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

Type I diabetes is a heterogeneous disorder and the causes of pancreatic beta-cell destruction are unknown. In 1-2% of all cases, viruses (e.g. coxsackie, rubella, mumps, or beta-cell poisons) have been implicated. Twin studies suggest at most 50% of genetic predisposition. In this review we describe the autoimmune components which, in association with inheritance of HLA-haplotypes in susceptible families, allow the future selection of predisposed sibs for possible preventive therapy to retard loss of insulin secretion. The known association of the endocrine autoimmune organ-specific disorders in 10% of Type I diabetics is the extreme expression of the other main genetic ingredient in the development of insulitis in this disease, irrespective of the triggering environmental components. In this "polyendocrine" subgroup and in the "juvenile-onset" cases there is a prolonged latency period during which pancreatic autoimmunity markers are present before clinical expression of the disease.
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PMID:Etiology of Type I diabetes mellitus: heterogeneity and immunological events leading to clinical onset. 634 51

In order to select a population at risk for the development of diabetes for a prospective study of the relationship of islet cell antibodies (ICA), islet cell surface antibodies ( ICSA ), and glucose tolerance after mumps infection, we carried out a screening program for diabetes. A diabetic survey was conducted among 1581 children (less than 16 yr of age) with mumps infection 14 mo before the survey, using a brief questionnaire combined with urinary glucose analysis. Responses to the screening program were obtained from 68.4% (N = 1080) of the children. Out of a total of 1080 subjects, 1069 (99%) had no diabetes mellitus, diabetic symptoms, or glucosuria. A "positive urine glucose screen" was obtained in 11 subjects (1%) of the study group. These individuals all had a normal oral glucose tolerance test according to the new WHO definition. A group of 86 children was randomly selected from the total group of 1080 children for follow-up glucose tolerance, ICA, and ICSA . Irrespective of the negative urine glucose screen impaired glucose tolerance was diagnosed in 3.5% (N = 3) of the 86 children. The prevalence of ICA and ICSA was 78% and 36%, respectively. The simultaneous prevalence of ICA and ICSA was 33%. The pathogenetic role of mumps infection and ICA/ ICSA and their possible relationship to slow progressive beta cell destruction remain to be elucidated.
Diabetes Care
PMID:Mumps infection and insulin-dependent diabetes mellitus (IDDM). 637 12

The detection of islet cell antibodies has led to an increasing interest in autoimmune mechanisms in Type I diabetes mellitus. Other phenomena, such as insulitis in juvenile diabetics and in experimental animals, cellular immune reactions and concommitant antibodies against other endocrine organs, antinuclear antibodies and circulating immune complexes have supported such speculations. HLA-association and viral-infections could be predisposing and inducing factors. However, with one exception, the occurrence of ICA in a group of mumps infected children did not result in the development of diabetes mellitus over 3-4 years, nor could it be correlated with HLA-pattern. The islet cell antibodies block glucose stimulated insulin secretion in vitro without complement, while Type I diabetic sera with complement are beta cell cytotoxic irrespective of their ICA concentration. It is still not clear whether these mechanisms play any role in vivo. Therapeutic intervention before the clinical manifestation of the disease is as yet not possible due to the lack of markers indicating a subclinical autoimmune process.
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PMID:Virus infection islet cell antibodies and islet cell function in type I diabetes mellitus. 638 56

To connect mumps and diabetes mellitus in children is an old problem in medical literature. The typical occurrence of ICA at the onset of diabetes in children, as well as the incidence of ICA approximately 3 weeks after mumps infection support the hypothesis of a direct relationship between virus infection and diabetes. But the mumps infection alone is not the key factor. Mumps vaccination may not provide protection against diabetes mellitus, it may even provoke it. (Genetic determination, expressed by the HLA-phenotype in all the patients reported, does not allow a differentiation.)
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PMID:Mumps, mumps vaccination, islet cell antibodies and the first manifestation of diabetes mellitus type I. 638 57

To investigate whether the development of islet-cell antibodies (ICA) in the course of mumps infection is associated with a "diabetes-like" immunogenetic condition, 45 children with mumps complications as well as 56 children with insulin-dependent diabetes mellitus (IDDM) were typed for HLA ABC and DR antigens. ICA were detected in 14 out of 35 mumps patients. In the IDDM group, significant deviations from antigen frequencies of normal controls were observed for HLA Bw39, DR2, DR3, and DR4. In contrast, in ICA positive mumps patients, the frequency of these antigens was normal, but Aw24 was significantly increased. Thus, no immunogenetic similarities of both groups of patients could be detected.
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PMID:Complications of mumps infection, islet-cell antibodies, and HLA. 639 72

There is good evidence that viruses may play a role in some animal models of diabetes. Since mumps virus seems to be the most likely candidate, we studied the possible relationship of islet cell antibodies, islet cell surface antibodies and glucose tolerance in 86 children and adolescents in whom mumps infection had occurred 14 months previously. Impaired glucose tolerance was diagnosed in 3.5% (n = 3) but symptomatic diabetes did not appear. No relationship existed between complications of antecedent mumps infection (pancreatitis, orchitis, meningitis) and glucose tolerance. The prevalence of ICA and ICSA was 78% and 36%, respectively. The simultaneous prevalence of ICA and ICSA was 33%. The pathogenetic role of mumps infection and ICA/ ICSA and their possible relation to slow progressive beta cell destruction remains to be elucidated.
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PMID:Prevalence of islet cell antibodies (ICA) and islet cell surface antibodies (ICSA) in children and adolescents with antecedent mumps infection). 653 20

A series of findings of animal experiments as well as epidemiological and clinical observation speak for the fact that viral infections may play a part as trigger mechanism within the etiopathogenesis of type I diabetes mellitus. Directly or via immune and/or autoimmune processes viruses might start a beta-cell-destructing process. A mumps infection is most frequently brought in connection with a diabetes manifestation. The attempt of a critical valuation of the arguments for a viral etiology of the type I diabetes mellitus is made. Including first preliminary results of the own working team, the authors get the opinion that at present it is not without doubt to prove a causal connection between mumps infection and the development of a type I diabetes mellitus. Prospective investigations including humoral and cellular immune phenomena in relation to the beta-cell-destructing process are to be demanded.
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PMID:[Mumps - risk for the manifestation of insulin-dependent (type I) diabetes mellitus?]. 664 31

Laboratory study fo 109 insulin-dependent diabetics younger than 17 yr of age and resident in greater Montreal at the time on onset of symptoms is reported. The cases were diagnosed during a 2-yr period (1976-1978). Sibling controls were obtained for 72 of the cases studied. Viral titers to coxsackie B, rubella, and mumps virus for the 72 patient-sibling pairs showed no difference in geometric mean titers or in change of titer between samples taken at the time of diagnosis and those taken 28 days later. The incidence of positive islet cell antibody in teh IDdM cases was 68.0% at the time of diagnosis compared with 56.(% 4 wk later. The comparative figures of sibling controls were 4.2% and 1.4%, respectively. The frequency of HLA B8, B15, B18, and B7 antigens were compared both with the sibling controls and a normal control population. Pairing of high risk HLA antigens were found more frequently in cases than controls. There was no difference in geometric mean viral titers in cases with risk risk haplotypes compared with those cases in which such haplotypes were absent.
Diabetes 1981 Jul
PMID:Prospective study of insulin-dependent diabetes mellitus. 701 64

A total of 1142 Massachusetts resident, insulin-dependent diabetics were identified from medical records of the Joslin Clinic. All patients were less than 21 years of age at onset and developed diabetes between 1 January, 1964 and 31 December, 1973. This group consisted of 598 males (52.4%) and 544 females (47.6%) with mean ages at onset (+/- SD) of 11.1 +/- 4.9 and 10.9 +/- 4.6 years respectively. The period between onset and diagnosis was less than two months in 634 cases (81.8%). A first degree family history was noted in 209 cases (18.3%), while an additional 689 cases (60.3%) had more distant relatives with diabetes. The seasonal distribution of onsets was examined in the total group, and in subgroups categorized by sex, type of onset, age of onset, and family history. Significant peaks were noted during the first six months (January-June) in the total group and in all subgroups except those less than five or greater than 14 years of age at onset. Maximum incidence occurred in either January or February. During the second six month period (July-December) strong peaks were noted only in females and in those with no family history. Maximum incidence occurred in late July and in August, respectively. Exceptionally pronounced seasonal variation was demonstrated in a subgroup of 129 diabetics less than 15 years of age with onsets less than two months prior to diagnosis, and with no family history. The distribution of year of onset, in this group, showed considerable variation which did not correlate with year to year fluctuations in the reported incidence of aseptic meningitis, rubeola or mumps.
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PMID:Seasonal incidence of insulin-dependent diabetes (IDDM) in Massachusetts, 1964-1973. 708 76

Recent observations have shown that insulin-dependent diabetes (JOD) may be the result of autoimmunity causing more or less rapid pancreatic isle cell destruction. This autoimmune process may be initiated in individuals who are genetically vulnerable to specific virus action. Several viruses have been implicated as causing JOD. Rubella and mumps viruses were the first viruses to be proved diabetogenic. A few years ago Coxsackie B viruses were added to the list. A prospective study of all new diabetics was undertaken in order to clarify the association of viral illness with JOD. 45 new insulin-dependent diabetics were studied (complement fixation, neutralizing antibodies or hemagglutination inhibition) within 3 days following admission. Screening for viral illnesses included the study for antibodies to the following: psittacosis, mycoplasma, Q fever, mumps, measles, herpes, CMV, rubella and chickenpox. Control bloods matched for sex, age, season and year with patients were obtained from individuals screened for viral illnesses during the same period. 18 JOD patients had antibodies against various Coxsackie B viruses. 4 patients had elevated rubella antibody titers.
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PMID:Are viral studies indicated in juvenile-onset diabetes? 711 Jul 40


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