Evaluation of Amodiaquin (Camoquin) in the Treatment of Relapsing Vivax Malaria

Love, Julian; Foulk, Richard; Williams, Robert G. W.; Mitchell, Ronald B.

doi:10.1097/00000441-195322510-00005

Cited by 1 publication

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“…Most of the reported cases have been associated with ingestion of relatively large doses; in only two other cases has agranulocytosis occurred after the dosage recommended for prophylaxis (cases 3 and 4, Booth et al, 1967). The pharmacology of amodiaquine is similar to that of chloroquine (Love et al, 1953;Goodman and Gilman, 1970;Grollman and Grollman, 1970). A plasma level of between 0-15 and 0-25 ,ug/ml would be expected after a single dose of 300 mg base, falling to between 0-02 and 0 04 vg/ml before the next dose one week later (Goodman and Gilman, 1970).…”

Section: Discussionmentioning

confidence: 99%

“…Of the 4-aminoquinolone antimalarials, amodiaquine (Love et al, 1953;Kennedy, 1955;Glick, 1957;Perry et al, 1962;Booth et al, 1967) and hydroxychloroquine (Polano et al, 1965;Chernof and Taylor, 1968) have been reported to cause agranulocytosis. Most of the reported cases have been associated with ingestion of relatively large doses; in only two other cases has agranulocytosis occurred after the dosage recommended for prophylaxis (cases 3 and 4, Booth et al, 1967).…”

Section: Discussionmentioning

confidence: 99%

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Amodiaquine-induced Agranulocytosis: Toxic Effect of Amodiaquine in Bone Marrow Cultures In Vitro

Lind¹,

Levi²,

Vincent³

1973

BMJ

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1971; Slapak et al., 1971) and our own findings make it possible to construct a probable sequence of events in the hyperacute rejection process. The first change appears to be damage to the capillary endothelium presumably by an antibody antigen complex with subsequent binding of complement. This is followed by platelets adhering to the damaged endothelium and subsequent aggregation in the glomerular and peritubular capillaries. Substances released from these damaged platelets could result in the intense vasoconstriction, which together with the platelet plugs themselves could cause acute haemostasis and immediate rejection. Thrombosis is probably a later and secondary change.The action of heparin in prolonging graft survival is probably due to its direct effect on the platelets. This is consistent with our findings of a reduced fall in the platelet count in the heparintreated dogs. Linn et al. (1971) suggested that substances released by the breakdown of complement contribute to the vasoconstriction during acute rejection. For this reason we established that our heparin preparation was free from anticomplementary activity. Modification of the rejection process with aspirin or cyproheptadine hydrochloride (Periactin) could also be explained by their antagonism to platelet aggregation (O'Brien, 1968; Burrows et al., 1970).

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Section: Discussionmentioning

confidence: 99%