The FACET (Formoterol and Corticosteroid Establishing Therapy) study established that there is a clear clinical benefit in adding formoterol to budesonide therapy in patients who have persistent symptoms of asthma despite treatment with low to moderate doses of an inhaled corticosteroid. We combined the clinical results from the FACET study with an expert survey on average resource use in connection with mild and severe asthma exacerbations in the U.K., Sweden and Spain. The primary objective of this study was to assess the health economics of adding the inhaled long-acting beta2-agonist formoterol to the inhaled corticosteroid budesonide in the treatment of asthma. The extra costs of adding the inhaled beta2-agonist formoterol to the corticosteroid budesonide in asthmatic patients in Sweden were offset by savings from reduced use of resources for exacerbations. For Spain the picture was mixed. Adding formoterol to low dose budesonide generated savings, whereas for moderate doses of budesonide about 75% of the extra formoterol costs could be recouped. In the U.K., other savings offset about half of the extra cost of formoterol. All cost-effectiveness ratios are within accepted cost-effectiveness ranges reported from previous studies. If productivity losses were included, there were net savings in all three countries, ranging from Euro 267-1183 per patient per year. In conclusion, adding the inhaled, long-acting beta2-agonist formoterol to low-moderate doses of the inhaled corticosteroid budesonide generated significant gains in all outcome measures with partial or complete offset of costs. Adding formoterol to budesonide can thus be considered to be cost-effective.
Metaplastic breast carcinomas (MBC) are rare primary breast malignancies characterized by the co-existence of carcinoma with non-epithelial cellular elements. They can be classified as monophasic spindle cell (sarcomatoid) carcinoma, biphasic carcinosarcoma, adenocarcinoma with divergent stromal differentiation (osseous, chondroid and rarely rhabdoid) as well as adenosquamous and pure squamous cell carcinomas. There is a paucity of information on clinically relevant pathologic features and clinical outcomes for these rare tumors. The aim of this study was to review the pathologic features and clinical outcomes of all cases of MBC seen at a single institution between 1971 and 2000.
A computerized search of the Queen Elizabeth II Health Sciences Center (QEII HSC) surgical pathology files was performed for the years 1971-2000. Tumor blocks from identified cases were reviewed and immunohistochemistry was performed for estrogen and progesterone receptors (ER/PR), HER2/neu protein overexpression and cytokeratin profile. Clinical outcome information was obtained from hospital files and telephone contact with treating physicians.
Twenty-six (26) cases were retrieved with only one case identified before 1990. All tumors were high grade with a median tumor size of 3.7 cm (range 1.4-9.5 cm). Thirteen cases had lymph node dissections available for evaluation, with 4 demonstrating nodal metastases. Five of 26 cases were ER positive within the adenocarcinomatous component, only two of which also expressed PR. Associated ductal carcinoma in situ (DCIS) was present in 11 cases. HER2/neu over-expression was seen in only one (1/26) adenosquamous carcinoma (3 + membranous staining of the malignant glandular component). At 23 months median follow-up, disease free survival (DFS) for the entire group was 53%.
Although a rare breast cancer subtype, MBC is of considerable interest due to its pathological heterogeneity and differences in clinical behavior compared to typical breast carcinomas. Increasing pathologic recognition of MBC as a discrete entity is suggested by the number of MBC diagnoses in the last decade compared to previous years. The poor DFS associated with MBC suggests that further research exploring mechanisms of carcinogenesis and identifying clinically relevant prognostic factors is needed to direct optimum clinical care. Importantly, MBC variants appear to rarely overexpress the HER2/neu oncoprotein.