EDITORIALS
Should we stop using intravenous gentamicin in patients with cystic fibrosis?
Correspondence to:
Dr C H Goss, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington Medical Center, Campus Box 356522, 1959 N E Pacific, Seattle, WA 98195, USA; goss@u.washington.edu
| The first 150 words of the full text of this article appear below. |
Patients with cystic fibrosis (CF) have shown continual annual improvement in survival in many countries.1–4 The improvements in outcome have been attributed to better treatments and a multidisciplinary approach to care focused in care centres with specific expertise in CF.5–8 As survival improves, we may start increasingly to see adverse events related to intensive treatments used to battle the chronic airway infections and airway inflammation in CF.
Because of chronic lung infections, patients with CF receive repeated courses of oral, inhaled and intravenous antibiotics, some of which are known to be nephrotoxic drugs such as aminoglycosides. The primary defect in CF, the cystic fibrosis transmembrane regulator protein (CFTR), is expressed in the kidney but its function is unknown.9 In this issue of Thorax, Smyth and colleagues10 present data on the association of intravenous aminoglycosides—particularly gentamicin—and acute renal failure (ARF) in the UK (see page 532). The authors
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Thorax 2008 63: 479.[Extract] [Full Text] [PDF]
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Thorax 2008 63: 532-535.[Abstract] [Full Text] [PDF]
This article has been cited by other articles:
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Balfour-Lynn, I. M
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