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Biomedical subjects

J Ditzel

Publications and source records attributed to J Ditzel.

At least 19 recordsLinked to original sources
PubMed1993

[Short-term and long-term effects on glycosylated hemoglobin after transition from conventional insulin treatment to multiple insulin injection regime in a diabetic outpatient clinic].

In order to examine the short- and long term effects of basal/bolus insulin therapy on the metabolic regulation assessed by glycosylated haemoglobin (HbA1c) the first 201 patients in the diabetes out-patient clinic of the Section of Endocrinology, Department of Medicine, Aalborg Hospital, assigned for this treatment were prospectively studied. In all 201 patients a significant decrease in mean HbA1c value was observed after 21 months on multiple injection therapy (8.5% vs 8.1%; p < 0.001). The higher the HbA1c value on conventional therapy, the greater was the observed decrease in HbA1c following six months on basal/bolus therapy (r = 0.57, p < 0.001). According to an anonymous questionnaire completed by the first 140 patients six months after the start of multiple injection therapy, 97% of the patients preferred to continue with basal/bolus therapy with NovoPen, and 87% felt that they had achieved a better general condition and that the basal/bolus regime made their daily life easier. It is concluded that basal/bolus therapy with NovoPen may combine the attainment of improved metabolic control assessed by a decrease in mean HbA1c in many poorly regulated patients and the subjective experience of an improved quality of life.

Adolescent↗
PubMed1993

Cytokine plasma levels and lymphocyte subsets in patients with newly diagnosed insulin-dependent (type 1) diabetes mellitus before and following initial insulin treatment.

Changes in the plasma concentrations of interleukin-1 beta (IL-1 beta), tumour necrosis factor alpha (TNF alpha), interleukin 2 (IL-2), and lymphocyte subsets were investigated in 19 persons with newly diagnosed (type 1) insulin-dependent diabetes mellitus (IDDM) from admission to hospital prior to insulin treatment and following 1 week and 1 month of treatment. Furthermore, the cytokines were measured 16-28 months after the presentation of IDDM. The mean TNF alpha values were all within the normal range, but demonstrated a slight increase in all the samples taken (Friedman 0.06). The mean plasma IL-1 beta value was initially at the upper normal limit, but gradually increased significantly from admission to hospital to 1 week, 1 month, and 16-28 months afterwards (Friedman 0.031). No IL-2 activity was detectable in the majority of the samples. No significant changes in total leukocyte and lymphocyte counts were found. The lymphocyte subsets (CD5+, CD8+, CD4+, CD16+, CD20+, HLA-DR+) did not show any significant changes from admission to after the start of insulin treatment. It is concluded that the gradual increase in IL-1 beta and TNF alpha plasma levels may reflect an ongoing autoimmune inflammatory reaction at the onset of IDDM.

Adolescent↗
PubMed1992

Normal lipoprotein(a) concentrations and apolipoprotein(a) isoforms in patients with insulin-dependent diabetes mellitus.

Lipoprotein(a) [Lp(a)] is an LDL particle in which apoliporotein B-100 is attached to a large plasminogen-like protein called apolipoprotein(a) [apo(a)]. Apo(a) has several genetically determined phenotypes differing in molecular weight, to which Lp(a) concentrations in plasma are inversely correlated, and plasma Lp(a) concentrations above 20-30 mg dl-1 are an independant risk factor for ischaemic heart disease (IHD). To investigate whether Lp(a) could be important for the high cardiovascular mortality rate in patients with insulin dependent diabetes mellitus (IDDM), we determined Lp(a) concentrations and phenotypes in a group of 108 men (median age 32 years) with IDDM without nephropathy. A group of 40-year-old men (n = 466) served as controls. The median Lp(a) concentration was 7.4 mg dl-1 [95% CI 4.9 to 11.7] in the diabetic patients and 6.3 mg dl-1 [95% CI 5.2 to 7.0] in controls. The Lp(a) concentration exceeded 30 mg dl-1 in 22% of IDDM patients and in 20% of controls (P = 0.13). Moreover, the distribution of apo(a) phenotypes did not differ between patients and control. Lp(a) levels and apo(a) phenotypes are thus apparently the same in IDDM patients without nephropathy and controls. These findings do not exclude the possibility that Lp(a) may be increased in patients with nephropathy in whom coronary artery disease frequently co-exist or that Lp(a) in a given concentration is more atherogenic in IDDM patients than in persons without IDDM.

Apolipoproteins↗
PubMed1991

The influence of maternal weight, smoking, vascular complications and glucose regulation on the birth weight of infants of type 1 diabetic women.

The influence of maternal blood glucose regulation, weight gain, pre-pregnancy weight, vascular complications and smoking on the birth weight of infants was investigated in 72 type 1 (insulin-dependent) pregnant diabetic women. In patients with vascular complications (n = 23) the birth weight was significantly lower than in patients without vascular involvement (n = 49) (mean 380 g, P less than 0.05). The mean RBWR (relative birth weight ratio) of infants of patients who smoked more than 10 cigarettes per day was statistically significant lower compared to the mean RBWR of infants of non-smokers (P less than 0.025). A significant correlation was present between haemoglobin A1c (HbA1c) and RBWR (r = 0.28, P less than 0.02) and between maternal net weight gain and RBWR (r = 0.36, P less than 0.005) and this correlation became even stronger when only patients without vascular lesions were considered (n = 49) (r = 0.51, P less than 0.005) and (r = 0.50, P less than 0.005), respectively. In contrast no correlation was found between pre-pregnancy weight and RBWR. The study suggests that factors other than maternal hyperglycaemia stimulate fetal growth and may explain why fetal macrosomia may occur despite of strict blood glucose regulation.

Adult↗
PubMed1990

Plasma 6-keto-PGF1 alpha, thromboxane B2 and PGE2 during diabetic ketoacidosis.

In 10 patients admitted to hospital with diabetic ketoacidosis plasma prostanoids 6-keto-PGF alpha, thromboxane B2 and PGE2 were studied before treatment and following recovery. During ketoacidosis the median plasma 6-keto-PGF1 alpha and PGE2 were significantly increased compared to those of a normal reference group: 5.2 pg/ml and 3.9 pg/ml versus 1.7 pg/ml and 0.4 pg/ml (p less than 0.01 and p less than 0.05). In response to therapy both prostanoids decreased significantly towards a normal level, 6-keto-PGF1 alpha: 0.5 pg/ml p less than 0.01 and PGE2: 0.08 p less than 0.05 respectively. The changes in plasma 6-keto-PGF1 alpha were negatively correlated to changes in pH, rho: -0.7788 p = 0.0135, whereas the changes in PGE2 were positively correlated to serum creatinine at admittance, rho: 0.6976, p = 0.0368 and to the amount of intravenous fluid and insulin used during treatment, rho: 0.7500 p = 0.0126 and rho: 0.8424, p = 0.0023 respectively. Plasma thromboxane B2 concentrations were not elevated and did not change after treatment of the ketoacidosis.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Long-term bone loss in insulin-dependent diabetes mellitus.

The bone mineral content (BMC) in patients with insulin-dependent diabetes is reduced by 10% early in the disease, but due to a lack of long-term longitudinal studies it is unknown whether this diabetic osteopenia develops further through life. Over a time period of 11 years we examined the BMC in a group of seven adult insulin-dependent diabetics, in whom physiological and pathological factors affecting bone metabolism had been excluded; the patients were well regulated without diabetic complications. The BMC was not significantly decreased at the initial examination. The longitudinal study revealed a small but statistically significant fall in BMC, mainly in trabecular bone. The narrow (95%) confidence interval of median end value (93.3-99.0% of initial BMC) indicates that the annual decrease in BMC in such patients is of the order of 0.5%, a reduction that is probably clinically insignificant.

Adult↗
PubMed1989

Serum beta 2-microglobulin levels in thyroid diseases.

Serum beta 2-microglobulin was measured in 38 patients with thyroid diseases. Serum levels of beta 2-microglobulin were significantly increased in patients with untreated Graves' disease (median: 200 nmol l-1; P less than 0.0002), and in patients with untreated toxic adenomas (222 nmol l-1; P less than 0.0005) compared to 60 healthy control subjects (147 nmol l-1). Following antithyroid treatment of euthyroidism, serum beta 2-microglobulin decreased significantly in both Graves' disease (162 nmol l-1) and toxic adenomas (175 nmol l-1); values which were not significantly different from that of the control group. The level of serum beta 2-microglobulin in 12 patients with hypothyroidism was not different from that of the control group. However, in untreated hypothyroidism serum beta 2-microglobulin was positively correlated with serum thyroxine (T4) (rho = 0.69; P less than 0.05) and free thyroxine index (FT4I) (rho = 0.72; P less than 0.02). It is concluded that elevated levels of serum beta 2-microglobulin may reflect the increased metabolism in patients with thyrotoxicosis. Increased levels in active Graves' disease may also partly be caused by immunological activation.

Adenoma↗
PubMed1989

The effect of n-3 polyunsaturated fatty acids on lipids, haemostasis, neutrophil and monocyte chemotaxis in insulin-dependent diabetes mellitus.

Insulin-dependent diabetes mellitus (IDDM) is associated with an increased risk of coronary artery disease (CAD). There is some evidence that polyunsaturated fatty acids of the marine n-3 type (n-3 PUFA's) may offer protection against CAD. We have studied the effect of short-term dietary supplementation with n-3 PUFAs on lipids, haemostasis, neutrophil and monocyte chemotaxis in 10 patients with IDDM. The patients were given 4 g daily of n-3 PUFAs (fish oil) for 6 weeks and were investigated before and after the supplement. No significant effects on platelets or haemostasis were observed. High density lipoprotein (HDL)-cholesterol significantly increased, and triglycerides and the ratio of total cholesterol to HDL-cholesterol significantly decreased. Monocyte chemotaxis was unaltered, while neutrophil chemotaxis significantly increased after fish oil. The finding of an improvement in neutrophil chemotaxis after supplementation with n-3 PUFAs to patients with IDDM needs to be confirmed in future studies.

Adult↗
PubMed1989

Renal sodium metabolism in relation to hypertension in diabetes.

Hypertension may eventually develop in response to chronic slight retention of sodium and expansion of the extracellular fluid volume, either due to intrinsic pathology or to neurohormonal influences of the kidneys. As almost half of all juvenile diabetic patients sooner or later will develop diabetic nephropathy and hypertension, data are discussed which tend to indicate that renal sodium metabolism is altered already early during the course of diabetes. Compared to healthy subjects the absolute total tubular sodium reabsorption is increased by approximately 30-40 per cent, as is the filtered sodium load. Insulin may stimulate sodium reabsorption in man through an effect on the distal nephron segment. However, by means of combined lithium and 51Cr-labelled EDTA clearances it has been clearly demonstrated that the excess sodium reabsorption in ambulatory insulin-dependent diabetics exclusively takes place in the proximal tubules, while the distal tubular function appears normal. In these studied patients the extracellular fluid volume was also significantly increased. The increased fractional sodium reabsorption of the proximal tubules remains unaffected by increasing duration of diabetes and is also demonstrable in patients with overt diabetic nephropathy. Glucose is reabsorbed in the early portion of the proximal tubules coupled to Na+ transport, utilizing a common carrier protein. An increased load of glucose will therefore be expected to induce an increase in the proximal tubular reabsorption rate of sodium and water, at least as long as the proximal tubular reabsorption capacity for glucose is not exceeded to a degree inducing significant osmotic diuresis. This deviation from normal in proximal renal sodium and fluid handling may be relevant to the development of hypertension in long-term insulin-dependent diabetes.

Diabetes Complications↗
PubMed1988

Early glomerular hyperfiltration and the development of late nephropathy in type 1 (insulin-dependent) diabetes mellitus.

We performed a follow-up study of the glomerular function in a series of 29 Type 1 (insulin-dependent) diabetic patients who had been studied 18 years previously. Initial median duration of diabetes was 2 years (range 0-9) and at follow-up 21 (17-27) years. At follow-up, 8 diabetic patients exhibited increased urinary albumin excretion rate 515 (32-3234) micrograms/min with glomerular filtration rates significantly lower than 21 diabetic patients with normal urinary albumin excretion (85 vs 126 ml/min/1.73 m2; p less than 0.01). The patients with increased urinary albumin excretion rate also had higher arterial blood pressure (145/90 vs 120/80) mm Hg; p less than 0.02) and increased frequency of proliferative retinopathy (7 out of 8 vs 2 out of 21; p = 0.0001) as compared to the group with normal urinary albumin excretion. However, we found no association of increased urinary albumin excretion rate (incipient or overt nephropathy) to early glomerular hyperfiltration as median initial glomerular filtration rate was 142 ml/min/1.73 m2 in the diabetic patients with increased urinary albumin excretion and 147 ml/min/1.73 m2 in the patients with normal excretion rate (p greater than 0.05).

Adolescent↗
PubMed1987

Plasma 6-keto-PGF1 alpha, thromboxane B2 and PGE2 in type 1 (insulin-dependent) diabetic patients during exercise.

The capacity of prostacyclin production determined as plasma 6-keto-PGF1 alpha was investigated in 12 type 1 (insulin-dependent) diabetic patients with a median duration of diabetes of 14 years during ordinary metabolic control. Using high pressure liquid chromatography preceding radioimmunoassay, the plasma concentration of 6-keto-PGF1 alpha, the stable metabolite of prostacyclin, was determined at rest and after a standardised bicycle exercise test. The plasma 6-keto-PGF1 alpha in diabetic patients at rest did not differ from that of 25 healthy volunteers; 2.9 pg/ml (range less than 0.2-15.3) versus 1.7 pg/ml (range less than 0.2-16.6). During the exercise test plasma 6-keto-PGF1 alpha increased significantly in the diabetic patients as well as in the control group (p less than 0.05). The increment of 6-keto-PGF1 alpha in the diabetic patients was neither related to the metabolic regulation, duration of diabetes nor to changes in platelet volume, platelet number or the production of thromboxane B2 and prostaglandin E2. Our results do not support the hypothesis that Type 1 diabetic patients have a decreased capacity of prostanoid production, as suggested from in vitro studies.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

The effect of buflomedil in diabetic retinopathy estimated by ocular fluorophotometry.

Tissue hypoxia is thought to be one of the possible factors involved in the etiology of diabetic retinopathy. Buflomedil has been reported to improve microvascular perfusion with a secondary increase in tissue oxygen pressure and may therefore be of interest in the study of diabetic retinopathy. We investigated 10 males with insulin-dependent diabetes and non-proliferative retinopathy, aged 24-46 with a duration of diabetes of 5-31 years. Buflomedil, 600 mg daily, or placebo was given for 4 weeks in a randomized, double-blind cross-over design, with a one-week washout in between. Patients were studied initially and at the end of each of the three periods. Ocular fluorophotometry was performed at each visit and a penetration index (PI) calculated by dividing the ocular measurements with the preceding average free fluorescein concentration. There was a slight, but significant decrease in the PI of the posterior vitreous while on buflomedil, from 10.6 +/- 13.4 (mean +/- SD) to 8.8 +/- 9.6 10(-4), p less than 0.05. No measurable changes were found in metabolic control as estimated by HbA1, and no side effects were observed. That the drug may act by increasing blood flow, was illustrated by measurements on capillary blood, where pH increased (7.43 +/- 0.01 to 7.45 +/- 0.01, p less than 0.05) and pCO2 decreased (5.48 +/- 0.4 to 5.15 +/- 0.24 kPa, p less than 0.05). Buflomedil may reduce the permeability of the posterior ocular barriers in diabetic retinopathy.

Adult↗
PubMed1986

Nontraumatic rhabdomyolysis during diabetic ketoacidosis.

The frequency of nontraumatic rhabdomyolysis in diabetic ketoacidosis was investigated by serial measurements of the serum levels of myoglobin and the serum activity of creatine kinase isoenzyme MM in 12 consecutively admitted ketoacidotic patients. In 5 patients (Group 1) we found hypermyoglobinaemia and elevated activity of creatine kinase isoenzyme MM on admission to hospital, whereas these two variables were normal in 7 patients (Group 2). On admission significantly higher median blood glucose levels and higher median serum osmolality were found in Group 1 than in Group 2 (for blood glucose: 49.6 mmol/l versus 19.0 mmol/l, p less than 0.02; for serum osmolality: 360 mosm/kg H2O versus 315 mosm/kg H2O, p less than 0.05). Decreased renal function was found in Group 1 as reflected by significantly higher beta 2-microglobulin serum concentrations in Group 1 compared with Group 2 on admission (median values 4.1 mg/l versus 1.7 mg/l, p less than 0.01) and during the first 3 days of therapy. The serum concentration of hypoxanthine (an indicator of the cellular energy state) was elevated in all patients on admission, with no difference between patients with or without hypermyoglobinaemia. In conclusion, our findings suggest that nontraumatic rhabdomyolysis with hypermyoglobinaemia and elevated serum activity of creatine kinase isoenzyme MM may be a hitherto unrecognized common feature of diabetic ketoacidosis.

Adult↗
PubMed1985

Hyperamylasemia, specific pancreatic enzymes, and hypoxanthine during recovery from diabetic ketoacidosis.

The contribution of the exocrine pancreas to hyperamylasemia in diabetic ketoacidosis was investigated by measuring total amylase, salivary and pancreatic isoamylases, cathodic trypsin-like immunoreactivity, and pancreatic lipase in 12 consecutive patients recovering from diabetic ketoacidosis. Hyperamylasemia was present in six of the patients [50%; expected incidence: 21.1-78.9% (95% confidence limits)]--in five with simultaneously increased activities of all three specific pancreatic enzymes, and in one with only increased salivary isoamylase. The serum concentration of hypoxanthine--an indicator of the cellular energy state--was above normal in all patients at admission. We found no differences in concentrations of hypoxanthine in serum of patients with or without hyperamylasemia or in patients with or without increases in the specific pancreatic enzymes. In none of the patients was the clinical course or the time--concentration curves of the pancreatic enzymes consistent with acute pancreatitis. The pathogenic mechanism leading to hyperamylasemia in diabetic ketoacidosis remains uncertain.

Adolescent↗
PubMed1985

Prevalence of macro- and microvascular disease as related to glycosylated hemoglobin in type I and II diabetic subjects. An epidemiologic study in Denmark.

The prevalence of macro- and microvascular disease and the distribution of glycosylated hemoglobin (Hb A1) were assessed in a representative Danish diabetes population living on the island of Falster with a population of 44.498 inhabitants. The diabetes population consisted of 533 diabetics of whom 166 were insulin-dependent (type I) and 367 non-insulin-dependent (type II). Among the 533 diabetics macrovascular complications as evidenced by myocardial infarction, gangrene or amputations and cerebrovascular catastrophes were present in 8%, 5% and 7%, respectively, while microvascular disease as evidenced by diabetic retinopathy was present in 53% of the cases. Multilogistic analysis showed no relationship between the macrovascular complications and the level of Hb A1, whereas there was a highly significant correlation between the level of Hb A1 and the presence of retinopathy in both patients with type I (P less than 0.01) and type II diabetes (P less than 0.001). The results emphasize the contention that the development of microvascular disease depends on the quality of blood glucose control while that of macrovascular disease seems unrelated to long-term hyperglycemia.

Blood Glucose↗