Proteína C reativa na deficiência isolada monogênica do hormônio de crescimento

• Ano de defesa: 2006
• Autor(a) principal: Marques-santos, Celi
• Orientador(a): Oliveira, Manuel Hermínio de Aguiar
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Sergipe
• Programa de Pós-Graduação: Pós-Graduação em Ciências da Saúde
• País: BR
• Palavras-chave em Português: Endocrinologia; Cardiologia; Proteína C Reativa; Inflamação; Aterosclerose; Deficiência do Hormônio de Crescimento; IGF-I; Síndrome metabólica; Nanismo hipofisário
• Palavras-chave em Inglês: C-reactive protein; Inflammation; Atherosclerosis; Growth hormone deficiency; IGF-I; Metabolic Syndrome
• Área do conhecimento CNPq: CNPQ::CIENCIAS DA SAUDE
• Link de acesso: https://ri.ufs.br/handle/riufs/3902

The present research has the objective to determinate the seric PCR concentrations in the monogenic isolated deficiency of the growth hormone (DIGH), test the hypothesis that DIGH is associated to the exacerbation of the inflammatory profile, identify the PCR elevation predictors, and evaluate the existence of an association between PCR and premature atherosclerosis. The growth hormone (GH) has as its main function the post-natal longitudinal growth; it interferes in the bone apposition, muscle mass growth, opposes to the action of insulin in the carbohydrates and lipids metabolism, and, in the cardiovascular system, helps the vascular and myocardial remodeling. IGF-I, GH primary mediator, plays a fundamental role in the growth regulation, cellular apoptosis and differentiation. The GH/IGF-I axis acts in the resistance to insulin and phenotypical expression of cardiovascular risk factors, associated to metabolic syndrome. IGF-I avoids the endothelial dysfunction, causes the increase of sensitivity to insulin, and avoids post-prandial dyslipidemia, besides presenting anti-inflammatory and anti-apoptotic activities. The decrease of IGF-I is associated to premature atherosclerosis and high cardiovascular risk. IGF-I role is controversial and its increase is related to the premature atherosclerosis in carotids. The deficiency of GH is associated to the increase of cardiovascular and brain vascular mortality. The inflammation plays an essential role in the atherosclerosis physiopathology from its initial phase up to atherotrombotic events in acute coronary syndromes. C - reactive protein, acute phase reagent of the inflammation, is produced by the liver, due mainly to the interleukin-6 stimulus. As a predictor and a mediator of atherosclerosis, among all circulating inflammatory markers, it is the most stable, the most studied and the one which presented the most constant relationship to future cardiovascular risk in various clinical situations, including asymptomatic individuals. In Itabaininha, Sergipe state we described a population with DIGH, with extremely low levels of IGF-I, high LDL-c and systolic arterial pressure and central obesity, a cluster of risk factors, highly susceptible to atherosclerosis ideal to this research. From this population, eighteen individuals were studied, eight male and ten female, with an average age of 45, compared to a control group composed of twenty individuals of the same region. After the clinical and metabolic characteristics were analyzed, the most relevant results were: PCR showed a meaningful difference between the groups (4,9 mg/l (4,7) vs 1,4 mg/l (2,2)); and IGF-I extremely low (1,0 ng/ml (1,0) vs 164,0 ng/ml (135,0)). The group predicts that PCR is independent from the other metabolic variables (R² = 0, 42), and that IGF-I is the main responsible for the increase of PCR in the DIGH. No association between PCR and the intimatemedia thickness of the carotids could be observed. Conclusion: it was demonstrated that the DIGH present high levels of PCR when compared to the control group; the variable group predicts this variation and IGF-I is the main responsible for the PCR variability. High PCR is not associated to premature atherosclerosis in this high risk differentiated group.