Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of epidemic influenza on hospitalizations because of influenza, pneumonia and diabetic acidosis in patients with diabetes mellitus was investigated. Data on the weekly incidence of influenza-like illness were obtained from the Continuous Morbidity Registration and the cumulative data on hospitalizations in short-stay hospitals were obtained from the National Medical Registration. Patients with duodenal ulcer were used as a control population. Epidemic elevations of influenza infections were observed in 1976 and 1978. The estimated relative risk for hospitalization because of influenza infection was 1.1 and 1.0 for the two non-epidemic years 1977 and 1979, respectively. For the epidemic years 1976 and 1978 this risk was calculated to be 5.7 and 6.2, respectively. An increased relative risk was also noted for pneumonia; being 25.6 for both epidemic years. The estimated relative risk of dying during hospitalization rose from 30.9 in 1977 to 91.8 in 1978. The number of hospitalizations for ketoacidosis was 50% higher in 1978 than in the other three years. During the epidemic years, 25.7% of patients hospitalized for pneumonia died, while this percentage was 14.6% in the non-epidemic years (P less than 0.05). Differences in mortality due to diabetic acidosis were similar: 25.4% in epidemic and 14.7% in non-epidemic years (P less than 0.01). During the 1978 epidemic, one out of every 1300 patients with diabetes mellitus was hospitalized because of pneumonia. It is estimated that 1 of every 260 patients with IDDM was hospitalized for diabetic acidosis. It is concluded that patients with diabetes mellitus have indeed a very high influenza-associated morbidity.
 ...
PMID:Effect of epidemic influenza on ketoacidosis, pneumonia and death in diabetes mellitus: a hospital register survey of 1976-1979 in The Netherlands. 190 98

The production of insulin autoantibodies (IAA) was studied after common viral infections in 12 children with type 1 diabetes mellitus and in their 18 healthy siblings. In addition, the production of IAA was measured after influenza vaccination with booster in 39 patients with type 1 diabetes mellitus and in 39 healthy controls. In 7 of the 12 diabetic children 13 viral infections were serologically confirmed. Among the siblings 14 periods of infection were noted in 9 individuals. A significant rise in IAA antibody titre was demonstrated in patients twice (IgG both times) and in siblings 11 times (IgM 5x, IgG 6x, difference significant P less than 0.05). In only three cases the rise in antibody titres occurred 6-12 wk after documented infection. There was a significant inverse correlation with age in both patients (r = 0.89, P less than 0.0001) and siblings (r = 0.67, P less than 0.001) for IgM IAA. After influenza vaccination a significant increase in IAA was noted twice: IgM IAA in a patient with diabetes and IgG IAA in a healthy volunteer. A four-fold decrease in IgG IAA was demonstrated in one diabetic patient. From these results it is concluded that IAA formation is not a direct sequela of viral infection or vaccination.
 ...
PMID:No evidence for the enhanced production of insulin autoantibodies after confrontation with common viral antigens in insulin dependent diabetes mellitus. 207 15

Insulin-dependent diabetes mellitus results from the autoimmune destruction of the insulin-producing beta cells of the pancreatic islets. The target antigen(s) involved in this immunopathological process has not been identified. Our strategy was to determine whether expression of a novel surface antigen by murine pancreatic beta cells would result in insulin-dependent diabetes mellitus. We have generated lines of transgenic mice (RIP-HA) that express the hemagglutinin of the A/Japan/305/57 strain of influenza virus on their insulin-producing beta cells. Hyperglycemia developed in mice derived from all three founders at a frequency varying from 13% to 27%, and was associated with lymphocytic infiltration of the islets and a humoral response against beta cell antigens, including hemagglutinin. These results suggest that the RIP-HA mice should provide a useful system in which to study the cellular interactions involved in the induction of self-tolerance and autoimmunity.
 ...
PMID:The expression of influenza virus hemagglutinin in the pancreatic beta cells of transgenic mice results in autoimmune diabetes. 218 89

The cytotoxic T-cell and humoral immune response to a commercially available influenza A-H1N1 subunit vaccine in 14 patients with type 1 diabetes mellitus was compared with the response in 13 healthy volunteers. Cytotoxic T-cell response to vaccination was poor in both patients and controls. At a calculated 50: 1 effector-target cell ratio, however, significantly more controls than patients showed an increase of over 5% cytotoxic T-cell mediated lysis after vaccination (P less than 0.05). In patients the cytotoxic T-cell response decreased with higher percentages of glycosylated haemoglobin (regression coefficient not equal to 0 with P less than 0.05). No significant difference was found between diabetic patients and control subjects with respect to antibody response after vaccination. Implications for vaccination strategy are discussed.
 ...
PMID:Cytotoxic T-cell response to influenza A subunit vaccine in patients with type 1 diabetes mellitus. 278 42

To assess the immunologic differences related to histocompatibility leukocyte antigen (HLA) haplotypes in patients with type 1 diabetes, trivalent killed influenza virus vaccine was given in the fall, when no influenza occurred, to 59 patients with diabetes (mean age 16 years) and 64 siblings without diabetes (mean age 36 years). All subjects had normal hemagglutination inhibition antibody responses at days 14 and 42 after vaccination, with no significant differences noted between patients with diabetes and those without diabetes. However, subjects with HLA haplotypes DR 3, DR 4, or both had lower antibody responses to influenza A/Chile and B/USSR at 14 days after vaccination (p less than 0.02) than DR x/x controls (who lacked 3 or 4). Lymphocyte transformation (LT) responses before and after vaccination were similar for patients with diabetes and those without diabetes. Of significance was that subjects with HLA haplotypes DR 3, DR 4, or both had 41.1% LT responders at 42 days after vaccination, compared with subjects with HLA-DR x/x (lacking 3 or 4) who had 22.6% responders (p less than 0.03), when influenza A/Chile was used as an antigen. Although not significant, influenza antigens A/Philippines and B/USSR each showed similar trends with increased postvaccine LT responses. The HLA associations were independent of sex, age, and the presence of diabetes. These studies suggest that HLA haplotypes DR 3 and DR 4, which were clearly linked to type 1 diabetes mellitus, were also associated with altered immune responsiveness to influenza viral proteins.
 ...
PMID:Immune responses to killed influenza vaccine in patients with type 1 diabetes: altered responses associated with HLA-DR 3 and DR 4. 326 55

An 11-year-old boy developed influenza with glucosuria. An oral glucose test performed during the infection revealed values within the diabetic range. Type 1 diabetes was wrongly diagnosed and insulin therapy initiated. A 19-year-old overweight adolescent developed pneumonia with hyperglycemia but without polydipsia or polyuria. Further investigation revealed incipient type 1 diabetes. As insulin therapy was not initiated the diabetes rapidly decompensated. It is recommended that further investigations be conducted in patients with hyperglycemia following infections.
 ...
PMID:[Diabetes or hyperglycemia?]. 335 3

Genetic, immunological and viral factors have been implicated in pathogenesis of Type 1 diabetes mellitus. The development of Type 1 diabetes in two siblings of patients with Type 1 diabetes studied as part of a large epidemiological study, is described. One case, a 13-year-old male not sharing either HLA haplotype with his diabetic sister, had virtually normal glucose tolerance 80 days before symptomatic presentation. He showed serological evidence of infection by Coxsackie CB4 (at diagnosis) and influenza A virus (soon after diagnosis). The other case, a 15-year-old male, had impaired glucose tolerance for over 500 days (i.e., since the diagnosis of diabetes in his HLA-identical brother) before symptomatic presentation which was not associated with serological evidence of acute viral infection. The former case was negative for islet cell antibody (cytoplasmic) when first seen though positive at diagnosis, while the latter was positive throughout. These two cases suggest contrasting interactions of the main pathogenetic factors associated with Type 1 diabetes.
 ...
PMID:The development of Type 1 (insulin-dependent) diabetes mellitus: two contrasting presentations. 631 59

Insulin-dependent diabetes mellitus (IDDM) results from selective autoimmune destruction of insulin producing beta-cells. T-cell reactivity and autoantibodies to several islet proteins such as insulin, GAD and IA-2 are associated with IDDM in mice and men. In NOD mice, the majority of T cells from insulitis specifically recognize the insulin B-chain peptide amino acid 9-22, in contrast to the periphery where the precursor frequency is much lower. It is important to note that these cells are diabetogenic. Surprisingly, the same insulin B-chain region contains epitopes recognized by protective T cells. In fact, autoimmune diabetes in NOD mice could be prevented by prophylactic treatment with this immunodominant T-cell epitope. In humans, however, no immunodominant regions of insulin have yet been defined. We have isolated and characterized a human insulin-specific T-cell clone that was derived from peripheral blood of a newly diagnosed IDDM patient. This patient displayed weakly positive primary T-cell responses to insulin. The peptide recognized by the clone was mapped to the insulin B chain (B:11-27). Functionally, the human insulin-specific CD4+ T cells displayed a Th1/0 like cytokine profile and were restricted by HLA-DR. The previously proposed alternative superantigen-like binding of insulin-B chain peptide outside of the peptide binding groove of HLA-DR could not be confirmed, since T-cell recognition was inhibited in competition experiments of insulin-B chain peptide with HLA-DR16 binding influenza peptide HA307-319. Our results indicate that human clonal T cells isolated from a recent onset IDDM patient recognize an epitope overlapping with the insulin B-chain region that is immunodominant and potentially therapeutic in NOD mice. This observation may be useful in studying the role of insulin-specific T cells in IDDM, and may eventually help to establish peptide-based immunotherapies in IDDM.
 ...
PMID:Cloned T cells from a recent onset IDDM patient reactive with insulin B-chain. 965 96

The objective of this article is to stratify interventions for diabetes according to their economic impact. We conducted a review of the literature to select articles that performed a cost-benefit analysis for 17 widely practiced interventions for diabetes. A scale for categorizing interventions according to their economic impact was defined. The 17 interventions were classified as follows: 1) clearly cost-saving, 2) clearly cost-effective, 3) possibly cost-effective, 4) non-cost-effective, or 5) unclear. Clearly cost-saving interventions included eye care and pre-conception care. Clearly cost-effective interventions included nephropathy prevention in type 1 diabetes and improved glycemic control. Possibly cost-effective interventions included nephropathy prevention in type 2 diabetes and self-management training. Non-cost-effective interventions were not identified. Interventions with unclear economic impact included case management, medical nutrition therapy, self-monitoring of blood glucose, foot care, blood pressure control, blood lipid control, smoking cessation, exercise, weight loss, HbA1c measurement, influenza vaccination, and pneumococcus vaccination. Widely practiced interventions for patients with diabetes can be clearly cost-saving and clearly cost-effective. These practices are attractive from both a medical and an economic perspective.
 ...
PMID:An economic analysis of interventions for diabetes. 1086 71

Many tissue-specific autoimmune diseases are mediated by the induction of autoantigen-specific T cells. These cells are believed to cause tissue damage through the production of cytokines, through direct lysis of cells expressing self-antigens, or through the induction of inflammatory responses. The escape from self-tolerance or anergy is a prerequisite for initiation of an autoimmune process. INS-HA (insulin-hemagglutinin) transgenic mice express the HA of A PR8 34 influenza virus in the pancreatic beta-cells under the rat insulin promotor. TCR-HA (T cell receptor-hemagglutinin) transgenic mice express the TCR specific for the immunodominant epitope HA110-120 from the same virus. Double transgenic (dTg) mice expressing both genes represent an excellent model for understanding the mechanism leading to autoimmune diabetes independently of susceptibility genes. In order to gain information on the breaking down of neonatal self-tolerance we studied the occurrence of insulin dependent diabetes mellitus (IDDM) after birth. Our results showed that newborn mice develop fulminant IDDM characterized by occurrence of insulitis as early as 3 days after birth, followed by hyperglycemia by 7 days, and significant hypoinsulinemia by 28 days. Such "double transgenic" mice expressing wild-type or targeted IL-4R alpha genes were examined for the onset of IDDM. Eight of eleven mice homozygous for the wild-type IL-4R alpha were hyperglycemic by 8 weeks of age, whereas only 1 of 16 mice homozygous for the targeted allele were hyperglycemic at this time. Most IL-4R alpha -/- mice remained normoglycemic to 36 weeks of age. Although only 10% of double transgenic mice homozygous for wild-type IL-4R alpha allele survived to 30 weeks, 80% of mice homozygous for the targeted allele did so. Even as late as 270 days of age, mice homozygous for the targeted allele had no insulitis or only peri-insulitis. Heterozygous mice displayed an intermediate frequency of diabetes. The IL-4R alpha chain acts as the high affinity binding chain and the principal signaling chain for IL-4; it also acts as the signaling chain for IL-13, but in this case the IL-13R alpha 1 chain conveys the bulk of the cytokine specificity. Thus, IL-4R alpha knock-out mice are unresponsive to both IL-4 and IL-13. The finding that the lack of IL-4R alpha chain protects TCR-HA, INS-HA double transgenic mice against diabetes, and death implies that either IL-4 or IL-13 plays a role in the progression of this disease. These studies demonstrate that TCR-HA, INS-HA double transgenic mice may provide a useful model to evaluate new strategies for the prevention of diabetes.
 ...
PMID:Cellular mechanisms involved in experimental insulin-dependent diabetes mellitus. 1216 74


1 2 3 4 5 6 7 Next >>