The effect of indacaterol during an acute exacerbation of COPD.

Some clinical trials have suggested that the inhaled long-acting ß2-agonists (LABAs) may be effective in the treatment of acute exacerbations of chronic obstructive pulmonary disease (AECOPD). Since indacaterol, the first once-daily LABA to be developed for the regular treatment of COPD, exhibits fast onset of action and 24-h duration of bronchodilation, we have investigated its effects in patients with AECOPD managed in the emergency department. In a randomised controlled pilot trial, we have enrolled 29 consecutive patients with a recent (i.e., within ≤ 4 d) history of AECOPD and requiring hospitalization. All patients received a standard protocol consisting of ipratropium bromide aerosol 500 µg three times a day, intravenous methylprednisolone 20 mg twice-daily and, if indicated, oral levofloxacin 500 mg once-daily. Moreover, they were randomly allocated to one of the two 5-day treatment groups (indacaterol maleate 300 µg once-daily or salbutamol nebulizer 1250 µg three times a day). The administration of indacaterol 300 µg to patients admitted to emergency department for an AECOPD resulted in a greater improvement of pulmonary function compared with traditional therapy, without cardiovascular side effects. Our results suggest that indacaterol could be a useful option in the treatment of AECOPD. However, further larger double-blinded randomized clinical trials are needed to validate the intriguing results obtained in this setting.

Peripheral graft infection due to Staphylococcus aureus without abnormal findings by 99mTc-HMPAO-labeled-leukocyte scan.

Here, we present the case of an extremely subtle peripheral graft infection caused by Staphylococcus aureus. The lack of local signs and the negativity of all imaging studies, including (99m)Tc-HMPAO-Labelled-Leukocyte Scan which is reported to have 100% sensitivity, delayed the diagnosis and therapy, which were both provided by surgery.

Diabetes in chronic liver disease: from old concepts to new evidence.

The liver is one of the principal organs involved in glucose metabolism together with skeletal muscle and adipose tissue. A link between diabetes and chronic liver disease (CLD) was first observed in the early half of the last century, but to date several questions remain unsolved. Altered glucose tolerance has been well described in alcoholic CLD, non-alcoholic fatty liver disease, chronic hepatitis C and portal hypertension. Moreover, insulin resistance is assuming an ever-growing importance in CLD; chronic hepatitis C has recently been proposed as a metabolic disease and insulin sensitivity as a predictive factor for liver fibrosis.CLD is also complicated by acquired growth hormone (GH) resistance, characterized by low concentrations of insulin-like growth factor-1 (IGF-1) with respect to normal or elevated GH levels. GH resistance in CLD is determined by several factors, including malnutrition, impaired liver function and reduced expression of hepatic GH receptors. We recently described the possible role of tumour necrosis factor-alpha (TNF-alpha) in blunting the hepatic response to GH in patients with chronic hepatitis C. The role of GH in impaired glucose metabolism is well known, and recent evidence suggests a receptor and/or post-receptor modulation of insulin signalling. Moreover, as in other chronic inflammatory conditions, pro-inflammatory cytokines may directly modulate the signal cascade that follows insulin binding to its receptor in the course of CLD. In this review, the proposed links between impaired glucose tolerance and CLD are analysed, special emphasis being focussed on the most recent findings concerning the interplay of chronic inflammation, GH resistance and insulin resistance.