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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Major advances in knowledge of immunological diseases have resulted from observation of transient effects on children borne by women with such diseases. The discoveries that in Graves' disease and myasthenia gravis there are IgG antibodies directed against receptors sites are examples of such developments, while "ikiopathic" thrombocytopenic purpura is now accepted as immunological owing to its behaviour during pregnancy. In some instances observations of transient neonatal forms do not correspond with the disease manifestations in the mother. These discrepancies may be due to surgical removal of an organ vital to the disease process; inactivating damage by the disease to such an organ; presence of a blocking antibody of a molecular type not transferred across the placenta; differing tissue-antigen specificity or differing lymphocyte cooperation based on genetic variation. At present there are unexplained observations of fetal/neonatal effects in relation to diabetes mellitus and systemic lupus erythematosus which suggest that study of immunological parameters might be profitable. Determination of the HLA status of mother/fetus pairs may give rewarding clues. In the elucidation of the diseases now proven as antibody-mediated in the antibodies first discovered often turned out to be irrelevant red herrings.
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PMID:Pregnancy: Nature's experimental system. Transient manifestation of immunological diseases in the child. 5 95

To gain further insight into the genetic determinants of diabetic small vessel disease, we studied 22 HLA antigens in 110 juvenile-onset, insulin-dependent diabetics with terminal glomerulosclerosis and retinopathy, who were being prepared for kidney transplant. HLA antigens were comtemporarily determined in non-diabetic kidney transplant recipients and healthy controls. The frequency of antigens A1 and B8 were significantly higher in diabetics than in controls (P less than .02 and .011), but the frequency of BW15 was normal. The data are compatible with the concept that juvenile diabetes with microangiopathy is one of the HLA-B8 associated disorders.
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PMID:Histocompatibility (HLA) antigens and diabetic microangiopathy. 5 63

The frequency of HLA-B8 was significantly increased in pancreatic islet cell antibody (P.I.C.A)-positive patients (61%) compared with P.I.C.A.-negative patients (35%) and a control population (28%). This increased frequency of HLA-B8 was even more striking in diabetics in whom P.I.C.A. persisted for more than 5 years (71%). Thus the association of HLA-B8 with diabetes may be related to the presence of P.I.C.A. in these patients.
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PMID:HLA and pancreatic islet cell antibodies in diabetes. 6 May 16

Pancreatic islet-cell antibodies (I.C.Ab) were detected in 31 patients with organ-specific autoimmune disorders, 4 first-degree relatives of I.C.Ab-positive diabetics, and 1 apparently normal subject, none of whom had clinical evidence of diabetes. 10 of these 36 subjects were found to have diabetic glucose-tolerance tests (G.T.T.S), 4 had lag storage, and 22 had normal G.T.T.S.2 had latent diabetes, as evidenced by diabetic G.T.T.S during pregnancy and thyrotoxicosis; another 2 subsequently developed insulin-dependent diabetes (I.D.D.) Serum from 26 subjects had been stored for 1-11 yr before the G.T.T.S were done. The titres in some were shown to rise and fall over the years, while in others they remained remarkably constant. There was no correlation between the titre, change in titre or the duration of I.C.Ab or the presence of HLA-B8, BW15, or CW3 and the result of the G.T.T. In addition to acting as a marker for asymptomatic and latent diabetes and prediabetes, it seems that the presence of I.C.Ab in the serum may define a new group of potential diabetics with normal G.T.T.S. Many such subjects have one or more organ-specific autoimmune disorders (irrespective of diabetic family history), but some are first-degree relatives of I.C.Ab-positive subjects (mainly I.D.D.). About 0-5% of the general population also have I.C.Ab in their serum.
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PMID:Pancreatic islet-cell antibody as a marker for asymptomatic and latent diabetes and prediabetes. 6 45

110 people in whom insulin-dependent diabetes developed when they were less than 30 years old were studied as soon as possible after diagnosis. There was evidence for clustering of cases with BW15-positive phenotypes during the winter peak (1976) but not during the autumn peak (1975). Subjects who were BW15-positive, and in particular those who were both B8 and BW15-positive, had higher neutralising antibody titres to Coxsackle virus types B1-B4 58% of cases had islet-cell antibodies (I.C.A.), but the presence of I.C.A. was not correlated with HLA phenotypes or viral antibody titres. In 41 subjects (37%), who gave a definite history of antecedent illness, evidence indicated that this was a precipitating infection and not the initiating event producing islet-cell damage. Nearly half the subjects had had diabetic symptoms for more than 4 weeks before diagnosis.
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PMID:Aetiology of juvenile-onset diabetes. A prospective study. 6 9

A classification of idiopathic diabetes based on autoimmunity suggests that two main types of disease process may result in this syndrome. Type 1 includes classic insulin-dependent juvenile-onset diabetes, insulin-dependent diabetes presenting in later life, and diabetes initially adequately controlled for at least 3 months on oral hypoglycaemic agents but with islet-cell antibody (I.C.A.) in the serum. Type II included classic maturity-onset insulin-independent diabetes and the rarer insulin-independent diabetes presenting at a younger age in patients whose serum is negative for I.C.A. at the time of diagnosis. In terms oer the main factor is a genetically determined diathesis towards islet-cell autoimmunity (type Ia), towards islet-cell damage by appropriate viral infection or other agent in the absence of islet cell autoimmunity (type Ic), or a combination of the two diatheses (type IB). Type-II diabetes has a different genetic basis and the environmental factor is a metabolic or other form of stress rather than viral infection. Both main types have an early potential phase indicated by the presence of I.C.A. in serum (type I) and, in the absence of I.C.A., in serum (type I) and, in the absence of I.C.A., by an appropriate family history of insulin-independent diabetes or giving birth to big babies (type II). Evidence to support this hypothesis comes from HLA and histological studies in man and viral studies in laboratory animals as well as from clinical observation.
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PMID:Classification of idiopathic diabetes. 6 40

20 out of 179 diabetics treated with oral hypoglycaemic agents (O.H.A.) within 3 mo of diagnosis had pancreatic-islet-cell antibodies (ICAb) in their sera at diagnosis or later. 13 of these 20, compared with only 14 of the remaining 159, subsequently required insulin at a mean follow-up of 2 yr 10 mo and 4 yr 11 mo, respectively (p less than 10(-7)). 5 of the 7 ICAb-positive diabetics still continuing on O.H.A. therapy after a mean follow-up of 4 yr 6 mo required maximum or near-maximum combined oral therapy, while only 34 of the 145 ICAb-negative diabetics continuing on O.H.A. did so at a mean follow-up of 5 yr 4 mo (p less than 0.02). In addition, 81 diabetics treated initially with diet for a mean time of 4 yr 7 mo before going on to O.H.A. therapy were studied. All were ICAb-negative when tested at a mean interval of 6 yr 10 mo from diagnosis. By the end of the mean follow-up period of 10 yr 3 mo, 27 were on combined oral therapy and 3 had been transferred to insulin treatment. ICAb-positive diabetics on O.H.A. had a high prevalence of a personal history of organ-specific autoimmune disease, thyrogastric antibodies, a family history of insulin-dependent diabetes and possibly of HLA-B8 comparable to that in insulin-dependent diabetes and higher than that expected in a control population or in diabetics controlled by diet alone. We believe that ICAb-positive diabetes controlled by O.H.A. is an earlier stage in the same disease process (type-I diabetes) that culminates in insulin-dependency.
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PMID:Clinical and pathogenic significance of pancreatic-islet-cell antibodies in diabetics treated with oral hypoglycaemic agents. 6 85

Ninety insulin-dependent diabetic children were HLA-typed in order to elucidate the role played by HLA complex-linked genes in the pathogenesis of diabetes mellitus of childhood. HLA-Aw30 and HLA-Bw35 were significantly increased and decreased, respectively, in the diabetic group as compared with controls. In relation to age at onset of diabetes, HLA-B8 was significantly increased in the 0-5-year group. By dividing the patients according to the season at onset of the disease, only HLA-Aw30 in the October-January group reached the level of significance.
Diabetes 1977 Sep
PMID:HLA antigens in diabetic children. 7 Mar 86

Familial multiple adenoma of pancreatic beta-cells is described for the first time. The occurrence of diabetes mellitus in different members of the family raises the possibility of a common genetic origin for the multiple islet-cell adenomas and the diabetic trait. The evidence suggests that this gene is autosomal and dominant, that it is not linked with the HLA antigens, and that is causes an abnormal sensitivity of the beta-cells, which become hyperplastic or hypofunctional.
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PMID:Familial islet-cell adenomatosis. 7 Jun 43

HLA-typing was performed in 149 patients with essential hypertension, 86 males and 63 females. In 66 patients with significantly elevated serum levels of immunoglobulins, HLA-B27 was increased to 18%, from 8% in the controls (P less than 0.007). This was not significant when correcting the P-value for the number of antigens analyzed, but confirms reports of an association of this antigen with serum levels of immunoglobulins. HLA-Bw15 was found to be increased two-fold in patients with a family history of hypertension (P corrected less than 0.05) and in patients with autoantibodies (not significant). This is discussed in relation to the increase of Bw15 in juvenile diabetes and in Systemic Lupus Erythematosus, diseases in which vascular damage also occurs.
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PMID:HLA antigens in essential hypertension. Relation to familiar disposition and serum immunoglobulins. 7 Aug 61


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