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Welcome Message Case#2: How the Pharmacist Talk with the Patient Medication Errors Corner: References. A physician prescribed Candesartan for a patient for his hypertension; the pharmacist dispensed the antiemetic Ondansetron instead of Candesartan. N.B. Candesartan Atacand ; : Angiotensin II Receptor Antagonist. UNDCP is committed to facilitate this process of change by continuing to provide a forum for policy consultations open to the civil society and the private sector. Through reports such as the Global Studies in Illicit Drug Markets, we hope to improve our services to analyse the trends of drug production, trafficking and abuse as well as the impact of drug control actions. In doing so we shall offer a neutral and excellent information base that policy-makers can utilise in order to decide appropriate strategies. Such studies will make drug control policy more transparent and credible to all parties, and will encourage more vital parts of the institutions and society to join the effort. These two paradigm shifts are creating a new drug control framework. This framework is gaining ground but it has yet to be consistently recognised and implemented throughout the whole region. Atacand is used to treat high blood pressure.

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The absorption, distribution, metabolism and excretion of DEHP have been extensively studied in rats, primarily after oral exposure, although disposition following inhalation, dermal, and intravenous exposures have been studied to a limited degree. Primates absorb DEHP from the gut less readily than rodents Rhodes, et al., 1982 ; . Younger animals may absorb DEHP to a greater degree than adults Gray and Gangolli, 1986 ; . Once absorbed, DEHP is widely distributed throughout the body. Fat, absorptive organs gastrointestinal tract ; and excretory organs liver, kidney, gastrointestinal tract ; are the major initial repositories for DEHP Kluwe, 1982 and KemI, 1998 ; . The heart, spleen, reproductive organs, lungs, muscles, and brain have also been shown to be repositories for DEHP and its metabolites KemI, 1998, Jaeger and Rubin, 1972 ; . Distribution of DEHP appears to be qualitatively similar across species KemI, 1998 ; . Distribution of the primary DEHP metabolites, while less well studied, is likely to be similar to that of DEHP Klewe, 1982, KemI, 1998 ; . Several studies indicate that DEHP can cross the placental barrier and distribute into fetal tissues. After a single dose of DEHP was administered to pregnant female rats, DEHP appeared in the placenta, fetal tissue and amniotic fluid within 24 hours Singh, et al., 1975, as cited in USCPSC, 1985 and KemI, 1998 ; . DEHP can also be distributed through breast milk into infants KemI, 1998 ; . Metabolism is the process of modifying a substance in the body so that it is more easily excreted for example, breaking it down into smaller molecules or making it more water soluble ; . The extent to which different DEHP metabolites are produced and excreted depends upon the species, the age of the animal, prior exposure to DEHP, the amount of DEHP administered, and the administation route KemI, 1998 ; . High levels of administered DEHP may saturate liver biotransformation capacity Syracuse Research, 1982 ; . DEHP is initially broken down to mono-ethylhexyl phthalate MEHP ; and 2-ethylhexanol 2-EH ; , primarily by hydrolysis in the lining of the intestinal tract. However, hydrolysis also occurs in the kidneys, lungs, plasma, pancreas and fat. Researchers have proposed that the toxicity of phthalates is governed to a great degree by the properties of these hydrolysis products, particularly MEHP Lake, et al., 1977, Foster, 1997, Li, et al., 1998 ; . Lake, et al. 1977 ; , concluded that the hydrolysis of phthalates is qualitatively similar between the rat, the ferret, the baboon, and humans, though it may differ somewhat quantitatively. These researchers suggested that all three animal models studied would be suitable for assessing the toxicity of phthalate diesters to humans. Approximately 80% of an oral dose of DEHP in rats undergoes hydrolysis into MEHP and 2ethylhexanol, while only about 1% of intravenously administered DEHP is converted Pollack, et al., 1985 ; . This means that intravenous exposure to DEHP may lead to less MEHP exposure and therefore less toxicity than an orally administered dose. Despite this, DEHP in stored blood has been demonstrated to undergo at least some hydrolysis to MEHP Vessman and Rietz, 1978, Sjoberg, et al., 1985a, b, Huber, et al., 1996 ; . MEHP has also been identified in the blood and tissues of human adults undergoing hemodialysis and neonates undergoing exchange transfusions Pollack, et al., 1985a, Sjoberg, et al., 1985 a, b ; . Pollack et al. 1985a ; found that time averaged circulating concentrations of MEHP during dialysis were similar to those of DEHP, which might be explained by altered metabolism of DEHP during renal failure or slow biotransformation after systemic intake of DEHP. Thus, humans are exposed to MEHP as a result of exposures from DEHP-containing medical devices. The liver appears to be the main organ for further metabolism of MEHP and 2-EH, occurring through many pathways, which differ across species. The organ toxicity of each of these metabolites, numbering more than 10, is largely unknown. Rats and mice metabolize MEHP and 2-EH primarily by and candesartan.

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Sales of SelokenTM Toprol-XLTM were up 21 percent in the first quarter, chiefly on the 24 percent increase in sales of Toprol-XLTM in the US. Sales for AtacandTM were up 7 percent in the first quarter. Sales outside the US were up 19 percent. Total prescriptions for AtacandTM in the US were down 9 percent, but reported sales were down 18 percent as a result of wholesaler stocking in the first quarter 2004. On 23 February, AtacandTM became the first angiotensin receptor blocker in the US to receive regulatory approval for heart failure, based on data that showed reductions in both cardiovascular mortality and hospitalisations in patients with heart failure. CrestorTM sales in the first quarter were 3 million, up 106 percent versus the first quarter last year. Sales in the last 12 months reached , 052 million. In markets outside the US, CrestorTM sales were 9 million in the quarter. Volume share of the statin market is now at double-digit levels in Canada 12.2 percent ; , Italy 11.8 percent ; , and the Netherlands 10.4 percent ; . Good progress continues in France, with market share reaching 5.0 percent in the latest month. Market share in the UK is 3.5 percent, down slightly from that reported at the year end and clomiphene. Neither merck nor pfizer was able to prove that their painkillers were substantially different from older medicines, wolfe said.

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Brewer, G.J. 1976 ; A view of the current status of antisickling therapy. Am. J. Hematol., 1, 121-128. Luskey, K.L. et al 1980 ; New approaches to the therapy of sickle cell disease. Tex. Rep. Biol. Med., 40, 305-312. Vichinsky, E.P. et al 1980 ; Sickle cell anaemia and related haemoglobinopathies. Pediatr. Clin. North Am., 27, 429-447. Bookchin, R.M. et al 1983 ; Red cell membrane abnormalities in sickle cell anaemia. Prog. Hematol., 13, 1-23. Chang, H. et al 1983 ; Comparative evaluation of fifteen anti-sickling agents. Blood, 61, 693-704. Warth, J.A. et al 1983 ; The increasing complexity of sickle cell anaemia. Prog. Hematol., 13, 25-47. Alavi, J.B. 1984 ; Sickle cell anaemia. Pathophysiology and treatment. Med. Clin. North Am., 68, 545-556. Aluoch, J.R. 1984 ; The treatment of sickle cell disease. A historical and chronological literature review of the therapies applied since 1910. Trop. Geogr. Med., 36, S1-26. Benjamin, L.J. 1989 ; Membrane modifiers in sickle cell disease. Ann. N. Y. Acad. Sci., 565, 247-261. Manning, J.M. 1991 ; Covalent inhibitors of the gelation of sickle cell haemoglobin and their effects on function. Adv. Enzymol. Relat. Areas. Mol. Biol., 64, 55-91. Buchanan, G.R. 1993 ; Sickle cell disease: recent advances. Curr. Probl. Pediatr., 23, 219-29. Cho, Y.W. et al 1996 ; Clinical Pharmacology for Pediatricians. II. Antisickling agents, with special reference to new vasoerythroactive drugs. J. Clin. Pharmacol. 22, 1-13.
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