Drugs
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Lanthanum carbonate is a novel, non-aluminium, non-calcium phosphate binding agent that forms a water-insoluble compound, lanthanum phosphate, in the gut. Lanthanum carbonate (elemental lanthanum 375-3000 mg/day) reduced serum phosphorus levels compared with placebo in two randomised, double-blind, multicentre 4-week trials in patients with chronic renal failure receiving regular haemodialysis. In two large, randomised trials in patients with chronic renal failure requiring haemodialysis, lanthanum carbonate (elemental lanthanum 375-3000 mg/day) was as effective as calcium carbonate and/or other conventional phosphate binders in reducing and maintaining serum phosphorus levels (< or =5.6 mg/dL over 6 months and < or =5.9 mg/dL over 2 years). ⋯ Most adverse events were mild-to-moderate in severity, with gastrointestinal events being the most common. The tolerability profile of lanthanum carbonate was similar to those of conventional phosphate binders; however, hypercalcaemic episodes occurred significantly less frequently over 6 months with lanthanum carbonate than with calcium carbonate. In a randomised 1-year trial, numerically fewer lanthanum carbonate (elemental lanthanum < or =3750 mg/day) recipients had renal bone disease at study end than at baseline; however, in the calcium carbonate < or =9000 mg/day group, numerically more patients had renal bone disease at study end compared with baseline.
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The US FDA has approved two drugs for the management of intermittent claudication: pentoxifylline and cilostazol. The mechanism of action that provides symptom relief with pentoxifylline is poorly understood but is thought to involve red blood cell deformability as well as a reduction in fibrinogen concentration, platelet adhesiveness and whole blood viscosity. The recommended dose of pentoxifylline is 400 mg three times daily with meals. ⋯ Policosanol is a mixture of fatty alcohols derived from honeybee wax which, according to very limited data, reduces symptoms of claudication. Amino acids, certain peptides and prostaglandins may have a therapeutic role. Finally, novel approaches including angiogenesis mediated by growth factors, are currently under investigation.
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In recent years, serious skin and soft tissue infections (SSTIs) caused by multidrug resistant pathogens have become more common. While the majority of SSTIs are caused by Staphylococcus aureus or beta-haemolytic streptococci that are methicillin/oxacillin susceptible, the emergence of methicillin-resistant and vancomycin-resistant community-acquired and nosocomial Gram-positive pathogens has created a need for different therapeutic agents, such as linezolid, quinupristin/dalfopristin, daptomycin, and newer generation carbapenems and fluoroquinolones. This review focuses on agents presently in clinical development for the treatment of SSTIs caused by Gram-positive pathogens such as staphylococci, streptococci and enterococci including methicillin-resistant S. aureus (MRSA) and vancomycin-resistant enterococci (VRE). ⋯ With their long half-lives, these agents have an advantage of less frequent dose administration with more rapid bactericidal activity and less likelihood for development of resistance. However, because of their proven activity against highly resistant organisms, these antibacterial agents should be reserved only for life-threatening situations and/or when resistant pathogens are suspected. Rational antimicrobial use coupled with awareness of infection control measures is paramount to avert the emergence of multidrug-resistant organisms.
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There are three stages in the management of gout: (i) treating the acute attack; (ii) lowering excess stores of uric acid to prevent flares of gouty arthritis and to prevent tissue deposition of urate; and (iii) providing prophylaxis to prevent acute flares. It is important to distinguish between therapy to reduce acute inflammation in acute gout and therapy to manage hyperuricaemia in patients with chronic gouty arthritis. During the acute gouty attack nonpharmacological treatments such as topical ice and rest of the inflamed joint are useful. ⋯ The effectiveness of colchicine prophylaxis as an isolated therapy is still to be confirmed by placebo-controlled trials. Another issue is prophylaxis with NSAIDs. There are no comparative studies with colchicine.