Dietary quality and associated factors among adults living in the state of São Paulo, Brazil

This study sought to analyze dietary quality and associated factors among adults living in regions of the State of São Paulo, Brazil. It was a cross-sectional population-based study of a sample of 3,454 adults ages 20 years and over who were included in the Household Health Survey. Dietary intake was measured by means of the 24-hour recall method, and dietary quality was assessed by means of the Healthy Eating Index (HEI), adapted to local realities. Probabilistic samples were obtained via multistage cluster samples from four regions in the State of São Paulo. Linear regression analyses were performed to evaluate the relationships between the HEI and the demographic, socioeconomic, and lifestyle variables. Among the individuals assessed, 5% had a good diet, 74% a diet that needed some degree of improvement, and 21% a poor diet. The means for HEI components were lowest for vegetables, fruits, and dairy products. The highest HEI scores were obtained by individuals who were nonsmokers, practiced physical activity, were retired, lived in houses or apartments, and had adequate living conditions surrounding them. In the multiple regression analysis, the variables of numbers of consumer durable goods, schooling of the head of the family, energy intake, and age had a positive association with the HEI. However, the association was inverse for the variables of smoking and body mass index. Higher dietary quality is associated with higher income, higher schooling level, better nutritional status, and being a nonsmoker. Knowledge of these factors is important for implementing programs for preventive nutrition or intervention.     

Hyperinsulinemic hypoglycemia evolving to gestational diabetes and diabetes mellitus in a family carrying the inactivating ABCC8 E1506K mutation

Vieira TC, Bergamin CS, Gurgel LC, Moisés RS. Hyperinsulinemic hypoglycemia evolving to gestational diabetes and diabetes mellitus in a family carrying the inactivating ABCC8 E1506K mutation. Congenital hyperinsulinism of infancy (CHI) is the most common cause of hypoglycemia in newborns and infants. Several molecular mechanisms are involved in the development of CHI, but the most common genetic defects are inactivating mutations of the ABCC8 or KCNJ11 genes. The classical treatment for CHI has been pancreatectomy that eventually leads to diabetes. More recently, conservative treatment has been attempted in some cases, with encouraging results. Whether or not the patients with heterozygous ABCC8 mutations submitted to conservative treatment may spontaneously develop type 2 diabetes in the long run, is a controversial issue. Here, we report a family carrying the dominant heterozygous germ line E1506K mutation in ABCC8 associated with persistent hypoglycemia in the newborn period and diabetes in adulthood. The mutation occurred as a de novo germ line mutation in the mother of the index patient. Her hypoglycemic symptoms as a child occurred after the fourth year of life and were very mild, but she developed glucose metabolism impairment in adulthood. On the other hand, in her daughter, the clinical manifestations of the disease occurred in the neonatal period and were more severe, leading to episodes of tonic–clonic seizures that were well controlled with octreotide or diazoxide. Our data corroborate the hypothesis that the dominant E1506K ABCC8 mutation, responsible for CHI, predisposes to the development of glucose intolerance and diabetes later in life.     

Association Between Mannose‐Binding Lectin Gene Polymorphisms and Pre‐eclampsia in Brazilian Women

Citation Vianna P, da Silva GK, dos Santos BP, Bauer ME, Dalmáz CA, Bandinelli E, Chies JAB. Association between Mannose‐Binding Lectin gene polymorphisms and pre‐eclampsia in Brazilian Women. Am J Reprod Immunol 2010 Problem Mannose‐binding lectin (MBL) is involved in the maintenance of an inflammatory environment in uterus. High MBL levels have been associated with successful pregnancies whereas low levels are involved in pre‐eclampsia (PE) development. Here, we evaluated MBL2 gene polymorphisms in the structural and promoter regions addressing their association with PE. Method of study DNA samples from 162 control pregnant women and 157 pregnant PE women were genotyped and data compared with demographic and clinical characteristics. Results High frequency of C and D alleles (related to low MBL levels) was observed in PE women when compared to controls (C: 0.08 versus 0.03, P = 0.006; D: 0.10 versus 0.05, P = 0.009). Grouping the MBL genotypes according to phenotype, a higher frequency of OO genotype was observed in PE women when compared to control women (0.15 versus 0.04, P = 0.007). Conclusion Our data suggest that women with genotypes associated with low MBL levels could be potential PE developers.     

Tissue inhibitor of metalloproteinase-3 is up-regulated by transforming growth factor-beta1 in vitro and expressed in fibroblastic foci in vivo in idiopathic pulmonary fibrosis

Idiopathic pulmonary fibrosis (IPF) is characterized by fibroblast expansion and extracellular matrix accumulation. However, the mechanisms involved in matrix remodeling have not been elucidated. In this study, the authors aimed to evaluate the expression of the tissue inhibitors of matrix metalloproteinases (TIMPs) in human fibroblasts and whole tissues from IPF and normal lungs. They also determined the role of mitogen-activated protein kinase (MAPK) in TIMP3 expression. TIMP1, TIMP2, and TIMP3 were highly expressed in lung fibroblasts. Transforming growth factor (TGF)-beta1, a profibrotic mediator, induced strong up-regulation of TIMP3 at the mRNA and protein levels. The authors examined whether the MAPK pathway was involved in TGF-beta1-induced TIMP3 expression. TGF-beta1 induced the phosphorylation of p38 and extracellular signal-regulated kinase (ERK)1/2. Biochemical blockade of p38 by SB203580, but not of the ERK MAPK pathway, inhibited the effect of this factor. The effect was also blocked by the tyrosine kinase inhibitor genistein and by antagonizing TGF-beta1 receptor type I (activin-linked kinase [ALK5]). In IPF tissues TIMP3 gene expression was significantly increased and the protein was localized to fibroblastic foci and extracellular matrix. Our findings suggest that TGF-beta1-induced TIMP3 may be an important mediator in lung fibrogenesis.     

Myositis-specific and myositis-associated antibodies in a series of eighty-eight Mediterranean patients with idiopathic inflammatory myopathy

OBJECTIVE: To determine the prevalence of myositis-specific autoantibodies (MSAs) and myositis-associated autoantibodies (MAAs) and their clinical and immunogenetic correlations in Mediterranean patients with idiopathic inflammatory myopathies. METHODS: Sera from 88 patients were studied for MSAs and MAAs by RNA and protein immunoprecipitation. HLA typing was performed by sequence-specific primer- and sequence-specific oligonucleotide-polymerase chain reaction and serology. Statistical analyses were performed with Student's t-test and Fisher's exact test. Cumulative survival probabilities were estimated by the Kaplan-Meier method and Cox regression analysis. RESULTS: Twenty-eight patients (30%) had MSAs, most commonly antisynthetase antibodies (23.9%). Six patients (7.5%) had anti-Mi-2 antibodies. No anti-signal recognition particles were found. Arthritis, mechanic's hands, interstitial lung disease, and sicca syndrome were more prevalent in patients with antisynthetase antibodies. Dysphagia and the need for more treatment courses were more frequent in patients who were anti-Mi-2 positive. Forty-three patients (48%) had MAAs, 20 (22%) with anti-Ro 60 and 18 (20.4%) with anti-Ro 52. Ten patients (11.4%) were positive for anti-PM-Scl, 6 (6.8%) for anti-RNP, and 1 for anti-Ku antibodies. Patients with PM-Scl, RNP, or Ro antibodies were more often classified as having overlap syndrome. Immunogenetic studies found a significant association between HLA-DR3 and the presence of antisynthetase antibodies (P = 0.049), anti-PM-Scl antibodies (P = 0.017), and interstitial lung disease (P = 0.03). No statistically significant differences in mortality, survival, or clinical course were observed between patients positive for MSAs or MAAs and the remaining patients. CONCLUSION: These results are consistent with those from other published series, although some differences warrant consideration. Autoantibody studies may be useful for defining more homogeneous groups of patients with idiopathic inflammatory myopathies.