Biomedical subjects
Publications and source records attributed to H J Mitzkat.
Capillary radioimmunoassay -- a modification of the coated tube technique -- is described. The assay is equivalent (accuracy, sensitivity, precision) to conventional methods for insulin determination; it overcomes, however, the necessity of centrifugation or filtration and offers the added bonus of being automation compatible.
Late results were obtained from the follow up of 48 patients with chronic pancreatitis, who underwent partial duodenopancreatectomy. We measured the rest function of the remaining B-cells after resection by daily glucose profile, i.v.-gtt, measurements of the glucagon stimulated C-peptide-output and the amount of C-peptide in the 24-h-urine. In 9% of the cases the operation induced diabetes in addition to the already existing 31%. 3/4 of the nondiabetics showed a latent diabetic metabolism (K value < 1.0). The cause of this, as shown by the C-peptide-analysis, was the loss of the endocrine functional reserve following pancreas resection because of chronic pancreatitis. Therapeutically great differences resulted in reaching and equilibrium of serum glucose in the pancreas resected insulin-dependent patients, because they were dependent on carbohydrates for energy. The tendency to hypoglycaemia represented an additional endangerment.
Computerized tomographic localization of insulinomas utilises the differences in radiodensity between the tumor and the adjacent pancreatic tissue. With the aid of this new technique four insulinomas have been localized preoperatively. All of the tumors had the same radiodensity. Firm, well encapsulated beta-islet-cell tumors were detected with the same ease as an insulinoma, which was soft and almost without encapsulation. The smallest tumor detected was 1.0 cm in diameter. Of the four insulinomas, localized by computer tomography of the body, only one was also detected angiographically and only two were detected sonographically.
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Documentation of insulinoma by computerized tomography and the diagnostic value of this new method compared with conventional radiography is discussed. The study of four cases demonstrates the capability of computer tomography to localize tumors in the pancreas.
Drugs used in obstetrics which affect carbohydrate metabolism are reviewed in regard to their mode of action and their effects on diabetic pregnancies. Hyperglycemic reactions can be expected following administration of diuretics (especially with long acting thiazides), diazoxide, beta-adrenergic stimulants (tocolytics), glucocorticoids, and prolactin. Hypoglycemic reactions can occur with high doses of acetylsalicylic acid and in the presence of insulin with beta-adrenergic blockers or other inhibitors of the sympathetic system such as guanethidine. Other drugs affecting the carbohydrate metabolism are listed in regard to their hypo- or hyperglycemic effects.
The aim of the present investigation was to examine the fetal and maternal blood glucose and insulin response following glucose infusion to the mother. The studies were performed on 11 primigravid patients with a gestational age of 38-40 weeks during the first stage of labor. Glucose was given intravenously by a bolus injection of 330 mg/kg body weight, followed by a glucose infusion of 27.5 mg/kg/min for 60 min. Glucose concentration, immuno-reactive insulin (IRI), pH and base excess of the maternal and fetal blood were measured before and during maternal glucose load. Maternal blood glucose rose within 10 min. up to 280.0 mg% (SD 25.9). This level could be fairly maintained throughout the experiment. The maternal glucose was after 60 min. infusion 326.5 mg% (SD 46.9). Fetal glucose concentration rose continuously from 65.8 mg% (SD 5.8) at control to 249.2 mg% (SD 23.3) after 60 min. The increase of maternal and fetal glucose was associated with an elevation of immuno-reactive insulin (IRI). The maternal insulin was 24.0 micronU/ml (SD 8.0). It was scattered over a wide range (55.4 micronU/ml-217.1 micronU/ml) after 60 min. glucose infusion. The fetal insulin was 17.0 micronU/ml (SD 5.2) at control and rose by 86.5% (SD 80.5) after 60 min. glucose load. One case of a mother with a subclinical diabetes mellitus deviated where the fetal insulin rose from 26.0 micronU/ml at control to 215.6 micronU/ml after 60 min. infusion. The increase of insulin per glucose rise was correlated to fetal body weight. During glucose infusion to the mother of both, fetal and maternal, acid base parameters remained unchanged. From these observations it may be concluded that in the human fetus insulin secretion following a single glucose load is generally low, however, it increases in cases where the maternal insulin response to glucose load is abnormal. This might be related to a chronic stimulation by glucose of the fetal pancreatic islet cells in poorly controlled diabetic and possibly prediabetic patients.
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Somatostatin, a peptide isolated from ovine hypothalami, prevents growth hormone secretion in vivo and in vitro. Moreover, somatostatin interferes with the secretion of various other hormones: TSH insulin, glucagon, gastrin, VIP and GIP. Under certain conditions a blunting effect on the secretion of prolactin and ACTH can be demonstrated.
The aim of the present paper was to investigate if the glucose concentration of the fetal blood is reduced already during parturition. It was further of interest if there is a relationship between the glucose concentration in the maternal blood and the acid-base-balance of the maternal and the fetal blood, respectively. The observations comprised 40 patients during labor. Blood was sampled from the hyperemized fetal scalp and the umbilical artery. The maternal blood was collected from the hyperemized earlobe and fingertip, respectively. The blood was analyzed for pH, PCO2, base excess and blood glucose. The dip area (DA) was taken from the cardiogram and measured by planimetry. During labor the blood glucose increased in the fetal blood from 67 mg% (SD 12) to 87 mg% (SD 23) (2 alpha less than 0,001) and in the maternal blood from 88 mg% (SD 14) to 113 mg% (SD 29) (2 alpha less than 0,02). There was a significant correlation between the fetal and maternal blood glucose concentrations. The increase of the fetal glucose concentration is, however, less with increasing maternal blood glucose. (b = 0,66). The base excess in the maternal and fetal blood fell significantly. The rise of the maternal and fetal base excess (= base deficit) was related to the increase of the glucose concentration (2 alpha less than 0,001). If the base excess was zero, the fetal and the maternal blood glucose was 46 mg% and 78 mg%, respectively. The difference between the maternal and fetal blood glucose was 28 mg%. With increasing DA the fetal blood glucose increased (2 alpha less than 0,001.). From the observations it is concluded that there developes no hypoglycemia during parturition. This is due to the correlation found between fetal and maternal blood glucose and due to the rise in fetal blood glucose during hypoxia. Obviously, the decrease in fetal glucose following delivery is caused by a lack of glycogen which is enduced during labor and strengthened by a deficit of enteral glucose supply.
Among a group of 286 patients with atherosclerotic arterial disease 35.3% had normal carbohydrate tolerance, 28% asymptomatic (biochemical or latent), and 36.7% overt diabetes mellitus. There was a tendency towards peripheral artery involvement and a greater incidence of coronary heart disease (myocardial infarction, changes in ST-T segment) among patients with asymptomatic or overt diabetes, figures being comparable for men and women. Most of the patients with atherosclerotic arterial disease without diabetes mellitus were in stage II, while in diabetics there was a shift towards stages I and IV. There was no significant correlation between incidence, symptoms, and location of atherosclerotic arterial disease, on the one hand, and duration of overt diabetes, on the other.
In order to investigate the androgen status of diabetics we determined in 39 patients, 18-60 years old, 17 of which suffered from potency disturbances, the basal total plasma testosterone, the free testosterone fraction and the unbound plasma testosterone as well as the testosterone binding capacity. In 39 of these patients we proved the response of Leydig cells to HCG. Between normal persons and patients with and without potency disturbances basal total plasma testosterone did not differ significantly (p greater than 0.10). After a 3-day stimulation with HCG the increase of basal total plasma testosterone was significantly lower in the two diabetic groups in comparison with the normal persons (p less than 0.0005). The group with potency disturbances had significantly lower values for the free testosterone fraction (p less than 0.005) and unbound plasma testosterone (p less than 0.0025) than normal persons whereas diabetics without potency disturbances did not reveal any significant differences (p greater than 0.25 and p greater than 0.40). Further there were significant differences between the patients with and without potency disturbances (p less than 0.025) and (p less than 0.025). Testosterone binding capacity was significantly increased in the group with potency disturbances (p less than 0.0005) and also in the group without potency disturbances (p less than 0.01) as compared with controls. Moreover was it significantly higher in the group with potency disturbances than that without potency disturbances (p less than 0.01). For none of the parameters a functional correlation of age or diabetes duration could be demonstrated. The results are discussed with regard to the causes of potency disturbances in male diabetics.
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