RESUMO
Dopamine-agonist cabergoline (CB) reduces prolactin (PRL) secretion and tumor size in 80% of patients with prolactin-secreting adenomas (PRL-omas) by binding type 2 dopamine receptor (DRD2). The mechanisms responsible for resistance to CB remain largely unknown. To assess the association of DRD2 with sensitivity to CB, TaqI-A1/A2, TaqI-B1/B2, HphI-G/T and NcoI-C/T genotypes were determined in a cross-sectional retrospective study, including 203 patients with PRL-oma. DRD2 alleles frequencies did not differ between patients and 212 healthy subjects. Conversely, NcoI-T allele frequency was higher in resistant rather than responsive patients, considering both PRL normalization (56.6 vs 45.3%, P=0.038) and tumor shrinkage (70.4 vs 41.4%, P=0.006). Finally, [TaqI A1-/TaqI B1-/HphI T-/NcoI T-] haplotype was found in 34.5% of patients normalizing PRL with < or =3 mg/week of CB vs 11.3% of resistants (P=0.021). In conclusion, resistance to CB was associated with DRD2 NcoI-T+ allele, consistent with evidence suggesting that this variant may lead to reduction and instability of DRD2 mRNA or protein.
Assuntos
Adenoma/tratamento farmacológico , Agonistas de Dopamina/uso terapêutico , Ergolinas/uso terapêutico , Neoplasias Hipofisárias/tratamento farmacológico , Polimorfismo Genético , Prolactina/metabolismo , Receptores de Dopamina D2/genética , Adenoma/genética , Adenoma/metabolismo , Adulto , Alelos , Cabergolina , Estudos Transversais , Feminino , Frequência do Gene , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Neoplasias Hipofisárias/genética , Neoplasias Hipofisárias/metabolismo , Estudos RetrospectivosRESUMO
Human cytomegalovirus (HCMV) is associated with several diseases in immunocompromised individuals. CMV infection can be diagnosed directly by demonstration of the virus or virus components in pathological materials or indirectly through serology. Molecular biology has allowed detailed studies of the viral genome and its antigenic gene products and has led to major advances in CMV diagnosis providing new tools for both the analysis of the CMV-specific immune response and the detection of virus-specific antigens or genetic material. In an attempt to provide a guide for the correlation between laboratory findings and clinical interpretation, we discuss in this work the clinical settings in which the presence of CMV needs to be diagnosed, and how a CMV diagnosis should be asked for or interpreted by the clinician in view of the variety of new or improved laboratory tests now available.
