Browsing by Author "Bastos, M"
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- Diabetes Mellitus após transplante renalPublication . Ruas, L; Bastos, M; Alves, R; Rodrigues, D; Barros, L; Mota, A; Carvalheiro, M; Ruas, A; Furtado, AL
- Hiperosmolaridade Diabética: análise retrospectiva de 60 casosPublication . Campos, MV; Bastos, M; Martins, T; Leitão, P; Lemos, MC; Carvalheiro, M; Ruas, AAIMS AND METHODS: Our aims were to determine the frequency of diabetic hyperosmolality (DH) in our Department, its causes, therapeutic implications and evolution. A five-years retrospective study was performed in 60 patients regarding age, sex, type and duration of diabetes mellitus (DM), previous antidiabetic therapy, underlying diseases, biochemical data, precipitating factors, therapeutic management and outcome. RESULTS: The hyperosmolar coma was responsible for 90% of the metabolic comas and for 3% of the diabetic patients. The median age of the cohort was 54.6 +/- 9.4 years, being females 61.7% and males 38.3% In 40% no prior diagnosis of DM was made and in the remaining patients the previous antidiabetic therapy was unknown in 61%. Altered consciousness was found in 90%, being 28% in coma. The metabolic acidosis was detectable in 22.2%, the average glycaemia was 956 +/- 267 mg/dl and the osmolality was 349.4 +/- 34.3 mosm/l. The precipitating factors were: poor metabolic control in all patients (HbA1C 12.5 +/- 2.75%), infections in 76.6%, suspension of antidiabetic therapy in 10% and concomitant hyperglycaemic drugs in 6.6% of patients. The global mortality was 20%. CONCLUSIONS: The majority of the situations could be preventable if an attempted screening and diagnosis of DM was made and precipitating factors avoid or promptly treated.
- Kidney transplantation and diabetes: posttransplantation malignancyPublication . Bastos, M; Baptista, C; Campos, MV; Alves, R; Freitas, L; Bastos, C; Leitão, P; Lemos, MC; Mota, A; Furtado, AL; Carvalheiro, M
- Kidney transplantation and posttransplantation diabetes: nutritional evaluationPublication . Loureiro, H; Silva, RS; Machado, C; Bastos, M; Baptista, C; Alves, R; Mota, A; Furtado, AL; Carvalheiro, M; Saldanha, MH
- Kidney transplantation with corticosteroid-free maintenance immunosuppression: a single center analysis of graft and patient survivalsPublication . Filipe, R; Mota, A; Alves, R; Bastos, C; Macário, F; Figueiredo, A; Roseiro, A; Parada, B; Sá, H; Nunes, P; Bastos, MThe purpose of this study was to assess the impact of a corticosteroid-free maintenance immunosuppression on graft survival in kidney transplantation. We analyzed 79 patients who were transplanted between June 1, 2006 and May 31, 2007. We excluded hyperimmunized patients, second transplantations, living donors, and black recipients. Patients underwent induction with thymoglobulin or basiliximab, followed by treatment with mycophenolate mofetil (MMF), tacrolimus, and methylprednisolone. On the 5th day, the patients were divided into 2 groups: group A (n = 45) discontinued steroid therapy; group B (n = 34) continued prednisone therapy. We performed a comparative analysis of incidence of delayed graft function (DGF), acute rejection episodes (ARE), renal function at 6 and 12 months, graft and patient survivals, causes of graft loss, and mortality. The 2 groups were similar for donor, recipient, and graft characteristics. The incidences of DGF were 8.9% in group A and 14.7% in group B; those for ARE were 2.3% in group A and 13.8% in group B (P = .077). The mean serum creatinine levels at 6 and 12 months were similar. There were 8 graft losses: 3 in group A (3 deaths with functioning grafts) and 5 in group B (1 death, 3 vascular causes, 1 kidney nonfunction). The 4 deaths were due to infection (n = 3) or neoplasia (n = 1). Graft survivals at 1 year were 98% in group A and 85% in group B, and patient survivals were 98% and 97%, respectively. An immunosuppressive regimen using antibody induction and steroid-free treatment proved to be effective in low-risk patients.
- Lack of association of vitamin D receptor gene polymorphisms with susceptibility to type 1 diabetes mellitus in the Portuguese populationPublication . Lemos, MC; Fagulha, A; Coutinho, E; Gomes, L; Bastos, M; Barros, L; Carrilho, F; Geraldes, E; Regateiro, FJ; Carvalheiro, MThe vitamin D receptor (VDR) gene is a candidate gene for susceptibility to autoimmune disorders. Association studies of VDR polymorphisms and risk of type 1 diabetes often produced conflicting results in different ethnic backgrounds. The aim of this study was to test for association between common VDR polymorphisms and the genetic susceptibility to type 1 diabetes in the Portuguese population. We genotyped 207 patients with type 1 diabetes and 249 controls for the FokI T>C (rs10735810), BsmI A>G (rs1544410), ApaI G>T (rs7975232), and TaqI C>T (rs731236) single nucleotide polymorphisms by polymerase chain reaction and restriction fragment length polymorphism analysis. The distribution of VDR genotype, allele, and haplotype frequencies did not differ significantly between patients and controls. These data suggest that the single nucleotide polymorphisms of the VDR gene are unlikely to contribute significantly to type 1 diabetes susceptibility in the Portuguese population.
- Nefropatia diabética: protocolo de estudo pré-transplantação renalPublication . Baptista, C; Bastos, M; Paiva, S; Martins, T; Leitão, P; Lemos, MC; Alves, R; Bastos, C; Mota, A; Carvalheiro, M; Furtado, AL; Ruas, ABetween May 1990 and October 1998, 67 diabetic patients with end-stage renal disease, on dialysis, were submitted to a standardized protocol in order to assess the coexistence and degree of other diabetic and nondiabetic complications that could affect transplantation. Some of the results were analysed. Type 2 diabetic patients had more abnormal results on the lower limbs doppler ultrasound and on the lower limbs arteriography than type 1 (p < 0.05). Type 2 diabetic patients had more cardiovascular complications so the decision to transplant should be taken on a case by case basis.
- Nefropatia diabética: taxa de filtração glomerular calculada e estimadaPublication . Guimarães, J; Bastos, M; Melo, M; Carvalheiro, MOBJECTIVE: To assess in diabetic nephropathy, the accuracy of estimated creatinine clearance (calculated with the Cockroft Gault formula) and the clearance of the Tc99m-DTPA, to measure the glomerular filtration rate (GFR). PATIENTS AND METHODS: We analysed the GFR measure by Tc99m-DTPA method and the estimated by the Cockroft Gault formula, in 21 subjects with type 1 or type 2 diabetes. RESULTS: There was a strong positive correlation between the two methods but the Cockroft Gault formula underestimated the GFR. CONCLUSIONS: The formula gives a accurate estimates of GFR, when GFR is <100 ml/min/1,73 m2. Beside the underestimation, the formula could be used in the management of diabetic nephropathy because the repeated isotope assessments of renal function are impracticable.
- Noninvasive analysis of hepatic glycogen kinetics before and after breakfast with deuterated water and acetaminophenPublication . Jones, JG; Fagulha, A; Barosa, C; Bastos, M; Barros, L; Baptista, C; Caldeira, MM; Carvalheiro, MThe contributions of hepatic glycogenolysis to fasting glucose production and direct pathway to hepatic glycogen synthesis were quantified in eight type 1 diabetic patients and nine healthy control subjects by ingestion of (2)H(2)O and acetaminophen before breakfast followed by analysis of urinary water and acetaminophen glucuronide. After overnight fasting, enrichment of glucuronide position 5 relative to body water (G5/body water) was significantly higher in type 1 diabetic patients compared with control subjects, indicating a reduced contribution of glycogenolysis to glucose production (38 +/- 3 vs. 46 +/- 2%). Following breakfast, G5/body water was significantly higher in type 1 diabetic patients, indicating a smaller direct pathway contribution to glycogen synthesis (47 +/- 2 vs. 59 +/- 2%). Glucuronide hydrogen 2 enrichment (G2) was equivalent to body water during fasting (G2/body water 0.94 +/- 0.03 and 1.02 +/- 0.06 for control and type 1 diabetic subjects, respectively) but was significantly lower after breakfast (G2/body water 0.78 +/- 0.03 and 0.82 +/- 0.05 for control and type 1 diabetic subjects, respectively). The reduced postprandial G2 levels reflect incomplete glucose-6-phosphate-fructose-6-phosphate exchange or glycogen synthesis from dietary galactose. Unlike current measurements of human hepatic glycogen metabolism, the (2)H(2)O/acetaminophen assay does not require specialized on-site clinical equipment or personnel.
- Novel FGFR1 mutations in Kallmann syndrome and normosmic idiopathic hypogonadotropic hypogonadism: evidence for the involvement of an alternatively spliced isoformPublication . Gonçalves, C; Bastos, M; Pignatelli, D; Borges, T; Aragüés, JM; Fonseca, F; Pereira, BD; Socorro, S; Lemos, MCOBJECTIVE: To determine the prevalence of fibroblast growth factor receptor 1 (FGFR1) mutations and their predicted functional consequences in patients with idiopathic hypogonadotropic hypogonadism (IHH). DESIGN: Cross-sectional study. SETTING: Multicentric. PATIENT(S): Fifty unrelated patients with IHH (21 with Kallmann syndrome and 29 with normosmic IHH). INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Patients were screened for mutations in FGFR1. The functional consequences of mutations were predicted by in silico structural and conservation analysis. RESULT(S): Heterozygous FGFR1 mutations were identified in six (12%) kindreds. These consisted of frameshift mutations (p.Pro33-Alafs*17 and p.Tyr654*) and missense mutations in the signal peptide (p.Trp4Cys), in the D1 extracellular domain (p.Ser96Cys) and in the cytoplasmic tyrosine kinase domain (p.Met719Val). A missense mutation was identified in the alternatively spliced exon 8A (p.Ala353Thr) that exclusively affects the D3 extracellular domain of FGFR1 isoform IIIb. Structure-based and sequence-based prediction methods and the absence of these variants in 200 normal controls were all consistent with a critical role for the mutations in the activity of the receptor. Oligogenic inheritance (FGFR1/CHD7/PROKR2) was found in one patient. CONCLUSION(S): Two FGFR1 isoforms, IIIb and IIIc, result from alternative splicing of exons 8A and 8B, respectively. Loss-of-function of isoform IIIc is a cause of IHH, whereas isoform IIIb is thought to be redundant. Ours is the first report of normosmic IHH associated with a mutation in the alternatively spliced exon 8A and suggests that this disorder can be caused by defects in either of the two alternatively spliced FGFR1 isoforms