Tight glucose control versus intermediate glucose control: a quasi-experimental study.

Intensive insulin treatment is associated with an increased risk of hypoglycaemia. The purpose of this study was to evaluate two different strategies: tight glucose control (TGC) versus intermediate glucose control (IGC). In this quasi-experimental study, 130 critically ill patients were assigned to receive either the TGC protocol (n=65), according to which blood glucose levels were maintained between 4.4 and 6.1 mmol/l, or the IGC protocol (n=65), according to which blood glucose levels were maintained between 4.4 and 8.0 mmol/l. A total of 52 subjects (40%) were diabetic and 63 (49%) were septic. In the IGC group, glucose levels were stabilised in the target range for a longer period of time when compared to the TGC group (63 vs. 41%, P < 0.001). The median capillary blood glucose level was 6.7 mmol/l in the TGC group (6.2 to 7.2) and 7.9 mmol/l (7.0 to 8.5) in the IGC group (P < 0.001). The incidence of hypoglyacemia less than 2.2 mmol/l was 21.5% in the TGC group and 1.5% in the IGC group (P < 0.001), and the incidence of hypoglycaemia less than 3.3 mmol/l was 67.7 and 26.2% (P < 0.001) in the two groups, respectively. Diabetes (odds ratio 2.88, CI 1.22 to 6.84) and the TGC protocol (odds ratio 7.39, CI 3.15 to 1735) were identified as independent risk factors for hypoglycaemia less than 3.3 mmol/l. Mechanical ventilation (odds ratio 4.33, CI 1.16 to 16.13), medical illness (odds ratio 2.88, CI 1.20 to 6.99) and hypoglycaemia (< 3.3 mmol/l) (odds ratio 299, CI 1.21 to 7.41) were independent factors associated with mortality. TGC is difficult to accomplish in routine intensive care unit settings and is associated with a significant increase in the incidence of hypoglycaemia. Hypoglycaemia < 3.3 mmol/l is an independent risk factor for in-hospital mortality.

Noncardiogenic pulmonary edema complicating diabetic ketoacidosis.

OBJECTIVE: To alert physicians to the possibility of pulmonary edema as a complication of diabetic ketoacidosis. METHODS: We report a case of adult respiratory distress syndrome after resuscitative efforts to compensate the first episode of diabetic ketoacidosis in a previously healthy young woman. RESULTS: In a 26-year-old woman with a 3-day history of malaise, polyuria, nausea, and vomiting, severe hypoxia and rales developed, and intubation and mechanical ventilation became necessary. Hemodynamic evaluation and striking electron microscopic findings on open-lung biopsy confirmed the diagnosis of adult respiratory distress syndrome. Despite adequate ventilatory support and hemodynamic management, death ensued and was attributed to irresponsive and progressive acute respiratory failure due to increased pulmonary capillary permeability edema. CONCLUSION: Clinicians should be aware of this possibly fatal pulmonary complication of diabetic ketoacidosis.

Exercício físico e diabete melito / Physical exercise and diabetes mellitus

O diabete melito acomete 7,6 por cento da populaçäo brasileira entre 30 e 69 anos. O exercício tem sido recomendado como parte do tratamento. Estudos recentes têm contribuído para a compreensäo dos seus efeitos metabólicos e hormonais, tanto em indivíduos normais como em diabéticos. nos indivíduos com diabete melito dependente de insulina, o exercício näo apresenta efeito importante sobre o controle glicêmico. Deve, no entanto, ser estimulado em relaçäo aos seus demais benefícios, näo diretamente racionados à glicemia . O principal risco associado ao exercício nesses indivíduos é a hipoglicemia, que pode ser reduzido com adequado ajuste de dieta e dose de insulina decorrentes das informaçöes obtdias por emio da adequada automonitorizaçäo da glicemia. Por outro lado, nos portadores de diabete melito näo-depende de insulina, a atividade física propricia melhora em vários aspectos relacionados a sua fisiopatogênese decorrentes de resistência insulínica, sendo, portanto, um importante fator no tratamno juntamente com dienta e/ou terapêutica medicamentosa indicada. Além dos benefícios diretos relacionados com o controle glicêmico, o exercício para o diabete melito näo-dependente de insulina traz outros pontos positivos. A subpopulaçäo de portadores de diabete melito näo-dependente de insulina com intolerância moderada à glicose é a que mais parece se beneficiar da atividade física. tanto no diabete melito dependente de insulina com intorlerância moderada à glicose é a que mais parece se beneficiar d aividade física. Tanto no diabete melito dependente de insulina como no diabete melito näo-dependente de insulina, deve ser realizada availaçäo médica inicial e educaçäo específica para que sejam atingidos os resultados esperados em relaçäo ao controle metabólico e à melhora na qualidade de vida. A atividade física é um importante fator adjuvante no tratamento diabete melito, com papel bastante distinto no diabete melito dependente de insulina e no diabete melito näo-dependente de insulina.

Inhibition of thyroxine 5'-deiodination type II in cultured human placental cells by cortisol, insulin, 3', 5'-cyclic adenosine monophosphate, and butyrate.

The regulation of conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) by the type II iodothyronine deiodinating pathway was studied in normal human placental cells cultured from the chorionic membrane. T4 5'-deiodination was measured in cell sonicates after intact cells were incubated with test agents for 24 to 48 hours. Stimulation of T4 5'-deiodination occurred to a similar degree after depriving cells of thyroid hormone in serum-free medium and in medium containing 10% calf serum. Cortisol at 10 to 100 nmol/L in serum-free medium inhibited T4 5'-deiodination up to 36%, and 1 to 100 nmol/L of insulin inhibited deiodination up to 50%. Dibutyryl-cyclic AMP (dbcAMP) inhibited deiodination, but this appeared to result from the inhibitory effects of butyrate. Addition to the culture media of 8-bromo-cAMP, cholera toxin, and theophylline each caused partial inhibition of T4 5'-deiodination, strongly suggesting an inhibitory effect of raised intracellular cAMP. Neither alpha- nor beta-adrenergic agonists had any effect when added to the culture medium, nor did glucagon or cysteamine. These results demonstrate a complex, multihormonal control of human placental type II iodothyronine deiodination, and suggest that changes in the activity of this pathway may result in altered intracellular, and conceivably circulating, T3 concentrations in states of cortisol excess and marked hyperinsulinism. The factor that regulates type II deiodination via cAMP remains to be identified.

Characteristics of thyroxine 5'-deiodination in cultured human placental cells. Regulation by iodothyronines.

Human and rat placental homogenates convert L-thyroxine (T4) to 3,5,3'-L-triiodothyronine (T3) via a pathway termed type II iodothyronine deiodination. To study regulation of this pathway, cell dispersions were prepared from human placental chorionic-decidual membrane. Dispersed cells deiodinated T4 and 3,3',5'-triiodothyronine (rT3), but not T3, at the 5' position. The reaction was only slightly inhibited by 1 mM 6-n-propylthiouracil, enhanced by dithiothreitol, and substantially inhibited by 50 nM iopanoic acid. Incubation of the cells in thyroid hormone-depleted medium induced a near doubling of T4 5'-deiodination in 36-48 h, with a significant rise seen as early as 12 h. Addition of T4, rT3, or T3 to hormone-depleted medium impaired the rise in type II deiodination in a dose-dependent fashion. T4 and rT3 were equipotent in this regard, and T3 was 2-3 times less potent. T4 was effective in physiological concentrations, 6.5-13 nM in medium containing 10% calf serum, and the effect of T4 was not due to its conversion to either T3 or rT3. In cells with deiodinase activity raised by 48 h incubation in thyroid hormone-depleted medium, addition of T4, T3, or rT3 reversed the increase in 8-24 h. Secretion of prolactin and beta hCG by the dispersed cells was not substantially affected by thyroid hormone deprivation. The increase in type II deiodination during thyroid hormone deprivation appears to depend on a signal from the thyroxine molecule, per se, and could potentially defend intracellular, and/or circulating, T3 pools in pathological states of mild-to-moderate hypothyroxinemia.

Ensaio do cortisol na saliva como um metodo para a avaliacao da fracao livre serica. / Measurement of saliva cortisol as a method for the evaluation of free serum fraction

A dosagem de hormonios esteroides na saliva seria representativa da fracao livre do soro que passaria para o liquido salivar atraves da membrana basal das celulas das glandulas salivares. Desenvolvemos um metodo para a dosagem de cortisol na saliva e o aplicamos numa populacao normal e em alguns pacientes com patologias adrenais.Foi observada boa correlacao, com valores de cortisol livre plasmatico em amostras colhidas concomitantemente (r = 0,95). Os valores encontrados em individuos normais foram: as 8:00h = 350 +/- 34ng/dl (media +/- erro padrao), as 17:00h = 133 +/- 13 ng/dl e apos 1mg de dexametasona: 19 +/- 2ng/dl. Concluimos ser a dosagem de cortisol na saliva de utilidade no diagnostico de patologias adrenocorticais

Adaptacao de um radioimunoensaio de cortisol para a dosagem da fracao livre do soro obtida por dialise. / Adaptation of a radioimmunoassay for cortisol for the measurement of the serum free fraction obtained by dialysis

Os autores apresentam o desenvolvimento de um metodo para a dosagem do cortisol livre do soro baseado na dosagem radioimunologica do cortisol livre obtido por dialise. A dialise e feita em celulas de teflon contra um tampao isomolar com equilibrio ocorrendo em 16 horas. Valores normais foram estabelecidos em amostras colhidas as 8:00, 17:00 horas e apos depressao com 1mg de dexametasona. Foram estudados tambem 6 pacientes com doenca de Cushing e 4 com insuficiencia adrenal primaria, mostrandose alta discriminacao entre os valores obtidos nesses pacientes e aqueles obtidos nos normais