[Microalbuminuria in diabetes mellitus].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J B Hoekstra.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The trials reviewed in this study investigated the effect of intravenous magnesium on arrhythmias and mortality in acute myocardial infarction. Nine trials were carried out in the pre-thrombolytic era. They varied in set-up, number of patients, dose of magnesium, follow-up and the type of arrhythmias analyzed. Magnesium reduced mortality in most studies, but the reduction was significant in only three of them. Two meta-analyses of the smaller studies revealed a 55% reduction in mortality. In the LIMIT-2, in which 2300 patients were enrolled, magnesium reduced mortality significantly by 24%. The effect of magnesium on arrhythmias was less clear. Preliminary results of ISIS-4, in which magnesium among others was administered together with thrombolytic agents, did not provide evidence of benefit in patients with suspected myocardial infarction. At present there are no arguments for the use of magnesium in acute myocardial infarction.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
FNA cytology of 112 patients with thyroid nodules seen in a 5-year period in a general hospital setting, and the histology obtained from the 53 operated patients, were retrospectively analysed. The inadequacy rate of FNA cytology was 11%, sensitivity was 84% (16/19), specificity was 52% (15/29), positive predictive value was 53% (16/30) and negative predictive value was 83% (15/18). Extrapolating these figures to the whole study group a negative predictive value of 95% is put forward as a more realistic figure. The results and the clinical pitfalls of the use of FNA cytology in diagnosing thyroid nodules are discussed. The authors conclude that FNA cytology is a reliable first diagnostic step in the diagnosis of thyroid nodules, even in a general hospital setting.
Hypoglycaemia is a severe complication of insulin-dependent diabetes mellitus, especially when it is not preceded by warning signs. A patient unaware of a low blood glucose concentration may not take any remedial action, becomes severely hypoglycaemic and may lapse into a potentially fatal coma. Hypoglycaemic unawareness is associated particularly with good glycaemic control. Hypoglycaemia unawareness was first related to diabetic autonomic neuropathy. Subsequently it emerged that well controlled diabetic patients suffered from hypoglycaemia unawareness more often than poorly controlled patients. Next to autonomic neuropathy and good glycaemic control, the transfer of more slowly resorbed beef and porcine insulin to more rapidly resorbed human insulin has been incriminated as causing an increased incidence of hypoglycaemia unawareness. Reviewing the scientific literature concerning the connection between hypoglycaemia unawareness and the use of human insulin, there is no rationale for supporting the hypothesis that human insulin leads to hypoglycaemia unawareness any longer. While the pathophysiology of hypoglycemia unawareness remains unclear in patients with insulin-dependent diabetes mellitus of long duration, it may well be related to impaired adrenaline secretion. The cause of this impaired adrenaline secretion during hypoglycaemia is unknown and it does not seem to be a result of diabetic autonomic neuropathy.
To establish the effects of a meal on portal venous flow and the prognostic value of this parameter, 46 patients with chronic liver disease and 28 healthy subjects were examined with duplex Doppler before and after a meal. The measurements were completed in 40 patients and 21 healthy subjects. Postprandial portal venous diameter, blood velocity and quantitative flow were measured for 60 min. Mean baseline values were: 11.4 mm versus 10.2 mm (p = 0.019), 10.8 cm.s-1 versus 13.4 cm.s-1 (p = 0.015) and 668 ml.min-1 versus 646 ml.min-1 (p = 0.7) respectively. Spleen size was 15.0 cm versus 10.6 cm (p = 0.0001) respectively. Postprandial diameter, velocity and flow increased significantly in patients and controls (p = 0.0001 for all). Mean postprandial flow could best be described by a polynomial equation with a parabolic curve. Patients' curves were more blunted than controls', with significantly different regression constants (p = 0.025 and p = 0.029). All subjects were followed up for survival and variceal haemorrhage. The mean follow-up time was 47 months. Early maximum postprandial velocity (p = 0.041) and large spleen size (p = 0.002) were significantly related to an unfavourable prognosis for survival. Early maximum velocity was also related to increased variceal haemorrhage. This study shows that postprandial portal venous flow is blunted in patients with chronic liver disease. Postprandial portal venous flow may have prognostic significance.
The evolution of portal venous flow in non-end-stage chronic liver disease with portal hypertension was assessed in 59 patients and compared with that in 55 control subjects and by means of duplex Doppler measurements by a single observer. All patients were prospectively followed up, and a repeated measurement was performed in a subgroup of 23 patients. The mean (+/- SD) portal venous diameter and velocity of patients versus controls were 11.2 (+/- 2.0) mm versus 10.1 (+/- 1.4) mm (p < 0.0005) and 11.0 (+/- 4.2) cm/sec versus 13.9 (+/- 4.1) cm/sec (p < 0.0005). The portal venous flow did not differ: 671 (+/- 291) ml/min versus 652 (+/- 203) ml/min. Diagnosis, Child class, and grade of varices did not influence the portal flow. Patients were followed up during a median (+/- SD) time of 47 (+/- 17) months. Nineteen (32%) patients died, and 14 (23%) had a variceal hemorrhage. Survival and hemorrhage were not correlated with the portal venous flow. Subsequent measurements in 23 patients showed a significant decrease in portal venous flow in 5 patients who died during follow-up. This was not found in the patients who survived. It is concluded that portal venous flow in chronic liver disease with portal hypertension is stable for a long time in the evolution of chronic liver disease. The existence of a 'portostat' is postulated. Only in the terminal stage of liver disease can a reduction of the portal venous flow be detected.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Abnormalities in lymphocyte subpopulations in patients with type 1 diabetes have been reported previously. To evaluate the effect of blood glucose levels on peripheral lymphocyte concentrations we studied the proportion and phenotypic composition of the T-cell population in 7 patients with type 1 and in 12 patients with type 2 diabetes at hospitalization because of metabolic dysregulation and in a period of restored control. Both the number of CD-4 and CD-8 positive cells increased significantly (p < 0.05), although no change in the CD-4:CD-8 ratio was observed. After restoring metabolic control there was a significant rise in the mean number of total lymphocytes (1760 +/- 759 x 10(6)/ml vs 2385 +/- 889 x 10(6)/ml, p < 0.05). The number of total lymphocytes increased in all patients but one. It is concluded that metabolic control can influence immunological parameters such as numbers of peripheral lymphocytes of various phenotypes.
The influence of epidemic influenza on hospitalizations because of influenza, pneumonia and diabetic acidosis in patients with diabetes mellitus was investigated. Data on the weekly incidence of influenza-like illness were obtained from the Continuous Morbidity Registration and the cumulative data on hospitalizations in short-stay hospitals were obtained from the National Medical Registration. Patients with duodenal ulcer were used as a control population. Epidemic elevations of influenza infections were observed in 1976 and 1978. The estimated relative risk for hospitalization because of influenza infection was 1.1 and 1.0 for the two non-epidemic years 1977 and 1979, respectively. For the epidemic years 1976 and 1978 this risk was calculated to be 5.7 and 6.2, respectively. An increased relative risk was also noted for pneumonia; being 25.6 for both epidemic years. The estimated relative risk of dying during hospitalization rose from 30.9 in 1977 to 91.8 in 1978. The number of hospitalizations for ketoacidosis was 50% higher in 1978 than in the other three years. During the epidemic years, 25.7% of patients hospitalized for pneumonia died, while this percentage was 14.6% in the non-epidemic years (P less than 0.05). Differences in mortality due to diabetic acidosis were similar: 25.4% in epidemic and 14.7% in non-epidemic years (P less than 0.01). During the 1978 epidemic, one out of every 1300 patients with diabetes mellitus was hospitalized because of pneumonia. It is estimated that 1 of every 260 patients with IDDM was hospitalized for diabetic acidosis. It is concluded that patients with diabetes mellitus have indeed a very high influenza-associated morbidity.
We investigated the variability of quantitative duplex Doppler measurements of portal flow. Measurements were validated in vitro using a flow phantom. The measured flow Q (ml/min), is related to the actual phantom output P (ml/min) according to the following formula: Q = 1.08 (P + 44) (r = 0.998). To estimate inter- and intra-observer variance, 38 subjects without portal hypertension were examined in two groups. Two observers examined the first group of subjects (n = 19), from a routine daily ultrasound schedule. Significant differences were found in mean +/- S.D. portal flow (692 +/- 182 ml/min vs. 613 +/- 185 ml/min, p = 0.04) and mean +/- S.D. velocity (15.3 +/- 3.9 cm/s vs. 13.2 +/- 2.6 cm/s, p = 0.01). The combined inter- and intra-observer coefficient of variation (S.D.) was 24% (158 ml/min), 9% (0.92 mm) and 24% (3.4 cm/s) for portal flow, diameter and velocity respectively. Non-systematic components of variance were the largest. Patient characteristics, age, sex, height, weight and body surface area did not influence measurement variations. In the second group of healthy volunteers (n = 19), where variance in measurements over 3 consecutive days was comparable to the combined variance in the first group, the non-systematic variance component was also the largest. We conclude that quantitative duplex Doppler measurements of portal venous flow are mainly subject to non-systematic variability. A coefficient of variation of 24% can be expected in diagnostic measurements in a single patient. Examination by a single observer is advisable. The value of this technique lies in the analysis of pathophysiological mechanisms in portal flow changes in large groups of subjects.
Herein, epidemiological data on influenza pneumonia and mortality, results of clinical studies, and the outcome of influenza vaccination trials are reviewed. All excess mortality studies that specify for underlying disease list diabetes as one of the major risk factors. During influenza epidemics, death rates among patients with diabetes mellitus may increase by 5-15%. Diabetes mellitus is also mentioned as a risk factor in most clinical studies, making up 3-14% of the patients studied. Even in recent studies, diabetes mellitus is only preceded as a risk factor by cardiovascular disease and chronic pulmonary disorders. To what extent cardiovascular disease and old age contribute to the increased influenza mortality and morbidity in diabetic patients remains unclear. The influence of epidemic influenza on the incidence of diabetic acidosis in combination with an impaired immune response to both Staphylococcus aureus and the influenza virus suggests that diabetes mellitus itself is the main risk factor. It is concluded that all patients with diabetes mellitus should receive annual vaccinations and that, in official recommendations, patients with diabetes mellitus should be mentioned as a separate risk group. Whole-virus vaccines are preferred over subunit vaccines.
The production of insulin autoantibodies (IAA) was studied after common viral infections in 12 children with type 1 diabetes mellitus and in their 18 healthy siblings. In addition, the production of IAA was measured after influenza vaccination with booster in 39 patients with type 1 diabetes mellitus and in 39 healthy controls. In 7 of the 12 diabetic children 13 viral infections were serologically confirmed. Among the siblings 14 periods of infection were noted in 9 individuals. A significant rise in IAA antibody titre was demonstrated in patients twice (IgG both times) and in siblings 11 times (IgM 5x, IgG 6x, difference significant P less than 0.05). In only three cases the rise in antibody titres occurred 6-12 wk after documented infection. There was a significant inverse correlation with age in both patients (r = 0.89, P less than 0.0001) and siblings (r = 0.67, P less than 0.001) for IgM IAA. After influenza vaccination a significant increase in IAA was noted twice: IgM IAA in a patient with diabetes and IgG IAA in a healthy volunteer. A four-fold decrease in IgG IAA was demonstrated in one diabetic patient. From these results it is concluded that IAA formation is not a direct sequela of viral infection or vaccination.
Explore the source record for details and available documents.
Explore the source record for details and available documents.