[Crystal meth - a new kid on the block]. / Crystal meth ­ een nieuwkomer.

In this article we describe epidemiological, pharmacological and clinical aspects of abuse of metamphetamines, also known as crystal meth. These aspects are illustrated by two cases of methamphetamine abuse and the complications associated with it. Metamphetamine abuse is often associated with sexual activity, a combination known as 'chemsex'. A chronic addiction to chemsex can have devastating effects on the user's social, psychological, and physical wellbeing. We describe a patient suffering from recurrent relapses in his addiction to chemsex. Acute crystal meth intoxications can result in very serious complications. We describe a patient suffering from severe neurological complications and rhabdomyolysis.

Towards elimination of parent-to-child transmission of syphilis in India: a rapid situation review to inform national strategy.

In February 2015, India's National AIDS Control Organisation, Ministry of Health and Family Welfare, launched a national strategy towards elimination of parent-to-child transmission (E-PTCT) of syphilis, with a goal to reduce the incidence of congenital syphilis to 0.3 cases per 1000 live births by 2017. As part of the development of the national strategy, a rapid situation analysis was undertaken to ascertain the current practices, challenges and barriers for E-PTCT of syphilis in India. The analysis was conducted during February and March 2014 in five states selected from five different regions of India. Key informant interviews were conducted with key stakeholders at facility, state and district level. Content analysis was used to identify the themes. Key barriers identified for E-PTCT of syphilis were: low priority for antenatal syphilis testing among providers, limited access to testing, untrained human resources, shortage of test kits and benzathine penicillin, nonadherence to the national protocol for syphilis testing, and poor recording and reporting of antenatal syphilis data. The analysis also identified opportunities for functional integration of E-PTCT within existing maternal and child health programmes. Health-care providers and programme managers expressed a need for training in the programme for E-PTCT of syphilis. The situation analysis identified that, for successful implementation of E-PTCT of syphilis, it is essential that state and district programme managers adopt this initiative; coordinate the programme; plan for an adequate budget in their programme implementation plan; ensure an uninterrupted supply of standardized diagnostics kits and drugs at all levels of health care; and adhere to E-PTCT guidelines when implementing the programme.

Hepatitis C virus core protein, cytochrome P450 2E1, and alcohol produce combined mitochondrial injury and cytotoxicity in hepatoma cells.

BACKGROUND & AIMS: Alcohol consumption exacerbates liver injury in chronic hepatitis C, and enhanced mitochondrial oxidative stress is one possible mechanism. The aim of this study was to determine whether hepatitis C virus core protein and alcohol-inducible cytochrome P450 2E1 contribute to reactive oxygen species production and cytotoxicity in human hepatoma cells. METHODS: Huh-7 cells expressing core protein, cytochrome P450 2E1, or both were exposed to 0.1 mmol/L tertiary butyl hydroperoxide, tumor necrosis factor alpha, and/or 25 mmol/L ethanol. Cytotoxicity, reactive oxygen species production, glutathione content, and mitochondrial membrane potential were measured. RESULTS: Expression of core/cytochrome P450 2E1 synergistically enhanced cell death induced by either tertiary butyl hydroperoxide or tumor necrosis factor alpha. After tertiary butyl hydroperoxide treatment, total reactive oxygen species production was increased more than 3-fold compared with cells that did not express core and cytochrome P450 2E1. Mitochondrial depolarization and reduced glutathione depletion occurred as well, and cell death was prevented by inhibition of mitochondrial permeability transition or caspase activity. Confocal microscopy showed that the mitochondria themselves were the origin of the reactive oxygen species. In the absence of core/cytochrome P450 2E1 expression, mitochondrial changes and cell death did not occur. Ethanol treatment further decreased mitochondrial reduced glutathione content and exacerbated mitochondrial reactive oxygen species production, depolarization, and cell death. All these effects were prevented by the antioxidant N -acetylcysteine. CONCLUSIONS: Mitochondrial reactive oxygen species production is induced by hepatitis C virus core and cytochrome P450 2E1, resulting in a reduction of mitochondrial antioxidant capacity and sensitivity to oxidants and tumor necrosis factor alpha. Alcohol further depletes mitochondrial reduced glutathione, which exacerbates depolarization and cell death. Sensitization of mitochondria to oxidative insults is thus a potential mechanism for alcohol-related exacerbation of liver injury in chronic hepatitis C.