Biomedical subjects
Publications and source records attributed to L Regeur.
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Alterations in circulating iodothyronines were studied in 15 juvenile type diabetic patients during the development of metabolic derangement after withdrawal of insulin. By means of measurements of circulating C peptide, one group of patients with and one without residual beta-cell function had been selected. In both groups there was a gradual decrease in serum T3 during the 12-hour period studied after withdrawal of insulin, while an increase in serum rT3 was observed after 4-6 hours. The alterations in serum T3 and the metabolic derangement were significantly more pronounced in patients without than with residual beta-cell function.
Eleven newly diagnosed insulin dependent patients were studied before and during the first 16 h after start of insulin treatment. All the patients were found to have significant amounts of C-peptide in plasma indicating residual insulin secretion. The fall in blood glucose after start of insulin therapy was followed by a parallel decrease in C-peptide (R = 0.99, P < 0.01) suggesting that the beta-cells may respond to variation in blood glucose. Eight of the patients were studied 1, 4, 7, 14, 90 and 180 days after start of insulin therapy. During the first 90 days of treatment an increasing maximal C-peptide concentration was found after a standard breakfast test meal. Two thirds of this improvement i beta-cell function was found after the initial 14 days with an average increase in maximal C-peptide of 260 per cent. The sensitivity to glucose improved.
The role of preserved beta-cell function in preventing ketoacidosis in type I insulin-dependent diabetes was assessed in eight patients with and seven patients without residual beta-cell function as determined from C-peptide concentrations. After 12 hours of insulin fatty-acid, and glycerol concentrations were all significantly higher in patients without beta-cell function than in those with residual secretion. Mean blood glucose concentrations reached 17.2 +/- SE of mean 1.3 mmol/l (310 +/- 23 mg/100 ml) in the first group compared with 8.8 +/- 1.4 mmol/l (159 +/- 25 mg/100 ml) in the second (P less than 0.01), while 3-hydroxybutyrate concentrations rose to 5.5 +/- mmol/l (57 +/- 5 mg/100 ml) and 1.4 +/- 0.3 mmol/l (15 +/- 3 mg/100 ml) in the two groups respectively (P less than 0.01). Individual mean C-peptide concentrations showed a significant inverse correlation with the final blood glucose values (r = -0.91; P less than 0.02). These findings strongly suggest that even minimal residual insulin secretion is important for metabolic wellbeing in diabetes and may prevent the development of severe ketoacidosis when insulin delivery is inadequate.
The kidney has been suggested as the main organ for the degradation of C-peptide. This hypothesis was tested in subjects with normal fasting blood glucose concentration and varying degrees of renal failure. Forty-nine subjects with endogenous creatinine clearance ranging from 0--25 ml/min were studied. The basal steady state concentrations of C-peptide (CP) and the immunoreactivity of insulin (IRI) were determined in plasma from fasting patients. The average IRI was similar to that found in normal subjects while a higher CP was found in all patients but two. The average CP in the nephrectomized patients was six times higher than the mean CP in normal subjects (0.35 pmol/ml). There was a significant inverse correlation between clearance and CP (r = 0.51, P less than 0.001) with the highest CP in nephrectomized patients. It is concluded that the increased CP in renal failure, and especially the markedly increased CP in the nephrectomized group supports the hypothesis of the kidney being the organ mainly responsible for the degradation of C-peptide also in man.
The influence of extracellular fluid volume expansion on the plasma aldosterone concentration (PAC) was investigated in five anephric and six non-nephrectomized patients on regular haemodialysis, and compared to a control group of four anephric and four non-nephrectomized patients. Plasma-renin activity, cortisol, Na+, and K+ were measured together with the PAC during the investigation. In anephric patients the PAC remained constant during the control period as well as during extracellular fluid volume expansion by infusion of 350 mmol of 20% mannitol. In the non-nephrectomized patients PAC diminished after mannitol infusion. The decline in PAC was correlated with the basal levels of PAC and the plasma renin activity. It is concluded that 5% extracellular fluid volume expansion has no direct influence on the regulation of PAC in patients without the renal renin-angiotensin system and that the regulation of PAC in anephric patients in the present investigation is probably mediated by changes in potassium and ACTH.
The pharmacokinetics of amikacin were examined in six bilaterally nephrectomized patients undergoing hemodialysis and in four patients with a minimal residual renal function undergoing peritoneal dialysis. The mean elimination half-life before the dialysis was 86.5 h in the anephric patients and 44.3 h in the patients with minimal residual kidney function. The results from the anephric patients suggest that some extrarenal elimination of amikacin may occur. The mean volume of distribution was about 25% of the total body weight. This is in accordance with values reported from subjects with normal renal function. During hemodialysis the half-life decreased to less than 10% (5.6 h) of the pretreatment value. The effectiveness of peritoneal dialysis was less as the half-life decreased to only about 30% (17.9 h) of the pretreatment value. During the dialyses a significant correlation between the half-life of amikacin and the decrease in blood urea and serum creatinine was demonstrated. The pharmacokinetic data were used to make dosage regimen recommendations for the treatment of patients undergoing intermittent hemodialysis or peritoneal dialysis.
Precise estimates of total neuron numbers in neocortices of 11 women, mean age 82.6 years (range 79-88) with severe senile dementia of the Alzheimer's type (SDAT) were compared with similar estimates in 10 cognitively normal women of comparable mean age (84.1 years; range 74-92). The total mean nerve cell number in the SDAT group was 16.9 x 10(9) with a coefficient of variation (CV = SD/mean) = 0.14, whereas mean total neuron number in the control group was 18.1 x 10(9), CV = 0.18. In a material of this size the reduction of 6% in neocortical cell number in the SDATs is neither statistically nor biologically significant. Nevertheless, all patients with SDAT were severely demented, having a mean score of 5.6 on a 1-7-scale of dementia. This contrasts with the nondemented individuals who had lived an independent life at home until shortly before death. The SDAT patients showed a rather consistent reduction in cortical volume by 14%, an atrophy that was solely due to a reduced cortical thickness. In addition, all had multiple neocortical plaques (Bielschowsky silver stain).