Plasmochin Toxicity: Analysis of 258 Cases

M, Hardgrove; Applebaum, Irving L.

doi:10.7326/0003-4819-25-1-103

Cited by 20 publications

(7 citation statements)

References 2 publications

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“…8AQs for which there are clinical data and for which published data are available from Rhesus monkeys include pamaquine, pentaquine and PQ. Pamaquine, used before the discovery of PQ, was customarily given at 10–20 mg doses 3 times a day for 5 days [ 22 ]. Pentaquine and isopentaquine were the subject of considerable investigation after World War II before PQ was discovered.…”

Section: Neurologic Toxicity Of 8aqs In Rhesus Monkeysmentioning

confidence: 99%

“… Data from [ 1 – 3 , 22 ] MED refers to the minimum effective dose for radical cure of P. cynomolgi in Rhesus monkeys in combination with a blood schizonticide All doses are the cumulative dose, i.e. the mg/kg/day × number of days dosed MND the minimum cumulative neurotoxic dose causing neurodegeneration or neurologic clinical signs, NA not appilicable, NTI neurologic therapeutic index NTI = MND/MED a Same neurologic signs as outlined in Column 3 …”

Section: Neurologic Toxicity Of 8aqs In Rhesus Monkeysmentioning

confidence: 99%

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Tafenoquine and primaquine do not exhibit clinical neurologic signs associated with central nervous system lesions in the same manner as earlier 8-aminoquinolines

Berman

Brown

Dow

et al. 2018

Malar J

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BackgroundTafenoquine was recently approved for Plasmodium vivax radical cure (KRINTAFEL™) and malaria prevention (ARAKODA™).MethodsA review of the non-clinical and clinical literature was conducted to assess whether tafenoquine (and primaquine) exhibit the same neurologic lesions and associated clinical signs as earlier 8-aminoquinolines, as has been alleged in recent opinion pieces.ResultsPlasmocid, pamaquine and pentaquine damage specific neuro-anatomical structures in Rhesus monkeys and humans leading to corresponding deficits in neurologic function. Neurologic therapeutic indices for these 3 drugs calculated based on monkey data were well correlated with human data. Despite 60 years of use, there is no evidence that primaquine exhibits similar neurotoxicity in humans.Discussion/conclusionsExtrapolation of data from Rhesus monkeys to humans, and the available clinical data, suggest that tafenoquine also does not exhibit pamaquine, pentaquine or plasmocid-like clinical neurologic signs in humans.

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Section: Neurologic Toxicity Of 8aqs In Rhesus Monkeysmentioning

confidence: 99%

Section: Neurologic Toxicity Of 8aqs In Rhesus Monkeysmentioning

confidence: 99%

Tafenoquine and primaquine do not exhibit clinical neurologic signs associated with central nervous system lesions in the same manner as earlier 8-aminoquinolines

Berman

Brown

Dow

et al. 2018

Malar J

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show abstract

“…In use as an antimalarial since the late 1920s (Hardgrove and Applebaum, 1946), a large review of 258 cases of toxic reactions to the drug failed to identify any symptoms suggestive of CNS toxicity (Hardgrove and Applebaum, 1946). However, pamaquine was found in some users to induce similar symptoms of vertigo and photophobia (U.S.…”

Section: Historical Evidence Of Quinoline Cns Toxicitymentioning

confidence: 99%

Idiosyncratic quinoline central nervous system toxicity: Historical insights into the chronic neurological sequelae of mefloquine

Nevin¹

2014

International Journal for Parasitology: Drugs and Drug Resistan

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“…The 8-aminoquinolines were among the first synthetic quinoline anti-malarials. Pamaquine (also known as plasmochin), developed by German scientists [ 222 , 223 ], and in use since the 1920s [ 224 ] was initially thought to be free of CNS toxicity, but a fatal case of fatal human toxicity, marked by symptoms of apprehension and restlessness, revealed evidence of extensive brain and brainstem neurotoxicity [ 225 ]. By the late 1940s, other synthetic 8-aminoquinoline anti-malarials in common use prior to WWII, or introduced during the WWII drug development effort, had been linked to a severe neurotoxic syndrome [ 226 – 228 ], potentially masking more subtle psychiatric effects, such as previously reported mild psychosis [ 229 , 230 ].…”

Section: Introductionmentioning

confidence: 99%

Psychiatric effects of malaria and anti-malarial drugs: historical and modern perspectives

Nevin

Croft

2016

Malar J

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The modern medical literature implicates malaria, and particularly the potentially fatal form of cerebral malaria, with a risk of neurocognitive impairment. Yet historically, even milder forms of malaria were associated in the literature with a broad range of psychiatric effects, including disorders of personality, mood, memory, attention, thought, and behaviour. In this article, the history of psychiatric effects attributed to malaria and post-malaria syndromes is reviewed, and insights from the historical practice of malariotherapy in contributing to understanding of these effects are considered. This review concludes with a discussion of the potentially confounding role of the adverse effects of anti-malarial drugs, particularly of the quinoline class, in the unique attribution of certain psychiatric effects to malaria, and of the need for a critical reevaluation of the literature in light of emerging evidence of the chronic nature of these adverse drug effects.

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Plasmochin Toxicity: Analysis of 258 Cases

Cited by 20 publications

References 2 publications

Tafenoquine and primaquine do not exhibit clinical neurologic signs associated with central nervous system lesions in the same manner as earlier 8-aminoquinolines

Tafenoquine and primaquine do not exhibit clinical neurologic signs associated with central nervous system lesions in the same manner as earlier 8-aminoquinolines

Idiosyncratic quinoline central nervous system toxicity: Historical insights into the chronic neurological sequelae of mefloquine

Psychiatric effects of malaria and anti-malarial drugs: historical and modern perspectives

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