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

We studied sera of 24 selected non-diabetic subjects in whom an antecedent mumps infection with either complications and/or with onset at older age occurred 10-27 month ago regarding the capability to lyse rat islets of Langerhans in vitro. Thirteen subjects were characterized by diabetes associated HLA antigens DR3 and/or DR4 whereas 11 of them had none of these HLA antigens. Islet cell surface antibodies (ICSA) could be detected in 11 out of 24 subjects. Isolated pancreatic islets from 8-10 days old Wistar rats were incubated in freshly prepared human serum. The insulin leakage under the conditions of pharmacologic blockade of insulin secretion by means of epinephrine and propranolol provides a measure of complement-mediated cytotoxicity of human serum against rats islets in vitro. Out of a total of 24 subjects the sera of 11 of them exhibited cytotoxicity. Mean cytolytic insulin leakage was significantly higher in subjects with DR3 and/or DR4 in comparison with subjects without these HLA antigens (6.82 +/- 0.77% vs 3.90 +/- 0.48%; p less than 0.05). Ten out of the 11 subjects with cytotoxic sera had HLA DR3 and/or DR4 whereas DR3 was present in three out of 13 subjects with non-cytotoxic sera. There was no relationship between beta cell function in vivo (fasting C-peptide concentration and insulin response to oral glucose challenge) and the capability of patients sera to damage islet cells in vitro. In conclusion the pathogenetic role of mumps virus and cytotoxic ICSA and their possible relation to slow progressive beta-cell destruction has still to be ascertained.
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PMID:Complement-mediated cytotoxic effects of islet cell surface antibodies in non-diabetic subjects with antecedent mumps infection and diabetic risk. 304 6

Mumps epidemics are followed by sporadic cases of insulin dependent diabetes mellitus (IDDM). We have studied beta-cell function in 11 subjects who had had a mumps infection. They had no clinical pancreatitis but were selected as they had abnormal pancreas iso-amylase values and/or glucosuria during the mumps virus infection. At the follow-up some years later the subjects were healthy. A few HbA1-values were noted in the upper part of the normal range. Total serum insulin values were normal, but the C-peptide values were low at first follow-up 1-3 years after infection in all but two patients. These values increased in 4/7 patients during the follow-up period but were subnormal in five subjects still 3-6 years after the infection. All five patients had HLA-DR 3 and/or 4. In 7 out of 11 patients islet cell surface antibodies could be demonstrated. Our results indicate that subclinical mumps pancreatitis may initiate a reaction towards the beta-cells recognized as subnormal C-peptide levels several years later in certain patients. This might contribute to manifest IDDM many years after infection.
Diabetes Res 1988 Dec
PMID:Mumps with laboratory signs of subclinical pancreatitis may cause a disturbed beta-cell function. 307 6

The epidemiology of Type 1 (insulin-dependent) diabetes was studied during a period starting after an unusually sharp epidemic of mumps. The number of diabetic cases increased significantly 2-4 years after the epidemic. Incidence rates were highest in geographical areas with the highest incidence of mumps and lowest in areas with the smallest numbers of reported mumps cases. Serological studies employing EIA-assays indicated recent mumps infections more often among newly diagnosed diabetic children than among matched controls although the incidence was low (13% of patients and 4% of controls had serological markers of recent mumps). Those patients, who had had serologically verified recent mumps had more often HLA-DR4 associated risk antigens (Dw4 and Dw14) than other patients. Also clinical history of mumps was obtained more often from diabetic children than from controls as 27% of the patients and 14% of the controls had had clinical mumps during the five years preceding the diagnosis of diabetes. These results confirm several earlier reports suggesting a connection between mumps and Type 1 diabetes and that the onset of diabetes may be delayed by several years.
Diabetes Res 1988 Nov
PMID:Mumps infections in the etiology of type 1 (insulin-dependent) diabetes. 324 43

In order to elucidate the possible relationship between insulin autoantibodies (IAA), conventional (ICA-IgG) and complement-fixing (CF-ICA) islet cell antibodies and Coxsackie-B4 and mumps virus-specific antibodies (IgG, IgM and IgA classes), we studied 194 children and adolescents with newly diagnosed Type 1 (insulin-dependent) diabetes. Sixty-one (31.4%) of the subjects were IAA-positive at diagnosis and 73.8% (45/61) of these also had ICA-IgG compared to 51.1% (68/113, p less than 0.01) of IAA-negative children. CF-ICA showed no significant association with IAA. The levels of IAA were significantly higher in the patients with ICA-IgG compared to those without [5.9 +/- 1.6% (SEM) vs 2.5 +/- 0.3%, p less than 0.01]. The patients positive for IAA were younger at diagnosis than the IAA-negative ones; (7.1 +/- 0.5 vs 9.3 +/- 0.3 years, p less than 0.001) and this was also true for ICA-IgG-positive children (8.1 +/- 0.4 vs 9.4 +/- 0.5 years, p less than 0.05) in comparison to ICA-IgG-negative subjects. No significant associations were found between IAA or ICA on the one hand and a positive family history of Type 1 diabetes or metabolic derangements at diagnosis on the other. Subjects negative for ICA were more frequently positive for mumps virus specific IgG antibodies than the ICA-positive patients (50/80 vs 53/111, p less than 0.05), and Coxsackie-B4 virus-specific IgA antibodies were more common in the CF-ICA-negative than the CF-ICA-positive children (53/111 vs 29/80, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship between serum insulin autoantibodies, islet cell antibodies and Coxsackie-B4 and mumps virus-specific antibodies at the clinical manifestation of type 1 (insulin-dependent) diabetes. 328 41

The sera of 127 non-diabetic children after mumps-infection were investigated for the presence of islet cell antibodies and islet cell surface antibodies. The study also included 4 children who developed diabetes mellitus shortly after an active mumps vaccination. 21 of the non-diabetic children and four of the vaccinated children exhibited islet cell cytoplasmic antibodies. Islet cell surface antibodies were observed more frequently, namely in 43 out of 68 patients studied after mumps infection and in 32 out of 44 patients studied after different viral diseases. With one exception, none of the mumps-infected children and none of the other viral infected patients developed diabetes mellitus.
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PMID:Islet cell antibodies and viral infections. 331 79

It has been suggested that the mumps virus may be involved in the etiopathogenesis of Type-I diabetes mellitus. Most studies have analyzed this relationship retrospectively. We, however, carried out a prospective study over a 4 year period after a mumps infection in two age groups (16 years and under [group A no = 32] and over 16 years [group B no = 18]). These subjects with "diabetic risk factors" (impaired glucose tolerance, low insulin response, ICSA and/or HLA-DR3/DR4) were selected from 1581 registered cases, in whom an antecedent mumps infection had occurred in 1980 and 1981. Glucose tolerance and insulin secretion did not change significantly during 4 years after a mumps infection. Overt diabetes was not observed in any of the cases. One year after a mumps infection 35% of children and 63% of adolescents/adults exhibited ICSA (control subjects = 5%; a serum was considered ICSA-positive if more than 25% of the intact rat islet cells showed distinct cell surface immunofluorescence). After 4 years the percentage of subjects with ICSA decreased significantly to 13% and 14%, resp. Only 21% of ICSA-positive sera were found to be cytotoxic on rat islet cells (51Cr-release assay). No relationship could be evaluated between complications resulting from a mumps infection and the appearance of ICSA. There was no correlation between ICSA, glucose tolerance, and insulin secretion. In fact, our prospective study did not reveal any relationship between a mumps infection and Type-I diabetes. ICSA would seem to be of no predictive value.
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PMID:Islet cell surface antibodies (ICSA) in subjects with a previous mumps infection--a prospective study over a 4 year period. 331 81

Cytoplasmic islet-cell antibodies, insulin antibodies, islet-cell surface antibodies and islet-cell specific cytotoxicity were determined in serum of the following groups: 131 patients with type I diabetes, 19 with type II diabetes, 29 with mumps, 29 with enterovirus infections, 18 with measles and 28 healthy controls. Cytoplasmic islet-cell antibodies were found predominantly in type I diabetics. Islet-cell surface antibodies, on the other hand, were relatively frequently (60-80%) present in sera of both diabetics and patients with various virus infections. Islet-cell specific cytotoxicity in vitro was found not only in sera of diabetics, but also of patients with mumps or enterovirus infections. Sera of five patients with measles, however, had cytotoxic reactions comparable to those of the controls. These results suggest that cytotoxic antibody reactions against islet cells in vitro occur also in sera of non-diabetic patients. Under certain circumstances, infections which induce such immune reactions may be of significance in the pathogenesis of diabetes.
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PMID:[Autoimmunity and viral infections in type-I diabetes mellitus]. 351 25

Islet cell antibodies were investigated in 127 non-diabetic children after mumps infection and in four out of seven children who developed diabetes mellitus shortly after active mumps vaccination. Twenty-one of the children who had mumps and all four vaccinated children who were tested had islet cell cytoplasmic antibodies. In contrast, islet cell surface antibodies were detected in 43 out of 68 patients with mumps infection and in 32 out of 44 patients with other viral diseases. All but one mumps-infected child and all the other viral infected patients investigated did not develop diabetes mellitus. The mumps-infected ICA positive children did not show those HLA-frequencies associated with Type 1 diabetes.
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PMID:Islet cell antibodies and the development of diabetes mellitus in relation to mumps infection and mumps vaccination. 351 41

Numerous experimental findings in animals as well as epidemiological and clinical observations support the hypothesis that certain viruses play a role in the pathogenesis of insulin-dependent diabetes mellitus (IDDM). Directly or via immune and/or autoimmune processes viruses might induce a beta-cell damage. An attempt is made to evaluate critically the arguments for the role of the mumps virus in the pathogenesis of IDDM. Based on their own experience, the authors hold the opinion that at present a causal connection between mumps infection and the development of IDDM cannot be proved beyond doubt. Prospective studies in humans including appropriate techniques of humoral and cellular immunity in relation to the beta-cell damage are required.
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PMID:Does mumps infection play a role in the etiology and pathogenesis of insulin-dependent diabetes mellitus? 354 75

The 1-yr incidence of insulin-dependent diabetes mellitus (IDDM) in a population of the Piedmont and Aosta Valley area of Italy was recorded. Anti-virus antibodies (e.g., Coxsackie B1-6, mumps, cytomegalovirus), islet cell antibodies (ICAs), and HLA-A, -B, -C, and -DR were determined in 74 IDDM patients (38 males, 36 females) and in controls. Total IDDM incidence was 5.0/100,000, and the incidence for those less than 20 yr of age was 11.6/100,000. Anti-virus antibody frequency was not different in IDDM patients and controls. ICAs were present in 58% of IDDM patients at onset and in 30% after 12 mo, and complement-fixing ICAs were found in 39 and 17%, respectively. IDDM was significantly and positively associated with DR3/DR4 and negatively associated with DR2 and DR5. ICA frequency was significantly higher in DR3/DR4 heterozygote patients than in patients without DR3 and DR4. These results suggest that in this IDDM population viral etiology is not evident, ICAs offer only a partial pathogenetic explanation, and genetic and immunologic heterogeneity is evident.
Diabetes 1987 Jul
PMID:Genetic, immunologic, and environmental heterogeneity of IDDM. Incidence and 12-mo follow-up of an Italian population. 355 83


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