PubMed Health⌕ Search

Biomedical subjects

K Bergis

Publications and source records attributed to K Bergis.

At least 19 recordsLinked to original sources
PubMed2004

Effects of improved glycaemic control maintained for 3 months on cognitive function in patients with Type 2 diabetes.

BACKGROUND AND AIM: In a previous study we failed to find beneficial short-term effects of improved glycaemic control on cognitive functioning in patients with Type 2 diabetes mellitus. A subgroup of the entire sample was tested again to examine the effect of longer-lasting improvement of metabolic control on cognitive functioning. METHODS: The cognitive performance of 26 patients with Type 2 diabetes was assessed at baseline and 3 months after discharge. Thirteen controls were tested at the similar time-points. Attention/concentration, psychomotor speed, verbal fluency, verbal memory and depressive symptoms were assessed. Improved glycaemic control was generally achieved with insulin therapy (20/26). RESULTS: At baseline, there was a trend for diabetic patients to perform worse than controls. Both groups improved significantly over 3 months in several measures. However, diabetic patients did not improve more than controls. CONCLUSIONS: In individuals with long-standing Type 2 diabetes, previous reports of improved cognitive capacity following restoration and maintenance of near-normoglycaemia were not confirmed. This might relate to the type of anti-diabetic therapy.

Blood Glucose↗
PubMed1997

[Nephropathy and hypertension in type II diabetes].

BACKGROUND: In Germany nephropathy in patients with type II diabetes has become the most frequent single cause of uremia requiring renal replacement therapy. This calls for effective measures of prevention. DIABETIC NEPHROPATHY AND HYPERTENSION: In patients with established diabetic nephropathy, hypertension is the most important pathogenetic factor which is susceptible to therapeutic intervention. Some pathogenetic mechanisms are discussed which impact on antihypertensive therapy. Interaction between hypertension and diabetic nephropathy is analyzed. CONCLUSION: Diabetic nephropathy in patients with type II diabetes has become the most frequent cause of endstage renal failure in Germany. Preventive measures, i. e. near normal glycemia and particularly antihypertensive treatment, have been proven to interfere with progression of renal failure in diabetic nephropathy. Early recognition is possible by testing for urinary albumin (microalbuminuria). In patients with diabetic nephropathy, blood pressure should be lowered to values well within the range of normotension by dietary salt restriction and antihypertensive drug therapy.

Combined Modality Therapy↗
PubMed1997

Pathogenesis and course of renal disease in IDDM/NIDDM: differences and similarities.

In the past the opinion prevailed that renal prognosis was less adverse in non-insulin-dependent diabetes mellitus (NIDDM) as compared with insulin-dependent diabetes mellitus (IDDM). This notion has to be revised in the light of recent evidence, based on epidemiologic data of NIDDM patients reaching endstage renal failure and a comparison of the cumulative prevalence of proteinuria and renal failure, respectively, in NIDDM as compared with IDDM. It has also been established that initial renal hemodynamic changes are quite comparable in NIDDM and in IDDM. It follows that past complacency about the renal sequelae of NIDDM is no longer justified and that preventive measures to interfere with the development of diabetic nephropathy are similarly important in NIDDM and IDDM.

Diabetes Mellitus, Type 1↗
PubMed1997

Abnormal pulsatile secretion of growth hormone in non-insulin-dependent diabetes mellitus.

OBJECTIVE: Studies of GH secretion in patients with non-insulin dependent diabetes mellitus (NIDDM) have produced conflicting results. We aimed to differentiate the effects of obesity and metabolic control on pulsatile GH secretion in patients with NIDDM. DESIGN: Blood sampling every 15 min from 22.00 hours to 08.00 hours after a fasting period of at least 3 h. PATIENTS: 13 male NIDDM patients, 9 healthy control subjects matched for age and BMI, and 6 lean subjects matched for age. MEASUREMENTS: Measurement of GH by a novel ultrasensitive chemiluminescence assay. Analysis of concentration vs time profiles by a multiparameter deconvolution technique. RESULTS: GH burst frequency was increased in the NIDDM (0.82 +/- 0.28 h-1) compared with both control groups (lean: 0.6 +/- 0.11; obese: 0.56 +/- 0.19). GH burst mass was decreased in patients (1.57 +/- 0.98 micrograms/l.min) and in obese controls (1.46 +/- 1.44) compared to lean controls (3.71 +/- 3.88). These differences resulted in a significantly higher nocturnal pulsatile GH secretion rate in the lean compared to the obese controls, whereas in the patient group enhanced GH burst frequency compensated for reduced burst mass. The characteristics of GH secretion were not related to nocturnal or early morning blood glucose concentrations. However, GH secretion rate was correlated positively with HbA1c (r = 0.57; P = 0.04), and negatively with plasma C peptide concentrations. CONCLUSIONS: The specific increase in GH burst frequency previously described in insulin-dependent diabetes mellitus is also present in NIDDM. However, GH hypersecretion does not occur because GH burst mass is reduced in proportion to the degree of obesity. The effect of diabetes on the hypothalamic control of GH release appears to be determined by the quality of long-term glycaemic control.

Analysis of Variance↗
PubMed1997

Excess of DD homozygotes in haemodialysed patients with type II diabetes. The Diabetic Nephropathy Study Group.

The role of the insertion/deletion polymorphism of the angiotensin-converting enzyme (ACE) gene in the genesis of diabetic nephropathy has been controversial. It has recently been proposed that progression occurs more rapidly in individuals with diabetic and non-diabetic renal disease who are homozygous for the D allele. We studied 658 patients with type II diabetes, 347 without diabetic nephropathy and 311 with various stages of diabetic nephropathy, and determined the I/D polymorphism of the ACE gene. Patients at the extremes of renal risk, i.e. normotensive patients without antihypertensive treatment and without nephropathy (n = 144), vs patients on dialysis (n = 61), differed with respect to genotype (DD 36.8% vs 57.4%; P = 0.007) and allele frequencies (D 0.59 vs 0.76; P < 0.001). In contrast, patients with and without presumed nephropathy as assessed by albuminuria did not differ with respect to DD genotype. In conclusion, in this study, which was limited by sample size, patients with the highest renal risk more frequently had the DD genotype. This would be compatible with a greater risk of (or rate of) progression to end-stage renal failure.

Adult↗
PubMed1997

Altered action of angiotensin II in patients with type 2 diabetes mellitus of recent onset.

OBJECTIVE: Angiotensin II (Ang II) increases insulin sensitivity in healthy volunteers. This effect is thought to be mediated, at least in part, by an increase in skeletal muscle blood flow. In the past it had been documented that some biological actions of Ang II are altered in diabetes. We addressed the issue of whether this is also true for its action on insulin sensitivity. DESIGN AND METHODS: Twelve healthy volunteers (aged 43+/-9 years) and 15 patients with type 2 diabetes mellitus (NIDDM) of recent onset (aged 45+/-9 years) were allocated in random order in a double-blind placebo-controlled design to be administered a sham infusion or an infusion of 2 ng Ang II/kg per min. Insulin-stimulated glucose uptake (the M value) was measured with the euglycaemic clamp technique, leg muscle blood flow (MBF) with plethysmography, blood pressure with a Dinamap device, and glomerular filtration rate and effective renal plasma flow with the steady-state inulin (Cin) and p-aminohippurate (CPAH) clearance methods, respectively. RESULTS: In volunteers the mean M-value after Ang II infusion (10.1+/-1.5 mg/kg per min) was significantly higher (P < 0.01) than that after sham infusion (8.2+/-0.9 mg/kg per min). In contrast, in diabetic patients it was not significantly different with Ang II (6.1+/-1.3 mg/kg per min) and sham infusion (5.5+/-1.2 mg/kg per min). The difference in the mean absolute increase in the M value (deltaM) between groups was significant (P< 0.02). The Ang II-induced increase in MBF under euglycaemic conditions was attenuated in diabetic patients (from 15.0+/-3.5 to 15.5+/-3.9 ml/100 ml per min, NS) compared with volunteers (from 16.8+/-3.3 to 19.1+/-3.7 ml/100 ml per min, P< 0.01). Again, the difference between the mean absolute increases in MBF (deltaMBF) in the groups was significant (P < 0.01). A significant correlation was found between deltaMBF and deltaM (r= 0.62, P<0.01). The absolute acute increase in mean arterial blood pressure with Ang II was similar in diabetic patients and volunteers. Mean Cin, CPAH and fractional sodium excretion values were significantly lower and renal vascular resistances and filtration fractions higher during the Ang II than they were during the placebo clamp period. This was observed in patients as well as in healthy subjects, but the effects of Ang II on renal haemodynamics and sodium handling were more pronounced in diabetic patients. CONCLUSIONS: In patients with NIDDM of recent onset the stimulatory effect of Ang II on insulin sensitivity and on skeletal muscle blood flow is attenuated. In contrast, the effects of Ang II on renal perfusion and sodium handling are more pronounced in patients with NIDDM than they are in healthy subjects.

Adult↗
PubMed1991

Prospective randomized two-years clinical study comparing additional metformin treatment with reducing diet in type 2 diabetes.

After a 2 weeks hospital treatment with a strong dietary regime 100 patients not sufficiently controlled (blood glucose fasting 120-180, pp 180-250 mg/100 ml), were randomly allocated to a purely dietary therapy or to a diet-metformin-combination for a duration of 2 years. After 1 and 2 years the patients were rehospitalized for an accurate evaluation. Additionally, HbA1 was controlled every 3 months, in case of problems after shorter periods. If HbA1 exceeded 10% for more than 4 weeks the patients were hospitalized for 5 days in order to decide whether the deterioration of metabolic control was due to the patients' non-compliance to treatment or to treatment failure. During 2 years of observation 30 patients were withdrawn from the treatment for external reasons. 13 patients (6 diet, 7 metformin + diet) were non-compliant with diet, 3 further patients were not metformin-compliant. Therapeutic failures were confirmed in 4 diet patients, none of the metformin + diet patients failed to respond to treatment. After excluding all these patients there was a group of 29 diet and 25 metformin + diet patients with a similar development of criteria of metabolic control during 2 years. Lipid levels deteriorated in the dietary group more noticeably than during additional metformin treatment although without reaching a statistically significant level, though. The stimulated C-peptide was significantly reduced by metformin in comparison to diet only, which supports former findings of an insulin-lowering effect of the drug.

Adult↗
PubMed1975

[The lithiasis of the gall bladder, a stepchild of the diagnosis of the epigastrium? (author's transl)].

An anamnestic questionnaire project at a hospital for gastroenterological diseases has proved, that in 100 patients cholelithiasis after a cholecystectomy was not diagnosed at first. In more than two thirds of the preliminary diagnoses (69.8 p.c.) stomach was concerned. The therapy required in these cases took 7.9 years on an average. Generally it took 12.6 years of complaints from the first symptom until cholecystectomy was performed. Even when cholelithiasis was diagnosed, the operation was not decided upon until 6.8 years had passed on an average. For the most part the patient himself delayed the operation. According to the patients questioned, chronic pancreatitis was the disease most frequent following cholecystectomy. Reasons for errors in diagnosis of epigastric pain are discussed. The undoubted value of early cholecystectomy is emphasized.

Adolescent↗