Day: 01/07/2011

The use of rapid onset opioids for breakthrough cancer pain: The challenge of its dosing

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Breakthrough cancer pain (BTcP) has been defined as a transitory increase in pain intensity on a baseline pain of moderate intensity in patients on analgesic treatment regularly administered. This review provides updated information about the use of opioids for the treatment of BTcP, with special emphasis on the use of new rapid onset opioids (ROOs).

Due to its slow onset to effect oral opioids cannot be considered an efficacious treatment for BTcP. Parenteral opioids may provide rapid onset of analgesia, but not always available particularly at home. Different technologies have been developed to provide fast pain relief with potent opioid drugs such fentanyl, delivered by non-invasive routes. Transmucosal administration of lipophilic substances has gained a growing popularity in the last years, due to the rapid effect clinically observable 10–15 min after drug administration, obtainable in non-invasive forms. Fentanyl is a potent and strongly lipophilic drug, which matches the characteristics to favour the passage through the mucosa and then across the blood–brain barrier to provide fast analgesia. Transmucosal, buccal, sublingual, and intranasal fentanyl showed their efficacy in comparison with oral morphine or placebo and are available for clinical use in most countries. All the studies performed with ROOs have recommended that these drugs should be administered to opioid-tolerant patients receiving doses of oral morphine equivalents of at least 60 mg. The choice of the dose of ROO to be prescribed as needed remains controversial. The need of titrating opioid doses for BTcP has been commonly recommended in all the controlled studies, but has never been substantiated in appropriate studies.

Proteinuria Raises Risk for Acute Kidney Injury

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AKI is related to both glomerular filtration rate and proteinuria level.

Acute kidney injury (AKI) raises risk for end-stage renal disease (ESRD) and renal-associated death. It often is iatrogenic (e.g., induced by drugs or contrast dye), and therefore often is preventable. Low estimated glomerular filtration rate (eGFR) predisposes patients to AKI, but the effect of proteinuria on risk for AKI has not been well characterized.

Researchers in Alberta, Canada, studied more than 900,000 adults without ESRD who underwent at least one outpatient measurement each of eGFR and proteinuria (by dipstick or albumin–creatinine ratio) from 2002 through 2006. Patients were stratified by baseline eGFR and proteinuria levels (normal, mild, or heavy) and were followed for a median of 35 months.

Within each eGFR stratum, patients with heavier proteinuria were significantly more likely to be hospitalized with AKI and to develop AKI that required dialysis. For most strata of baseline eGFR and proteinuria, rates of all-cause mortality and the composite outcome of ESRD or chronic doubling of serum creatinine were significantly higher in patients who were hospitalized for AKI than in those who were not. The effect of AKI on these outcomes was weaker for patients with low eGFR and heavy proteinuria at baseline, who were at excess risk even without AKI.

Comment: This study suggests that proteinuria as well as eGFR should be considered in assessing risk for AKI, and it adds to growing evidence that proteinuria should play a greater role in the definition of chronic kidney disease.

— Bruce Soloway, MD

Published in Journal Watch General Medicine January 6, 2011