In a sample of 1.033 diabetic patients characteristics of 10 group specific systems (ABO, MNS, Rh, P, K and Fy blood groups and Hp, Gc and Gm serum types) were tested in order to verify any association of hereditary group specific traits and diabetes.
In a sample of 1.033 diabetic patients characteristics of 10 group specific systems (ABO, MNS, Rh, P, K and Fy blood groups and Hp, Gc and Gm serum types) were tested in order to verify any association of hereditary group specific traits and diabetes.
In a sample of 1.033 diabetic patients characteristics of 10 group specific systems (ABO, MNS, Rh, P, K and Fy blood groups and Hp, Gc and Gm serum types) were tested in order to verify any association of hereditary group specific traits and diabetes.
In a sample of 1.033 diabetic patients characteristics of 10 group specific systems (ABO, MNS, Rh, P, K and Fy blood groups and Hp, Gc and Gm serum types) were tested in order to verify any association of hereditary group specific traits and diabetes.
In a sample of 1.033 diabetic patients characteristics of 10 group specific systems (ABO, MNS, Rh, P, K and Fy blood groups and Hp, Gc and Gm serum types) were tested in order to verify any association of hereditary group specific traits and diabetes.
There was a tendency toward an increased incidence of cancer in families with infants who had elevated CEA levels and a reverse trend was noted with respect to diabetes; however, these associations were not statistically significant.
This suggests that there may be a gene closely linked with the HLA-A locus which plays a role in the expression of diabetes in the Pimas by contributing to an earlier age of onset.
If extended to human insulin and different HLA-DR and HLA-B antigen patterns, these finding should help in the therapeutic selection of the appropriate insulin and thus reduce the induction of an anti-insulin response in patients with diabetes.
HLA-A, B, C, and DR antigen frequencies in relation to development of diabetes and variations in white cell antibody formation in highly transfused thalassemia patients.
Newer terminology identifies those uncommon patients with true insulin deficiency as having insulin-dependent diabetes (IDDM), while the majority of patients with diabetes have some residual insulin secretion but may have a disorder of insulin receptor number or affinity.
These results do not define a clear cataract-SORD deficiency etiopathogenic relationship, nevertheless, they strongly suggest activity polymorphism in human red cell SORD, which would be highly relevant not only to the study of cataracts but of other major complications in diabetes.
However, we did find interactions between GM, HLA-DR, and Type 1 diabetes (significant or of borderline significance after considering the effect of multiple tests): possession of Glm(2) appeared to increase susceptibility to diabetes in individuals who had HLA-DR3 but not HLA-DR4, while possession of G3m(5) appeared to increase susceptibility in individuals who had HLA-DR4 but not HLA-DR3.
The greater the severity of the diabetes (greater fasting hyperglycemia) the greater the post-receptor defect, and in those patients with more significant fasting hyperglycemia the post-receptor defect is the predominant abnormality leading to the insulin resistant state.
The greater the severity of the diabetes (greater fasting hyperglycemia) the greater the post-receptor defect, and in those patients with more significant fasting hyperglycemia the post-receptor defect is the predominant abnormality leading to the insulin resistant state.
In order to study the heterogeneity of Type 2 (noninsulin-dependent) diabetes, we determined HLA antigens and measured B-cell function as C-peptide response to intravenous glucagon in 217 patients with onset of non-ketotic diabetes after the age of 40 years.
The presence of albumin antibodies was neither related to the presence of diabetic late complications, islet cell antibodies, HLA-status nor duration of diabetes.
The etiological fraction (EF) values indicated that HLA D/DR alleles were the best markers for IDDM, the observed EF for HLA-DR4 in diabetes was as high as 0.70.
Islet cell antibodies (ICA-IgG and complement-fixing-ICA), parietal cell antibodies (PCA), intestinal epithelial cell antibodies (IECA), thyroglobulin (TgA) and thyroid microsomal antibodies (MsA), antinuclear (ANA) and reticulin antibodies (RA), were studied in 55 insulin-dependent diabetic patients (30 males and 25 females), aged 2-19 years with diabetes from a few days up to 14 years.
We conclude that increased fasting proinsulin levels precede abnormalities of insulin secretion, and are an early indication of minor B-cell damage in these twins irrespective of their risk of developing diabetes.
In a multivariate analysis glutamic pyruvic transaminase, blood glucose, body mass index, bilirubin, systolic blood pressure, uric acid and a family history of diabetes were all significantly associated with the development of diabetes.