Soosamma Varghese, SEPT, Weller Wing, Ampthill Road, Bedford, Bedfordshire, UK.
Although as an element PI3K phosphorylation Lithium had been discovered in the 1800s and used in the fields of rheumatology and psychiatry since this time, it was not until 1949 that the first academic work on lithium in psychiatry appeared. This work showed that lithium had a significant effect in a case

series of 10 patients with mania presenting with ‘psychotic excitement’ [Garrod, 1859; Lange, 1886; Cade, 1949; Schioldann, 2011]. By 1950 a hospital-based trial had led to the development of indicators for safe lithium doses and initial signs of toxicity, including gastric disturbances, muscular Inhibitors,research,lifescience,medical weakness, ataxia and slurred speech [Ashburner, 1950; Noack and Trautner, 1951; Malhi and Gershon, 2009]. However, by 1951 lithium’s use in medicine had been somewhat discredited by reports of deaths

in the USA and Australia after the widespread use of lithium salts as a table salt substitute [Corcoran Inhibitors,research,lifescience,medical and Taylor, 1949]. Despite being somewhat discredited by the early 1970s, lithium was first registered by the US Food and Drug Administration (FDA) for long-term prophylactic use in bipolar disorder with approval in the UK occurring by 1985 [FDA, 2012]. Lithium has since been licensed in the UK for the treatment and prophylaxis of mania and hypomania, prophylactic treatment of recurrent affective disorders, treatment of recurrent bipolar depression when the use of alternative antidepressants Inhibitors,research,lifescience,medical has been ineffective, and the treatment of aggressive or self-mutilating Inhibitors,research,lifescience,medical behaviour [Norgine Ltd, 2011; Rosemont Pharmaceuticals Ltd, 2011; Sanofi-Aventis, 2012]. Renal function is import for the elimination

of lithium, as it is primarily renally excreted, and a declining estimated glomerular filtration rate (eGFR) will increase any Inhibitors,research,lifescience,medical risks of lithium intoxication due to accumulation. Although a little evidence supports the theory that lithium is responsible for progressive glomerular damage, there are still conflicting opinions of the effect of long-term lithium use on eGFR [Waller and Edwards, 1985; Tredget et al. 2010]. Most evidence suggests that although there is not a definitive correlation between lithium therapy and glomerular function decline leading to renal failure, there does appear to be some association between lithium therapy and urinary concentrating ability [McKnight et al. 2012]. Only a small number of patients on long-term lithium therapy Org 27569 go on to develop renal insufficiency or end-stage renal disease caused by lithium [Coşkunol et al. 1997; Markowitz et al. 2000; Tredget et al. 2010]. Lithium monitoring in the UK Until 2003 with the publication of the British Association of Psychopharmacology (BAP) guidelines and later in 2006 with the National Institute for Health and Clinical Excellence (NICE) bipolar guidance there were no nationally recognized guidelines covering lithium monitoring outside of the recommendations in the BNF [NICE, 2006; BAP, 2009].

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