Navegando por Palavras-chave "Addison's disease"
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- ItemSomente MetadadadosAutoantibodies against glutamic acid decarboxylase and 21-hydroxylase in Brazilian patients with Type 1 diabetes or autoimmune thyroid diseases(Editrice Kurtis S R L, 2003-06-01) Silva, R. C.; Sallorenzo, Carolina [UNIFESP]; Kater, Claudio Elias [UNIFESP]; Dib, Sergio Atala [UNIFESP]; Falorni, A.; Universidade Federal de São Paulo (UNIFESP); Univ PerugiaAutoimmune thyroid diseases (ATD) are often associated with Type 1 diabetes mellitus (T1DM) and Addison's disease (AD), characterizing the autoimmune polyendocrine syndrome. We evaluated the frequency of autoantibodies against glutamic acid decarboxylase isoform. 65 (GAD65Ab) and 21-hydroxylase (21OHAb) in the sera of 65 [58 females (F)/7 males (M), 17-70 yr] patients with Graves' disease (GD) and 47 (45 F/2 M, 12-77 yr) with Hashimoto's thyroiditis (HT), none of whom had either diabetes or AD. The sera of 30 recently diagnosed T1DM patients (16 M/14 F, 1-39 yr) and of 97 (54 F/43 M, 7-69 yr) healthy controls were also examined. GAD65Ab were detected in the sera of 18 (60%) T1DM, 8 (12%) GD and in none of the HT patients or the controls (p=0.03 for GD vs HT, p=0.002 for GD vs controls, and p<0.001 for GD vs T1DM). 21OHAb were detected in the sera of 2 (3%) GD, 1 (2%) HT and in none of the T1DM patients or the controls. GAD65Ab levels were significantly lower in GD than in T1DM patients (median: -0.06 vs 0.28,p<0.001). Six of the 8 GD GAD65Ab-positive patients submitted to an intravenous glucose tolerance test showed no diminished first phase insulin secretion. All 21OHAb positive patients had normal basal cortisol and adrenocorticotropin (ACTH), normal cortisol response after ACTH stimulation, but high plasma renin activity. In conclusion, despite the genetic diversity of the Brazilian population, the frequency of GAD65Ab and 21OHAb in our patients is similar to that observed in other countries. GAD65Ab were more prevalent in GD than in HT patients, suggesting a difference in the immune response between these disorders. Long-term follow-up is necessary to determine the clinical relevance of these autoantibodies in the Brazilian population. (C) 2003, Editrice Kurtis.
- ItemAcesso aberto (Open Access)Detection of adrenocortical autoantibodies in Addison's disease with a peroxidase-labelled protein A technique(Associação Brasileira de Divulgação Científica, 1998-09-01) Silva, Reinaldo Correia [UNIFESP]; Faiçal, Samir [UNIFESP]; Laureti, Stefano; Falorni, Alberto; Dib, Sergio Atala [UNIFESP]; Kater, Claudio Elias [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); University of PerugiaAdrenocortical autoantibodies (ACA), present in 60-80% of patients with idiopathic Addison's disease, are conventionally detected by indirect immunofluorescence (IIF) on frozen sections of adrenal glands. The large-scale use of IIF is limited in part by the need for a fluorescence microscope and the fact that histological sections cannot be stored for long periods of time. To circumvent these restrictions we developed a novel peroxidase-labelled protein A (PLPA) technique for the detection of ACA in patients with Addison's disease and compared the results with those obtained with the classical IIF assay. We studied serum samples from 90 healthy control subjects and 22 patients with Addison's disease, who had been clinically classified into two groups: idiopathic (N = 13) and granulomatous (N = 9). ACA-PLPA were detected in 10/22 (45%) patients: 9/13 (69%) with the idiopathic form and 1/9 (11%) with the granulomatous form, whereas ACA-IIF were detected in 11/22 patients (50%): 10/13 (77%) with the idiopathic form and 1/9 (11%) with the granulomatous form. Twelve of the 13 idiopathic addisonians (92%) were positive for either ACA-PLPA or ACA-IIF, but only 7 were positive by both methods. In contrast, none of 90 healthy subjects was found to be positive for ACA. Thus, our study shows that the PLPA-based technique is useful, has technical advantages over the IIF method (by not requiring the use of a fluorescence microscope and by permitting section storage for long periods of time). However, since it is only 60% concordant with the ACA-IIF method, it should be considered complementary instead of an alternative method to IIF for the detection of ACA in human sera.
- ItemAcesso aberto (Open Access)Doença de addison de etiologia auto-imune(Sociedade Brasileira de Endocrinologia e Metabologia, 1998-12-01) Silva, Regina do Carmo [UNIFESP]; Kater, Claudio Elias [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Autoimmune Addison's disease is a rare and potentially, fatal endocrinopathy, that can occur either isolated or as part of the types I and II polyglandular autoimmune syndromes (PAS). Adrenocortical autoantibodies are considered sensitive immunological markers of the destructive autoimmune process, and can identify individuals in the pre-clinical stage of the disease. The steroidogenic enzyme 21-hydroxylase (P450c21) represents the major adrenal autoantigen, although other P450 cytochromes (17a-hydroxylase and side chain cleavage) can also trigger an autoimmune response, mainly in the PAS type I and in Addison's disease with associated premature ovarian failure. The role of P45021 autoantibodies in the pathogenesis of the adrenal failure is not yet well established, and the same happens with the anti-ACTH receptor antibodies.
- ItemSomente MetadadadosGH-releasing peptide (GHRP-6)-induced ACTH release in patients with Addison's disease: Effect of glucocorticoid withdrawal(Editrice Kurtis S R L, 2003-02-01) Martins, Manoel Ricardo Alves [UNIFESP]; Pinto, ACAR [UNIFESP]; Brunner, E. [UNIFESP]; Silva, MRD [UNIFESP]; Lengyel, AMJ [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)GH releasing peptide (GHRP-6) is a synthetic hexapeptide with potent GH releasing activity both in man and in animals. This peptide is also able to stimulate ACTH and cortisol (F) release. It has been suggested that the ACTH responsiveness to GHRP-6 is modulated by circulating glucocorticoid levels. To further clarify this hypothesis, we studied the effect of GHRP-6 (1 ug/kg, iv) on ACTH and F release in patients with Addison's disease (no.=6) during replacement therapy and after 72 h of glucocorticoid withdrawal. Seven controls were also submitted to a single GHRP-6 test. In control subjects, ACTH values (pmol/l; mean+/-SE) increased from 2.9+/-0.8 to 4.7+/-1.4 (peak). AUC (pmol.min/l) values were 170.3+/-48.8. F (nmol/l) values increased from 257.0+/-42.9 to 367.0+/-50.8. In patients with Addison's disease there was an increase in ACTH levels from 38.1+/-7.1 to 174.9+/-79.4 after GHRP-6 administration. AUC values were 5490.4+/-2269.1. After 72 h withdrawal of glucocorticoid, there was an increase in basal ACTH values (1191.2+/-97.3), and a trend toward an increase in ACTH levels after GHRP-6 (p=0.053). Patients with Addison's disease on therapy showed a significantly higher ACTH response to GHRP-6 when compared to controls. Our results show that in patients with Addison's disease on replacement there is an increased ACTH release after GHRP-6 administration, compared to controls. After 72 h glucocorticoid withdrawal, this enhanced responsiveness is not maintained. Our data suggest that circulating glucocorticoids modulate GHRP-6-induced ACTH release and that multiple mechanisms may be involved in this process. (C) 2003, Editrice Kurtis.
- ItemAcesso aberto (Open Access)Insuficiência adrenal primária no adulto: 150 anos depois de Addison(Sociedade Brasileira de Endocrinologia e Metabologia, 2004-10-01) Silva, Regina do Carmo [UNIFESP]; Castro, Margaret de; Kater, Claudio Elias [UNIFESP]; Cunha, Andréa Aparecida; Moraes, Andréia M. de; Alvarenga, Daniela B. de; Moreira, Ayrton C.; Elias, Lucila L.k.; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)Thomas Addison first described, 150 years ago, a clinical syndrome characterized by salt-wasting and skin hyperpigmentation, associated with a destruction of the adrenal gland. Even today, over a century after Addison's report, primary adrenal insufficiency can present as a life-threatening condition, since it frequently goes unrecognized in its early stages. In the 1850 s, tuberculous adrenalitis was present in the majority of patients, but nowadays, autoimmune Addison's disease is the most common cause of primary adrenal insufficiency. In the present report, we show the prevalence of different etiologies, clinical manifestations and laboratorial findings, including the adrenal cortex autoantibody, and 21-hydroxylase antibody in a Brazilian series of patients with primary adrenal insufficiency followed at Divisão de Endocrinologia da Universidade Federal de São Paulo (UNIFESP) and at Faculdade de Medicina de Ribeirão Preto - USP (FMRP-USP).