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Journal articles on the topic 'Primaquin'

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Published: 4 June 2021
Last updated: 18 February 2022

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1

Hang, Zhang Zhong. "Elimination of the gametocytes of Theileria annulata of cattle by primaquin phosphate." Veterinary Parasitology 23, no. 1-2 (1987): 11–21. http://dx.doi.org/10.1016/0304-4017(87)90021-5.

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2

Vinnemeier, Christof, and Thierry Rolling. "Prophylaxe und Therapie der Malaria: aktuelle Empfehlungen." DMW - Deutsche Medizinische Wochenschrift 143, no. 07 (2018): 472–75. http://dx.doi.org/10.1055/s-0044-100818.

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Was ist neu? Epidemiologie Weltweit sind die Malaria-Inzidenzen rückläufig. Die Zahl der nach Deutschland importierten Fälle blieb zuletzt auf hohem Niveau stabil. Von größter Bedeutung ist es gut bekannte Risikogruppen mit Beratungsangeboten zu erreichen, z. B. Reisende auf Verwandtenbesuch in Endemiegebieten. Prophylaxe Mefloquin steht seit 2013 in Deutschland nur noch als Einzelimport zur Verfügung, bleibt jedoch für bestimmte Personengruppen weiter ein wichtiges Prophylaktikum. Die notfallmäßige Selbsttherapie der Malaria, die gängige Praxis für Reisende in Länder mit niedrigem und mittlerem Übertragungsrisiko ist, wird in der Reisemedizin zunehmend kritisiert und sollte zielgerichteter eingesetzt werden. Therapie der Malaria tropica Patienten mit einem höheren Körpergewicht müssen nach einer Therapie engmaschig nachbeobachtet werden, da sie ein höheres Risiko einer Rekrudeszenz haben. Artesunat ist Mittel der Wahl zur Therapie der komplizierten Malaria tropica. Auch hier ist eine konsequente Kontrolle nach Therapieende notwendig, um eine mit Artesunat assoziierte hämolytische Anämie frühzeitig zu erfassen. Malaria tertiana Seit 2014 gab es in Deutschland eine Zunahme von Patienten mit einer Malaria tertiana, insbesondere bei Migranten aus Eritrea. Aufgrund der unzureichenden Gesundheitsversorgung der Flüchtenden haben nicht alle Patienten die bei Plasmodium vivax notwendige Rezidivprophylaxe mit Primaquin erhalten.
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3

Octabiano G, Reinaldi, I. Nyoman Yesaya C, Zega Agustian, et al. "Mixed Infection of Vivax and Falciparum Malaria with Severe Manifestations of Malaria at the General Hospital of the Christian University of Indonesia: A Case Report." Journal of Asian Multicultural Research for Medical and Health Science Study 2, no. 2 (2021): 28–32. http://dx.doi.org/10.47616/jamrmhss.v2i2.96.

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Malaria is still a health problem in Indonesia. The number of malaria cases according to the 2018 RISKESDAS reached 8076 cases, and the highest number was obtained from Papua province with 3,334 cases. Multiple infection malaria in Indonesia according to RISKESDAS 2018, has a rate of 0.01% of the total cases, namely Plasmodium Falciparum malaria and Plasmodium non Falciparum malaria. A 47 year old man was referred from the clinic with complaints of high fever preceded by chills 10 days before being admitted to the hospital. Accompanied by shortness of breath, unable to get off the treatment bed due to feeling very weak, nauseous, sick and having a bulging stomach. Physical examination revealed a pale conjunctiva, ronkhi in the lower field of the right lung, dim percussion in the basal of the left lung, hepatomegaly, splenomegaly, shifting dullness. ring form vivax, on chest X-ray found a left pleural effusion. It is known that the patient previously lived in Papua from September 2018 to May 2019. During treatment, the patient was given artesunate injection therapy, dihydroartemisin + piperaquine and primaquin for seven days of treatment. At the end of the treatment, another chest X-ray was performed and re-examination of the peripheral blood smear, no more pleural effusions were found and no parasites were found on re-examination of the peripheral blood smear. Mixed infection of vivax and falciparum malaria, is a rare case that may occur in endemic areas where both plasmodium can be found. The prevalence in Indonesia according to RISKESDAS is only about 0.01% of all malaria cases in Indonesia.
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4

Pareek, Anil, Nitin Chandurkar, Nithya Gogtay, et al. "Sustained Release Formulation of Primaquine for Prevention of Relapse of Plasmodium vivax Malaria: A Randomized, Double-Blind, Comparative, Multicentric Study." Malaria Research and Treatment 2015 (August 20, 2015): 1–8. http://dx.doi.org/10.1155/2015/579864.

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Background. Primaquine is used to eradicate latent Plasmodium vivax parasite from liver, with administration of standard dose daily up to 14 days. We studied efficacy, safety, and tolerability of sustained release (SR) formulation of primaquine in comparison with conventional primaquine in preventing relapse of P. vivax malaria. Methods. Microscopically confirmed cases of P. vivax malaria received chloroquine therapy for three days. Aparasitemic and asymptomatic patients were then randomized to receive either conventional primaquine 15 mg for 14 days or primaquine SR 15 mg for 14 days, or primaquine SR 30 mg for seven days. Results. Of the 360 patients, who received chloroquine therapy, 358 patients were randomized. Two-hundred eighty-eight patients completed six-month follow-up and four patients (three: conventional primaquine 15 mg (2.86%), one: primaquine SR 30 mg (0.93%)) showed relapse confirmed by PCR genotyping. Drug compliance was significantly better in primaquine SR 30 mg group (95.57%, p=0.039) without any serious adverse events. Conclusion. Primaquine SR 15 mg and primaquine SR 30 mg could be an effective alternative to conventional primaquine 15 mg due to their comparable cure rates and safety profile. Shorter treatment duration with primaquine SR 30 mg may increase patient compliance and may further reduce relapse rates. Clinical Trial Registration. This trial is registered with CTRI/2010/091/000245.
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5

Sutanto, Inge, Bagus Tjahjono, Hasan Basri, et al. "Randomized, Open-Label Trial of Primaquine against Vivax Malaria Relapse in Indonesia." Antimicrobial Agents and Chemotherapy 57, no. 3 (2012): 1128–35. http://dx.doi.org/10.1128/aac.01879-12.

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ABSTRACTRadical cure ofPlasmodium vivaxinfection applies blood schizontocidal therapy against the acute attack and hypnozoitocidal therapy against later relapse. Chloroquine and primaquine have been used for 60 years in this manner. Resistance to chloroquine by the parasite now requires partnering other blood schizontocides with primaquine. However, the safety and efficacy of primaquine against relapse when combined with other drugs have not been demonstrated. This randomized, open-label, and relapse-controlled trial estimated the efficacy of primaquine against relapse when administered with quinine or dihydroartemisinin-piperaquine for treatment of the acute infection. Among 650 soldiers who had returned to their malaria-free base in Java, Indonesia, after 12 months in malarious Papua, Indonesia, 143 with acuteP. vivaxmalaria were eligible for study. One hundred sixteen enrolled subjects were randomized to these treatments: artesunate (200-mg dose followed by 100 mg/day for 6 days), quinine (1.8 g/day for 7 days) plus concurrent primaquine (30 mg/day for 14 days), or dihydroartemisinin (120 mg) plus piperaquine (960 mg) daily for 3 days followed 25 days later by primaquine (30 mg/day for 14 days). Follow-up was for 12 months. One hundred thirteen subjects were analyzable. Relapse occurred in 32 of 41 (78%) subjects administered artesunate alone (2.71 attacks/person-year), 7 of 36 (19%) administered quinine plus primaquine (0.23 attack/person-year), and 2 of 36 (6%) administered dihydroartemisinin-piperaquine plus primaquine (0.06 attack/person-year). The efficacy of primaquine against relapse was 92% (95% confidence interval [CI] = 81% to 96%) for quinine plus primaquine and 98% (95% CI = 91% to 99%) for dihydroartemisinin-piperaquine plus primaquine. Antirelapse therapy with primaquine begun a month after treatment of the acute attack with dihydroartemisinin-piperaquine proved safe and highly efficacious against relapse byP. vivaxacquired in Papua, Indonesia.
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6

&NA;. "Primaquine." Reactions Weekly &NA;, no. 1324 (2010): 29–30. http://dx.doi.org/10.2165/00128415-201013240-00089.

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7

&NA;. "Primaquine." Reactions Weekly &NA;, no. 428 (1992): 11. http://dx.doi.org/10.2165/00128415-199204280-00056.

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8

&NA;. "Primaquine." Reactions Weekly &NA;, no. 1095 (2006): 23. http://dx.doi.org/10.2165/00128415-200610950-00079.

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9

&NA;. "Primaquine." Reactions Weekly &NA;, no. 314 (1990): 10. http://dx.doi.org/10.2165/00128415-199003140-00055.

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10

&NA;. "Primaquine." Reactions Weekly &NA;, no. 731 (1998): 10. http://dx.doi.org/10.2165/00128415-199807310-00034.

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11

&NA;. "Primaquine." Reactions Weekly &NA;, no. 1247-1248 (2009): 29–30. http://dx.doi.org/10.2165/00128415-200912470-00097.

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12

&NA;. "Primaquine." Reactions Weekly &NA;, no. 1422 (2012): 40–41. http://dx.doi.org/10.2165/00128415-201214220-00134.

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13

Jittamala, Podjanee, Sasithon Pukrittayakamee, Elizabeth A. Ashley, et al. "Pharmacokinetic Interactions between Primaquine and Pyronaridine-Artesunate in Healthy Adult Thai Subjects." Antimicrobial Agents and Chemotherapy 59, no. 1 (2014): 505–13. http://dx.doi.org/10.1128/aac.03829-14.

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ABSTRACTPyronaridine-artesunate is a newly introduced artemisinin-based combination treatment which may be deployed together with primaquine. A single-dose, randomized, three-sequence crossover study was conducted in healthy Thai volunteers to characterize potential pharmacokinetic interactions between these drugs. Seventeen healthy adults received a single oral dose of primaquine alone (30 mg base) and were then randomized to receive pyronaridine-artesunate alone (540−180 mg) or pyronaridine-artesunate plus primaquine in combination, with intervening washout periods between all treatments. The pharmacokinetic properties of primaquine, its metabolite carboxyprimaquine, artesunate, its metabolite dihydroartemisinin, and pyronaridine were assessed in 15 subjects using a noncompartmental approach followed by a bioequivalence evaluation. All drugs were well tolerated. The single oral dose of primaquine did not result in any clinically relevant pharmacokinetic alterations to pyronaridine, artesunate, or dihydroartemisinin exposures. There were significantly higher primaquine maximum plasma drug concentrations (geometric mean ratio, 30%; 90% confidence interval [CI], 17% to 46%) and total exposures (15%; 6.4% to 24%) during coadministration with pyronaridine-artesunate than when primaquine was given alone. Pyronaridine, like chloroquine and piperaquine, increases plasma primaquine concentrations. (This study has been registered at ClinicalTrials.gov under registration no. NCT01552330.)
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14

Hanboonkunupakarn, Borimas, Elizabeth A. Ashley, Podjanee Jittamala, et al. "Open-Label Crossover Study of Primaquine and Dihydroartemisinin-Piperaquine Pharmacokinetics in Healthy Adult Thai Subjects." Antimicrobial Agents and Chemotherapy 58, no. 12 (2014): 7340–46. http://dx.doi.org/10.1128/aac.03704-14.

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ABSTRACTDihydroartemisinin-piperaquine is an artemisinin-based combination treatment (ACT) recommended by the WHO for uncomplicatedPlasmodium falciparummalaria, and it is being used increasingly for resistant vivax malaria where combination with primaquine is required for radical cure. The WHO recently reinforced its recommendations to add a single dose of primaquine to ACTs to reduceP. falciparumtransmission in low-transmission settings. The pharmacokinetics of primaquine and dihydroartemisinin-piperaquine were evaluated in 16 healthy Thai adult volunteers in a randomized crossover study. Volunteers were randomized to two groups of three sequential hospital admissions to receive 30 mg (base) primaquine, 3 tablets of dihydroartemisinin-piperaquine (120/960 mg), and the drugs together at the same doses. Blood sampling was performed over 3 days following primaquine and 36 days following dihydroartemisinin-piperaquine dosing. Pharmacokinetic assessment was done with a noncompartmental approach. The drugs were well tolerated. There were no statistically significant differences in dihydroartemisinin and piperaquine pharmacokinetics with or without primaquine. Dihydroartemisinin-piperaquine coadministration significantly increased plasma primaquine levels; geometric mean ratios (90% confidence interval [CI]) of primaquine combined versus primaquine alone for maximum concentration (Cmax), area under the concentration-time curve from 0 h to the end of the study (AUC0–last), and area under the concentration-time curve from 0 h to infinity (AUC0–∞) were 148% (117 to 187%), 129% (103 to 163%), and 128% (102 to 161%), respectively. This interaction is similar to that described recently with chloroquine and may result in an enhanced radical curative effect. (This study has been registered at ClinicalTrials.gov under registration no. NCT01525511.)
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15

Pukrittayakamee, Sasithon, Kesinee Chotivanich, Arun Chantra, Ralf Clemens, Sornchai Looareesuwan, and Nicholas J. White. "Activities of Artesunate and Primaquine against Asexual- and Sexual-Stage Parasites in Falciparum Malaria." Antimicrobial Agents and Chemotherapy 48, no. 4 (2004): 1329–34. http://dx.doi.org/10.1128/aac.48.4.1329-1334.2004.

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ABSTRACT The activities of primaquine in combination with quinine or artesunate against asexual- and sexual-stage parasites were assessed in 176 adult Thai patients with uncomplicated Plasmodium falciparum malaria. Patients were randomized to one of the six following 7-day oral treatment regimens: (i) quinine alone, (ii) quinine with tetracycline, (iii) quinine with primaquine at 15 mg/day, (iv) quinine with primaquine at 30 mg/day, (v) artesunate alone, or (vi) artesunate with primaquine. Clinical recovery occurred in all patients. There were no significant differences in fever clearance times, rates of P. falciparum reappearance, or recurrent vivax malaria between the six treatment groups. Patients treated with artesunate alone or in combination with primaquine had significantly shorter parasite clearance times (mean ± standard deviation = 65± 18 versus 79 ± 21 h) and lower gametocyte carriage rates (40 versus 62.7%) than those treated with quinine (P ≤ 0.007). Primaquine did not affect the therapeutic response (P > 0.2). Gametocytemia was detected in 98 patients (56% [22% before treatment and 34% after treatment]). Artesunate reduced the appearance of gametocytemia (relative risk [95% confidence interval] = 0.34 [0.17 to 0.70]), whereas combinations containing primaquine resulted in shorter gametocyte clearance times (medians of 66 versus 271 h for quinine groups and 73 versus 137 h for artesunate groups; P≤ 0.038). These results suggest that artesunate predominantly inhibits gametocyte development whereas primaquine accelerates gametocyte clearance in P. falciparum malaria.
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16

Healy, Sara A., Sean C. Murphy, Jen C. C. Hume, et al. "Chemoprophylaxis Vaccination: Phase I Study to Explore Stage-specific Immunity to Plasmodium falciparum in US Adults." Clinical Infectious Diseases 71, no. 6 (2019): 1481–90. http://dx.doi.org/10.1093/cid/ciz1010.

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Abstract Background Chemoprophylaxis vaccination with sporozoites (CVac) with chloroquine induces protection against a homologous Plasmodium falciparum sporozoite (PfSPZ) challenge, but whether blood-stage parasite exposure is required for protection remains unclear. Chloroquine suppresses and clears blood-stage parasitemia, while other antimalarial drugs, such as primaquine, act against liver-stage parasites. Here, we evaluated CVac regimens using primaquine and/or chloroquine as the partner drug to discern whether blood-stage parasite exposure impacts protection against homologous controlled human malaria infection. Methods In a Phase I, randomized, partial double-blind, placebo-controlled study of 36 malaria-naive adults, all CVac subjects received chloroquine prophylaxis and bites from 12–15 P. falciparum–infected mosquitoes (CVac-chloroquine arm) at 3 monthly iterations, and some received postexposure primaquine (CVac-primaquine/chloroquine arm). Drug control subjects received primaquine, chloroquine, and uninfected mosquito bites. After a chloroquine washout, subjects, including treatment-naive infectivity controls, underwent homologous, PfSPZ controlled human malaria infection and were monitored for parasitemia for 21 days. Results No serious adverse events occurred. During CVac, all but 1 subject in the study remained blood-smear negative, while only 1 subject (primaquine/chloroquine arm) remained polymerase chain reaction–negative. Upon challenge, compared to infectivity controls, 3/3 chloroquine arm subjects displayed delayed patent parasitemia (P = .01) but not sterile protection, while 3/11 primaquine/chloroquine subjects remained blood-smear negative. Conclusions CVac-primaquine/chloroquine is safe and induces sterile immunity to P. falciparum in some recipients, but a single 45 mg dose of primaquine postexposure does not completely prevent blood-stage parasitemia. Unlike previous studies, CVac-chloroquine did not produce sterile immunity. Clinical Trials Registration NCT01500980.
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17

Gultom, Febryan, Weny I. Wiyono, and Heedy Tjitrosantoso. "STUDI PENGGUNAAN OBAT PADA PASIEN MALARIA DI INSTALASI RAWAT INAP RSUD KABUPATEN MIMIKA." PHARMACON 8, no. 2 (2019): 498. http://dx.doi.org/10.35799/pha.8.2019.29319.

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ABSTRACT Malaria is an infectious disease caused by the Plasmodium parasite (class of Sporozoa) that attacks red blood cells. In indonesia, there are 4 (four) species of malaria parasites, namely Plasmodium falciparum as the cause of tropical malaria which often causes brain malaria with death, Plasmodium vivax as the cause of malaria tertiana, Plasmodium malariae as the cause of malaria quartana and Plasmodium ovale as the cause of ovale malaria. This study aims to determine the patient characteristics and treatment patterns in malaria patients at the inpatient installation of the Mimika District Hospital in period June – December 2018. This study was a descriptive study with retrospective data collection against 68 medical records of malaria patients who were hospitalized inclusion criteria. There were more men group than women, 41 patiensts (60,29%). Most of malaria patients are in the 0 – 5 year age group with 30 patients (44,12%). The most common type of malaria is uncomplicated vivax malaria 21 patients (33,82%). The most drug use of patients was Primaquin as many as 57 (83,82%) of 68 patients. The exact percentage of drug use for patients is 100%, right drug 89.71%, right dose 92.65%, timely 97.06% and right route 100%. Keywords : Malaria, Drug Utilization Study, Hospitalization. ABSTRAK Malaria merupakan penyakit menular disebabkan oleh parasit Plasmodium (kelas Sporozoa) yang menyerang sel darah merah. Di Indonesia dikenal 4 (empat) macam spesies parasit malaria yaitu Plasmodium falciparum sebagai penyebab malaria tropika yang sering menyebabkan malaria otak dengan kematian, Plasmodium vivax sebagai penyebab malaria tertiana, Plasmodium malariae sebagai penyebab malaria quartana dan Plasmodium ovale sebagai penyebab malaria ovale. Penelitian ini bertujuan untuk mengetahui karakteristik pasien dan pola pengobatan penyakit malaria pada pasien malaria di instalasi rawat inap RSUD Kabupaten Mimika periode bulan Juni – Desember 2018. Penelitian ini merupakan penelitian deskriptif dengan pengambilan data secara retrospektif terhadap 68 data rekam medik pasien malaria rawat inap yang memenuhi kriteria inklusi. Jumlah pasien laki-laki lebih banyak dibandingkan perempuan yaitu sebanyak 41 pasien (60,29%). Pasien Malaria kebanyakan berada pada kelompok usia 0-5 tahun sebanyak 30 pasien (44,12%). Jenis malaria yang paling sering terjadi adalah Malaria vivax tanpa komplikasi sebanyak 23 pasien (33,82%). Penggunaan obat pasien paling banyak yaitu Primakuin sebanyak 57 (83,82%) dari total 68 pasien. Persentase ketepatan penggunaan obat yang tepat pasien 100%, tepat obat 89,71%, tepat dosis 92.65%, tepat waktu 97,06% dan tepat rute 100%. Kata kunci : Malaria, Studi Penggunaan Obat, Rawat Inap.
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18

Chu, Cindy S., Germana Bancone, Nay Lin Soe, Verena I. Carrara, Gornpan Gornsawun, and François Nosten. "The impact of using primaquine without prior G6PD testing: a case series describing the obstacles to the medical management of haemolysis." Wellcome Open Research 4 (February 6, 2019): 25. http://dx.doi.org/10.12688/wellcomeopenres.15100.1.

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Radical cure of Plasmodium vivax malaria in glucose-6-phosphate dehydrogenase (G6PD) deficient individuals employs weekly primaquine dosing. This is the only recommended regimen for this patient sub-group. If national malaria programs mandate daily primaquine dosing (the recommended regimen for G6PD normal individuals), then G6PD testing before prescription is necessary to avoid iatrogenic haemolysis in G6PD deficient individuals. In this case series, two P. vivax infected patients with unknown G6PD status from two different countries were prescribed primaquine as per national malaria program guidelines. During treatment both patients presented to the clinic with symptoms of anaemia after taking primaquine incorrectly. The clinical management of the iatrogenic severe haemolysis that occurred in these patients demonstrates the various adverse effects primaquine can cause, that other common medical treatments also have haemolytic potential, and how the diagnosis of G6PD deficiency can be elusive during acute haemolysis. Health care providers should provide careful instructions about primaquine dosing, be watchful for haemolysis, and have a high index of suspicion for G6PD deficiency in the presence of haemolysis if the G6PD status is previously unknown.
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Chu, Cindy S., Germana Bancone, Nay Lin Soe, Verena I. Carrara, Gornpan Gornsawun, and François Nosten. "The impact of using primaquine without prior G6PD testing: a case series describing the obstacles to the medical management of haemolysis." Wellcome Open Research 4 (April 9, 2019): 25. http://dx.doi.org/10.12688/wellcomeopenres.15100.2.

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Radical cure of Plasmodium vivax malaria in glucose-6-phosphate dehydrogenase (G6PD) deficient individuals employs weekly primaquine dosing. This is the only recommended regimen for this patient sub-group. If national malaria programs mandate daily primaquine dosing (the recommended regimen for G6PD normal individuals), then G6PD testing before prescription is necessary to avoid iatrogenic haemolysis in G6PD deficient individuals. In this case series, two P. vivax infected patients with unknown G6PD status from two different countries were prescribed primaquine as per national malaria program guidelines. During treatment both patients presented to the clinic with symptoms of anaemia after taking primaquine incorrectly. The clinical management of the iatrogenic severe haemolysis that occurred in these patients demonstrates the various adverse effects primaquine can cause, that other common medical treatments also have haemolytic potential, and how the diagnosis of G6PD deficiency can be elusive during acute haemolysis. Health care providers should provide careful instructions about primaquine dosing, be watchful for haemolysis, and have a high index of suspicion for G6PD deficiency in the presence of haemolysis if the G6PD status is previously unknown.
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20

Jansongsaeng, Somruedee, Nitipol Srimongkolpithak, Jutharat Pengon, Sumalee Kamchonwongpaisan, and Tanatorn Khotavivattana. "5-Phenoxy Primaquine Analogs and the Tetraoxane Hybrid as Antimalarial Agents." Molecules 26, no. 13 (2021): 3991. http://dx.doi.org/10.3390/molecules26133991.

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The rapid emergence of drug resistance to the current antimalarial agents has led to the urgent need for the discovery of new and effective compounds. In this work, a series of 5-phenoxy primaquine analogs with 8-aminoquinoline core (7a–7h) was synthesized and investigated for their antimalarial activity against Plasmodium falciparum. Most analogs showed improved blood antimalarial activity compared to the original primaquine. To further explore a drug hybrid strategy, a conjugate compound between tetraoxane and the representative 5-phenoxy-primaquine analog 7a was synthesized. In our work, the hybrid compound 12 exhibited almost a 30-fold increase in the blood antimalarial activity (IC50 = 0.38 ± 0.11 μM) compared to that of primaquine, with relatively low toxicity against mammalian cells (SI = 45.61). Furthermore, we found that these 5-phenoxy primaquine analogs and the hybrid exhibit significant heme polymerization inhibition, an activity similar to that of chloroquine, which could contribute to their improved antimalarial activity. The 5-phenoxy primaquine analogs and the tetraoxane hybrid could serve as promising candidates for the further development of antimalarial agents.
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21

Strous, G. J., A. Du Maine, J. E. Zijderhand-Bleekemolen, J. W. Slot, and A. L. Schwartz. "Effect of lysosomotropic amines on the secretory pathway and on the recycling of the asialoglycoprotein receptor in human hepatoma cells." Journal of Cell Biology 101, no. 2 (1985): 531–39. http://dx.doi.org/10.1083/jcb.101.2.531.

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We studied the intracellular transport of secretory and membrane proteins in the human hepatoma cell line HepG-2 infected with vesicular stomatitis virus. Cells were pulse-labeled in the presence of [35S]methionine and chased in the presence of the lysosomotropic agent primaquine. At a concentration of 0.3 mM primaquine effectively inhibited the secretion of albumin and, to a lesser extent, that of orosomucoid and transferrin. The drug also prevented the budding of virus particles at the cell surface. The intracellular transport to the Golgi complex of the membrane protein VSV-G was not affected by primaquine as it acquires resistance to endo-beta-N-acetylglucosaminidase H at the same rate as in control cells. Addition of primaquine at various times after the initiation of the chase period indicates that the effect of primaquine occurs just before secretion. In confirmation of the biochemical data, immunocytochemical localization of albumin in cells treated with NH4Cl demonstrated that albumin accumulated in vesicles at the trans side of the Golgi complex. The effect of primaquine on secretion was also compared with its effect on receptor recycling. The dose-response characteristics of the effect of primaquine on receptor recycling are identical to those of the effects on protein secretion and virus budding. These results indicate that both processes involve the same transport mechanism, and/or that they occur via at least one identical intracellular compartment.
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22

Brito-Sousa, Jose Diego, Thalie C. Santos, Sara Avalos, et al. "Clinical Spectrum of Primaquine-induced Hemolysis in Glucose-6-Phosphate Dehydrogenase Deficiency: A 9-Year Hospitalization-based Study From the Brazilian Amazon." Clinical Infectious Diseases 69, no. 8 (2019): 1440–42. http://dx.doi.org/10.1093/cid/ciz122.

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Abstract Despite glucose-6-phosphate dehydrogenase (G6PD) deficiency prevalence of 5% in the Amazon, primaquine is administered without G6PD screening. This is an important cause of hospitalization among Plasmodium vivax–infected individuals, leading to life-threatening anemia and acute renal failure across endemic areas. In Manaus, the frequency of primaquine-induced hemolysis was 85.2 cases per 100 000 primaquine users.
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23

Dembélé, Laurent, Jean-François Franetich, Valérie Soulard, et al. "Chloroquine Potentiates Primaquine Activity against Active and Latent Hepatic Plasmodia Ex Vivo: Potentials and Pitfalls." Antimicrobial Agents and Chemotherapy 65, no. 1 (2020): e01416-20. http://dx.doi.org/10.1128/aac.01416-20.

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ABSTRACTFor a long while, 8-aminoquinoline compounds have been the only therapeutic agents against latent hepatic malaria parasites. These have poor activity against the blood-stage plasmodia causing acute malaria and must be used in conjunction with partner blood schizontocidal agents. We examined the impacts of one such agent, chloroquine, upon the activity of primaquine, an 8-aminoquinoline, against hepatic stages of Plasmodium cynomolgi, Plasmodium yoelii, Plasmodium berghei, and Plasmodium falciparum within several ex vivo systems—primary hepatocytes of Macaca fascicularis, primary human hepatocytes, and stably transformed human hepatocarcinoma cell line HepG2. Primaquine exposures to formed hepatic schizonts and hypnozoites of P. cynomolgi in primary simian hepatocytes exhibited similar 50% inhibitory concentration (IC50) values near 0.4 μM, whereas chloroquine in the same system exhibited no inhibitory activities. Combining chloroquine and primaquine in this system decreased the observed primaquine IC50 for all parasite forms in a chloroquine dose-dependent manner by an average of 18-fold. Chloroquine also decreased the primaquine IC50 against hepatic P. falciparum in primary human hepatocytes, P. berghei in simian primary hepatocytes, and P. yoelii in primary human hepatocytes. Chloroquine had no impact on primaquine IC50 against P. yoelii in HepG2 cells and, likewise, had no impact on the IC50 of atovaquone (hepatic schizontocide) against P. falciparum in human hepatocytes. We describe important sources of variability in the potentiation of primaquine activity by chloroquine in these systems. Chloroquine potentiated primaquine activity against hepatic forms of several plasmodia. We conclude that chloroquine specifically potentiated 8-aminoquinoline activities against active and dormant hepatic-stage plasmodia in normal primary hepatocytes but not in a hepatocarcinoma cell line.
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&NA;. "Chloroquine/primaquine." Reactions Weekly &NA;, no. 1320 (2010): 17. http://dx.doi.org/10.2165/00128415-201013200-00053.

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&NA;. "Clindamycin/primaquine." Reactions Weekly &NA;, no. 457 (1993): 8. http://dx.doi.org/10.2165/00128415-199304570-00030.

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&NA;. "Dapsone/primaquine." Reactions Weekly &NA;, no. 620 (1996): 6. http://dx.doi.org/10.2165/00128415-199606200-00016.

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Khandelia, Vikash, Pavankumar Pyarsabadi, Umashankar Nama, Saurabh Chittora, Yogesh Swami, and Hemant Richariya. "The potential nephrotoxic effect of single tablet of 15 mg primaquine in G6PD deficient Hadoti region population of India." International Journal of Advances in Medicine 4, no. 2 (2017): 605. http://dx.doi.org/10.18203/2349-3933.ijam20170899.

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Primaquine is used in prevention of relapse of plasmodium vivax and ovale. It is known to cause haemolysis induced acute kidney injury in patients with glucose-6-phosphate dehydrogenase (G-6-PD) enzyme deficiency. Primaquine is widely used in the remote areas of Hadoti region of India by many non-registered practitioners for treatment of febrile illnesses without prior testing of G-6-PD status. Due to this practice, many patients land up with the grave consequences with significant health care burden. We report 8 such cases, which were referred to our hospital, New hospital medical college, Kota, Rajasthan, India. Our study included a series of 8 cases which were referred to our hospital with significantly deranged renal function test due to use of primaquine without prior testing of G-6-PD status. Routine blood investigations including renal function tests and G-6-PD status were measured. In our study, we found that patients with febrile illness and G-6-PD deficiency developed acute kidney injury even with a single tablet of 15 mg of primaquine. The use of even a single dose of 15 mg primaquine may not be safe in population of Hadoti region of India. Hence they should not be exposed to primaquine without prior G-6-PD testing.
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Shah, Naman K., Allan Schapira, Jonathan J. Juliano, et al. "Nonrandomized Controlled Trial of Artesunate plus Sulfadoxine-Pyrimethamine with or without Primaquine for Preventing Posttreatment Circulation of Plasmodium falciparum Gametocytes." Antimicrobial Agents and Chemotherapy 57, no. 7 (2013): 2948–54. http://dx.doi.org/10.1128/aac.00139-13.

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ABSTRACTArtemisinin combination therapies eliminate immaturePlasmodium falciparumgametocytes but not mature gametocytes, which may persist for up to 1 month posttreatment. A single dose of primaquine, which is inexpensive and effective against mature gametocytes, could be added to further reduce the potential for posttreatment parasite transmission. Currently, we have few data regarding the effectiveness or safety of doing so. We collected data from 21 therapeutic efficacy trials of the National Antimalarial Drug Resistance Monitoring System of India conducted during 2009 to 2010, wherein 9 sites used single-dose primaquine (0.75 mg/kg of body weight) administered on day 2 along with artesunate plus sulfadoxine-pyrimethamine (AS+SP) while 12 did not. We estimated the effect of primaquine on posttreatment gametocyte clearance and the total number of gametocyte-weeks as determined by microscopy. We compared the median area under the curve for gametocyte density and reported adverse events. One thousand three hundred thirty-five patients completed the antimalarial drug treatment. Adjusting for region, primaquine increased the rate of gametocyte clearance (hazard ratio, 1.9; 95% confidence interval [CI], 1.1 to 3.3), prevented 45% (95% CI, 19 to 62) of posttreatment gametocyte-weeks, and decreased the area under the gametocyte density curve over the 28-day follow-up compared to AS+SP alone (Pvalue = 0.01). The results were robust to other adjustment sets, and the estimated effect of primaquine increased during sensitivity analysis on the measurement of exposure time. No serious adverse events were detected. In conclusion, the addition of primaquine to AS+SP was effective in reducing the posttreatment presence ofP. falciparumgametocytes. Primaquine was well tolerated and could be administered along with an artemisinin combination therapy as the first-line therapy.
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29

Pukrittayakamee, Sasithon, Joel Tarning, Podjanee Jittamala, et al. "Pharmacokinetic Interactions between Primaquine and Chloroquine." Antimicrobial Agents and Chemotherapy 58, no. 6 (2014): 3354–59. http://dx.doi.org/10.1128/aac.02794-13.

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ABSTRACTChloroquine combined with primaquine has been the standard radical curative regimen forPlasmodium vivaxandPlasmodium ovalemalaria for over half a century. In an open-label crossover pharmacokinetic study, 16 healthy volunteers (4 males and 12 females) aged 20 to 47 years were randomized into two groups of three sequential hospital admissions to receive a single oral dose of 30 mg (base) primaquine, 600 mg (base) chloroquine, and the two drugs together. The coadministration of the two drugs did not affect chloroquine or desethylchloroquine pharmacokinetics but increased plasma primaquine concentrations significantly (P≤ 0.005); the geometric mean (90% confidence interval [CI]) increases were 63% (47 to 81%) in maximum concentration and 24% (13 to 35%) in total exposure. There were also corresponding increases in plasma carboxyprimaquine concentrations (P≤ 0.020). There were no significant electrocardiographic changes following primaquine administration, but there was slight corrected QT (QTc) (Fridericia) interval lengthening following chloroquine administration (median [range] = 6.32 [−1.45 to 12.3] ms;P< 0.001), which was not affected by the addition of primaquine (5.58 [1.74 to 11.4] ms;P= 0.642). This pharmacokinetic interaction may explain previous observations of synergy in preventingP. vivaxrelapse. This trial was registered at ClinicalTrials.gov under reference number NCT01218932.
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30

Somasundaram, B., J. C. Norman, and M. P. Mahaut-Smith. "Primaquine, an inhibitor of vesicular transport, blocks the calcium-release-activated current in rat megakaryocytes." Biochemical Journal 309, no. 3 (1995): 725–29. http://dx.doi.org/10.1042/bj3090725.

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The whole-cell patch-clamp technique was used to study the effect of primaquine, an inhibitor of vesicular transport, on the calcium-release-activated current (Icrac) in rat megakaryocytes. Addition of primaquine, before emptying of internal Ca2+ stores by ionomycin, prevented the development of Icrac, with a half-maximal concentration of near 100 microM. Maximal inhibition (> or = 83%) was observed at 0.6-1 mM primaquine. At 1 mM, chloroquine, a related compound which is less effective at blocking vesicular secretion, had no effect on Icrac. Primaquine (0.8 mM) added after sustained activation of Icrac caused a gradual block of current, with maximal inhibition of 50% observed after 2-3 min. At 1 mM, internal guanosine 5′-[gamma-thio]triphosphate reduced Icrac by 65 +/- 13%. Neither 1 mM GTP nor 2 mM guanosine 5′-[beta-thio]diphosphate had any significant effect on Icrac. The recognized role of GTPases in the regulation of vesicular trafficking, together with block of Icrac activation by primaquine, provide evidence that the channels carrying Icrac may be stored in a vesicular membrane compartment and transferred to the plasma membrane following store depletion.
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31

Bunnag, Danai, Juntra Karbwang, Aurathai Thanavibul, et al. "High dose of primaquine in primaquine resistant vivax malaria." Transactions of the Royal Society of Tropical Medicine and Hygiene 88, no. 2 (1994): 218–19. http://dx.doi.org/10.1016/0035-9203(94)90305-0.

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32

Zorc, Branka, Zrinka Rajić, and Ivana Perković. "Antiproliferative evaluation of various aminoquinoline derivatives." Acta Pharmaceutica 69, no. 4 (2019): 661–72. http://dx.doi.org/10.2478/acph-2019-0048.

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Abstract Four classes of aminoquinoline derivatives were prepared: primaquine ureas 1a–f, primaquine bis-ureas 2a–f, chloroquine fumardiamides 3a–f and mefloquine fumardiamides 4a–f. Their antiproliferative activities against breast adeno-carcinoma (MCF-7), lung carcinoma (H460) and colon carcinoma (HCT 116 and SW620) cell lines were evaluated in vitro, using MTT cell proliferation assay. The results revealed a low activity of primaquine urea and bis-urea derivatives and high activity of all fumardiamides, with IC50 values in low micromolar range against all tested cancer cell lines.
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Chu, Cindy S., Aung Pyae Phyo, Claudia Turner, et al. "Chloroquine Versus Dihydroartemisinin-Piperaquine With Standard High-dose Primaquine Given Either for 7 Days or 14 Days in Plasmodium vivax Malaria." Clinical Infectious Diseases 68, no. 8 (2018): 1311–19. http://dx.doi.org/10.1093/cid/ciy735.

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Chloroquine or dihydroartemisinin-piperaquine with either 7- or 14-day primaquine regimens provided highly effective radical cure of vivax malaria on the Thailand-Myanmar border. Short course higher dose primaquine regimens for vivax malaria radical cure may improve efficacy by improving adherence.
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34

Vale-Costa, Sílvia, Nuno Vale, Joana Matos, et al. "Peptidomimetic and Organometallic Derivatives of Primaquine Active against Leishmania infantum." Antimicrobial Agents and Chemotherapy 56, no. 11 (2012): 5774–81. http://dx.doi.org/10.1128/aac.00873-12.

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ABSTRACTThe current treatment of visceral leishmaniasis is made difficult by the low efficacy, elevated costs, low bioavailability, and high toxicity of many of the available drugs. Primaquine, an antimalarial 8-aminoquinoline, displays activity againstLeishmaniaspp., and several of its derivatives have been developed as potential antileishmanial drugs. However, primaquine exhibits low oral bioavailability due to oxidative deamination of its aliphatic chain. We previously developed peptidomimetic and organometallic derivatives of primaquine, with higher resistance to proteolytic degradation and oxidative deamination, which presented significant activity against primaquine-sensitive pathogens such asPlasmodiumorPneumocystis. In light of these relevant findings, we decided to evaluate these compounds against both the promastigote and intramacrophagic amastigote forms ofLeishmania infantum, the agent of Mediterranean visceral leishmaniasis. We found that several of these compounds had significant activity againstL. infantum. One of the peptidomimetic (3c) and one of the organometallic (7a) derivatives of primaquine were active against the clinically relevant intramacrophagic amastigote form of the parasite, causing >96% reductions in the number of amastigotes per 100 macrophages at 60 and 40 μM, respectively, while being less cytotoxic for host cells than the reference drugs sitamaquine and miltefosine. Hence, compounds 3c and 7a represent new entries toward the development of new antileishmanial leads.
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Lee, Woo-Yul, Dong-Woo Chae, Choon-Ok Kim, et al. "Population Pharmacokinetics of Primaquine in the Korean Population." Pharmaceutics 13, no. 5 (2021): 652. http://dx.doi.org/10.3390/pharmaceutics13050652.

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While primaquine has long been used for malaria treatment, treatment failure is common. This study aims to develop a population pharmacokinetic model of primaquine and its metabolite, carboxyprimaquine, and examine factors influencing pharmacokinetic variability. The data was obtained from a clinical study in 24 Korean subjects randomly assigned to normal and obese groups. The participants received primaquine 15 mg daily for 4 days and blood samples were collected at day 4. Pharmacokinetic modeling was performed with NONMEM and using simulations; the influences of doses and covariates on drug exposure were examined. A minimal physiology-based pharmacokinetic model connected with a liver compartment comprehensively described the data, with CYP450 mediated clearance being positively correlated with the body weight and CYP2D6 activity score (p < 0.05). In the simulation, while the weight-normalized area under drug concentration for primaquine in the obese group decreased by 29% at the current recommended dose of 15 mg, it became similar to the normal weight group at a weight-normalized dose of 3.5 mg/kg. This study has demonstrated that the body weight and CYP2D6 activity score significantly influence the pharmacokinetics of primaquine. The developed model is expected to be used as a basis for optimal malaria treatment in Korean patients.
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36

&NA;. "Doxorubicin/paclitaxel/primaquine." Reactions Weekly &NA;, no. 1291 (2010): 20. http://dx.doi.org/10.2165/00128415-201012910-00060.

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37

&NA;. "Mefloquine/primaquine overdose." Reactions Weekly &NA;, no. 727 (1998): 9–10. http://dx.doi.org/10.2165/00128415-199807270-00026.

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38

&NA;. "Cotrimoxazole/clindamycin/primaquine." Reactions Weekly &NA;, no. 1139 (2007): 10. http://dx.doi.org/10.2165/00128415-200711390-00032.

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39

Jordán de Luna, C., M. Palomo Navarro, M. Pérez Cebrián, and J. L. Poveda Andrés. "Metahemoglobinemia por primaquina." Farmacia Hospitalaria 35, no. 5 (2011): 278–79. http://dx.doi.org/10.1016/j.farma.2010.08.004.

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40

Raman, Jyothi, Shruti Mody, and R. P. Khubchandani. "Primaquine induced Methemoglobinemia." Indian Journal of Pediatrics 70, no. 6 (2003): 521. http://dx.doi.org/10.1007/bf02723149.

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41

Matos, Joana, Filipa P. da Cruz, Élia Cabrita, et al. "Novel Potent Metallocenes against Liver Stage Malaria." Antimicrobial Agents and Chemotherapy 56, no. 3 (2011): 1564–70. http://dx.doi.org/10.1128/aac.05345-11.

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ABSTRACTNovel conjugates of the antimalarial drug primaquine (compound 1) with ferrocene, named primacenes, have been synthesized and screened for their activities against blood stage and liver stage malariain vitroand host-vector transmissionin vivo. Both transmission-blocking and blood-schizontocidal activities of the parent drug were conserved only in primacenes bearing a basic aliphatic amine group. Liver stage activity did not require this structural feature, and all metallocenes tested were comparable to or better than primaquine in this regard. Remarkably, the replacement of primaquine's aliphatic chain by hexylferrocene, as in compound 7, led to a ∼45-fold-higher level activity against liver stage parasitemia than that of primaquine.
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42

Chotivanich, Kesinee, Jetsumon Sattabongkot, Rachanee Udomsangpetch, et al. "Transmission-Blocking Activities of Quinine, Primaquine, and Artesunate." Antimicrobial Agents and Chemotherapy 50, no. 6 (2006): 1927–30. http://dx.doi.org/10.1128/aac.01472-05.

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ABSTRACT The infectivity of Plasmodium falciparum gametocytes after exposure in vitro to quinine, artesunate, and primaquine was assessed in Anopheles dirus, a major vector of malaria in Southeast Asia. Mature gametocytes (stage 5) of a Thai isolate of P. falciparum were exposed to the drugs for 24 h in vitro before membrane feeding to A. dirus. After 10 days, the mosquito midguts were dissected and the oocysts were counted. In this system, artesunate showed the most potent transmission-blocking activity; the mean (standard deviation [SD]) 50% and 90% effective concentrations (EC50, and EC90, respectively, in nanograms per milliliter) were 0.1 (0.02) and 0.4 (0.15), respectively. Transmission-blocking activity of quinine and primaquine was observed at relatively high concentrations (SDs): EC50 of quinine, 642 (111) ng/ml; EC50 of primaquine, 181 (23) ng/ml; EC90 of quinine, 816 (96) ng/ml; EC90 of primaquine, 543 (43) ng/ml. Artesunate both prevents the maturation of immature P. falciparum gametocytes and reduces the transmission potential of mature gametocytes. Both of these effects may contribute to reducing malaria transmission.
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43

Elbashir, Abdalla A., Bahruddin Saad, Abdussalam Salhin Mohamed Ali, and Muhammad Idiris Saleh. "Development of a Capillary Electrophoresis Method for the Enantioselective Estimation of Primaquine in Pharmaceutical Formulations." Journal of AOAC INTERNATIONAL 91, no. 3 (2008): 536–41. http://dx.doi.org/10.1093/jaoac/91.3.536.

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Abstract A capillary electrophoresis (CE) method has been developed that allows the separation and estimation of primaquine enantiomers using hydroxypropyl--cyclodextrin (HP--CD) as a chiral selector. The influence of chemical and instrumental parameters on the separation, such as type and concentration of CD, buffer concentration, buffer pH, applied voltage, capillary temperature, and injection time, were investigated. Good separation of the racemic mixture of primaquine was achieved using a fused-silica capillary (52.5 cm effective length 50 m id) and a background electrolyte composed of tris-phosphate buffer solution (50 mM, pH 2.5) containing 15 mM HP--CD as a chiral selector. The recommended applied voltage, capillary temperature, and injection time were 15 kV, 25C, and 6 s, respectively. Within-day and interday reproducibility of peak area and migration time gave relative standard deviation values ranging from 1.053.30. Good recoveries (range of 96.8104.9) were obtained from the determination of placebos that were spiked with 0.251.00 mg/L primaquine. The proposed CE method was successfully applied to the assay of primaquine diphosphate in pharmaceutical formulations (tablets).
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44

Dijanic, Christopher, Jillian Nickerson, Sunita Shakya, Amanda Dijanic, and Marilyn Fabbri. "Relapsing Malaria: A Case Report of Primaquine Resistance." Case Reports in Infectious Diseases 2018 (2018): 1–3. http://dx.doi.org/10.1155/2018/9720823.

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Primaquine (an 8-aminoquinoline malarial therapy) is the only FDA-approved therapy to treat the hypnozoite stage of P. vivax. We think of relapse occurring because of parasitic resistance or poor compliance secondary to drug toxicities. However, in patients with repeated treatment failure, we must consider CYP-450 mutations affecting drug metabolism as an important cause of relapse. A 47-year-old man who travelled to a jungle in Venezuela was diagnosed with P. falciparum and P. vivax in July 2015. He was treated with seven rounds of primaquine-based therapy in the following year, all resulted in relapse without further exposure to endemic areas. On his eighth presentation, he was found to have CYP-4502D6 mutation that affected the metabolism and activation of primaquine. Thereafter, he was treated without relapse. Primaquine efficacy depends on many factors. Understanding the mechanism responsible for malaria relapse is paramount for successful treatment and reduction in morbidity and mortality. This case illustrates the importance of considering cytochrome mutations that affect drug efficacy in cases of relapsing malaria.
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45

GREGORY, Roland B., and Greg J. BARRITT. "Store-activated Ca2+ inflow in Xenopus laevis oocytes: inhibition by primaquine and evaluation of the role of membrane fusion." Biochemical Journal 319, no. 3 (1996): 755–60. http://dx.doi.org/10.1042/bj3190755.

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The role of membrane fusion in the activation of store-activated Ca2+ channels (SACCs) in the plasma membrane of Xenopus laevis oocytes was investigated with primaquine, an inhibitor of vesicle trafficking, reagents that disrupt the cytoskeleton, and reagents that activate or inhibit the functions of monomeric and trimeric GTP-binding regulatory proteins. Ca2+ inflow was assessed by measuring the rate of increase in the fluorescence of the intracellular Ca2+ chelator fluo-3 after the addition of extracellular Ca2+ to oocytes previously incubated in the absence of added Ca2+. Primaquine inhibited the 3-deoxy-3-fluoro-Ins(1,4,5)P3 (Ins(1,4,5)P3F)-stimulated increase in Ca2+o-induced fluo-3 fluorescence with no detectable effect on the release of Ca2+ from intracellular stores. The effect of primaquine was observed within 1.5 min, showed similarity to the inhibition induced by Gd3+, was reversible, and was observed when primaquine was added either before or after activation of the SACCs. The degree of inhibition of Ca2+ inflow by primaquine was halved when the extracellular concentration of Ca2+ was increased from 3.1 to 12.5 mM. Primaquine also inhibited Ca2+ inflow through cholera toxin-activated divalent cation channels and Drosophila Trpl channels (expressed in oocytes after injection of trpl cRNA). These results indicate that primaquine inhibits open SACCs, possibly by directly inhibiting Ca2+ flow through the channel pore. Colchicine plus cytochalasin B, Brefeldin A, the peptide Arf-1 (2–17) (introduced by microinjection), lovastatin or pertussis toxin did not inhibit the Ins(1,4,5)P3F-stimulated increase in fluo-3 fluorescence. In contrast, guanosine 5´-[γ-thio]triphosphate (GTP[S]), guanosine 5´-[β,γ-imido]triphosphate (p[NH]ppG) and AlF4-, but not guanosine 5´-[β-thio]diphosphate, inhibited the Ins(1,4,5)P3F-stimulated increase in fluo-3 fluorescence. Co-administration of GTP did not prevent the inhibition by GTP[S] or AlF4-. Staurosporine largely prevented the inhibition of store-activated Ca2+ inflow by GTP[S]. It is concluded that membrane fusion processes are unlikely to be involved in the link between the release of Ca2+ from the endoplasmic reticulum and activation of SACCs. The idea that this link is achieved by direct interaction of a protein(s) in the endoplasmic reticulum membrane with the SACC protein is briefly discussed.
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46

Rodrigues, Letícia Norma Carpentieri, Sayuri Pereira Watanabe, and Humberto Gomes Ferraz. "Perfil de dissolução in vitro de comprimidos de primaquina disponíveis para tratamento de malária no Brasil." Revista da Sociedade Brasileira de Medicina Tropical 41, no. 1 (2008): 41–45. http://dx.doi.org/10.1590/s0037-86822008000100008.

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A ineficácia clínica de muitos medicamentos tem servido de alerta para estudos mais profundos sobre os componentes da formulação, processos empregados e características físico-químicas dos fármacos. O objetivo deste trabalho foi avaliar a liberação in vitro de comprimidos de fosfato de primaquina disponíveis no Brasil para tratamento da malária, e o desenvolvimento de novas formulações de liberação convencional. Embora os comprimidos de fosfato de primaquina estudados tenham sido aprovados pelos critérios propostos pela Farmacopéia Americana (2006) para o teste de dissolução, não apresentaram desempenho adequado para o perfil de dissolução, mostrando retenção do fármaco durante a liberação. Os resultados indicam a existência de problemas nos comprimidos de fosfato de primaquina analisados, podendo sugerir como um dos fatores responsáveis pelo aparecimento de resistência dos parasitas.
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47

GIOVANELLA, FRANCIANNE, GABRIELA K. FERREIRA, SAMIRA D. T. DE PRÁ, et al. "Effects of primaquine and chloroquine on oxidative stress parameters in rats." Anais da Academia Brasileira de Ciências 87, no. 2 suppl (2015): 1487–96. http://dx.doi.org/10.1590/0001-3765201520140637.

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Primaquine and chloroquine are used for the treatment of malaria; evidence from the literature suggests that these drugs may induce oxidative stress. In this study we investigated the effects of primaquine and chloroquine on oxidative damage and DNA damage in brain, liver and kidney of rats after 7, 14 and 21 days of administration. Our results demonstrated that primaquine causes DNA damage in brain after 7, 14 and 21 days, and in liver after 7 and 14 days. Moreover, primaquine increases TBARS levels in the kidney and protein carbonyls in the brain after 14 days, and decreases protein carbonyls in the liver after 7 days. Whereas chloroquine causes DNA damage in the kidney after 7 and 14 days, and in the liver after 14 and 21 days, increases TBARS levels in the kidney after 7 days, and decreases TBARS levels in the brain after 21 days. Moreover, decreases protein carbonyls in the liver after 7 and 14 days, and in the brain after 7 and 21 days. However, chloroquine treatment for 14 days increases protein carbonyls in the brain and kidney. In conclusion, these results showed that prolonged treatment with antimalarial may adversely affect the DNA.
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48

Chen, Eugene H., Keiichi Tanabe, Andrew J. Saggiomo, and Edward A. Nodiff. "Modifications of primaquine as antimalarials. 4. 5-Alkoxy derivatives of primaquine." Journal of Medicinal Chemistry 30, no. 7 (1987): 1193–99. http://dx.doi.org/10.1021/jm00390a012.

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49

Heppner, D. Gray. "Primaquine Prophylaxis against Malaria." Annals of Internal Medicine 130, no. 6 (1999): 536. http://dx.doi.org/10.7326/0003-4819-130-6-199903160-00009.

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50

Barry, Michele. "Primaquine Prophylaxis against Malaria." Annals of Internal Medicine 130, no. 6 (1999): 536. http://dx.doi.org/10.7326/0003-4819-130-6-199903160-00010.

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