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Biomedical subjects

K Irsigler

Publications and source records attributed to K Irsigler.

At least 91 records · Page 5Linked to original sources
PubMed1980

[Dietary treatment of hypertriglyceridemia (author's transl)].

The wide spread of hypertriglyceridemias throughout the population can be most convincingly referred to defective or over-nourishment. Consequently the possibilities of correcting this symptom by a change of diet are considerable. In discussing the relevant diets, the 200 calorie protein diet, the SO3D diet and the null diet (for hospital patients) and guiding principles for outpatients are refered to. The assumption that increased blood lipids can be corrected exclusively through a low fat diet is only true for the rare type 1 hypertriglyceridemia.

Diet, Reducing↗
PubMed1979

[Comparison of glibenclamide, gliquidone, glisoxepide and placebo in maturity onset diabetics of differing degrees of severity (author's transl)].

The purpose of the study was to investigate whether the potency of effect on the beta cell differs with type of sulfonylurea (SU) and with degree of severity of diabetes. 12 maturity onset diabetics were classed according to fasting blood glucose (FBG) in three groups of 4 patients each. Each patient served as his own control. Glibenclamide, Gliquidone, Glusoxepide and placebo were administered in random order with degree dosage adjusted according to degree of severity of diabetes. All patients were given a standardized diet with 150 g carbohydrates per day. Fullday profiles of blood glucose, insulin, C-peptide and sulfonylurea level in serum were made on the third day under each preparation. Results showed that with proper nutrition and sufficient weight reduction, patients in group I (FBG 80--130 mg/dl) needed no oral medication and in fact showed a tendency towards hypoglycaemic episodes under oral therapy. In group II (FBG 130--200 mg/dl) the effect of nutrients on beta cell secretion appeared to be both enhanced and accelerated by SU administration. Satisfactory metabolic control was achieved with SU, but not with placebo. This group seems to represent the type of patient most likely to benefit from SU therapy. In spite of high dosage levels, satisfactory control was not achieved with SU in any patient in group III (FBG greater than 200 mg/dl). Depending on individual factors such as ketosis-proneness, vascular complications, age and psycho-social aspects, insulin administration should be considered for these patients. There were not differences between the individual SU preparations in the parameters studied. There was insufficient evidence for a pharmacokinetic differential diagnosis.

Blood Glucose↗
PubMed1979

[Diabetic coma].

Explore the source record for details and available documents.

Adult↗
PubMed1979

[Blood sugar self-profiles. Improvement in diabetes control in outpatients (author's transl)].

15 insulin-dependent diabetics who had been hospitalised for evaluation and modification of their treatment regimen were trained to take their own blood samples with 10 microliter glass capillaries. Blood sugar self-profiles were analysed from each patient twice in hospital and afterwards at home. Urine samples were also self-tested for sugar. The profiles were carried out reliably and seem to cause a minimum of trouble to the patient. This method of feedback, with comparison of blood and urine sugar values, increased the patient's understanding and ability to vary his own insulin dosis. The analysis of 3 daily profiles for each patient showed increasing improvement in metabolic control. This also increased motivation to keep to a regimen in which insulin dosage, physical activity, and nutrition are in balance. For the first time daily profiles were introduced which could be carried out under the normal conditions of the patient's daily life.

Ambulatory Care↗
PubMed1979

[Biguanide-induced and - associated lactic acidosis: serum and tissue biguanide levels in hyperlactaemia and lactic acidosis (author's transl)].

An investigation was carried out on 30 diabetic patients in an attempt to clarify the relationship between serum biguanide levels and raised lactate. No consistent relationship was demonstrable between the serum biguanide level, administered dosage and time of administration. There was also no correlation between biguanide and lactate increase. It is not justifiable to quote a specific serum level of biguanides in defining lactic acidosis. A causal association between biguanide medication and lactic acidosis seems to be possible only by determination of serum and tissue levels. Determination of biguanide levels was carried out in the serum and tissue of a patient who had died as a result of lactic acidosis after phenformin administration. While the serum levels were only slightly higher than the therapeutic range, both liver and kidney tissue showed highly toxic levels. Furthermore, the amount of biguanides in the body was calculated in another patient successfully treated for lactic acidosis after buformin therapy. A differentiation should be made between biguanide-induced and biguanide-associated lactic acidosis. In both forms serum levels can be within relatively low ranges. In the former condition, the biguanides alone are responsible for the development of lactic acidosis by blocking the respiratory chain. In the latter condition they aggravate an already existing pathological condition, and can, therefore, represent a lethal factor.

Acidosis↗
PubMed1979

Calorimetric results in man: energy output in normal and overweight subjects.

In order to test the practicability of 24-hr investigations with the gradient-free Vienna Whole-Body Calorimeter, energy output was measured over 24-hr periods in 18 human subjects. Heat loss was partitioned into dry and evaporative components. Sixteen female subjects were divided into normal-weight (less than 100% according to the Broca index), overweight (100%--120%), and obese (over 120%) groups. A male with severe hypothyroidism, and a female with no signs of impairment of thyroid function who had weight problems that were suspected to be due to low energy expenditure, were studied separately. Subjects reported that the calorimeter chamber was sufficiently comfortable for at least a 24-hour investigation. Overweight and obese subjects showed both greater total heat output and greater inter-individual variability than the normal weight group. Normal and overweight subjects were on steady levels of food intake that were representative of usual intake. For normal subjects there was a relatively close correspondence between energy intake and output, but not for overweight subjects. Thyroid hormone therapy produced a large increase in energy output in the hypothyroid patient. Energy expenditure was found to be unusually low in the patient with weight problems and was increased by about 50% after thyroid hormone administration.

Adult↗
PubMed1979

Long-term continuous intravenous insulin therapy with a portable insulin dosage-regulating apparatus.

A portable insulin dosage-regulating apparatus (PIDRA) was used with five volunteer diabetic subjects for periods ranging from 1 wk to more than 3 months to explore the possibilities of achieving near normoglycemic control over long time periods with such an apparatus. PIDRA consists of a matchbox size pump with insulin reservoir and a pocket size electronic control box. It can infuse a preprogrammed basal rate of insulin plus externally manipulated supplementary doses in rectangular profiles. The quality of blood glucose control was monitored with the Miles Biostator and through self-testing by the patient in the outpatient phases. Under inpatient conditions, the relatively simple PIDRA insulin administration profile was almost as effective in achieving normoglycemia as the Biostator, and good control could be maintained over long periods of time. The apparatus allows considerably greater ease in variation of insulin dosage with less risk of hypoglycemic epidoses as compared with conventional subcutaneous injections. Several technical problems remain to be solved, but it is concluded that PIDRA represents a viable alternative as a means of achieving tight control, at least as a step toward the goal of an implanted glucose-contingent insulin infusion system.

Adolescent↗
PubMed1979

Preprogrammed insulin infusion with a portable pump system.

A glucose-controlled insulin infusion system (Biostator) was used to determine patient insulin requirement for clinical evaluation of a portable pump system (technical development by Siemens AG). Results from 6 insulin-dependent diabetics with respect to quality of control, carbohydrate/insulin ratio, and insulin requirement are shown. Preprogrammed insulin infusion with the portable system was carried out for up to 117 days.

Adolescent↗
PubMed1979

Use of glucose-controlled insulin infusion system for improvement of subcutaneous insulin regimen.

The use of an artificial pancreas for blood glucose monitoring and feedback correction for evaluation and improvement of subcutaneous insulin therapy facilitates the process of finding an optimal therapy regime for the individual patient. The frequency of hypoglycemic episodes can be reduced while maintaining good control, and hospital stays can be considerably shortened. This procedure is particularly useful in achieving tight control in pregnant diabetics.

Adolescent↗
PubMed1979

Treament of biguanide-induced lactic acidosis with dichloroacetate. 3 case histories.

The administration of dichloroacetate (DCA) in cases of biguanide-induced lactic acidosis (LA) improves pyruvate oxidation and therefore increases energy production from glucose. Preliminary results of treatment of LA in humans are reported. A continuous fall in pyruvate was observed in all 3 cases after administration of at least 20 g of DCA (4 g i.v. bolus, then continuously 12 g/h). In Case 1, in which no supplementary measures for controlling the acidosis were applied, the acidosis did not improve and the patient died. In Case 2, despite administration of tris-buffer and dialysis, pH-values could not be raised sufficiently. The production of hydrogen ions persisted and lactate continued to rise. This patient also died. Case 3 was admitted in the beginning stages of a phenformin-induced LA, and in this case therapy was successful. The decline in pyruvate was accompanied by a slow fall in lactate, and a further fall in pH was averted. The clinical condition of the patient improved markedly after i.v. administration of a total of 34 g of DCA.

Acetates↗
PubMed1978

[Diabetic control with a portable insulin infusion pump for 7 weeks (author's transl)].

A portable insulin infusion pump was used to achieve diabetic control over a period of 7 weeks in a juvenile onset-type diabetic. Insulin was infused at a basal rate and further doses could be triggered externally by the patient. Insulin requirement had been previously determined by means of an artifical beta-cell (Glucose Controlled Insulin Infusion System). This method of insulin administration resulted in a clear improvement in diabetic control. Some problems did arise in connection with materials from which the instrument and catheter were constructed. However, it was shown that a portable insulin pump can be used with out-clinic patients for a number of weeks and is also justified for at least certain cases.

Adult↗
PubMed1978

[The risk of lacticate acidosis: a comparison of the 3 biguanides in treatment of diabetics (authors' transl)].

Hyperlactaemia was induced by means of a standard exercise test in 10 diabetics receiving normal treatment with biguanides (either buformin, metformin, or phenformin) in combination with either a sulfonylurea or insulin. The treatment regimen was then continued without biguanides for 3 weeks and the exercise test was repeated at the end of this period. All 3 biguanide preparations induce hyperlactaemia in diabetics. Physical stress leads to an additional increase in lactate, which reaches pathological proportions. Discontinuation of biguanide treatment leads to a significant decrease in resting and stress values. In a comparison of the 3 biguanide products, phenformin induced significantly higher lactate values in response to exercise than buformin. Of the biguanides, phenformin appears to carry the greatest risk of causing hyperlactaemia in susceptible patients, induced by concurrent circumstances, with progression to severe lacticate acidosis. The special pharmacokinetic properties of phenformin and the 8-fold higher incidence of lacticate acidosis than under buformin or metformin therapy support this observation.

Acidosis↗
PubMed1978

[Four cases of fatal lactic acidosis during biguanide therapy (author's transl)].

Four case reports of lactic acidosis occurring during biguanide treatment (2 with phenormin, 2 with buformin) are analysed. Three of the patients died in a toxic state of lactic acidosis, whilst the fourth patient survived lactic acidosis, but died 11 days later due to myocardial infarction. In spite of serum biguanide levels within the therapeutic range, one patient had highly toxic hepatic levels of phenformin (13,500 ng/g tissue). Two factors are essential for the treatment of lactic acidosis: 1. rapid diagnosis: history of biguanide intake; clinical symptoms; acid-base imbalance; rapid lactate determination to establish the diagnosis. 2. therapy: correction of acidosis, insulin and glucose; shock treatment; forced diuresis and/or haemodialysis. From the high numbers of biguanide-treated diabetics and the incidence of lactic acidosis in other countries it can be assumed that this toxic side effect of biguanide treatment occurs relatively frequently in Austria too, but remains largely undetected.

Acidosis↗
PubMed1977

[No free water in the treatment of "hyperosmolar diabetic coma": treatment control by comparing serum and CSF (author's transl)].

Some serum and CSF concentrations were measured in five patients with severe hyperosmolar coma (mean blood sugar = 58.9 mmol/l; osmolarity = 406 mosmol/l). A gradual decrease of serum osmolarity prevented the development of an osmotic gradient between CSF and extracellular space. Insulin treatment (1-20 IU/h) with a motor infusion pump and infusion of hypertonic solutions decreased serum osmolarity by 2-4 mosmol/l X h. The faster fall of glucose in the extracellular space was compensated by hypertonic saline infusions (up to 365 mosmol/l). All patients survived.

Adult↗