[Pandoraea sputorum colonization in a patient with cystic fibrosis]. / Colonización por Pandoraea sputorum en un paciente con fibrosis quística.

Cystic fibrosis (CF) is a disease produced by a defect in the transmembrane conductance regulator protein, CFTR. Currently, the morbidity and mortality associated with CF are fundamentally related with the lung affectation that is a consequence of this defect. With the progression of the disease, there is an increase in the isolation of non-fermenting gram-negative bacilli colonizing these patients. The genus Pandoraea arises from a reclassification of species included within the "Burkholderia cepacia complex". It is made up of 9 species susceptible only to tetracycline, imipenem and cotrimoxazole. We report the first clinical case in Spain of colonization by Pandoraea sputorum in a patient diagnosed with CF at the age of eleven. After several previous colonizations by different Pseudomonas species in September 2005, a gram-negative bacillus was isolated in sputum, which was identified by sequencing and mass spectrometry (MALDITOF-MS) as P. sputorum, only sensitive to piperacillin-tazobactam, cotrimoxazole and imipenem. From 2005 to 2008, chronic colonization by this microorganism was associated with deterioration in lung function that was recuperated after treatment with piperacillin-tazobactam and imipenem. In 2010, this microorganism was once again isolated and treated with imipenem, to which the patient responded favorably. Currently, it is not known whether this microorganism is a chronic colonizer, whether it produces a transitory infection or whether it constitutes an important problem in CF patients, but given its special characteristics of sensitivity to anti-microbial drugs, the correct identification of this genus is essential. Mass spectrometry seems to be a valid technique that is faster than sequencing methods for identifying these species.

Comparison of tinzaparin and acenocoumarol for the secondary prevention of venous thromboembolism: a multicentre, randomized study.

The objective of the present study was to evaluate the efficacy, safety and healthcare resource utilization of long-term treatment with tinzaparin in symptomatic patients with acute pulmonary embolism as compared to standard therapy. In this open-label trial, 102 patients with objectively confirmed pulmonary embolism were randomized to receive, after initial treatment with tinzaparin, either tinzaparin (175 IU/kg/day) or international normalized ratio-adjusted acenocoumarol for 6 months. Clinical endpoints were assessed during the 6 months of treatment. A pharmacoeconomic analysis was carried out to evaluate the cost of the long-term treatment with tinzaparin in comparison with the standard one. In an intention-to-treat analysis, one of 52 patients developed recurrent venous thromboembolism in the tinzaparin group compared with none of the 50 patients in the acenocoumarol group. One patient in each group had a major haemorrhagic complication. Six patients in the acenocoumarol group had minor bleeding compared with none in the tinzaparin group (P = 0.027). Median hospital length of stay was shorter in the tinzaparin group compared to the acenocoumarol group (7 versus 9 days; P = 0.014). When all the direct and indirect cost components were combined for the entire population, we found a slight, nonstatistically significant (mean difference €345; 95% CI 1382-2071; P = 0.69) reduction in total cost with tinzaparin. Symptomatic acute pulmonary embolism treatment with full therapeutic doses of tinzaparin for 6 months is a feasible alternative to conventional treatment with vitamin K antagonists.