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S Ivarsson

Publications and source records attributed to S Ivarsson.

At least 19 recordsLinked to original sources
PubMed2006

Common variants in MODY genes increase the risk of gestational diabetes mellitus.

AIMS/HYPOTHESIS: Impaired beta cell function is the hallmark of gestational diabetes mellitus (GDM) and MODY. In addition, women with MODY gene mutations often present with GDM, but it is not known whether common variants in MODY genes contribute to GDM. SUBJECTS AND METHODS: We genotyped five common variants in the glucokinase (GCK, commonly known as MODY2), hepatocyte nuclear factor 1-alpha (HNF1A, commonly known as MODY3) and 4-alpha (HNF4A commonly known as MODY1) genes in 1,880 Scandinavian women (648 women with GDM and 1,232 pregnant non-diabetic control women). RESULTS: The A allele of the GCK -30G-->A polymorphism was more common in GDM women than in control subjects (odds ratio [OR] 1.28 [95% CI 1.06-1.53], p=0.008, corrected p value, p=0.035). Under a recessive model [AA vs GA+GG], the OR increased further to 2.12 (95% CI 1.21-3.72, p=0.009). The frequency of the L allele of the HNF1A I27L polymorphism was slightly higher in GDM than in controls (1.16 [95% CI 1.001-1.34], p=0.048, corrected p value, p=0.17). However, the OR increased under a dominant model (LL+IL vs II; 1.31 [95% CI 1.08-1.60], p=0.007). The rs2144908, rs2425637 and rs1885088 variants, which are located downstream of the primary beta cell promoter (P2) of HNF4A, were not associated with GDM. CONCLUSIONS/INTERPRETATION: The -30G-->A polymorphism of the beta-cell-specific promoter of GCK and the I27L polymorphism of HNF1A seem to increase the risk of GDM in Scandinavian women.

Adult↗
PubMed2005

Association of the E23K polymorphism in the KCNJ11 gene with gestational diabetes mellitus.

AIMS/HYPOTHESIS: Gestational diabetes mellitus (GDM) and type 2 diabetes share a common pathophysiological background, including beta cell dysfunction and insulin resistance. In addition, women with GDM are at increased risk of developing type 2 diabetes later in life. Our aim was to investigate whether, like type 2 diabetes, GDM has a genetic predisposition by studying five common polymorphisms in four candidate genes that have previously been associated with type 2 diabetes. MATERIALS AND METHODS: We studied 1,777 unrelated Scandinavian women (588 with GDM and 1,189 pregnant non-diabetic controls) for polymorphisms in the genes encoding potassium inwardly rectifying channel subfamily J, member 11 (KCNJ11 E23K), insulin receptor substrate 1 (IRS1 G972R), uncoupling protein 2 (UCP2 -866G-->A) and calpain 10 (CAPN10 SNP43 and SNP44). RESULTS: The EE, EK and KK genotype frequencies of the KCNJ11 E23K polymorphism differed significantly between GDM and control women (31.5, 52.7 and 15.8% vs 37.3, 48.8 and 13.9%, respectively; p=0.050). In addition, the frequency of the K allele was increased in women with GDM (odds ratio [OR]=1.17, 95% CI 1.02-1.35; p=0.027), and this effect was greater under a dominant model (KK/EK vs EE) (OR=1.3, 95% CI 1.05-1.60; p=0.016). Analysis of the IRS1 G972R polymorphism showed that RR homozygosity was found exclusively in women with GDM (91.0, 8.3 and 0.7% vs 90.7, 9.3 and 0.0% for GG, GR and RR genotypes, respectively; p=0.014). The genotype and allele frequencies of the other polymorphisms studied were not statistically different between the GDM and control women. CONCLUSIONS/INTERPRETATION: The E23K polymorphism of KCNJ11 seems to predispose to GDM in Scandinavian women.

Adult↗
PubMed2004

Genotypic and phenotypic differences between Arabian and Scandinavian women with gestational diabetes mellitus.

AIMS/HYPOTHESIS: Gestational diabetes mellitus is a heterogeneous disorder characterised by impaired insulin secretion and action. Our aim was to study whether autoimmunity, variations in genes affecting insulin secretion and action, or both, contribute to the development of gestational diabetes and whether the pathogenesis of the disease differs between women with a Scandinavian or Arabian background. METHODS: We studied a total of 500 unrelated women with gestational diabetes (400 Scandinavian and 100 Arabian) and 550 unrelated pregnant non-diabetic control women (428 Scandinavian and 122 Arabian) matched for ethnicity. RESULTS: Arabian women with gestational diabetes were 50% more insulin resistant for the same BMI compared with Scandinavian women with the disease (homeostasis model assessment [HOMA-IR]; 3.2+/-0.3 vs 2.2+/-0.2, p=0.02). Both Scandinavian (4.2% vs 0.9%, p=0.008) and Arabian (4.6% vs 0.0%, p=0.03) women with gestational diabetes had a higher frequency of GAD antibodies (GAD65Ab) than the matched controls. The frequency of HLA-DQB1 risk genotypes was slightly higher in Scandinavian women with gestational diabetes than in the Scandinavian controls (46.3% vs 38.8%, p=0.03) but no significant difference was found between the Arabian women with gestational diabetes and the Arabian controls (47% vs 51.6%, p=0.47). There were no significant differences in the frequency of the insulin gene variable number of tandem repeat ( INS VNTR) alleles and genotypes or the peroxisome proliferator-activated receptor-gamma 2 ( PPAR gamma 2-Pro12Ala) polymorphism between the women with gestational diabetes and the control women either in Arabian or in Scandinavian women. CONCLUSIONS/INTERPRETATION: Gestational diabetes mellitus was associated with the presence of GAD65Ab in both study groups. Scandinavian women with gestational diabetes may share some genetic features with Type 1 diabetes. In addition, Arabian women with gestational diabetes are more insulin resistant than Scandinavian women with gestational diabetes and with the same BMI.

Adult↗
PubMed1999

Effect of growth hormone (GH) during puberty in GH-deficient children: preliminary results from an ongoing randomized trial with different dose regimens.

This paper reports results from an ongoing, randomized, multicentre national trial. The aim is to elucidate whether a dose of growth hormone (GH) of 0.2 IU/kg (0.07 mg/kg), given either as once-daily or twice-daily injections during puberty, is more effective than a once-daily dose of 0.1 IU/kg/day (0.03 mg/kg/day) in improving final height in children with GH deficiency (GHD). The twice-daily regimen comes closer to the spontaneous GH secretion pattern in puberty. Ninety-two children with GHD who had been receiving GH therapy for at least 1 year, and with spontaneous puberty or who were prepubertal and due to be started on replacement therapy to induce puberty, were randomly assigned to receive GH as follows: group A, 0.1 IU/kg/day (0.03 mg/kg/day), administered once daily; group B, 0.2 IU/kg/day (0.07 mg/kg/day), administered once daily; and group C, 0.2 IU/kg/day (0.07 mg/kg/day), divided into two equal injections given at 12-hour intervals. Pubertal height gain was 0.7, 0.7 and 1.3 SDS for groups A, B and C, respectively. The gain in height during puberty was thus most marked in group C. Mean final height, when corrected for parental height, was between 0 and 1 SDS in all treatment groups. All but seven children reached a final height within +/- 2 SD of the general population. There was a wide range of final heights in all three treatment groups. This variation in response suggests the need to individualize treatment in order to achieve an appropriate final height for most individuals.

Adolescent↗
PubMed1995

Maternal enteroviral infection during pregnancy as a risk factor for childhood IDDM. A population-based case-control study.

Using the nationwide childhood-onset diabetes register in Sweden, we were able to trace children who contracted diabetes before the age of 15 years and who were born at a specific hospital in Sweden where maternal sera from delivery had been stored during the years 1969-1989. Sera obtained at delivery from 57 mothers of diabetic children were compared with sera from 203 mothers of control subjects who were delivered at the same hospital during the same time period. The sera were analyzed blindly using a group-specific enzyme-linked immunosorbent assay for enteroviral IgG and IgM antibodies before and after urea wash as an avidity test. On the same plates, IgG antibodies to herpes, mumps, and toxoplasmosis were analyzed. The mean absorbance values of enteroviral IgG antibodies against enteroviral antigens (echo30, coxsackie B5, and echo9) were significantly higher among mothers whose children later developed diabetes (P = 0.002, P = 0.02, and P = 0.04, respectively). When reduction in activity after urea wash, indicating recently formed antibodies, was compared, the differences were even more pronounced (P < 0.001 for all three antigens). No significant differences were found for antibodies against herpes (all types), herpes type 2, mumps, or toxoplasmosis. When IgM activity and/or a significant decrease in avidity index, an indication of recent enterovirus infection, was used as a risk exposure, the odds ratio standardized for year of birth (95% confidence interval) was 3.19 (1.39-7.30). We conclude that the results of this study indicate that enteroviral infection during pregnancy is a risk factor for childhood-onset diabetes in the offspring.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Viral↗
PubMed1992

Cholelithiasis during the first year of life: case reports and literature review.

Five cases are reported of children with gallstones diagnosed by ultrasound during their first 7 months of life. Of the four with symptomatic gallstones, one subsequently developed vitamin K deficiency syndrome with profuse bleedings. The children, who belonged to a defined population, were all diagnosed within an 18-month span, suggesting the frequency of early gallstone formation to be higher than formerly supposed. One child had haemolytic anaemia, but none of the conventional risk factors for stone formation was present in the other four cases.

Child, Preschool↗
PubMed1985

Bombesin, neurotensin and pro-gamma-melanotropin immunoreactants in human milk.

The concentration of bombesin-like, neurotensin-like and pro-gamma-melanotropin-like immunoreactants in human skim milk was measured by radioimmunoassay and found to be 235 pg/ml (mean, n = 13, range 60-430 pg/ml), 63 pg/ml (mean, n = 13, range 20-105 pg/ml) and 2.4 ng/ml (mean, n = 6, range 1.2-5 ng/ml), respectively. The concentrations were 5-10 times higher than in plasma. High performance liquid chromatography showed that the neurotensin and pro-gamma-melanotropin immunoreactants co-eluted with the authentic peptides. Bombesin gave three peaks, one co-eluting with authentic bombesin and one with porcine gastrin releasing peptide 14-27, whereas another one had a shorter elution time, suggesting a less hydrophobic fragment, possibly even smaller than gastrin releasing peptide 14-27.

Bombesin↗
PubMed1985

Excretion of radionuclides in human breast milk after the administration of radiopharmaceuticals.

The fraction of injected activity that was excreted through the breast milk of nursing mothers at different times after the injection of various radiopharmaceuticals has been measured in 21 patients. For 99mTc-labeled radiopharmaceuticals the total excreted fraction was 10% for pertechnetate and 1.5-3% for MAA, plasmin, diethylenetriaminepentaacetic acid (DTPA), and methylene diphosphonate (MDP). For [125I]hippuran and [131I]hippuran the corresponding value was 3%. For the above mentioned radiopharmaceuticals the activity concentration in the milk decreased exponentially with an effective half-life of approximately 4 hr. For chromium-51 ethylenediaminetetraacetic acid ([51Cr]EDTA) and [99mTc]RBC, much smaller amounts were excreted in the breast milk. The absorbed dose to various organs of the baby has been calculated. We conclude that when [99mTc]pertechnetate, [99mTc]MAA, [99mTc]plasmin, [125I]hippuran, or [131I]hippuran are used the child should be fed just before the administration of the radionuclide to the mother and the next three milk fractions should not be used. For [99mTc]DTPA and [99mTc]MDP as well as [51Cr]EDTA, only the first fraction should not be used. According to our earlier investigations breast feeding has to be stopped for at least 3 wk after investigations with [125I]fibrinogen.

Breast Feeding↗
PubMed1983

Tri-iodothyronine and thyroxine in human milk.

The concentration of tri-iodothyronine (T3) and thyroxine (T4) in human milk was determined by radioimmunoassay (RIA). The analysis of T3 was performed on unextracted milk and on ethanol extracts of defatted milk. Analysis of unextracted milk was complicated by artifacts. Reliable and reproducible results were achieved only with the milk extracts. In 10 colostral milk samples the mean T3 levels +/- SD were 0.80 +/- 0.52 nmol/l before feeding (early milk) and 0.93 +/- 0.62 after feeding (hind milk). The T3 concentration in colostrum did not change significantly during the feeding to the infant. In 12 mature milk samples collected between infant feedings, the mean T3 +/- SD was 1.19 +/- 0.42 nmol/l. T4 was not detected in any of the samples analysed (detection limit 3 nmol/l).

Colostrum↗
PubMed1977

The Larsen syndrome and glial proliferation in the brain.

A case of the Larsen syndrome is reported in which postmortem examination of the brain revealed glial proliferation resembling tuberous sclerosis. The differential diagnosis of the syndrome and the possible significance of the lesions are discussed.

Abnormalities, Multiple↗
PubMed1976

On the occurrence of lipoprotein-x in non-hemolytic jaundice.

In cholestasis, serum lipids are altered. The alterations could at least partially be ascribed to the occurrence of an abnormal lipoprotein, LP-X. In 103 patients with jaundice, out of whom 16 had extra-hepatic cholestasis, the presence of LP-X was tested and semi-quantificated (by visual grading) utilizing an immunological technique. In extra-hepatic cholestasis, all patients showed LP-X in serum, while in intra-hepatic drug-induced cholestasis 87% revealed this phenomenon. At the initial stage of acute hepatitis, in drug-induced cholestasis, and in extra-hepatic cholestasis, the semi-quantificated LP-X correlated with alkaline phosphatase values. In extra-hepatic cholestasis, LP-X disappeared soon after the obstruction was relieved by operation.

Bilirubin↗