Coartem has a potential to prolong the QT interval, so combinations with other drugs having that property can cause irregular heartbeat, potentially leading to lethal ventricular fibrillation. The combination with halofantrine, another antimalarial, can cause a life-threatening QT prolongation. Drugs and other substances influencing the activity of the liver enzyme CYP3A4, including grapefruit juice, can either increase or lower blood levels of artemether/lumefantrine, depending on the sort of substance. This can either lead to more severe side effects or to reduced efficiency. History
In 2001, the first fixed dose artemisinin-based combination therapy to meet the World Health Organizations (WHO) pre-qualification criteria for efficacy, safety and quality was created. It is approved in over 80 countries worldwide, including various countries in Africa, as well as Swissmedic, the European Medicines Agency (EMA) and the U.S. Food and Drug Administration (FDA). Society and culture
Access to treatment
Coartem is provided without profit to developing countries using grants from the Global Fund to Fight AIDS, Tuberculosis and Malaria, US Presidents Malaria Initiative along with other donors. Novartis has lowered the price of Coartem by 50% since 2001, increasing access to patients around the world. The first significant price reduction occurred in 2006, when the price of Coartem decreased from an average of US$1.57 to US$1.00. In 2006, due to an improved supply situation for the natural ingredient artemisinin, Novartis was able to undertake the pharmaceutical industrys most aggressive manufacturing scale-up of its kind from 4 million treatments in 2004 to 62 million treatments in 2006.
Frontotemporal dementia (Picks disease)
Gerstmann–Sträussler–Scheinker syndrome
Huntingtons disease
Lytico-bodig disease (ALS complex of Guam)
Multiple system atrophy (Shy–Drager syndrome)
Neuroacanthocytosis
Neuronal ceroid lipofuscinosis
Olivopontocerebellar atrophy
Pantothenate kinase-associated neurodegeneration, also known as neurodegeneration with brain iron accumulation
Parkin mutation (hereditary juvenile dystonia)
Parkinsons disease
Parkinsons disease dementia
Progressive supranuclear palsy
Wilsons disease
X-linked dystonia parkinsonism (Lubag syndrome)

Drug-induced ("pseudoparkinsonism")
About 7% of people with parkinsonism developed symptoms as a result of side effects of medications, mainly neuroleptic antipsychotics especially the phenothiazines (such as perphenazine and chlorpromazine), thioxanthenes (such as flupenthixol and zuclopenthixol) and butyrophenones (such as haloperidol), and rarely, antidepressants. Yet another drug that can induce parkinsonism is the antihistaminic medication cinnarizine, usually prescribed for motion sickness; this is because besides antagonizing histamine receptors this drug antagonizes the dopamine D2 receptors. The incidence of drug-induced parkinsonism increases with age. Drug-induced parkinsonism tends to remain at its presenting level and does not worsen like Parkinsons disease.Implicated medications include:

Antipsychotics
Lithium
Metoclopramide
MDMA addiction and frequent use
Tetrabenazine
Cinnarizine

Infectious
Creutzfeldt–Jakob disease
Encephalitis lethargica
HIV infection and AIDS

Toxins
Evidence exists of a link between exposure to pesticides and herbicides and PD; a two-fold increase in risk was seen with paraquat or maneb/mancozeb exposure.Chronic manganese (Mn) exposure has been shown to produce a parkinsonism-like illness characterized by movement abnormalities. This condition is not responsive to typical therapies used in the treatment of PD, suggesting an alternative pathway than the typical dopaminergic loss within the substantia nigra. Manganese may accumulate in the basal ganglia, leading to the abnormal movements. A mutation of the SLC30A10 gene, a manganese efflux transporter necessary for decreasing intracellular Mn, has been linked with the development of this parkinsonism-like disease.