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Biomedical subjects

W Grzeszczak

Publications and source records attributed to W Grzeszczak.

At least 19 recordsLinked to original sources
PubMed1999

The role of aldose reductase gene in the susceptibility to diabetic nephropathy in Type II (non-insulin-dependent) diabetes mellitus.

The dinucleotide repeat polymorphism (5'-ALR2) in the promoter region of the aldose reductase gene on chromosome 7q35 has been implicated in the development of diabetic nephropathy in Type I (insulin-dependent) diabetes mellitus, and markers flanking the aldose reductase locus have given evidence suggestive of a linkage between diabetic nephropathy and Type II (non-insulin-dependent) diabetes mellitus in Pima Indians. To examine whether the 5'-ALR2 polymorphism in the aldose reductase gene is involved in the development of diabetic nephropathy in Caucasians with Type II diabetes, we carried out a large association study. Patients with Type II diabetes from one outpatient clinic were screened for diabetic nephropathy and divided into three groups according to the degree of this disease: 179 patients with normoalbuminuria, 225 patients with microalbuminuria and 70 patients with proteinuria. Patients with normoalbuminuria were included in the study only if they had had Type II diabetes for 10 or more years. DNA from all patients was genotyped for the 5'-ALR2 polymorphism using a previously established polymerase chain reaction protocol. The frequency of the putative risk allele Z-2 was 34.6%, 34.2% and 33.6% in the normoalbuminuria, microalbuminuria and proteinuria groups, respectively. Similarly no difference among groups was found for the frequency of the putative protective allele Z + 2. In conclusion, the results of our association study in Caucasian patients with Type II diabetes do not support the hypothesis that the 5'-ALR2 polymorphism in the aldose reductase gene contributes to susceptibility to diabetic nephropathy.

Age of Onset↗
PubMed1998

Reduced insulin-mediated glucose uptake by euglycemic clamp in offspring of patients with type 2 diabetes.

Family studies point to an important genetic element in the genesis of type 2 diabetes. A variety of metabolic abnormalities have been documented in offspring of patients with type 2 diabetes. It has not been shown, however, at what age reduced insulin sensitivity is demonstrable using the sensitive the euglycemic clamp technique. To address this issue we screened 425 consecutive type 2 diabetic patients and examined all available (n = 48) normotensive, normoglycemic, non-smoking offspring (mean age 31.4+/-0.9 years) and compared them to 22 healthy offspring of non-diabetic parents (controls). The two groups were of similar age and BMI. Measurements in offspring and controls included baseline IRI, tissue glucose uptake (TGU, using euglycemic hyperinsulinemic clamp technique), and 24 hour ambulatory blood pressure (ABP). TGU was significantly (p < 0.001) lower in offspring of diabetic parents (338.8+/-19.9 (mol/kg/min) when compared to controls (516.6+/-22.2 micromol/kg/min). 24 h systolic ABP was significantly higher (p < 0.02) in propositi compared to controls (121.2+/-2.2 mm Hg and 113.8+/-1.7 mm Hg, respectively). No difference in triglycerides concentration was found. A borderline negative correlation was observed, however, between triglyceride levels and TGU (R = -0.48, p < 0.001). TGU was not related to the presence or absence of diabetic nephropathy in the parents. We conclude: Insulin resistance and various facets of the metabolic syndrome are demonstrable even at age 30 years in young non-obese, normotensive offspring of patients with type 2 diabetes. These disturbances are not related to the presence of microvascular complications in parents.

Adult↗
PubMed1998

A polymorphism in the gene for the atrial natriuretic peptide and diabetic nephropathy. Diabetic Nephropathy Study Group.

BACKGROUND: Atrial natriuretic peptide is involved in blood pressure regulation via its vasodilating and natriuretic actions. Since diabetic nephropathy and hypertension are closely related, ANP is a reasonable candidate gene for diabetic nephropathy (DN). METHODS: We genotyped 410 patients with type I diabetes (without DN n = 307; with DN n = 103) and 658 patients with type II diabetes (without DN n = 464; with DN n = 194). In the patients the duration of diabetes was at least 10 years. Diabetic nephropathy was defined as urinary albumin excretion of > or = 30 mg/24 h. The HpaII polymorphism in intron 2 of the ANP gene was determined using PCR amplification followed by restriction digest. Alleles were separated on agarose gels stained with ethidium bromide. RESULTS: We compared genotype distribution and allele frequencies between patients with and without nephropathy. No significant difference was observed either in type I (allele frequency without DN H1, 0.02/H2, 0.98 vs with DN H1, 0.05/H2, 0.95; P = 0.132) or in type II diabetes (allele frequency without DN H1, 0.04/H2, 0.96 vs with DN H1, 0.05/H2, 0.95; P = 0.551). CONCLUSIONS: The polymorphism in the gene for the atrial natriuretic peptide does not seem to play a major role in the development of diabetic nephropathy in either type I or in type II diabetes.

Adult↗
PubMed1998

Angiotensin I-converting enzyme gene polymorphisms: relationship to nephropathy in patients with non-insulin dependent diabetes mellitus.

Nephropathy is a frequent complication of long-term diabetes. Strong evidence exists that genetic predisposition plays a major role in the development of diabetic nephropathy. The role of the angiotensin I-converting enzyme gene (ACE) in the susceptibility to nephropathy in diabetes, especially in non-insulin dependent diabetes mellitus (NIDDM), remains unclear. This study examines the association of two ACE polymorphisms: a 287-bp insertion/deletion (I/D) in intron 16 and PstI (A/G substitution in intron 7; alleles P/M) with renal complications in 941 NIDDM patients. From this group, for further analysis 127 patients were selected with overt proteinuria or chronic renal failure, 335 patients with microalbuminuria, and a control group of 254 normoalbuminuric patients with a diabetes duration of at least 10 yr. No significant differences in the distribution of ACE I/D and PstI genotypes or allele frequencies were observed between the examined groups. The results of this study strongly suggest that there is no association between the ACE gene I/D and PstI polymorphisms and nephropathy in NIDDM.

Aged↗
PubMed1998

[Natural killer cell count in hemodialysis patients].

UNLABELLED: The patients with chronic renal failure present an immunodeficiency state manifested by prolonged tolerance to allografts, increased incidence of infections and abnormally high incidence of neoplasia. The present study aimed to assess the effect of chronic uraemia and haemodialysis treatment on the natural killer cells (NK cells) count. Peripheral blood NK cells (CD3-, CD16+), total lymphocytes, leukocytes, monocytes and granulocytes of 24 hemodialyzed patients with chronic renal failure and 32 healthy subjects were studied using flow cytometry. In the investigated group of patients with chronic renal failure treated with haemodialysis the count of NK cells (CD3-, CD16+) in the peripheral blood was significantly decreased in comparison to healthy subjects (137 +/- 11 versus 229 +/- 13, p < 0.001) and a significant negative correlation (r = -0.391, p < 0.05) was observed between the duration of haemodialysis treatment and the count of NK cells (CD3-, CD16+). CONCLUSIONS: 1) Chronic uraemia and haemodialysis treatment exerts a negative effect on NK cells (CD3-, CD16+) count in the peripheral blood. 2) The count of NK cells (CD3-, CD16+) in the peripheral blood in patients with chronic renal failure treated with haemodialysis could be a prognostic marker of susceptibility to infections and malignancy.

Adult↗
PubMed1998

[Lack of relationship between angiotensinogen gene m235t polymorphism and gene insertion/deletion (I/D-intron 16) and Pst I RFLP (P/M-intron 7) polymorphisms of the angiotensin I converting enzyme(ACE) gene and the development of H-gestosis. Preliminary results].

Genetic and familial factors may predispose to H-gestosis. The aim of our study was to answer the question if angiotensinogen gene m235t polymorphism, and ACE gene I/D and Pst I RFLP polymorphisms may be markers of genetic predisposition to the H-gestosis. 246 pregnant women (median age 26 years) were studied (the studied group consisted of 116 women with H-gestosis and the control group consisted of 130 healthy pregnant women). Genotyping was performed using polymerase chain reaction method. Statistical analysis was done by means of Statistica for Windows. Genotype distribution was analyzed using chi 2 test. P < 0.05 was considered as statistically significant. In our study we did not receive statistically significant differences in ACE and angiotensinogen genes genotype distributions and allele frequencies between the investigated groups. Based on results of the study we may suggest that I/D and Pst I RFLP ACE gene polymorphism and angiotensinogen gene m235t polymorphism do not play any significant role in the pathogenesis of H-gestosis.

Adolescent↗
PubMed1998

[The influence of salmon calcitonin on changes in thyroid hormone concentration and on TSH secretion. I].

The aim of this investigation was determination of salmon calcitonin (sCT) influence on changes of thyroid hormones levels in serum. The investigation was carried out on a group of 26 patients. The group was divided in two different ways: into people younger and older than 65 years, and into men and women. Investigation protocol consists of 4 days. On the 1st day patients received 100U of SC, on the 2nd day--100U of SC and 0.4 mg TRH, on the 3rd day--0.4 mg TRH, on the 4th day--0.9% solution of NaCl and 5% solution of human albumin. T3, T4 fT3 and fT4 concentrations in serum were determined by RIA method.

Adult↗
PubMed1998

[Influence of salmon calcitonin on changes in thyroid hormone concentration and on TSH secretion. II].

The aim of this investigation was determination of salmon calcitonin (SC) administration influence on hypothalamus-pituitary-thyroid axis. The investigation was carried out on a group of 26 patients. The group was divided in two different ways: into people younger and older than 65 years, and into men and women. Investigation protocol consists of 4 days. On the 1st day patients received 100U of SC, on the 2nd day--100U of SC and 0.4 mg TRH, on the 3rd day--0.4 mg TRH, on the 4th day--0.9% solution of NaCl and 5% solution of human albumin. TSH serum concentrations were determined by RIA method. Infusion of SC caused TSH serum concentration increase in all groups. This effect is qualitatively similar but quantitatively different in investigated groups. Administration of SC with TRH causes significantly smaller growth of TSH concentration than observed after infusion of TRH alone. The mechanism of SC influence on pituitary may be similar to the one of TRH.

Adolescent↗
PubMed1998

[Use of doxazosin (Cardura-Pfizer), alpha 1-adrenoreceptor antagonist, in treatment of hypertension in patients with diabetes].

Doxazosin (Cardura-Pfizer) is a alpha 1-adrenoreceptor antagonist. This drug significantly decreases the blood pressure in subjects with hypertension. Despite decreasing blood pressure, doxazosin has a beneficial effect on many disorders observed in subjects with diabetes mellitus. Doxazosin 1) improves the regulation of lipids disturbances, 2) improves tissue sensitivity to insulin, 3) decreases the frequency of sexual disorders. In this situation Doxazosin is a good choice in the treatment of hypertension in diabetic subjects, in subjects with hypertension and hypercholesterolemia, with left ventricular hypertrophy, in old male subjects with hypertension and benign prostatic hypertrophy.

Adrenergic alpha-Antagonists↗
PubMed1998

[The significance of candidate genes' polymorphism in the development of diabetic nephropathy].

Poor metabolic control, hemodynamic factors and long duration of diabetes may predispose to the development of diabetic nephropathy. Recently the hypothesis that genetic factors may play certain role in the pathogenesis of diabetic nephropathy has been also proposed. The angiotensin I converting enzyme (ACE) gene has been the main candidate gene predisposing to the development of diabetic nephropathy. One of its polymorphisms--insertion/deletion seems to be particularly associated with long-term diabetic complications. There are many candidate genes taking probable part in the pathogenesis of diabetic nephropathy. Among them we must think about: the HLA system genes, cations transporters genes, renin-angiotensin system genes, insulin sensibility dependent genes, genes coding basement membrane, genes taking part in apoprotein synthesis regulation. If there would be strong evidence that genetic factors play certain role in the pathogenesis and progression of diabetic nephropathy, the high risk diabetics could be selected and the adequate prevention could be applied.

Diabetic Nephropathies↗
PubMed1998

[Genetic aspects of diabetic retinopathy].

Poor metabolic control, hemodynamic factors and long duration of diabetes may predispose to the development of diabetic retinopathy. Recently the hypothesis that genetic factors may play certain role in the pathogenesis of diabetic retinopathy has been also proposed. The angiotensin I converting enzyme (ACE) gene has been the main candidate gene predisposing to the development of diabetic retinopathy. One of its polymorphisms--insertion/deletion seems to be particularly associated with long-term diabetic complications. The HLA system genes, TNF-beta gene, IGF-1 gene and PAI-1 gene are the other candidate genes. If there would be strong evidence that genetic factors play certain role in the pathogenesis and progression of diabetic retinopathy, the high risk diabetics could be selected and the adequate prevention could be applied.

Diabetic Retinopathy↗
PubMed1998

[The role of oxidative stress in development of diabetic angiopathies].

Oxidative stress is an imbalance between free radicals production and lipid peroxidation on the one hand, and the activity of antioxidant systems (enzymatic and non-enzymatic) on the other hand. It seems that oxidative stress may cause the development and complications of several diseases including diabetes, atherosclerosis, neoplasms, inflammation, hypertension etc. Prooxidant--antioxidant imbalance in diabetes may be due to non-enzymatic protein glycation, glucose autooxidation, increased sorbitol pathway, decreased activity of antioxidant enzymes and depletion of some non-enzymatic scavengers. It seems that we may partially diminish the development and progression of diabetic angiopathies decreasing oxidative stress by means of scavengers supplementation, use of hypotensive drugs with antioxidant properties and antidiabetic oral agents with antiperoxidative activity.

Antioxidants↗
PubMed1998

[Microangiopathic complications in type 2 diabetes].

The current knowledge concerning macroangiopathic complications of type 2 diabetes was presented in the review. The prevalence of atherosclerosis in coexistence with diabetes was indicated as well as the factors involved in the increased progression of the complication. The clinical differences in the course of particular types of atherosclerosis were described. The risk factors of atherosclerosis and the potential possibilities of the prevention were also analyzed.

Arteriosclerosis↗
PubMed1998

[Treatment of lipid metabolism disorders in the elderly].

Positive correlation between cholesterol concentration and morbidity of circulatory system diseases is not questioned and has a large evidence in literature. Aging is associated with increasing mean concentration of serum lipids, especially LDL cholesterol fraction. But the risk of coronary heart disease in patients at advanced age with hypercholesterolemia is less significant than in younger ones. In the therapy of hyperlipidemia the usage of hypolipemic drugs (statin) is not practical recommended in the elderly. Possible usage of these drugs should not reduce the comfort of life. Diet is an alternative and also effective method of lipid-lowering therapy.

Aged↗
PubMed1997

Nephropathy of type II diabetes: evidence for hereditary factors?

Family studies point to an important genetic element in the genesis of diabetic nephropathy, but it is not known whether renal abnormalities are present prior to the onset of diabetes. To address this issue we examined all consecutive patients suffering from type II diabetes with a duration of more than 10 years who attended a diabetes outpatient clinic. Ninety-four patients had nephropathy, 307 did not. All offspring who were phenotypically normal (no hypertension, normal oral glucose tolerance, non-smoking) and agreed to participate were examined, 26 from nephropathic and 30 from non-nephropathic diabetic parents. They were compared with 30 offspring matched for age, gender and BMI from non-diabetic parents as controls. We measured urinary albumin excretion under baseline conditions and at several time points after ingestion of 300 g cooked beef and submaximal treadmill exercise, respectively. In addition, casual blood pressure, ambulatory blood pressure, urinary albumin and urinary alpha-1-microglobulin were measured. Primary renal disease was excluded by clinical examination. Under baseline conditions, median urinary albumin excretion rate (AER; microgram/min) was significantly (P < 0.005) higher in offspring of nephropathic type II diabetic patients (7.8; range 1.04 to 19.5) than in the offspring of non-nephropathic type II diabetic patients (4.8; 0.36 to 17.5) and controls (4.4; 0.16 to 18.4). Submaximal treadmill exercise caused a greater proportional increase of AER in offspring of nephropathic type II diabetics (median 16-fold) than in offspring of non-nephropathic diabetic patients (6.3-fold) or controls (4.8-fold). In offspring of nephropathic diabetic patients casual and particularly ambulatory systolic blood pressures were significantly higher, but AER was not correlated with blood pressure. In summary, higher values, albeit within the normal range, for baseline and postexercise albuminuria were noted in phenotypically normal offspring of parents with type II diabetes and nephropathy. The observation suggests that changes in transglomerular albumin traffic are demonstrable prior to the onset of diabetes and diabetic nephropathy in subjects with a potential genetic predisposition to these conditions.

Adult↗
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↗