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G Soltész

Publications and source records attributed to G Soltész.

At least 19 recordsLinked to original sources
PubMed2003

Diabetes in the young: a paediatric and epidemiological perspective.

The spectrum of diabetes in the young has widened; it now includes monogenic diseases, for example the various forms of permanent and transient neonatal diabetes and MODY as well as the emerging obesity-associated Type 2 diabetes in late childhood, but the main form is still Type 1 diabetes. Age-related major medical, physiological, social and emotional problems make the clinical management of diabetes in children and adolescents a difficult task for the physician and the family. Overall glycaemic control remains moderate or poor despite a treatment schedule, which interferes with several elements of "normal" childhood. There is an up to tenfold geographical variation in the incidence of childhood Type 1 diabetes within Europe with relatively stable incidence rates in some countries (mainly northern), but dynamic increases in incidence in other countries (mainly central European).A number of nongenetic (environmental) factors have been associated with the risk of Type 1 diabetes. Among these, perinatal factors, early nutrition, growth and vaccinations, atopic diseases and vitamin D are discussed in detail. The important interplay between genes, organism and environment is illustrated with new genetic data supporting the importance of environmental pressures in the evolution of this major disease.Although Type 1 diabetes usually accounts for only a minority of the total impact of diabetes in a population, it is the predominant form of the disease in younger age-groups in most developed countries. It is estimated that on an annual basis almost 100 000 children younger than 15 years of age develop Type 1 diabetes worldwide. The autoimmune destruction of the pancreatic beta cells in Type 1 diabetes leads to absolute insulin dependence and a high rate of complications typically occurring at a relatively young age. Therefore, Type 1 diabetes places a particularly heavy burden on the individual, the family and health services.

Child↗
PubMed2001

Is childhood-onset type I diabetes a wealth-related disease? An ecological analysis of European incidence rates.

AIMS/HYPOTHESIS: To describe the epidemiology of childhood-onset Type I (insulin-dependent) diabetes mellitus in Europe, the EURODIAB collaborative group established prospective, geographically-defined registers of children diagnosed under 15 years of age. A total of 16,362 cases were registered by 44 centres during the period 1989-1994. The registers cover a population of approximately 28 million children with most European countries represented. METHODS: In most centres a primary and a secondary source of ascertainment were used so that the completeness of registration could be assessed by the capture-recapture method. Ecological correlation and regression analyses were used to study the relationship between incidence and various environmental, health and economic indicators. RESULTS: The standardised average annual incidence rate during the period 1989-94 ranged from 3.2 cases per 100,000 person-years in the Former Yugoslavian Republic of Macedonia to 40.2 cases per 100,000 person-years in Finland. Indicators of national prosperity such as infant mortality (r = -0.64) and gross domestic product (r = 0.58) were most strongly and significantly correlated with incidence rate and previously-reported associations with milk consumption (r = 0.58), coffee consumption (r = 0.51) and latitude (r = 0.40) were also observed. CONCLUSION/INTERPRETATION: The wide variation in childhood Type I diabetes incidence rates within Europe could be partially explained by indicators of national prosperity. These indicators could reflect differences in environmental risk factors such as nutrition or lifestyle that are important in determining a country's incidence rate.

Adolescent↗
PubMed2001

HLA alleles and IDDM in children in Hungary: a comparison with Finland.

It has been postulated that variation in the distribution of human leukocyte antigen (HLA)-encoded susceptibility alleles for insulin-dependent diabetes mellitus (IDDM) is the genetic basis for variation in the incidence of the disease between populations. The aim of this study was to characterize HLA-encoded susceptibility to IDDM in Hungary and to identify whether HLA-DRB1/DQ-encoded susceptibility could account for the five times lower incidence of disease in Hungary compared with Finland. The haplotypes DRB1*03-DQA1*05-DQB1*02 (DRB1*03-DQ2) and DRB1*04-DQA1*0301-DQB1*0302 (DRB1*04-DQ8) were significantly associated with disease in both populations. Three genotypes incorporating either or both of these haplotypes accounted for over 70% of the diabetic population in both races. The combined background frequency and the degree of risk as measured by odds ratios of these HLA-DRB1-DQ genotypes were not significantly different in the two countries. Comparison of the DRB1*0401-DQ8 haplotype between the two races suggested a role for HLA-B alleles in susceptibility. These data indicate that the susceptibility associated with high risk DRB1-DQ genotypes alone is insufficient to account for the fivefold variation in incidence of IDDM between Hungary and Finland. Other genetic and/or environmental influences must be involved.

Alleles↗
PubMed2000

[Pathogenesis and types of neonatal diabetes].

Studies on pathogenesis of neonatal diabetes may lead to better understanding of pancreatic beta-cell maturation and regulation of insulin secretion. The purpose of this study was to examine the clinical course, immunologic and genetic background of the transient and permanent form of neonatal diabetes. Clinical data (onset and duration of diabetes, C peptide levels, duration of insulin treatment, associated disorders) were collected, islet cell specific antibodies (islet cell antibody and glutamate decarboxylase antibody) were determined and genetic analyses (HLA DQA1-DQB1 typing and microsatellite mapping on chromosome 6) were performed in three patients with permanent and three patients with transient neonatal diabetes. None of the six patients had HLA DQ diabetes susceptibility alleles and most infants were negative for islet cell autoantibodies indicating that no pancreatic islet-cell specific autoimmunity exists in the two forms of neonatal diabetes mellitus. Complete paternal uniparental isodisomy of chromosome 6 has been identified in a transient neonatal diabetes case with macroglossia. The permanent neonatal diabetes cases and the other two cases with transient form did not possess this chromosome anomaly. It is concluded, that none of the two forms neonatal diabetes is of autoimmune origin. They have different genetic background and represent different disease entities. Transient neonatal diabetes is probably caused by alteration of expression of an imprinted gene on chromosome 6 which might play role in fetal growth and pancreatic beta-cell maturation and insulin secretion. Permanent neonatal diabetes is probably a more heterogenous phenotype, the cause of which remains to be clarified in the future.

Autoantibodies↗
PubMed2000

Isodicentric Y chromosome in an Ullrich-Turner patient without virilization.

We report on a 17-year-old young woman with Ullrich-Turner syndrome (UTS), who was found to have a karyotype 45,X/46,X,idic(Y)(q11). She had age-appropriate genitalia without virilization in spite of the presence of the Y-derived marker chromosome and SRY locus in 70% of her lymphocytes. Having reviewed the literature, we conclude that a possible explanation for the lack of virilization in these mosaic patients is most likely an uneven distribution of tissue mosaicism (gonadal mosaicism).

Adolescent↗
PubMed2000

Correlation of blood-spot 17-hydroxyprogesterone daily profiles and urinary steroid profiles in congenital adrenal hyperplasia.

OBJECTIVE: To compare the value of blood-spot 17-hydroxyprogesterone (17-OHP) daily profiles and urinary steroid excretion in untreated and treated patients with congenital adrenal hyperplasia (CAH). PATIENTS: Ten patients with CAH were investigated during steroid replacement therapy (Group 1), and 11 patients were investigated without treatment (Group 2). METHODS: Capillary blood samples were collected for measurement of blood-spot 17-OHP values by non-chromatographic radioimmunoassay. Steroid profiles of 24-h urine samples were analyzed by gas chromatography. RESULTS: There was a close correlation between the individual daily means of blood-spot 17-OHP measurements and the pregnanetriol/ tetrahydrocortisone ratio in both groups of patients (Group 2: r=0.839, p<0.001; Group 1: r=0.686, p<0.001). Almost the same correlation was found between the blood-spot 17-OHP value and the sum of three 17-hydroxyprogesterone metabolites/the sum of three cortisol/cortisone metabolites ratio (Group 2: r=0.918, p<0.001; Group 1: r=0.741, p<0.001). CONCLUSIONS: Blood-spot 17-OHP measurements and 24-h urinary steroid profile have the same impact in identification and monitoring therapy of children with CAH.

17-alpha-Hydroxyprogesterone↗
PubMed2000

Transient but not permanent neonatal diabetes mellitus is associated with paternal uniparental isodisomy of chromosome 6.

OBJECTIVES: The factors determining the pathogenesis of transient and permanent neonatal diabetes mellitus are poorly characterized. The purpose of this study was to examine the role of chromosome 6 in the pathogenesis of neonatal diabetes mellitus and to detect differences between these 2 phenotypes. METHODS: Microsatellite markers (D6S334, D6S286, D6S310, D6S308, D6S292, D6S311, and D6S403) and human leukocyte antigen DQ alleles were examined using polymerase chain reaction and DNA fragment electrophoresis in 3 patients with transient and 3 patients with permanent neonatal diabetes mellitus. Humoral markers of islet cell autoimmunity and clinical characteristics were analyzed in the 2 groups. RESULTS: A patient with transient neonatal diabetes mellitus (TND) and macroglossia carrying paternal uniparental isodisomy (UPD) of chromosome 6 has been identified. The isodisomy affected the whole chromosome; no maternal chromosome 6 sequences were detected. The permanent neonatal diabetes mellitus cases and the other 2 cases with TND did not have UPD. None of the patients had high-risk type 1 diabetes human leukocyte antigen DQ alleles and most infants were negative for islet cell-specific autoantibodies indicating that none of the 2 forms of neonatal diabetes mellitus is likely to be of autoimmune origin. An association of TND and persistent granulocytopenia is described for the first time. CONCLUSIONS: We propose that transient and permanent forms of neonatal diabetes mellitus have different genetic background and represent different disease entities. TND is associated with UPD of chromosome 6 suggesting that an imprinted gene on chromosome 6 is responsible for this phenotype. It seems that 2 copies of the paternal allele are necessary for the development of TND; therefore, it is likely that overexpression of a putative gene located on chromosome 6 alters pancreatic beta-cell maturation and insulin secretion.

Chromosomes, Human, Pair 6↗
PubMed1999

[Incidence of type 1 childhood diabetes in Hungary (1978-1997). Hungarian Committee on the Epidemiology of Childhood Diabetes].

The incidence of Type 1 diabetes in 2417 children aged 0-14 years was studied between 1978 and 1997. Statistical analysis of the data in the twenty-year period showed a steady increase in incidence of Type 1 diabetes with an average rate of 4.8% (95% CI 4.0-5.5) per annum. The incidence rate was lowest in children aged 0 to 4 years and the highest in the age group 10 to 14 years. This increase in incidence was similar for all age groups, but it was most pronounced in the 10 to 14 year-old age group. One hundred and twenty one of the 1239 families (9.7%), one of parents was also reported to have Type 1 diabetes and in 3 (0.2%) families both parents had Type 1 diabetes. Twenty two (2.3%) of the diabetic families had a sibling with Type 1 diabetes. The nearly three-fold increase in incidence during the last two decades (3.8 per 100,000 per year in 1978; 10.7 per 100,000 per year) was probably due to environmental factors, while the high degree of familial clustering emphasises the role of genetic factors in the etiology of Type 1 diabetes.

Adolescent↗
PubMed1999

Fetal type lymphocytes in insulin dependent diabetes mellitus.

CD5+ B and gamma/delta T lymphocytes constituting a major population in the fetus and newborn infant, represent two small subsets of the B and T lymphocyte compartment in healthy adults. There is evidence for their potential involvement and relative expansion in autoimmune disorders. In insulin-dependent diabetes mellitus (IDDM) CD5+ B lymphocyte counts have been found to be increased or normal. The aim of our study was to determine the percentage of both "fetal type" lymphocyte subsets in peripheral blood of 22 recently diagnosed children with IDDM, in that of 13 high risk subjects (islet cell antibody (ICA) positive non-diabetic Ist degree relatives of diabetic children) and in 43 healthy controls. The percentage of gamma/delta TCR+ cells and of CD5+ B lymphocytes was found to be significantly (p < 0.0001 and p = 0.03, respectively) higher in the diabetic and prediabetic groups as compared to controls. Young children with IDDM associated antibodies carry a higher risk of developing clinical IDDM than older individuals. In our hands, the percentage of both CD5+ B and gamma/delta T lymphocytes was higher in the younger population. However, age-dependent decrease for both lymphocyte subpopulations in IDDM-prediabetic patients was less than in healthy controls. Since the above subpopulations are supposed to play a role in immune response to conserved structures, these observations would suggest a higher capacity of older individuals to 'natural autoimmunity" and would explain at least in part the increased risk of antibody positive young children to develop IDDM.

Adolescent↗
PubMed1997

[Clinical diagnosis of childhood insulin dependent diabetes mellitus. Hungarian Epidemiological Group for Childhood Diabetes].

The aim of this study was to describe the clinical presentation and severity of the disease at onset in childhood during 1994. Based on the prospective national incidence registry, data were collected (using a modified version of the EURODIAB ACE questionnaire) from all diabetic children diagnosed during a full calendar year (1994). The ascertainment was 91%. Polyuria, polydipsia and weight loss were the most frequent clinical symptoms, but fatigue, abdominal pain and personality changes were also often reported. Almost one quarter of the children presented with diabetic ketoacidosis. There was no correlation between age, duration of symptoms, blood glucose levels and the severity of disease. The unacceptably high incidence of presentation ketoacidosis called for an urgent improvement of the diagnostic acumen of the physicians dealing with children.

Age Factors↗
PubMed1994

Non-genetic risk determinants for type 1 (insulin-dependent) diabetes mellitus in childhood. Hungarian Childhood Diabetes Epidemiology Study Group.

Using the prospective Hungarian childhood diabetes register, a nationwide case-control study was carried out to investigate the possible role of various non-genetic factors as risk determinants for type 1 diabetes in childhood. A questionnaire (covering family characteristics, social status, fetal and perinatal events, breast-feeding habits, infectious diseases and stressful life events) was sent by mail to all incident diabetic children in 1990 (n = 163) and to two referent children (for each diabetic child), matched for age, sex and county. Diabetic children had a tendency to have mothers > 35 years of age (odds ratio (OR) = 3.52; 95% confidence intervals (CI) 0.74-16.79), a lower proportion of their mothers had higher education (OR = 1.69; 95% CI 0.95-3.0) and these children tended to move home more frequently (OR = 1.99; 95% CI 0.97-4.1). Although the duration of exclusive breast feeding was similar in both groups, the proportion of diabetic children who received no breast milk tended to be higher (OR = 1.76; 95% CI 0.91-3.4). A higher proportion of diabetic children reported non-specific infections (OR = 2.94; 95% CI 1.19-7.21) and the number of stressful life events was higher in diabetic children aged 10-14 years (OR = 3.9; 95% CI 1.14-13.27). As the risk determinants for childhood insulin-dependent diabetes mellitus identified in our low-risk population appear to be similar to those detected in the genetically different, high-risk Swedish population, our study strongly supports an etiological role for these non-genetic risk factors in IDDM.

Adolescent↗