Uso do prontuário eletrônico na assistência pré-natal às portadoras de diabetes na gestação

Objetivo Apresentar e validar um registro eletrônico de saúde (RES) multifuncional para atendimento ambulatorial a portadoras de endocrinopatias na gestação e comparar a taxa de preenchimento de informações de saúde com o prontuário convencional. Métodos Desenvolvemos um RES denominado Ambulatório de Endocrinopatias na Gestação eletrônico (AMBEG) para registro sistematizado das informações de saúde. O AMBEG foi utilizado para atendimento obstétrico e endocrinológico de gestantes acompanhadas no ambulatório de endocrinopatias na gestação na maternidade referência em gestação de alto risco na Bahia, no período de janeiro de 2010 a dezembro de 2013. Aleatoriamente foramselecionadas 100 pacientes atendidas como AMBEG e 100 pacientes atendidas comprontuário convencional comregistro em papel e comparou-se a taxa de preenchimento de informações clínicas. Resultados Foram realizados 1461 atendimentos com o AMBEG: 253, 963 e 245 respectivamente, admissões, consultas de seguimento e puerpério. Eram portadoras de diabetes 77,2% e sendo 60,1% portadoras de diabetes pré-gestacional. O AMBEG substituiu, satisfatoriamente, o prontuário convencional. O percentual de informações clínicas registradas em ambos os prontuários foi significativamente maior no AMBEG: queixas clínicas (100 versus 87%, p < 0,01), altura uterina (89 versus 75%, p = 0,01), ganho de peso total (91 versus 40%, p < 0,01) e dados específicos sobre o diabetes (dieta, esquema de insulina, controle glicêmico e manejo de hipoglicemias) revelando diferença significativa (p < 0,01). A possibilidade de exportar dados clínicos para planilhas facilitou e agilizou a análise estatística de dados. Conclusões O AMBEG é uma ferramenta útil no atendimento clínico a mulheres portadoras de endocrinopatias na gestação. A taxa de preenchimento de informações clínicas foi superior à do prontuário convencional.

Correlação das dosagens de frutosamina e de hemoglobina glicosilada com o perfil glicêmico em gestantes com diabetes mellitus

Objetivo Avaliar se há correlação das dosagens de frutosamina e de hemoglobina glicosilada (HbA1c) com as frequências de desvios de glicemia capilar em gestantes com diabetes mellitus. Métodos estudo observacional, retrospectivo, de corte transversal, incluindo todas as gestantes comdiabetes que iniciaram o pré-natal emhospital terciário de ensino durante o ano de 2014 e que apresentavam pelo menos 20 dias de auto monitoramento glicêmico previamente às dosagens séricas de frutosamina e de HbA1c. Os desvios de glicemia capilar foram considerados "hipoglicemias" quando menores que 70mg/dL ou "hiperglicemias" quando acima do alvo glicêmico terapêutico para o horário. Foram testadas as correlações lineares par a par das dosagens de frutosamina e de HbA1c com as frequências de hipoglicemias e de hiperglicemias capilares pelo teste Tau-b de Kendall. Na sequência, foi avaliada a regressão linear entre as dosagens de HbA1c e de frutosamina e as frequências de hipoglicemias e de hiperglicemias. Resultados Foram incluídas 158 gestantes que contribuíram com 266 amostras para dosagem sérica de frutosamina e HbA1c. As dosagens de frutosamina e de HbA1c apresentaram, respectivamente, coeficientes τ de Kendall de 0,29 (p < 0,001) e 0,5 (p < 0,001) com a frequência de hiperglicemias, e de 0,09 (p = 0,04) e 0,25 (p < 0,001) com a frequência de hipoglicemias capilares. No modelo de regressão linear, as dosagens de frutosamina e de HbA1c apresentaram, respectivamente, coeficientes de determinação R2 = 0,26 (p < 0,001) e R2 = 0,51 (p < 0,001) para a predição de hiperglicemias, e R2 = 0,03 (p = 0,003) e R2 = 0,059 (p < 0,001) para a predição de hipoglicemias. Conclusão As dosagens de frutosamina e de HbA1c apresentam correlação fraca a moderada com as frequências de hiperglicemias e hipoglicemias capilares no auto monitoramento glicêmico e não são capazes de traduzir com precisão os desvios da meta glicêmica no tratamento de gestantes com diabetes.

Estudo comparativo das estruturas do segmento anterior de olhos de cães normais e com catarata, portadores ou não de Diabetes mellitus, avaliados por biomicroscopia ultrassônica

A catarata representa uma das principais causas de cegueira em cães, sendo que as alterações metabólicas provocadas pelo Diabetes mellitus (DM), constituem a segunda causa mais comum de catarata nesta espécie. A biomicroscopia ultrassônica (UBM) é um método ultrassonográfico de alta frequência (50 MHz) que permite a obtenção de imagens do modo B de qualidade microscópica. Este estudo objetivou, por meio do uso da UBM, comparar as estruturas do segmento anterior de olhos de cães com catarata, diabética e não-diabética, às de cães normais, para verificar possíveis alterações decorrentes do DM. Os parâmetros avaliados foram espessura da córnea, profundidade da câmara anterior, aumento de celularidade no interior da câmara anterior e medida do ângulo iridocorneal. Foram realizados exames de 87 olhos de 47 animais da espécie canina, divididos em 3 grupos: grupo controle (GCO), grupo de portadores de catarata não-diabéticos (GCAT) e o grupo dos diabéticos (GDM). Os resultados revelam que o grupo dos diabéticos apresentou maiores espessuras de córnea que os demais grupos enquanto o grupo controle apresentou maiores câmaras anteriores. Encontrou-se aumento de celularidade em câmara anterior apenas nos grupos com catarata. Quando analisadas as medidas do ângulo iridocorneal, não houve diferença entre os 3 grupos. Com base no que foi aferido, permite-se concluir que olhos de cães diabéticos com catarata apresentam maior espessura de córnea central que olhos de cães com catarata de outras etiologias e de cães normais, que há diminuição da câmara anterior, com aumento de celularidade, em olhos de cães com catarata, quando comparados a cães normais e que não há diferença na medida do ângulo iridocorneal em olhos de cães com catarata, diabética ou não, e de cães normais.

Standardization of a computerized method for calculating autonomic function test responses in healthy subjects and patients with diabetes mellitus

The objectives of the present study were 1) to compare results obtained by the traditional manual method of measuring heart rate (HR) and heart rate response (HRR) to the Valsalva maneuver, standing and deep breathing, with those obtained using a computerized data analysis system attached to a standard electrocardiograph machine; 2) to standardize the responses of healthy subjects to cardiovascular tests, and 3) to evaluate the response to these tests in a group of patients with diabetes mellitus (DM). In all subjects (97 healthy and 143 with DM) we evaluated HRR to deep breathing, HRR to standing, HRR to the Valsalva maneuver, and blood pressure response (BPR) to standing up and to a sustained handgrip. Since there was a strong positive correlation between the results obtained with the computerized method and the traditional method, we conclude that the new method can replace the traditional manual method for evaluating cardiovascular responses with the advantages of speed and objectivity. HRR and BPR of men and women did not differ. A correlation between age and HRR was observed for standing (r = -0.48, P<0.001) and deep breathing (r = -0.41, P<0.002). Abnormal BPR to standing was usually observed only in diabetic patients with definite and severe degrees of autonomic neuropathy.

Pituitary-thyroid axis in short- and long-term experimental diabetes mellitus

Short-term experimental diabetes mellitus (DM) produces a significant decrease in serum thyroid hormones, a decreased or normal serum thyroid-stimulating hormone (TSH) and a reduction in hepatic and renal T4-5'-deiodination. However, little is known about the effects of chronic diabetes mellitus on the pituitary-thyroid axis function. We evaluated the changes induced by very short-term (6 days), short-term (15 days) and chronic (6 months) streptozotocin-induced diabetes mellitus in 3-month old female Dutch-Miranda rat serum T4, serum TSH and T4-5'-deiodinase activity in the thyroid and pituitary glands. Serum hormones were determined by specific radioimmunoassays. Iodothyronine-5'-deiodinase activities were assayed in the thyroid and pituitary microsomal fractions using 2 µM T4 as substrate. Mean serum T4 was significantly decreased from 3.3 to 2.0 µg/dl 6 days after diabetes mellitus induction, and from 2.2 to 1.5 µg/dl after 15 days of DM, with no significant changes in serum TSH, indicating a decreased pituitary TSH responsiveness to the diminished suppression by T4, even though pituitary T4-5'-deiodinase activity was unchanged. Thyroid T4-5'-deiodinase was unchanged after 6 days of diabetes mellitus, but was significantly increased from 20.6 to 37.0 pmol T3/mg protein after 15 days. Six months after diabetes mellitus induction, both serum T4 and thyroid T4-5'-deiodinase returned to normal ranges and serum TSH was unchanged, although pituitary T4-5'-deiodinase was now significantly decreased from 2.7 to 1.7 pmol T3/mg protein. These findings indicate that some kind of adaptation to chronic insulinopenia may occur at the thyroid level, but this does not seem to be true for the pituitary

Factors associated with the development of renal complications of diabetes mellitus in São Paulo city

The incidence of diabetic end-stage renal failure (ESRF) varies worldwide and risk factors have been demonstrated in several populations. The objective of the present study was to identify possible factors associated with the risk of development of ESRF in patients with diabetes mellitus (DM). Two groups of diabetic subjects were included in a case-control study: 1) one group was submitted to renal replacement therapies, attending dialysis centers in São Paulo city and 2) the same number of controls without clinical nephropathy (two negative dipstick tests for urine protein), matched for duration of DM, were obtained from an outpatient clinic. A standardized questionnaire was used by a single investigator and additional data were obtained from the medical records of the patients. A total of 290 diabetic patients from 33 dialysis centers were identified, and 266 questionnaires were considered to contain reliable information. Male/female ratios were 1.13 for ESRF and 0.49 for the control group. A higher frequency of men was observed in the ESRF group when compared with controls (53 vs 33%, P<0.00001), although logistic regression analysis did not confirm an association of gender and diabetic nephropathy (DN). Similar proportions of non-white individuals were found for both groups. Patients with insulin-dependent diabetes mellitus (IDDM) were less common than patients with non-insulin-dependent diabetes mellitus (NIDDM), particularly in the control group (3.4 vs 26.3%, P<0.00001, for controls and ESRF patients, respectively); this type of DM was associated with a higher risk of ESRF than NIDDM, as determined by univariate analysis or logistic regression (OR = 4.1). Hypertension by the time of the DM diagnosis conferred a 1.4-fold higher risk of ESRF (P = 0.04), but no difference was observed concerning the presence of a family history. Association between smoking and alcohol habits and increased risk was observed (OR = 4.5 and 5.9, respectively, P<0.001). A 2.4-fold higher risk of ESRF was demonstrated in patients with multiple hospitalizations due to DM decompensation, which suggested poor metabolic control. Photocoagulation and neuropathy were found to be strongly associated with ESRF but not with macrovascular disease. Data collected in our country reinforce the higher risk attributable to IDDM and the association between hypertension and the progression of DN. Indirect evidence for an association with metabolic control is also suggested

Autoradiographic thyroid evaluation in short-term experimental diabetes mellitus

Previous studies have shown that in vitro thyroid peroxidase (TPO) iodide oxidation activity is decreased and thyroid T4-5'-deiodinase activity is increased 15 days after induction of experimental diabetes mellitus (DM). In the present study we used thyroid histoautoradiography, an indirect assay of in vivo TPO activity, to determine the possible parallelism between the in vitro and in vivo changes induced by experimental DM. DM was induced in male Wistar rats (about 250 g body weight) by a single ip streptozotocin injection (45 mg/kg), while control (C) animals received a single injection of the vehicle. Seven and 30 days after diabetes induction, each diabetic and control animal was given ip a tracer dose of 125I (2 µCi), 2.5 h before thyroid excision. The glands were counted, weighed, fixed in Bouin's solution, embedded in paraffin and cut. The sections were stained with HE and exposed to NTB-2 emulsion (Kodak). The autohistograms were developed and the quantitative distribution of silver grains was evaluated with a computerized image analyzer system. Thyroid radioiodine uptake was significantly decreased only after 30 days of DM (C: 0.38 ± 0.05 vs DM: 0.20 ± 0.04%/mg thyroid, P<0.05) while in vivo TPO activity was significantly decreased 7 and 30 days after DM induction (C: 5.3 and 4.5 grains/100 µm2 vs DM: 2.9 and 1.6 grains/100 µm2, respectively, P<0.05 ). These data suggest that insulin deficiency first reduces in vivo TPO activity during short-term experimental diabetes mellitus

Distribution of HLA-DRB1 alleles in a mixed population with insulin-dependent diabetes mellitus from the Southeast of Brazil

HLA class II genes are strongly associated with susceptibility and resistance to insulin-dependent diabetes mellitus (IDDM). The present study reports the HLA-DRB1 genotyping of 41 IDDM patients and 99 healthy subjects from the Southeast of Brazil (Campinas region). Both groups consisted of an ethnic mixture of Caucasian, African Negro and Amerindian origin. HLA-DRB1*03 and *04 alleles were found at significantly higher frequencies among IDDM patients compared to the controls (DRB1*03: 48.8% vs 18.2%, P<0.005, RR = 4.27; DRB1*04: 43.9% vs 15.1%, P<0.008, RR = 4.37) and were associated with a susceptibility to the disease. DRB1*03/*04 heterozygosity conferred a strong IDDM risk (RR = 5.44). In contrast, the HLA-DRB1*11 allele frequency was lower among IDDM patients (7.3% vs 26.3% in controls), but the difference was not significant. These data agree with those described for other populations and allow genetic characterization of IDDM in Brazil

Abnormal nocturnal blood pressure fall in normotensive adolescents with insulin-dependent diabetes is ameliorated following glycemic improvement

Lack of the physiological nocturnal fall in blood pressure (BP) has been found in diabetics and it seems to be related to the presence of diabetic complications. The present study examined the changes in the nocturnal BP pattern of 8 normotensive insulin-dependent diabetic adolescents without nephropathy following improvement in glycemic control induced by an 8-day program of adequate diet and exercise. The same number of age- and sex-matched control subjects were studied. During the first and eighth nights of the program, BP was obtained by ambulatory BP monitoring. After a 10-min rest, 3 BP and heart rate (HR) recordings were taken and the mean values were considered to represent their awake values. The monitor was programmed to cuff insufflation every 20 min from 10:00 p.m. to 7:00 a.m. The glycemic control of diabetics improved since glycemia (212.0 ± 91.5 to 140.2 ± 69.1 mg/dl, P<0.03), urine glucose (12.7 ± 11.8 to 8.6 ± 6.4 g/24 h, P = 0.08) and insulin dose (31.1 ± 7.7 to 16.1 ± 9.7 U/day, P<0.01) were reduced on the last day. The mean BP of control subjects markedly decreased during the sleeping hours of night 1 (92.3 ± 6.4 to 78.1 ± 5.0 mmHg, P<0.001) and night 8 (87.3 ± 6.7 to 76.9 ± 3.6 mmHg, P<0.001). Diabetic patients showed a slight decrease in mean BP during the first night. However, the fall in BP during the nocturnal period increased significantly on the eighth night. The average awake-sleep BP variation was significantly higher at the end of the study (4.2 vs 10.3%, P<0.05) and this ratio turned out to be similar to that found in the control group (10.3 vs 16.3%). HR variation also increased on the eighth night in the diabetics. Following the metabolic improvement obtained at the end of the period, the nocturnal BP variation of diabetics was close to the normal pattern. We suggest that amelioration of glycemic control may influence the awake-sleep BP and HR differences. This effect may be due at least in part to an attenuated insulin stimulation of sympathetic activity

Incidence of type 1 diabetes mellitus in Passo Fundo, RS, Brazil

To establish the incidence of type 1 diabetes among children (infants to 14 years of age) in the city of Passo Fundo, Rio Grande do Sul, Brazil (population under 15 years = 50,098), during the period of January to December 1996, a retrospective and prospective population-based registry was established, using physician reports of newly diagnosed patients under 15 years of age with type 1 diabetes as the primary source of case identification. Primary and nursery schools and a general call through the media (newspapers, radio and television) was the secondary source. Data were calculated according to the methods recommended by the WHO (1990). Six new cases were identified. Case ascertainment was estimated at 100%. The incidence of type 1 diabetes in the year 1996 was 12/100,000 inhabitants. These data indicate that the incidence of childhood type 1 diabetes in a subtropical region in the Southern part of Brazil was similar to that observed in developed countries throughout the world. The inability to demonstrate the North-South gradient is probably due to the European origin of inhabitants of the city.

Frequency of islet cell autoantibodies (IA-2 and GAD) in young Brazilian type 1 diabetes patients

Type 1 diabetes, as an autoimmune disease, presents several islet cell-specific autoantibodies such as islet cell antibody (ICA), anti-insulin, anti-glutamic acid decarboxylase (GAD) and the antibody (Ab) against tyrosine phosphatase (PTP)-like protein known as ICA-512 (IA-2). In order to determine the frequency of the anti-GAD and anti-IA-2 autoantibodies in Brazilian type 1 diabetes patients we studied 35 diabetes mellitus (DM) type 1 patients with recent-onset disease (£12 months) and 37 type 1 diabetes patients with long-duration diabetes (>12 months) who were compared to 12 children with normal fasting glucose. Anti-GAD65 and anti-IA-2 autoantibodies were detected with commercial immunoprecipitation assays. The frequency of positive results in recent-onset DM type 1 patients was 80.0% for GADAb, 62.9% for IA-2Ab and 82.9% for GADAb and/or IA-2Ab. The long-duration type 1 diabetes subjects presented frequencies of 54.1% for GADAb and IA-2Ab, and 67.5% for GAD and/or IA-2 antibodies. The control group showed no positive cases. Anti-GAD and IA-2 assays showed a high frequency of positivity in these Brazilian type 1 diabetes patients, who presented the same prevalence as a Caucasian population.

Transforming growth factor beta activity in urine of patients with type 2 diabetes and diabetic nephropathy

Diabetic nephropathy (DN) is characterized structurally by progressive mesangial deposition of extracellular matrix (ECM). Transforming growth factor-ß (TGF-ß) is considered to be one of the major cytokines involved in the regulation of ECM synthesis and degradation. Several studies suggest that an increase in urinary TGF-ß levels may reflect an enhanced production of this polypeptide by the kidney cells. We evaluated TGF-ß in occasional urine samples from 14 normal individuals and 23 patients with type 2 diabetes (13 with persistent proteinuria >500 mg/24 h, DN, 6 with microalbuminuria, DMMA, and 4 with normal urinary albumin excretion, DMN) by enzyme immunoassay. An increase in the rate of urinary TGF-ß excretion (pg/mg UCreat.) was observed in patients with DN (296.07 ± 330.77) (P<0.001) compared to normal individuals (17.04 ± 18.56) (Kruskal-Wallis nonparametric analysis of variance); however, this increase was not observed in patients with DMMA (25.13 ± 11.30) or in DMN (18.16 ± 11.82). There was a positive correlation between the rate of urinary TGF-ß excretion and proteinuria (r = 0.70, a = 0.05) (Pearson's analysis), one of the parameters of disease progression.

Pancreatic nitric oxide and oxygen free radicals in the early stages of streptozotocin-induced diabetes mellitus in the rat

The objective of the present study was to explore the regulatory mechanisms of free radicals during streptozotocin (STZ)-induced pancreatic damage, which may involve nitric oxide (NO) production as a modulator of cellular oxidative stress. Removal of oxygen species by incubating pancreatic tissues in the presence of polyethylene glycol-conjugated superoxide dismutase (PEG-SOD) (1 U/ml) produced a decrease in nitrite levels (42%) and NO synthase (NOS) activity (50%) in diabetic but not in control samples. When NO production was blocked by N G-monomethyl-L-arginine (L-NMMA) (600 µM), SOD activity increased (15.21 ± 1.23 vs 24.40 ± 2.01 U/mg dry weight). The increase was abolished when the NO donor, spermine nonoate, was added to the incubating medium (13.2 ± 1.32). Lipid peroxidation was lower in diabetic tissues when PEG-SOD was added (0.40 ± 0.02 vs 0.20 ± 0.03 nmol/mg protein), and when L-NMMA blocked NOS activity in the incubating medium (0.28 ± 0.05); spermine nonoate (100 µM) abolished the decrease in lipoperoxide level (0.70 ± 0.02). We conclude that removal of oxygen species produces a decrease in pancreatic NO and NOS levels in STZ-treated rats. Moreover, inhibition of NOS activity produces an increase in SOD activity and a decrease in lipoperoxidation in diabetic pancreatic tissues. Oxidative stress and NO pathway are related and seem to modulate each other in acute STZ-induced diabetic pancreas in the rat.

Lack of antidiabetic effect of a Eugenia jambolana leaf decoction on rat streptozotocin diabetes

Streptozotocin-diabetic rats were treated for 17 days with a decoction of Eugenia jambolana (Myrtaceae) leaves (15%, w/v) as a substitute for water. Body weight, food and fluid intake, urine volume, glycemia, urinary glucose and urea were evaluated every 5 days. The animals were sacrificed by decapitation and blood samples collected for the determination of glycemia, serum cholesterol, HDL-cholesterol, triglycerides and angiotensin-converting enzyme. The weight of adipose and muscle tissues was also determined. There were no statistically significant differences between treated and untreated rats for any of the biochemical or physiological parameters. We conclude that, at least in this experimental model, Eugenia jambolana leaf decoction has no antidiabetic activity.

Is pancreas development abnormal in the non-obese diabetic mouse, a spontaneous model of type I diabetes?

Despite extensive genetic and immunological research, the complex etiology and pathogenesis of type I diabetes remains unresolved. During the last few years, our attention has been focused on factors such as abnormalities of islet function and/or microenvironment, that could interact with immune partners in the spontaneous model of the disease, the non-obese diabetic (NOD) mouse. Intriguingly, the first anomalies that we noted in NOD mice, compared to control strains, are already present at birth and consist of 1) higher numbers of paradoxically hyperactive ß cells, assessed by in situ preproinsulin II expression; 2) high percentages of immature islets, representing islet neogenesis related to neonatal ß-cell hyperactivity and suggestive of in utero ß-cell stimulation; 3) elevated levels of some types of antigen-presenting cells and FasL+ cells, and 4) abnormalities of extracellular matrix (ECM) protein expression. However, the colocalization in all control mouse strains studied of fibroblast-like cells (anti-TR-7 labeling), some ECM proteins (particularly, fibronectin and collagen I), antigen-presenting cells and a few FasL+ cells at the periphery of islets undergoing neogenesis suggests that remodeling phenomena that normally take place during postnatal pancreas development could be disturbed in NOD mice. These data show that from birth onwards there is an intricate relationship between endocrine and immune events in the NOD mouse. They also suggest that tissue-specific autoimmune reactions could arise from developmental phenomena taking place during fetal life in which ECM-immune cell interaction(s) may play a key role.