title: Expression of TRAIL and Fas in Primary Hyperparathyroidism.
abstract: OBJECTIVE
  Differentiating between parathyroid lesions is still difficult and ambiguous. In cases of primary hyperparathyroidism, appropriate and prompt diagnosis is of great importance for effective treatment and follow-up. A great amount of mechanisms contribute to the pathogenesis of primary hyperparathyroidism, such as disturbance in balance between pro- and anti-apoptotic factors. Therefore, we examined whether immunohistochemical expression of apoptotic factors, TNF-related apoptosis-inducing ligand (TRAIL) and Fas, could have clinical utility as a marker of proliferative lesions of parathyroid gland.
  
  
  METHODS
  Parathyroid specimens of 58 consecutive patients who had undertaken surgery due to primary hyperparathyroidism were incubated with purified mouse monoclonal antihuman antibodies: anti-TRAIL and anti-Fas. Staining was considered positive when at least 5% of the cells showed immunoreactivity.
  
  
  RESULTS
  The percentage of cells which were positively stained for TRAIL in parathyroid hyperplasia was 9.65%, in parathyroid adenoma 8.31%, and in normal controls 2.24%. Immunoreactivity for TRAIL was detected in 91.89% of parathyroid hyperplasias, 85.71% of parathyroid adenomas, and none in healthy glands. The percentage of cells with a positive reaction to Fas in parathyroid hyperplasia was 8.92%, in parathyroid adenoma 8.09%, and in normal tissue 1.9%. The expression of Fas was found in 94.59% of parathyroid hyperplasias, 90.48% of parathyroid adenomas, and none in healthy glands.
  
  
  CONCLUSIONS
  In our study, hyperplasias demonstrated the highest expression of TRAIL and Fas, whereas in adenomas it was increased compared to normal tissue, but lower than in hyperplasias. These factors could be an additive tool in the differential diagnosis of parathyroid lesions.
authors.affiliation: a Department of Histology and Embryology , School of Medicine with the Division of Dentistry, Medical University of Silesia , Jordana 19, Zabrze , Poland.
authors.forename: Oliwia Anna
authors.initials: OA
authors.lastname: Segiet
authors.affiliation: b Department of General and Endocrine Surgery , School of Medicine with the Division of Dentistry, Medical University of Silesia , Stefana Batorego 15, Bytom , Poland.
authors.forename: Mariusz
authors.initials: M
authors.lastname: Deska
authors.affiliation: a Department of Histology and Embryology , School of Medicine with the Division of Dentistry, Medical University of Silesia , Jordana 19, Zabrze , Poland.
authors.forename: Łukasz
authors.initials: Ł
authors.lastname: Mielańczyk
authors.affiliation: a Department of Histology and Embryology , School of Medicine with the Division of Dentistry, Medical University of Silesia , Jordana 19, Zabrze , Poland.
authors.forename: Marlena
authors.initials: M
authors.lastname: Brzozowa-Zasada
authors.affiliation: b Department of General and Endocrine Surgery , School of Medicine with the Division of Dentistry, Medical University of Silesia , Stefana Batorego 15, Bytom , Poland.
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Buła
authors.affiliation: b Department of General and Endocrine Surgery , School of Medicine with the Division of Dentistry, Medical University of Silesia , Stefana Batorego 15, Bytom , Poland.
authors.forename: Jacek
authors.initials: J
authors.lastname: Gawrychowski
authors.affiliation: a Department of Histology and Embryology , School of Medicine with the Division of Dentistry, Medical University of Silesia , Jordana 19, Zabrze , Poland.
authors.forename: Romuald
authors.initials: R
authors.lastname: Wojnicz
mesh_terms: D000328:Adult; D000368:Aged; D006801:Humans; D049950:Hyperparathyroidism, Primary / Q000378:metabolism*; D008875:Middle Aged; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000378:metabolism*; D019014:fas Receptor / Q000378:metabolism*
chemical_list: C491901:FAS protein, human; D053221:TNF-Related Apoptosis-Inducing Ligand; D019014:fas Receptor
keywords: Fas receptor; TNF-related apoptosis-inducing ligand; apoptosis; parathyroid neoplasms; primary hyperparathyroidism