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Biomedical subjects

J Ludvigsson

Publications and source records attributed to J Ludvigsson.

At least 109 records · Page 6Linked to original sources
PubMed1992

C-peptide profiles in patients with non-insulin-dependent diabetes mellitus before and during insulin treatment.

The objective of the study was to evaluate the effect of insulin treatment on insulin secretion in patients with non-insulin-dependent diabetes mellitus (NIDDM). Ten patients with NIDDM were first investigated while still taking oral hypoglycemic agents, and then randomized to a crossover study with two eight-week periods of insulin treatment (oral treatment having been stopped) given either as mainly intermediate-acting insulin twice daily (2-dose) or as preprandial regular insulin and intermediate-acting insulin at bedtime (4-dose). In the patients treated with oral agents the 24-h C-peptide area under the curve was similar to that in the controls, but the profile was different with a rise at breakfast but with almost absent meal peaks during the rest of the day. Insulin treatment improved glycemic control markedly, lowered urinary C-peptide excretion and the serum C-peptide concentrations being reduced by more than 50%. The shape of the C-peptide profiles was unaltered and there were no significant differences between the two insulin regimens. The decrease in serum C-peptide concentration during insulin treatment correlated with the change in blood glucose. Fasting serum C-peptide concentrations correlated closely with the 24-h C-peptide area under the curve. In conclusion, insulin treatment of NIDDM patients with secondary failure to oral agents greatly reduces the insulin secretion, probably owing to the reduction in blood glucose.

Aged↗
PubMed1992

Prevalence and clinical picture of IDDM in Nigerian Igbo schoolchildren.

OBJECTIVE: To evaluate the prevalence and clinical picture of IDDM in Nigerian Igbo schoolchildren born and living in continental Africa. RESEARCH DESIGN AND METHODS: In three school districts (Ezza, Ishielu, Ohaukwu), 77,862 schoolchildren aged 5-17 yr answered our questionnaires on age, sex, known disease, drugs being taken, family history, and diabetic symptoms like polyuria, polydipsia, polyphagia, and weight loss. Positive respondents were given glucosuric tests, and glucosuric subjects had hyperglycemic tests. Diagnosis of IDDM was established in hyperglycemic patients by referred hospital clinicians based on insulin requirements. RESULTS: Twelve new cases of IDDM were found in addition to 14 previously diagnosed cases, giving a CPR of 0.33/1000. Ishielu had a CPR of 0.46/1000 compared with 0.25 (P less than 0.01) for Ohaukwu. Boys had a CPR of 0.38/1000 compared with 0.25/1000 (P less than 0.06) for girls. Boy-to-girl prevalence ratio was approximately 3:1. CONCLUSIONS: The relatively high prevalence of IDDM in this poor African population, despite potential deaths caused by minimal medical attention, may be because of long-term protein malnutrition and endemic childhood infections, which have been implicated in the etiology of IDDM in similar malnourished populations.

Adolescent↗
PubMed1992

Islet cell surface antibodies in diabetic children determined with 125I-labelled anti-IgG as tracer.

We have developed an assay for ICSA using fixed beta-cells as target cells and 125-I-Anti-IgG as tracer. Interassay variation was 9.5% and intraassay variation was 9.9%. For high titers of ICSA specificity was 100% but sensitivity then only 70%. Our technique enables a laboratory assistant to determine 200 samples in one week. Absorption of the samples with rat beta-cells as well as rat fibroblasts showed that ICSA are beta-cell specific and does not crossreact with rat fibroblasts. We found a significant difference in prevalence of high titer ICSA between healthy school children (4%) and newly diagnosed diabetic children (19%) (p < 0.001). That difference had disappeared after 18 months duration of IDDM when the B-cell mass and thus the amount of antigen had decreased. No difference was seen between healthy children and adult blood donors. There was no seasonal variation of ICSA titers in healthy children.

Adolescent↗
PubMed1992

Maternal smoking and irradiation during pregnancy as risk factors for child leukemia.

The effect of joint exposure to diagnostic X-rays and maternal smoking during pregnancy was compared in a case-control study of 216 children with cancer (128 cases with acute lymphoblastic leukemia [ALL] and 88 with solid tumors) and 301 control children with insulin-dependent diabetes mellitus (IDDM). Exposure to diagnostic X-rays combined with smoking of ten or more cigarettes per day gave a relative risk of 3.6 (95% CI, 1.8 to 7.0) and a positive dose response relation for ALL in the offspring (p less than 0.001). When examined alone, X-rays gave a relative risk of 1.8 (95% CI, 1.1 to 3.1), and smoking a relative risk of 2.2 (95% CI, 1.1 to 4.5). No similar trend was seen for solid tumors. Potential confounding was examined after stratification on maternal smoking-diagnostic X-ray exposure and each of potential confounders, but there was little change in the risk ratio. We conclude that the risk of ALL in the offspring was more than threefold higher when smoking was combined with diagnostic X-ray during pregnancy.

Adolescent↗
PubMed1992

Molecular analysis of Philadelphia-positive childhood chronic myeloid leukemia.

The breakpoints in chromosome 22 were determined in five children with Philadelphia-positive chronic myeloid leukemia. All had rearrangements within the major breakpoint cluster region (M-bcr). Four patients had breakpoints in the 5' region of M-bcr (zones 1-3), whereas one had a rearrangement in the 3' region (zone 4). The patient with the 3' rearrangement was the only one to develop a lymphoid blast crisis; he also had a substantially longer survival (102 months) than the others (11-54 months).

Child↗
PubMed1991

Relating homology between the Epstein-Barr virus BOLF1 molecule and HLA-DQw8 beta chain to recent onset type 1 (insulin-dependent) diabetes mellitus.

A role for the Epstein-Barr virus in initiating Type 1 (insulin-dependent) diabetes mellitus has been proposed since Epstein-Barr virus BOLF1 (497-513) AVTPL RIFIVPPAAEY has an 11 amino acid identity with HLA-DQw8 beta (49-60) AVTPL GPPAAEY. Rabbit antisera to the BOLF1 (496-515) peptide crossreacted with the homologous DQw8 beta (44-63) peptide but not with the related DQw7 beta (44-63) peptide, which differed from the DQw8 peptide only in an ALA to ASP substitution in position 57. Antisera to DQw8 beta (49-60) reacted with the DQw8 beta (44-63) peptide and BOLF1 (496-515), but not with DQw7 beta (44-63). The antiserum to the BOLF1 peptide bound to denatured class II major histocompatibility complex beta chains from Epstein-Barr virus-transformed DQw8-positive lymphocytes in an immunoblotting analysis. Epstein-Barr virus antibodies were detected at equal frequencies and similar titres in sera of 30 patients with Type 1 diabetes (16 of 30; 63%) and in sera of 20 non-diabetic control subjects (13 of 20; 65%). Sera from diabetic patients did not bind to DQw8 beta (44-63) or BOLF1 (496-515) peptides. From these data we conclude that there is no simple relationship between serological evidence of Epstein-Barr virus infection and crossreactions between homologous Epstein-Barr virus and class II major histocompatibility complex peptides.

Adolescent↗
PubMed1991

Särimner: a computer model of diabetes physiology for education of physicians and patients.

Often diabetic patients have developed their skills by some trial-and-error-like training over a long period of time. To minimize this inconvenience we have made a mathematical model to facilitate diabetes education. The model consists of a number of blocks involved in diabetes physiology: digestion, blood (transport), pancreas, injected insulin absorption, liver, muscles, kidneys, metabolism and insulin sensitivity. The model serves as a demonstration object and the user can change meals, exercise and injections and see the resulting blood glucose level. A more experienced user can search for further explanations of different phenomena deeper in the physiology of the model. The model does not solve any problem for the user, but creates a learning situation in which the user, led by his own curiosity, successively increases his experience of diabetes physiology. Särimner is implemented as an easy-to-use menu driven computer program for IBM PC-clones with Hercules, EGA or VGA graphics.

Adolescent↗
PubMed1991

Raised IgG and IgM in "epidemic" IDDM suggest that infections are responsible for the seasonality of type I diabetes.

Serum levels of immunoglobulins G, A and M were quantitatively measured at diagnosis and at regular intervals for four years in 92 type I (insulin-dependent) diabetes patients. The patients were 0.8-15.99 years of age at diagnosis. Thirty-six of them got diabetes during periods of high incidence (the "epidemic" group) and 56 of them were diagnosed during periods of seemingly low incidence (the non-"epidemic" patients). Fifty percent (18/36) of the "epidemic" group had infections less than two months preceding diagnosis as compared to 29% (16/56) (p less than 0.01) of the non-"epidemic" patients. At diagnosis immunoglobulins G, and M in the "epidemic" group were 11.28 +/- 2.0 and 1.97 +/- 0.77 as compared to 9.9 +/- 2.3 (p less than 0.01) and 1.31 +/- 0.58 (p less than 0.001) respectively in the non-"epidemic" patients. The same highly significant differences were observed when mean values of IgG and IgM were compared between children who had infections less than two months before diagnosis and those without preceding infections. Except for slightly higher (p less than 0.12) total (OKT3) T-lymphocytes and higher (p less than 0.03) B-lymphocytes at diagnosis in the "epidemic" group, there were no significant differences in quantitative T- and B-lymphocyte subpopulations between various groups. 6.3% (2/32) of the patients who had preceding infections had HLA-DR3/non-DR4 genotypes as compared to 30.6% (15/49); p less than 0.001, of those patients without preceding infections.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Islet cell surface antibodies preferentially inhibit glucose-stimulated insulin release in vitro.

The effect of islet surface antibodies (ICSA) on in vitro insulin release was studied. Isolated rat islets were incubated in the presence of immunoglobulin preparations from patients with insulin-dependent and non-insulin-dependent diabetes mellitus (IDDM, NIDDM) and healthy subjects, and stimulated with D-glucose, L-arginine or tolbutamide. After incubation, the amount of insulin release from the rat islets was determined. The immunoglobulin preparations from 5 newly diagnosed IDDM patients who were positive for ICSA, and from 5 age-matched healthy subjects were examined. Even in the absence of complement or lymphocytes, immunoglobulin fractions positive for ICSA significantly inhibited low and high concentrations of glucose-stimulated insulin release compared with normal control (P less than 0.02), but had little influence on insulin release after stimulation with tolbutamide. Arginine-stimulated insulin release was almost the same in ICSA-positive immunoglobulin fractions and the control. Immunoglobulin fractions negative for ICSA either from four patients with recently diagnosed IDDM or from four newly diagnosed NIDDM patients had only negligible effect on insulin release after stimulation with glucose. These results suggest that ICSA in IDDM patients, even in the absence of complement or lymphocytes, may preferentially interfere with the mechanisms of glucose-stimulated insulin release in the pancreatic B cells.

Adolescent↗
PubMed1990

HLA heterozygosity in insulin-dependent diabetes is most frequent at the DQ locus.

Restriction fragment length polymorphism using an HLA-DQ beta-chain genomic probe showed that 63 children with insulin-dependent (type 1) diabetes mellitus (IDDM) were all (100%) positive for the BamH1 fragments 12 kb and/or 4 kb compared to 98% (62/63) for HLA-DR3 and/or 4 and 75% (47/63) for HLA-B8 and/or 15. The 36 (56%) DR3-positive children were all 4-kb-positive; however, a total of 44 (70%) children were 4-kb-positive (P less than 0.02). The 55 (87%) DR4-positive children were all 12-kb-positive, but a total of 56 (89%) were 12-kb-positive (NS). The heterozygosity at the HLA region increased from 11/63 (18%) for HLA-B8/15 to 29/63 (46%) for HLA-DR3/4 (P less than 0.0004) and to 37/63 (59%) for the HLA-DQ 4 kb/12 kb fragments (P less than 0.02). The test of an equal probability of a positive result under the adjacent pair of tests indicates that the increased risk of developing IDDM in association with HLA-DQ is to a great extent due to heterozygosity at this locus. There were no differences between the 4 kb/12 kb and the DR3/4-positive IDDM children with respect to fasting or meal-stimulated C peptide, insulin requirement, or levels of insulin antibodies formed during the first 12 months of insulin therapy. Our results support the hypothesis that HLA-DQ is closely associated with an increased risk of childhood IDDM, and when typed for at this locus parameters of the clinical course were homogeneous, suggesting that factors other than HLA-DQ may determine previously observed differences between IDDM children in clinical or functional parameters.

Adolescent↗
PubMed1990

Vitreous fluorophotometry in juvenile diabetics with and without retinopathy in relation to metabolic control: insulin antibodies and c-peptide levels.

Vitreous fluorophotometry was performed in 56 juvenile insulin-dependent diabetic patients aged 9-23 years (median: 16 years), diabetes duration 1-20 years (median: 8 years). Fundus photography showed mild background retinopathy in 5 patients, while 51 patients had no signs of retinopathy. Abnormal leakage into the posterior vitreous body was found in 4/5 patients with background retinopathy and in 24/51 with normal fundi. We found a significantly positive correlation between abnormal leakage and duration of diabetes and HbA1 with Kendall rank-order correlation coefficients T = 0.21 (P = 0.01) and 0.19 (P = 0.02) resp. No significant correlation was found between leakage and age, actual blood glucose level or insulin antibodies expressed as insulin binding capacity of IgG, but a significantly negative correlation between abnormal leakage and low levels of fasting c-peptide/s T = 0.437 P less than 0.001. Kendall partial rank-order correlation analysis showed that c-peptide/s significantly explained the leakage when HbA1 or duration was kept constant. Duration could only explain leakage when HbA1 was fixed but not when c-peptide/s was kept constant. HbA1 could also explain leakage when duration or c-peptide was fixed.

Adolescent↗
PubMed1989

Seasonality of type 1 (insulin-dependent) diabetes mellitus: values of C-peptide, insulin antibodies and haemoglobin A1c show evidence of a more rapid loss of insulin secretion in epidemic patients.

According to month of diagnosis, 165 children who developed Type 1 (insulin-dependent) diabetes mellitus at the age of 0-16.2 years (mean +/- SD, 7.6 +/- 4.1 years) could be divided into 69 patients diagnosed during peak seasons (epidemic cases) and 96 patients diagnosed during months of low incidence (non-epidemic cases). Seasonality of onset of symptoms and of diagnosis was observed in both sexes in all age groups. The patients diagnosed during peak seasons had shorter duration of symptoms (13.2 +/- 8.1 days) as compared to 22.9 +/- 10.3 days; p less than 0.001 in the patients diagnosed during months of low incidence. At diagnosis, 88.4% (61/69) of the epidemic group had ketonuria as compared to 71.9% (69/96); p less than 0.06 in the non-epidemic patients. The values of C-peptide, insulin antibodies, haemoglobin A1c and HLA-DR phenotype frequencies in the 69 epidemic patients were compared with those of the 96 non-epidemic patients. In the epidemic patients, the C-peptide values of 0.11 +/- 0.05 mmol/l at diagnosis had increased to 0.12 +/- 0.05 mmol/l at one month and 0.13 +/- 0.06 mmol/l at 3 months. These values were significantly lower (p less than 0.001) than in the non-epidemic patients at the same time points: 0.17 +/- 0.08 nmol/l; p less than 0.001, 0.23 +/- 0.11 nmol/l; p less than 0.001, and 0.22 +/- 0.10 nmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗