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

BB rats were found to have autoantibodies to gastric parietal cells, thyroid colloid antigens, smooth muscle, and thymocytes. No autoantibodies reactive with pancreatic islet cells (cytoplasmic), thyroid epithelial cells, adrenal cortex, testes, or anterior pituitary sections were identified. BB rats with gastric parietal autoantibodies had modest degrees of lymphocytic gastritis, but none developed iron or vitamin B12 deficiencies. These results suggest that BB rats have an underlying autoimmune diathesis. In addition, reports of peripheral T lymphopenia in such rats were confirmed, and markedly reduced helper T cell and cytotoxic-suppressor T cell subsets were demonstrated. Histological studies also revealed depletions of the T cell areas of spleen and lymph nodes. Furthermore, BB rats exhibited a profound inability to reject skin grafts across major and minor histocompatibility barriers. This was confirmed by mixed lymphocyte culture studies in vitro. BB-rat lymphocytes from either spleen or peripheral blood also showed profoundly reduced responses to T cell mitogens. Although BB-rat lymphocytes could produce normal levels of interleukin-2, they were unable to respond to this T cell growth factor. However, examination of thymuses from BB rats showed largely normal histologies, normal numbers of thymocyte subsets, and good mitogenic responses to con A. Thus, it appears that BB rats may have a thymic or post thymic defect in T lymphocyte maturation. The relevance of the immunologic lesion to the etiology of IDD in BB rats remains to be shown.
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PMID:Autoimmune diatheses and T lymphocyte immunoincompetences in BB rats. 634 99

One hundred and seventy-seven patients with insulin dependent diabetes mellitus (IDDM) diagnosed at the pediatric age were investigated for the presence of gastric parietal cell autoantibodies (PCA). The objective was to evaluate the prevalence of PCA seropositivity and to know whether Helicobacter pylori could be a reason for a higher presence of PCA in IDDM children and adolescents. Twelve of 177 patients (6.77%; confidence interval: 3.1-10.3) had detectable PCA. Gastric pathology was studied in eight of these patients and in seven patients without PCA. Diagnosis of H. pylori infection was made on antral biopsies. None of the patients had an atrophic gastritis. Six of the eight patients with PCA had gastric mucosa colonization by H. pylori and/or chronic gastritis. According to these results, we suggest that H. pylori can be the cause of the presence of PCA positive results in diabetic children and adolescents, and diabetic patients with detectable PCA should be screened for H. pylori.
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PMID:Helicobacter pylori infection with parietal cell antibodies in children and adolescents with insulin dependent diabetes mellitus. 940 8

Although much is known about the pathology of human chronic atrophic (type A, autoimmune) gastritis, its cause is poorly understood. Mouse experimental autoimmune gastritis (EAG) is a CD4+ T cell-mediated organ-specific autoimmune disease of the stomach that is induced by neonatal thymectomy of BALB/c mice. It has many features similar to human autoimmune gastritis. To obtain a greater understanding of the genetic components predisposing to autoimmune gastritis, a linkage analysis study was performed on (BALB/cCrSlc x C57BL/6)F2 intercross mice using 126 microsatellite markers covering 95% of the autosomal genome. Two regions with linkage to EAG were identified on distal chromosome 4 and were designated Gasa1 and Gasa2. The Gasa1 gene maps within the same chromosomal segment as the type 1 diabetes and systemic lupus erythematosus susceptibility genes Idd11 and Nba1, respectively. Gasa2 is the more telomeric of the two genes and was mapped within the same chromosomal segment as the type 1 diabetes susceptibility gene Idd9. In addition, there was evidence of quantitative trait locus controlling autoantibody titer within the telomeric segment of chromosome 4. The clustering of genes conferring susceptibility to EAG with those conferring susceptibility to type 1 diabetes is consistent with the coinheritance of gastritis and diabetes within human families. This is the first linkage analysis study of autoimmune gastritis in any organism and as such makes an important and novel contribution to our understanding of the etiology of this disease.
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PMID:A major linkage region on distal chromosome 4 confers susceptibility to mouse autoimmune gastritis. 1022 80

Helicobacter pylori (Hp) infection plays a role in gastric emptying (GE) in type 1 diabetic patients and may have implications for glycaemic control. The aim of our study was to investigate this relationship. Gastric emptying was studied in 13 patients with type 1 diabetes and Hp infection. The Hp infection status was assessed by serology and urease breath test (UBT). In addition upper gastrointestinal endoscopy with gastric mucosal biopsy was performed to look for gastritis. A radionuclide-labeled solid meal was used to study GE before and after eradication therapy (amoxicillin, clarithromycin and omeprazole) for Hp infection. All patients were evaluated for autonomic and peripheral neuropathy and were asked for symptoms of gastrointestinal motor dysfunction. Blood glucose levels were determined before the meal and at 30,60,90 and 120 min after the start of the meal. Home blood glucose self-monitoring and HbA(1c) were performed to document glycaemic control during the study. Three months after treatment, five patients were free of Hp infection and were without gastritis (group I: no Hp infection, no gastritis); eight of the patients continued to have gastritis after treatment (group II) and of these eight patients, six had gastritis without Hp infection and two had gastritis plus persistent Hp infection. These last two patients were re-treated with eradication therapy. Patients with gastritis were re-evaluated 6 months after initial treatment; at which time four were now free of gastritis and were added to group I (n=9) while four continual to have gastritis although without Hp infection (group II, n=4). In group I, GE half-time showed an increase (30.6+/-10.3 min vs. 60.2+/-15.4 min; P<0.05) while no change (28.8+/-9.5 vs. 26.9+/-8.7 min; n.s.) was observed in group II. GE half-time was not altered by autonomic and peripheral neuropathy or blood glucose during solid meal test. HbA(1c) did not change significantly after treatment in either groups but the blood glucose levels were more stable in group I compared to group II. A delay in GE was observed with disappearance of gastritis associated to H. pylori infection after eradication treatment in patients with type 1 diabetes. This change in GE could help to stabilise the blood glucose levels in these patients treated with insulin before each meal.
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PMID:Effect of the treatment of Helicobacter pylori infection on gastric emptying and its influence on the glycaemic control in type 1 diabetes mellitus. 1118 11

Helicobacter pylori infection has been described in association with increases in glycated hemoglobin (HbA(1c)) levels in patients with type 1 diabetes. The purpose of the present study was to use an animal model of Helicobacter infection to test, under controlled conditions, the hypothesis that infection is associated with high HbA(1c) levels. Diabetes was induced in C57BL/6 mice by administration of streptozotocin, and the mice were orally inoculated with H. felis. Six weeks after inoculation, infected mice (n=10) showed gastritis scores significantly greater (P=.01) than those of uninfected mice (n=10). HbA(1c) levels were significantly higher in infected mice with gastritis (11.6%; n=6) than in infected mice without gastritis (8.4%; n=4) or uninfected mice (7.6%; n=10). It was concluded that gastritis induced by H. felis is associated with increased HbA(1c) levels in the mouse model of streptozotocin-induced diabetes.
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PMID:Association between Helicobacter felis-induced gastritis and elevated glycated hemoglobin levels in a mouse model of type 1 diabetes. 1199 82

A familial component to the tendency to develop autoimmune gastritis has long been recognized. Although linkage to certain HLA alleles and an association with the endocrine autoimmune diseases thyroiditis and type 1 diabetes have been reported, little further progress has been achieved in clinical studies. In contrast, the mouse model of gastritis induced in the BALB/c strain by thymectomy in the third day of life has identified four linkage regions; two on distal chromosome 4 (Gasa1 and Gasa2), one on chromosome 6 (Gasa3) and one in the H2 (Gasa4). Three of these four genes colocalize with NOD mouse diabetes susceptibility genes--the strongest concordance identified to date between any two autoimmune diseases--reflecting the association between autoimmune diabetes and type 1 gastritis in humans.
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PMID:Genetic control of susceptibility to autoimmune gastritis. 1576 89

Type 1 diabetes mellitus (DM1), autoimmune thyroid disease (ATD) and autoimmune gastritis often occur together forming the so-called autoimmune polyendocrine syndrome (APS) type 3. Thyroid autoimmunity is evident in up to one third and gastric autoimmunity in up to a quarter of patients with DM1. Also relatives of DM1 patients, particularly mothers, have higher frequencies of these autoimmune conditions. Vice versa, gastric autoimmunity is present in one third of ATD patients and islet autoimmunity in one out ten. The BB-DP rat, the NOD mouse, the OS chicken and the neonatal thymectomy mouse model are animal models of APS type 3. In these models the autoimmune destruction of the various target tissues has been shown to be a multi-step process in which several genetic polymorphisms need to converge to induce both local anomalies in the target gland and anomalies in the immune system. With regard to environmental factors, excess iodine is well known to elicit/aggravate thyroid autoimmunity in these animal models. Screening DM1 patients and their relatives (particularly females) for thyroid autoimmunity is recommended. If positive, excess iodine should be avoided and thyroxin treatment considered. Whether autoimmune thyroiditis and autoimmune gastritis patients should be screened for islet Ab is not clarified.
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PMID:The association between autoimmune thyroiditis, autoimmune gastritis and type 1 diabetes. 1643 10

Autoimmune diseases such as type 1 diabetes and multiple sclerosis pose a significant health burden on our society. As a whole, autoimmune diseases affect approximately 6% of the population and are the third largest disease burden after heart disease and cancer. Such pathologic manifestations arise by way of damaging reactions of B-cell derived antibodies and/or T-cells to self-antigens and are triggered by genetic and environmental factors. Currently there is no known cure, with treatment restricted to toxic, long-term immunosuppressive regimes, replacement therapy and in intractable cases, transplantation of autologous or allogeneic haematopoietic stem cells. In experimental models of autoimmunity, gene therapeutic approaches have demonstrated promise in treating the autoimmune diseases. These include delivery of anti-inflammatory cytokines and exploitation of regulatory T cells. However, none of these approaches provide lasting, long-term benefit. We hypothesise that therapeutically transduced haematopoietic stem cells followed by transplantation is an alternative strategy to establish permanent immune tolerance that can not only prevent autoimmunity but also cure these diseases. Our approach is focused on directing autoimmune disease-specific autoantigen expression in the thymus by genetic manipulation of haematopoietic stem cells to establish molecular chimeras. Our hypothesis originates from experimental studies with a mouse model of experimental autoimmune gastritis (EAG) and more recently with the non-obese diabetic (NOD) mouse model for type 1 diabetes (T1D).
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PMID:Gene therapy strategies towards immune tolerance to treat the autoimmune diseases. 1647 45

Vitiligo is a common skin disease characterized by depigmented maculae resulting from a reduction of the number and function of melanocytes. Many studies suggest that vitiligo might be an autoimmune disease. Vitiligo has been frequently described in association with other autoimmune diseases. Among the diseases described in association with vitiligo are the so-called autoimmune polyglandular syndromes (APS). Vitiligo can be present in all types of APS but the most frequent association appears to be in APS-3. APS-3 was defined as the association between autoimmune thyroiditis and another autoimmune disease. Here we report one patient with thyroiditis, vitiligo and autoimmune gastritis (APS-3B+C), one patient with chronic autoimmune thyroiditis, vitiligo and alopecia (APS-3C), and one case of a young patient with type 1 diabetes mellitus and vitiligo (APS-4), according to the newest classification. We stress the importance of a thorough assessment for autoimmune diseases in selected patients with vitiligo.
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PMID:Vitiligo associated with other autoimmune diseases: polyglandular autoimmune syndrome types 3B+C and 4. 1680 62

Helicobacter pylori [H. pylori], one of the most common chronic infections worldwide, is the main etiologic agent of gastritis, peptic ulcer and gastric cancer. Patients with diabetes mellitus are often affected by chronic infections. Many studies have evaluated the prevalence of H. pylori infection in diabetic patients and the possible role of this condition in their metabolic control. Some studies found a higher prevalence of the infection in diabetic patients and a reduced glycaemic control, while others did not support any correlation between metabolic control and H. pylori infection. There are only a few studies on the eradication rate of H. pylori in diabetic patients. Most of these papers concluded that standard antibiotic therapy allows a significantly lower H. pylori eradication rate than is observed in control groups matched for sex and age. Changes in the microvasculature of the stomach with a possible reduction of antibiotic absorption, the presence of gastroparesis and the frequent use of antibiotics for recurrent bacterial infections with the development of resistant strains could be some of the mechanisms underlying this phenomenon. A quadruple therapy may be used as the second line approach with a good eradication rate, even if an antibiotic selected according to a specific H. pylori antibiogram is considered the gold standard in these patients. As regards the gastrointestinal symptoms of H. pylori infected individuals, many studies showed that they are as frequent in patients with type 1 diabetes as in the general population. The incidence of H. pylori recurrence after 12 months follow-up is significantly higher in type 1 diabetic subjects when compared to controls. Reduced lymphocyte activity, neutrophil dysfunction with failure of chemotaxis and a possible reservoir of H. pylori in dental plaque may explain the higher rate of re-infection in these patients.
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PMID:The role of H. pylori infection in diabetes. 1822 Jun 10


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