RESUMO
OBJECTIVE: To analyze the aberrant expression of the GIPR and LHCGR in different forms of adrenocortical hyperplasia: ACTH-independent macronodular adrenal hyperplasia (AIMAH), primary pigmented nodular adrenocortical disease (PPNAD) and diffuse adrenal hyperplasia secondary to Cushing's disease (DAHCD). METHODS: We quantified GIPR and LHCGR expressions using real time PCR in 20 patients with adrenocortical hyperplasia (seven with AIMAH, five with PPNAD, and eight with DAHCD). Normal adrenals tissues were used as control and the relative expression was compared with beta-actin. RESULTS: GIPR and LHCGR expressions were demonstrated in all tissues studied. Median GIPR and LHCGR mRNA levels were 1.6; 0.4; 0.5 and 1.3; 0.9; 1.0 in adrenocortical tissues from AIMAH, PPNAD and DAHCD respectively. There were no differences between GIPR and LHCGR expressions in all tissues studied. CONCLUSIONS: GIPR and LHCGR overexpression were not identified in the studied cases, thus suggesting that this molecular mechanism is not involved in adrenocortical hyperplasia in our patients.
Assuntos
Doenças do Córtex Suprarrenal/metabolismo , Glândulas Suprarrenais/patologia , Hipersecreção Hipofisária de ACTH/metabolismo , Receptores dos Hormônios Gastrointestinais/metabolismo , Receptores do LH/metabolismo , Actinas/metabolismo , Adolescente , Doenças do Córtex Suprarrenal/genética , Glândulas Suprarrenais/metabolismo , Adulto , Idoso , Feminino , Humanos , Hiperplasia/metabolismo , Masculino , Pessoa de Meia-Idade , Hipersecreção Hipofisária de ACTH/genética , Reação em Cadeia da Polimerase , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Receptores dos Hormônios Gastrointestinais/genética , Receptores do LH/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Adulto JovemRESUMO
OBJECTIVE: To analyze the aberrant expression of the GIPR and LHCGR in different forms of adrenocortical hyperplasia: ACTH-independent macronodular adrenal hyperplasia (AIMAH), primary pigmented nodular adrenocortical disease (PPNAD) and diffuse adrenal hyperplasia secondary to Cushing's disease (DAHCD). METHODS: We quantified GIPR and LHCGR expressions using real time PCR in 20 patients with adrenocortical hyperplasia (seven with AIMAH, five with PPNAD, and eight with DAHCD). Normal adrenals tissues were used as control and the relative expression was compared with β-actin. RESULTS: GIPR and LHCGR expressions were demonstrated in all tissues studied. Median GIPR and LHCGR mRNA levels were 1.6; 0.4; 0.5 and 1.3; 0.9; 1.0 in adrenocortical tissues from AIMAH, PPNAD and DAHCD respectively. There were no differences between GIPR and LHCGR expressions in all tissues studied. CONCLUSIONS: GIPR and LHCGR overexpression were not identified in the studied cases, thus suggesting that this molecular mechanism is not involved in adrenocortical hyperplasia in our patients.
OBJETIVO: Analisar a expressão aberrante do GIPR e do LHCGR em diferentes formas de hiperplasias adrenocorticais: hiperplasia adrenal macronodular independente de ACTH (AIMAH), doença adrenocortical nodular pigmentada primária (PPNAD) e hiperplasia adrenal difusa secundária à doença de Cushing (DAHCD). MÉTODOS: Quantificou-se por PCR em tempo real a expressão desses receptores em 20 pacientes: sete com AIMAH, cinco com PPNAD e oito com DAHCD. Adrenais normais foram utilizadas como controle e a expressão relativa desses receptores foi comparada à expressão da β-actina. RESULTADOS: A expressão desses receptores foi demonstrada em todos os tecidos estudados. A mediana da expressão do GIPR e do LHCGR foi de 1,6; 0,4; 0,5 e de 1,3; 0,9; 1,0 nos tecidos dos pacientes com AIMAH, PPNAD e DAHCD, respectivamente. Não houve diferença significativa na expressão desses receptores nos tecidos estudados. CONCLUSÕES: Hiperexpressão do GIPR e do LHCGR não foi observada, sugerindo que esse mecanismo não está envolvido na patogênese molecular da hiperplasia adrenal nesses pacientes.
Assuntos
Adolescente , Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem , Doenças do Córtex Suprarrenal/metabolismo , Glândulas Suprarrenais/patologia , Hipersecreção Hipofisária de ACTH/metabolismo , Receptores dos Hormônios Gastrointestinais/metabolismo , Receptores do LH/metabolismo , Actinas/metabolismo , Doenças do Córtex Suprarrenal/genética , Glândulas Suprarrenais/metabolismo , Hiperplasia/metabolismo , Reação em Cadeia da Polimerase , Hipersecreção Hipofisária de ACTH/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Receptores dos Hormônios Gastrointestinais/genética , Receptores do LH/genética , Adulto JovemRESUMO
Primary pigmented nodular adrenocortical disease is a rare cause of Cushing's syndrome in children and young adults. It is characterized by hypercorticolism resistant to dexamethasone suppression and at microscopic examination by multiple small black cortical nodules containing large cells with eosinophilic cytoplasm and lipofuscin with internodular cortical atrophy. Its pathogenesis is unknown. Bilateral adrenalectomy is the treatment of choice. We report a case of Cushing's syndrome due to primary pigmented nodular adrenocortical disease in a 32 year old female and review the literature.
Assuntos
Doenças do Córtex Suprarrenal/complicações , Síndrome de Cushing/etiologia , Doenças do Córtex Suprarrenal/metabolismo , Adulto , Síndrome de Cushing/metabolismo , Feminino , Humanos , Hidrocortisona/metabolismoRESUMO
La hiperplasia nodular pigmentaria primaria es una causa rara de síndrome de Cushing, con predilección en adultos jóvenes del género femenino. En el laboratorio está caracterizada por un hipercortisolismo independiente de ACTH; en el estudio histopatológico por múltiples nódulos corticales pequeños y obscuros, de células grandes, citoplasma con eosinofilia y lipofuscina que le dan una particularidad distintiva; además puede encontrarse una atrofia internodular el tratamiento de elección es la adrenalectomía bilateral. En este reporte damos a conocer el caso de una mujer de 32 años de edad con hiperplasia nodular pigmentaria primaria; además presentamos una revisión de la literatura
Assuntos
Humanos , Feminino , Adulto , Doenças do Córtex Suprarrenal/diagnóstico , Doenças do Córtex Suprarrenal/metabolismo , Doenças do Córtex Suprarrenal/fisiopatologia , Síndrome de Cushing/etiologia , Síndrome de Cushing/fisiopatologiaRESUMO
GH receptor (GHR) has been reported to express in both normal rat and human adrenals. However, no study examined GHR expression in diseased human adrenal cortex. We quantitated, with RT-PCR, GHR messenger RNA (mRNA) in both normal and diseased human adrenal cortex with the following results: GHR mRNA levels in four histologically normal, not steroid-stimulated, control adrenal cortices was 1.5-11 x 10(4) molecules/microgram total RNA; in three diffusely hyperplastic adrenals (DH): 6.7-17.7 x 10(4); in two nonfunctioning tumors (NF): 0.84-1.9 x 10(4); in five androgen-producing neoplasms (AP): 4.6-34 x 10(4); and in five glucocorticoid-producing neoplasms (GP): 6.7-87 x 10(4). GHR transcript levels among adrenal cortices, DH, NF, AP, and GP reached statistically significant difference (P < 0.03). The GP group exhibited higher GHR mRNA levels than controls (P < 0.006). NF, as well as GP and AP, tumors had less GHR mRNA than their histologically normal adjacent cortex (P < 0.05). A positive correlation between urinary cortisol and GHR messenger RNA (mRNA) levels from GP and DH was observed (r = 0.93, P < 0.003). Our data suggest that GHR is expressed in both normal and diseased adrenal cortex and that GHR mRNA accumulation is less efficient in adrenocortical neoplasm than their adjacent nonneoplastic cortex. GHR expression in adrenal cortex provides an evidence of direct GH action in this tissue.