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Biomedical subjects

K Asplund

Publications and source records attributed to K Asplund.

At least 181 records · Page 10Linked to original sources
PubMed1983

Glibenclamide-associated hypoglycaemia: a report on 57 cases.

In the largest series of patients with glibenclamide-associated hypoglycaemia reported so far, 51 cases reported to the Swedish Adverse Drug Reactions Advisory Committee and six additional cases are reviewed and related to sales and prescription data of glibenclamide. Median age of the patients with hypoglycaemia was 75 years and 21% were 85 years or above. For comparison, the median age of a random sample (1 in 288 of all patients prescribed glibenclamide) was 70 years and only 5% were 85 years or older. In eight out of 40 cases where duration of glibenclamide treatment was recorded, the hypoglycaemic event occurred during the first month of treatment. The median daily dose of glibenclamide prescribed was 10 mg both in the hypoglycaemic cases and in the prescription sample. Coma or disturbed consciousness was the most common clinical presentation in this series and the minimum blood glucose value was 1.3 mmol/l (median). Twenty-two patients responded immediately to treatment, 24 had protracted hypoglycaemia of 12-72 h duration and 10 died. Fatal outcome was observed even with small doses of glibenclamide (2.5-5 mg/day). Previous strokes and cardiac disorders were isolated as two independent determinants of a serious course of the hypoglycaemia. Other contributing factors included impaired renal function, low food intake, diarrhoea, alcohol intake and interaction with other drugs. Thus, it is not uncommon for glibenclamide, like the first-generation sulphonylureas, to cause serious, protracted and even fatal hypoglycaemic events.

Aged↗
PubMed1983

Respiratory alkalosis early after stroke: its relation to loco-motor function.

In 27 acute stroke patients with hemi-motor deficit blood gases (paO2, paCO2 and blood pH) were determined within 72 hours and related to level of consciousness, site of brain lesion, findings of haemorrhage into the cerebral spinal fluid, extent of motor impairment and concomitant medical disorders. Sixteen subjects were followed for three weeks with repeated blood-gas sampling and assessment of motor control. Respiratory alkalosis occurred in 37%, hypoxia in 7% but acidosis in none. Blood gas abnormalities were significantly and positively associated only with the extent of motor impairment. Only small changes in blood gases were found during the three weeks follow-up. Initial findings of respiratory alkalosis predicted poor motor recovery during the follow-up period.

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PubMed1982

Nutritional status of medical patients on emergency admission to hospital.

The nutritional status was assessed in 75 consecutive patients acutely admitted to a general medical ward. Weight-for-height, triceps skinfold thickness, arm muscle circumference, plasma albumin and serum transferrin were used as nutritional indicators. By combining abnormalities in two or more of these variables, we found obesity in 9% and undernutrition in 22% of the patients on admission. Energy deficiencies as well as acute and chronic protein undernutrition were observed. Age over 75 years, lack of own teeth and a reason for admission other than circulatory disorders or diabetes were tentatively identified as risk factors for undernutrition-some of them conceivably interdependent. Living conditions and regular medication seemed to be less important determinants in this group of patients. We conclude that undernutrition is prevalent among hospitalized medical patients in Sweden as in other industrialized countries. Patients with "hospital malnutrition" are partly recruited from a population of malnourished elderly people outside the hospital. Adequate nutritional support is an essential objective of hospital care in patients wih medical disorders.

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PubMed1982

Hyperosmolar non-ketotic coma in diabetic stroke patients.

Hyperosmolar non-ketotic coma in diabetes is a life-threatening condition. We describe three patients, aged 59-67 years, who developed hyperosmolar coma during the first ten days after admission for stroke. Common to all three were normal plasma osmolality and slightly elevated plasma creatinine levels on admission, treatment with diuretics, parenteral dextrose administration before and low urinary glucose output during the coma. In the five days preceding the coma, total fluid deficits were 3.8, 6.5 and 9.4 1, respectively. In one patient the rate of glucose delivery had clearly exceeded utilization during adequate insulinization, in another a marked reduction in urinary glucose output preceded extreme hyperglycaemia and coma. Two of the three patients died, both from extensive thrombus formation in cerebral arteries and multiple emboli to the lungs. We conclude that enhanced endogenous glucose production and reduced renal clearance of glucose may contribute to precipitate hyperosmolar non-ketotic coma. A close monitoring of fluid and dextrose administration seems mandatory in diabetic stroke patients, in particular if renal function is impaired or if diuretics are given. Insulin treatment should be considered in all diabetic patients during the first days after a stroke.

Aged↗
PubMed1981

Nutritional assessment of psychogeriatric patients.

The nutritional status of 91 patients on four psychogeriatric wards was assessed by anthropometric measurements and determination of circulating proteins. The patients had low mean values for weight, arm muscle circumference, plasma albumin and serum transferrin. Indicators of malnutrition were combined to define the nutritional status in each individual. Energy and/or protein undernutrition was found in 30% and obesity in 4%. Energy undernutrition was more common than protein deficiency. Undernutrition was quite common during the first year of hospitalization and did not correlate with the duration of hospital stay. Subjects with their own teeth had a lower prevalence of undernutrition than edentulous patients. Food intake was similar in patients with and without undernutrition. The possible interactions between malnutrition and chronic psychiatric disorders in the elderly are discussed.

Aged↗
PubMed1980

The natural history of stroke in diabetic patients.

A five-year follow-up of 53 diabetic patients admitted for their first stroke in 1972--73 has been performed. They were compared with two groups of 53 non-diabetic patients each with cerebrovascular disease (CVD), one randomly selected and one matched with the diabetics for age, sex and diagnosis of CVD at discharge. All patients could be traced at follow-up. The mean age at the time of first stroke was 66.5 years in male and 73.2 years in female diabetics. Manifest diabetes was diagnosed in 19% during hospitalization for stroke; of the remainder, 74% had had diabetes since less than ten years. In 85% of the diabetics there were no signs of severe angiopathy affecting eyes, kidneys or lower extremities. The majority of diabetic as well as non-diabetic CVD patients had a history of hypertension and/or heart disease. Few were overweight. Case fatality rate was significantly higher in diabetics than in non-diabetics throughout the follow-up (p less than 0.01 for diabetics vs. matched non-diabetics, p less than 0.001 for diabetics vs. randomly selected non-diabetics). The presence of heart disorder predicted mortality in the diabetic subjects. Surprisingly, hypertension diagnosed before stroke involved a more favourable long-term prognosis in all three groups (p less than 0.05). The major causes of death in diabetic CVD patients were cardiac disorders (50%) and stroke (47%). Previous investigations have identified diabetes as a risk factor for stroke. This study shows that diabetes also adversely affects the short-term as well as the long-term outcome in stroke.

Age Factors↗
PubMed1979

Effects of glucose, chloromercuribenzene-p-sulphonic acid and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid on phosphate efflux from pancreatic islets.

Collagenase-isolated pancreatic islets of non-inbred ob/ob mice, containing more than 90% beta-cells, were labelled with radioactive orthophosphate (32P or 33P) and then subjected to non-recirculating perifusion. The basal D-glucose concentration in the perifusion medium was 2.8 mM. When the concentration was suddenly raised to 5.6, 8.3 or 16.7 mM, D-glucose promptly elicited a transient and dose-dependent release of radiophosphate. In the presence of 2.8 mM D-glucose, 0.1 mM of the poorly permeating sulphydryl blocker, chloromercuribenzene-p-sulphonic acid, also evoked a phosphate flush resembling the one induced by D-glucose. The basal radiophosphate release was partially inhibited by 1 mM 4-acetamido-4-'-isothiocyanostilbene-2,2'-disulphonic acid. However, the phosphate flush induced by 16.7 mM D-glucose was not noticeably inhibited by 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid. It is concluded that the phosphate flush emanates from beta-cells and that membrane sulphydryl groups may participate in its regulation. Although at least the basal phosphate release may in part represent transmembrane transport through 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid-sensitive anion channels, other mechanisms are also likely to participate in the glucose-induced phosphate flush.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1978

Insulin production by pancreatic islets of obese-hyperglycemic mice cultured for one week in different glucose concentrations.

Culture of pancreatic islets isolated from obese-hyperglycemic mice (gene symbol ob) for one week in media containing widely different concentrations of glucose (3.3, 5.6 or 16.7 mM) was found to markedly influence the functional behaviour of the islet B-cells. Thus, the insulin content of islets cultured at 3.3 or 16.7 mM glucose (subphysiological or supraphysiological glucose concentrations respectively) was markedly reduced. Islets cultured in 5.6 or 16.7 mM glucose displayed a normal insulin secretory response when stimulated with glucose, whereas islets cultured in a subnormal glucose concentration (3.3 mM) showed a reduced insulin response to glucose stimulation in batch type incubations and also lacked a second phase of insulin secretion in islet perifusion experiments. The rate of insulin biosynthesis of non-cultured ob/ob islets was higher than that of islets from their lean siblings but culture for one week in 3.3 mM glucose induced a pronounced impairment of the insulin biosynthesis in islets of obese as well as lean mice. The present data indicate that the hyperfunction of the islets of the ob/ob mouse at least in part is a reversible phenomenon, suggesting that inherent properties of islet B-cells do not act as "primary" factors in the development of the obese-hyperglycemic syndrome.

Animals↗
PubMed1978

32P-labeling patterns in rat pancreatic islets: tissue source of the radiophosphate released after glucose stimulation.

Immediately after stimulation with glucose in vitro, isolated rat pancreatic islets prelabeled with [32P]orthophosphate release a pulse of [32P]orthophosphate into the media (the "phosphate flush"). Islets have been rapidly frozen before, during, and after this pulse to assess the concurrent changes in the distribution of tissue radioactivity. Under the present experimental conditions, approximately 90% of the islet radioactivity was soluble in perchloric acid (PCA-soluble) immediately before stimulation and slightly more than half of that was present as [32P]orthophosphate. The tissue pool of [32P]orthophosphate declined 55% and 62% after 7 and 14 min of stimulation which, respectively, incorporated the peak and the end of the heightened efflux of radioactivity. The net decrementa in tissue orthophosphate could account for all of the radioactivity which was released during the "phosphate flush." During the 14-min period of stimulation, labeled ATP and GTP (which had accounted for 13% and 4% of total PCA-soluble radioactivity before stimulation) increased 51% and 35%, respectively, and labeled ADP and AMP (which had accounted for 5.4% and 1.5% of PCA-soluble counts) fell 36% and 77%, respectively. Certain other PCA-soluble components, such as phosphorylcholine and phosphorylethanolamine, and total PCA-insoluble radioactivity were not demonstrably altered. The findings indicate that the "phosphate flush" originates from a labile pool of tissue orthophosphate. It remains to be established whether the simultaneous changes in the turnover of selected nucleotides are coupled to the translocation of orthophosphate or are mediated separately.

Animals↗
PubMed1978

Phosphate metabolism and glucose-initiated efflux of phosphate ions in islets of fetal pancreas.

Elsewhere we have proposed that the rapid transient efflux of 32P orthophosphate that occurs when prelabeled pancreatic islets are exposed to nutrient secretagogues (the "phosphate flush") reflects one of the earliest steps in islet stimulus-secretion coupling. We have now shown that the "phosphate flush" is much smaller with islets from fetal rats 21 1/2 days old. This could be attributed to decreased cellular stores of radioactivity, especially inorganic orthophosphate (32P), at the onset of stimulation, which may have been due, in part, to the diminished ability of fetal islets to retain the radiophosphorus accumulated during the labeling period. Certain other differences in phosphate metabolism were also observed. With prelabeled islets from adult rats, exposure to 3.0 mg. per milliliter glucose effected acute increases in the tissue content of AT32P and GT32P. Comparable stimulation of prelabeled fetal islets with 3.0 mg. per milliliter glucose did not elicit detectable changes in the labeling of ATP or GTP. The findings indicate that selected aspects of phosphate metabolism may be immature in fetal islets and, perhaps, implicated in their obtunded secretion of insulin in response to stimulation with glucose.

Adenosine Triphosphate↗