ABSTRACT
Background: Prolonged hospitalization after tonsillectomy up to three nights was implemented to decrease mortality due to post-tonsillectomy hemorrhage.Aims: To assess if extension of postoperative inpatient observation time from one to three nights results in potential benefits following tonsillectomy.Subjects and methods: Patients who stayed only one night post-tonsillectomy between 1994 and 2006 (Group A) were compared to 1570 patients who stayed three nights postoperatively between 2008 and 2016 (Group B). Complication rate and expense of hospitalization were compared.Results: Published data show that 114 (1.78%) out of 6400 patients in group A had post-tonsillectomy hemorrhage. In this patient group 75.4% (n = 86) of all bleedings occurred after discharge from hospital. However, in group B post-tonsillectomy hemorrhage occurred in 70 (4.5%) and of those only 0.38% (n = 6) developed bleeding episodes on the second or third postoperative day (POD). As observed in group A, the majority of hemorrhage (n = 57; 81.4%) was observed after discharge. Cost analysis reveals a difference of approximately 6 million for all 32 ENT departments per year in Austria.Conclusions and significance: Extending postoperative hospitalization from one to three nights reveals no benefit after tonsillectomy. Comparison reveals substantial increase of costs for an extended 3 nights inpatient stay.
Subject(s)
Cost-Benefit Analysis , Length of Stay/economics , Postoperative Hemorrhage/surgery , Tonsillectomy/adverse effects , Adolescent , Adult , Austria , Child , Child, Preschool , Comorbidity , Female , Hospitalization , Humans , Male , Peritonsillar Abscess/surgery , Postoperative Hemorrhage/economics , Sleep Apnea, Obstructive/surgery , Tonsillitis/surgeryABSTRACT
The anti-apoptotic protein Mcl-1 is highly expressed in various types of malignant tumors. Overexpression is reported to correlate with poor prognosis and disease progression. We report the expression levels of Mcl-1 in tumor samples of the parotid gland. A retrospective study containing 108 patients was performed. A tissue microarray of six malignancies of the parotid gland and pleomorphic adenoma as control was constructed. Parotid gland tumor samples were immunohistochemically stained for Mcl-1 and expression intensities were assessed. Statistical analysis included correlation to patients' clinical data and comparison of malignancies to the adenoma. All malignancies had significantly higher expression of Mcl-1 than the pleomorphic adenomas. The intensity, however, had no significant correlation to overall survival. Our immunohistochemical findings indicate that parotid gland malignancies produce high levels of Mcl-1 protein. Therefore, Mcl-1 might serve as a predictive co-marker in tumors of the parotid gland.
Subject(s)
Biomarkers, Tumor/metabolism , Parotid Neoplasms/pathology , Proto-Oncogene Proteins c-bcl-2/metabolism , Adenoma/metabolism , Adenoma/pathology , Adolescent , Adult , Aged , Aged, 80 and over , Biopsy , Carcinoma/metabolism , Carcinoma/pathology , Case-Control Studies , Data Interpretation, Statistical , Female , Gene Expression Regulation, Neoplastic , Humans , Immunohistochemistry/methods , Male , Middle Aged , Myeloid Cell Leukemia Sequence 1 Protein , Parotid Neoplasms/metabolism , Retrospective Studies , Up-Regulation , Young AdultABSTRACT
BACKGROUND AND OBJECTIVES: This retrospective study was performed to evaluate the status of p53 in pleomorphic adenomas and carcinomas ex pleomorphic adenoma in the parotid gland. As loss or mutation of p53 can cause malignant transformation, the possible degeneration of pleomorphic adenomas to carcinomas ex pleomorhic adenoma was investigated by mutational analysis. METHODS: Twenty-five Patients including 14 patients with pleomorphic adenomas and 11 patients with carcinoma ex pleomorphic adenoma of the parotid gland were examined for p53 status. DNA was extracted out of paraffin-embedded tissue and PCR was performed for the coding exons 2-11. Denaturing gradient gel electrophoresis (DGGE) was carried out for mutational analysis and DNA sequencing was performed in case of a suspected mutation. RESULTS: Fourteen pleomorphic adenomas and 11 carcinomas ex pleomorphic adenoma were screened for p53 status and potent mutations. Subsequent sequencing of the distinct exons showed no mutation. CONCLUSION: We could not detect mutations of p53 neither in benign nor malignant parotid tumors and we therefore assume that p53 plays no role in the transformation from pleomorphic adenoma to carcinoma ex pleomorphic adenoma.
