Environmental Fate and Toxicology of Dimethoate.

The insecticide dimethoate, an organophosphate, was first introduced in 1962 for broad spectrum control of a wide range of insects including mites, flies, aphids, and plant hoppers. It inhibits AChE activity, resulting in nerve damage, which may lead to death. It is considered highly toxic to insects although dimethoate resistance has been observed. Dimethoate has both a low vapor pressure (0.247 mPa) and Henry's law constant (l.42x10(-6) Pa m3/mol), thus volatilization is not a major route of dissipation from either water or moist soils. Photolysis is considered a minor dissipation pathway. However, studies have shown that in the presence of a catalyst, the rate of photolysis does increase. The insecticide has high water solubility (39,800 mg/L) and under alkaline conditions, hydrolysis predominates representing a major degradation pathway. It has a low soil sorption capacity (Koc=20) which varies by soil type and organic matter content. Dimethoate is degraded by microbes under anaerobic conditions and bacterial species have been identified that are capable of using dimethoate as a carbon source. Although many intermediate by-products have been identified by abiotic and biotic processes, the major degradation product is omethoate. Dimethoate has been found to adversely impact many organisms. In plants, photosynthesis and growth are highly impacted, whereas birds exhibit inhibition in brain enzyme activity, thus sublethal effects are apparent. Furthermore, aquatic organisms are expected to be highly impacted via direct exposure, often displaying changes in swimming behavior. Toxicity results include inhibition in growth and more importantly, inhibition of acetylcholinesterase activity.

Real-life outcomes of maraviroc-based regimens in HIV-1-infected individuals.

PURPOSE: The use of maraviroc in our unit was reviewed with regard to efficacy and safety and also reviewed with regard to how our experience reflects the data presented in clinical trials. METHODS: We utilized the pharmacy dispensary system to identify any patient dispensed maraviroc and conducted a case note review. RESULTS: We identified 27 patients who have been prescribed maraviroc as part of their antiretroviral treatment. In all, 81% were men and 81% were white British. There were 26 treatment-experienced patients and 1 treatment-naive patient. At the time of switching to maraviroc, 17 patients had detectable HIV viral loads and 10 had HIV RNA levels <40 copies/mL. At completion, 6 undetectable patients maintained undetectability and 10 viremically detectable patients achieved viral suppression. Maraviroc was discontinued in 18.5% of patients and the only adverse drug reaction reported was a rash. CONCLUSIONS: The experience of using maraviroc by our study participants shows similarity in terms of efficacy and safety to the MERIT and MOTIVATE clinical trials.

Managing hepatitis B/HIV co-infected: adding entecavir to truvada (tenofovir disoproxil/emtricitabine) experienced patients.

BACKGROUND: Combination emtricitabine (FTC) or lamivudine (LAM) with tenofovir disoproxil (TDF) is the recommended first-line regime for treatment in chronic hepatitis B virus (HBV)/HIV co-infection. However, in those failing to suppress, few data exist regarding further management. In HBV/HIV co-infection, there are no published data describing outcomes when entecavir (ETV) is then added to TDF-based regimes in patients no longer suppressing their HBV. We report the first series of patients using ETV with truvada-based HAART in HBV/HIV co-infected patients with previous HBV therapy failure, including inadequate suppression. METHODS: A prospective observational study. RESULTS: Thirteen HIV/HBV co-infected patients (all male, hepatitis B e antigen positive and hepatitis B e antibody negative) were commenced on ETV in addition to background truvada. All patients were previously exposed to LAM or FTC and TDF (median 53 months, range 6−123). Seven patients had LAM monotherapy prior to TDF/LAM or FTC combination; the remaining six patients were exposed to FTC or LAM and TDF combination. Median time of follow-up was 74 weeks (range 16−159) and median HBV decline was 2.53 log(10) IU/ml (range 1.28−7.36). Thirty-eight percent of patients achieved undetectable HBV DNA level by the end of the study and eight of 13 (62%) achieved normal alanine aminotransferase (ALT) levels with median reduction −28 U/l (range −152 to 37). TDF was stopped in one patient because of renal toxicity. ETV was well tolerated with no change of estimated glomerular filtration rate during the study. CONCLUSION: Entecavir can be considered in addition to TDF/FTC in HBV/HIV co-infected treatment-experienced patients failing to fully suppress their HBV viral load.

Milk alkali syndrome associated with excessive ingestion of Rennie: case reports.

Milk alkali syndrome is a cause of hypercalcaemia, renal failure and alkalosis, and is potentially reversible if detected early and the calcium and alkali source withdrawn. It was originally described in patients ingesting large amounts of calcium containing milk for the treatment of peptic ulcer disease. We present a modern day version of the syndrome in three cases which were associated with excessive intake of Rennie, a calcium carbonate containing antacid.