ABSTRACT
BACKGROUND: Plasmodium vivax malaria is a leading cause of morbidity in Ethiopia. The first-line treatment for P. vivax is chloroquine (CQ) and primaquine (PQ), but there have been local reports of CQ resistance. A clinical study was conducted to determine the efficacy of CQ for the treatment of P. vivax malaria in southern Ethiopia. METHODS: In 2021, patients with P. vivax mono-infection and uncomplicated malaria were enrolled and treated with 25 mg/kg CQ for 3 consecutive days. Patients were followed for 28 days according to WHO guidelines. The data were analysed using per-protocol (PP) and KaplanâMeier (KâM) analyses to estimate the risk of recurrent P. vivax parasitaemia on day 28. RESULTS: A total of 88 patients were enrolled, 78 (88.6%) of whom completed the 28 days of follow-up. Overall, 76 (97.4%) patients had adequate clinical and parasitological responses, and two patients had late parasitological failures. The initial therapeutic response was rapid, with 100% clearance of asexual parasitaemia within 48 h. CONCLUSION: Despite previous reports of declining chloroquine efficacy against P. vivax, CQ retains high therapeutic efficacy in southern Ethiopia, supporting the current national treatment guidelines. Ongoing clinical monitoring of CQ efficacy supported by advanced molecular methods is warranted to inform national surveillance and ensure optimal treatment guidelines.
Subject(s)
Antimalarials , Chloroquine , Malaria, Vivax , Malaria, Vivax/drug therapy , Chloroquine/therapeutic use , Ethiopia , Humans , Antimalarials/therapeutic use , Male , Adult , Female , Adolescent , Young Adult , Child , Middle Aged , Child, Preschool , Plasmodium vivax/drug effects , Treatment Outcome , Aged , Parasitemia/drug therapyABSTRACT
Organ dysfunction after cardiopulmonary bypass (CPB) still is a major problem in patients undergoing cardiovascular surgery. Studies have demonstrated that systemic inflammatory response (SIR) remains one of the major causes of CPB-associated organ injury. The mechanism of SIR during CPB includes the interaction of blood and artificial surface and endotoxemia. The interaction of blood and artificial surface is initiated by protein adsorption. As a result of series of chain reactions, the numerous powerful inflammatory mediators, including hormones and autacoids, are formed and released. Subsequently, the contact system, coagulation system, complement system, fibrinolysis system, and leukocytes, platelets, and endothelial cells, are all activated to participate in the interaction of blood and artificial materials. These activations of different systems and blood cells can interact and magnify each other. CPB-associated endotoxemia has been demonstrated to intensify and deteriorate SIR during CPB. SIR leads to organ injury. In clinical setting, the most common SIR-related organ damage is pulmonary dysfunction, which often is manifested by decreasing of lung compliance, rise in shunt fraction, work of breathing, and likelihood of atelectasis and pneumonia. Strategies to control CPB-related SIR have been developed, such as improvement of biocompatibility of artificial surface (new biomaterials), temporary inhibition of blood cells activation ("blood anesthesia") during CPB, and blockage of the bioactivities and effects of inflammatory mediators.