual parasites per microliter of blood. The average parasite clearance time was 5.9 days, and the average duration of fever was 3.8 days. After 7 days of treatment, 81.8% of patients were parasite negative, while one patient had a recrudescence after 17 days (RI). Three infections were resistant at the RII level. By prolongation of the observations to day 10, the parasitaemia was cleared in all patients, i.e. all infections were sensitive to quinine plus tetracycline. Thirty-four patients with falciparum malaria were screened for in-vitro resistance to chloroquine, mefloquine and quinine using the WHO standard micro-test.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Quinine poisoning in children.

The accidental ingestion of quinine by children causes significant morbidity and mortality. We have reviewed quinine poisoning as presented in the medical literature and our experience of paediatric quinine poisoning during the period from January 1975 to September 1986. The clinical features that were seen in our patients were similar to those that are described in larger series. In our series, 13 children were identified, of whom 11 children were aged one to two years. Ten children either remained asymptomatic or made a complete recovery. Two children had a persisting major deficit and one died. Once ingestion of quinine has occurred, absorption should be prevented by the emptying of the stomach with ipecacuanha or gastric lavage promptly and then by the administration of activated charcoal. Once toxicity develops, supportive therapy should be given, but there is no specific therapy to reduce toxicity or to enhance elimination. Physicians who prescribe quinine should be aware of the potential dangers to small children.

Adolescent↗
PubMed1999

Enantiomeric separation of N-protected amino acids by non-aqueous capillary electrophoresis using quinine or tert-butyl carbamoylated quinine as chiral additive.

A capillary electrophoretic (CE) method for the enantioseparation of N-protected chiral amino acids was developed using quinine and tert-butyl carbamoylated quinine as chiral selectors added to nonaqueous electrolyte solutions (NACE). A series of various N-derivatized amino acids were tested as chiral selectands, and in order to optimize the CE enantioseparation of these compounds, different parameters were investigated: the nature of the organic solvent, the combination of different solvents, the nature and the concentration of the background electrolyte, the selector concentration, the capillary temperature, and the applied voltage. The influence of these factors on the separation of the analyte enantiomers and the electroosmotic flow was studied. Generally, with tert-butyl carbamoylated quinine as chiral selector, better enantioseparations were achieved than with unmodified quinine. Optimum experimental conditions were found with a buffer made of 12. 5 mM ammonia, 100 mM octanoic acid, and 10 mM tert-butyl carbamoylated quinine in an ethanol-methanol mixture (60:40 v/v). Under these conditions, DNB-Leu enantiomers could be separated with a selectivity factor (alpha) of 1.572 and a resolution (Rs) of 64.3; a plate number (N) of 127,000 and an asymmetry factor (As) of 0.93 were obtained for the first migrating enantiomer.

Amino Acids↗
PubMed2001

Controlled trial of 3-day quinine-clindamycin treatment versus 7-day quinine treatment for adult travelers with uncomplicated falciparum malaria imported from the tropics.

We conducted a randomized, double-blind, placebo-controlled trial to compare a 3-day quinine-clindamycin regimen (group QC) with a 7-day quinine regimen (group Q) for the treatment of uncomplicated Plasmodium falciparum malaria in travelers returning from the tropics. A total of 55 and 53 patients in groups Q and QC were analyzed, respectively. Adverse effects were similar in both groups, although two patients in group Q had severe adverse reactions, leading to the cessation of treatment. The 28-day cure rate for the evaluated patients (per-protocol analysis) was 100% for group QC, whereas it was 96.3% for group Q (P = 0.5). The 28-day cure rate in the intention-to-treat analysis was 96.2% for group QC, whereas it was 94.6% for group Q (P = 1). There were no significant differences between the two regimens with regard to parasite and fever clearance times. Our study shows that the 3-day quinine-clindamycin regimen is well tolerated and compares favorably with a 7-day quinine treatment. This short-term regimen had previously been evaluated only in areas of endemicity. According to our results, the 3-day quinine-clindamycin regimen may be an alternative for the treatment of imported uncomplicated P. falciparum malaria in travelers returning from the tropics.

Adult↗
PubMed1991

Infection of Anopheles darlingi fed on patients with Plasmodium falciparum before and after treatment with quinine or quinine plus tetracycline.

Anopheles darlingi fed on eight falciparum malaria patients with gametocytes before and after treatment with quinine sulfate or quinine sulfate plus tetracycline became infected. Quinine and quinine plus tetracycline had no apparent sporontocidal or gametocytocidal effect on late stage immature and mature gametocytes. Plasmodium falciparum gametocytes are persistent and infected mosquitoes for up to 21 days after patients were treated with quinine plus tetracycline. Sporogonic development was similar for groups of mosquitoes fed before and after patients were treated with these schizontocides. The percentages of infected mosquitoes that developed salivary gland infections were also similar for groups of mosquitoes fed before and after treatment. Twenty-four hours after treatment with 45 mg of primaquine phosphate, falciparum malaria patients were not infective to An. darlingi.

Animals↗
PubMed1987

Controlled trial of initial slow intravenous quinine vs conventional quinine infusion in the treatment of highly parasitized falciparum malaria in adult patients.

A total of 10 patients (adults) with highly parasitized falciparum malaria were treated initially with intravenous quinine (10 mg per kg quinine diluted in 20 ml normal saline injected very slowly with a syringe taking not less than 20 minutes). Six control patients were treated with quinine infusion standard method (quinine 10 mg/kg diluted in 500 ml of normal saline given as slow drip taking 4 hours for the drug to enter the patient's body). Both two groups of patients were followed by oral quinine 10 mg/kg three times a day for 7 days.

Adult↗
PubMedDate not supplied

Towards optimal regimens of parenteral quinine for young African children with cerebral malaria: unbound quinine concentrations following a simple loading dose regimen.

Nine children with severe falciparum malaria were treated with an intravenous quinine regimen which did not require burettes or infusion pumps, to determine its practicability and to ensure that therapeutic drug concentrations were achieved and maintained throughout the dose interval. The regimen comprised quinine dihydrochloride (15 mg/kg; 12.5 mg/kg of the free base), which was added to a bag of intravenous fluid (after wastage of all but 100 mL), and given via standard giving sets over 2 h. Blood was drawn sequentially during the infusion, and for 12 h thereafter; plasma water was obtained by ultrafiltration of samples at the bedside, and quinine concentration was measured, in plasma and plasma water, by high performance liquid chromatography. Drug administration was practicable without burettes or infusion pumps; unbound drug concentrations exceeded the 99% inhibitory concentration for local parasites within 0.5 h, and remained within the therapeutic range for the entire dose interval. This loading dose regimen can now be recommended for young children in African hospitals; maintenance doses of 10 mg/kg should be given at 12 h intervals until oral antimalarial drugs are possible. These recommendations will need to be modified if susceptibility to quinine declines.

Child↗