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

Chronic infection may increase the risk for ischemic stroke. Presently, it is insufficiently established whether Helicobacter pylori infection represents a risk factor for ischemic stroke. We analyzed IgG antibodies against H. pylori in 109 patients with acute cerebral ischemia and 82 age- and sex-matched control patients with non-vascular and non-inflammatory neurological diseases. Antibody titers were significantly higher in patients than in control subjects (p=0.007). H. pylori seropositivity tended to be more common in patients (odds ratio (OR) 1.55, 95% confidence interval (ci) 0.87-2.76), but this trend was further attenuated in multivariate analysis (OR 1.42; 95% 0.75-2.67) with hypertension, diabetes mellitus, current or previous smoking, previous cerebral ischemia and low socioeconomic status. H. pylori seropositivity increased the odds for cerebral ischemia of atherothrombotic origin in univariate (OR 3.63; 95% ci 1.37-9.65) and multivariate analysis (OR 3.53; 95% ci 1.09-11.4). H. pylori seropositivity may be an independent risk factor for stroke of atherothrombotic origin.
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PMID:Helicobacter pylori infection as an independent risk factor for cerebral ischemia of atherothrombotic origin. 1141 64

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

The persistent inflammation of the stomach induced by Helicobacter pylori infection can have consequences on the rest of the body. In the last few years, many studies have been performed on the implication of H. pylori in the pathogenesis of extra-gastric diseases attempting to establish if this association is real. Many diseases may be associated with H. pylori, e.g. vascular diseases, autoimmune diseases, skin diseases, sideropenic anemia, diabetes, Parkinson disease, and bronchiectasis. The number of important studies revealing such associations suggests that pathogenic mechanisms may link this infection with many diseases of unknown etiology. Unfortunately, the quality of the studies performed is not homogeneous, and more rigorous investigations are required to show whether a causal link exists between H. pylori infection and the pathogenic processes of these extra-digestive diseases.
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PMID:[Helicobacter pylori infection as a cause of extra-digestive diseases: myth or reality?]. 1270 May 3

Helicobacter pylori infection is the most common cause of gastritis with its associated sequelae. Gastritis secondary to other bacteria is rare. This report describes Enterococcus-associated gastritis in a 59-year-old diabetic man. Nine months after receiving treatment for H. pylori-associated gastritis, he underwent endoscopy to confirm H. pylori eradication and to evaluate the status of previously seen ulcers. Mucosal biopsy specimens revealed severe active but focal gastritis adjacent to gram-positive coccobacilli in short to long chains with no H. pylori. Culture grew an Enterococcus similar to E. hirae and E. durans. No treatment was given, and endoscopy done 2 months later showed complete resolution of the gastritis and absence of H. pylori or enterococci. Our patient's gastritis represents a previously undescribed manifestation of Enterococcus infection. It is possible that the presence of NSAID gastric mucosal injury and diabetes predisposed this individual to the development of transient Enterococcus gastritis.
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PMID:Enterococcus gastritis. 1456 92

This paper provides a review of current literature on Helicobacter pylori infection in diabetes mellitus. According to majority of studies there is no difference of Helicobacter pylori infection prevalence between diabetes mellitus and general population. There is no role of Helicobacter pylori in etiopathogenesis of diabetes. The only finding of Helicobacter pylori itself has not been an indication for eradication therapy in diabetes. In case of anti-helicobacter therapy (due to another indication) eradication rate is lower in diabetics (compared to non-diabetics) and there is a higher risk of re-infection (compared to general population). Several issues (especially dysmotility disorders of the stomach and influence of Helicobacter pylori eradication for the control of diabetes) remain controversial.
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PMID:[Clinical importance of Helicobacter pylori infection in patients with diabetes mellitus]. 1530 30

Iron deficiency is a known complication of achlorhydria and may precede the development of pernicious anemia. Among 160 patients with autoimmune gastritis identified by hypergastrinemia and strongly positive antiparietal antibodies, we explored the overlap between 83 subjects presenting with iron deficiency anemia (IDA), 48 with normocytic indices, and 29 with macrocytic anemia. Compared with macrocytic patients, patients with IDA were 21 years younger (41 +/- 15 years versus 62 +/- 15 years) and mostly women. All groups had a high prevalence of thyroid disease (20%) and diabetes (8%) suggestive of the autoimmune polyendocrine syndrome. Stratification by age cohorts from younger than 20 years to older than 60 years showed a regular and progressive increase in mean corpuscular volume (MCV) from 68 +/- 9 to 95 +/- 16 fl, serum ferritin levels from 4 +/- 2 to 37 +/- 41 microg/L, gastrin level from 166 +/- 118 to 382 +/- 299 pM/L (349 +/- 247 to 800 +/- 627 pg/mL), and a decrease in cobalamin level from 392 +/- 179 to 108 +/- 65 pg/mL. The prevalence of Helicobacter pylori infection was 87.5% at age younger than 20 years, 47% at age 20 to 40 years, 37.5% at 41 to 60 years, and 12.5% at age older than 60 years. These findings challenge the common notion that pernicious anemia is a disease of the elderly and imply a disease starting many years before the establishment of clinical cobalamin deficiency, by an autoimmune process likely triggered by H pylori.
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PMID:Variable hematologic presentation of autoimmune gastritis: age-related progression from iron deficiency to cobalamin depletion. 1700 59

The results of prospective studies of the association between dietary salt intake and gastric cancer occurrence remain controversial. To examine this issue in a cohort study of a general population, 2,476 subjects aged 40 years or older were stratified into 4 groups according to the amount of daily salt intake: namely, <10.0, 10.0-12.9, 13.0-15.9, and > or = 16.0 per day and were followed up prospectively for 14 years. During the follow-up period, 93 subjects developed gastric cancer. The age- and sex-adjusted incidence was significantly higher in the second to fourth groups than in the first group (age- and sex-adjusted hazard ratio [95% confidence interval], 2.42 [1.24-4.71] for the second group; 2.10 [1.03-4.30] for the third group; 2.98 [1.53-5.82] for the fourth group). This association remained substantially unchanged even after adjusting for other confounding factors such as age, sex, Helicobacter pylori infection, atrophic gastritis, medical history of peptic ulcer, family history of cancer, body mass index, diabetes, total cholesterol, physical activity, alcohol intake, smoking habit and other dietary factors. In the stratified analysis, a significant salt-cancer association was observed only in subjects who had both Helicobacter pylori infection and atrophic gastritis (age- and sex-adjusted hazard ratio, 2.87 [1.14-7.24]). Our findings suggest that high dietary salt intake is a significant risk factor for gastric cancer; moreover, this association was found to be strong in the presence of Helicobacter pylori infection with atrophic gastritis.
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PMID:A prospective study of dietary salt intake and gastric cancer incidence in a defined Japanese population: the Hisayama study. 1645 Mar 97

Previous studies have lacked sufficient power to assess associations between early-life socioeconomic position and adult cause-specific mortality. The authors examined associations of parental social class at age 0-16 years with mortality among 1,824,064 Swedes born in 1944-1960. Females and males from manual compared with nonmanual childhood social classes were more likely to die from smoking-related cancers, stomach cancer, respiratory disease, cardiovascular disease, and diabetes. Males from manual compared with nonmanual social classes were more likely to die from unintentional injury, homicide, and alcoholic cirrhosis. The association with stomach cancer was little affected by adjustment for parental later-life and own adult social class or education. For other outcomes, educational attainment resulted in greater attenuation of associations than did adjustment for adult social class. Early-life social class was not related to suicide or to melanoma, colon, breast, brain, or lymphatic cancers or to leukemia. With the exception of stomach cancer, caused by Helicobacter pylori infection acquired in childhood, poorer social class in early life was associated with diseases largely caused by behavioral risk factors such as smoking, physical inactivity, and an unhealthy diet. Educational attainment may be important in reducing the health inequalities associated with early-life disadvantage.
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PMID:Association of childhood socioeconomic position with cause-specific mortality in a prospective record linkage study of 1,839,384 individuals. 1698 23

The aim of this investigation was to determine the seroprevalence of H. pylori in patients with coronary artery disease (CAD). Patients with coronary artery disease (n = 90) and control group (n = 90) were enrolled into this randomized, multi-centre study. CAD risk factors analyzed included age, male gender, diabetes mellitus, systemic hypertension, cigarette smoking, hypercholesterolemia and socioeconomic status. The results of this study showed a higher seroprevalence of Helicobacter pylori infection in patients with CAD compared to controls (78.8% versus 58.3%, p < 0.05). However, Helicobacter pylori seropositivity was not associated with coronary artery risk factors (smoking, body mass index, diabetes mellitus, hypertension, total cholesterol and socioeconomic status) either in the whole study population or in the patients and control subjects analyzed separately (P > 0.05). Further study are needed to clarify the precise role of Helicobacter pylori infection on the development of coronary artery disease.
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PMID:Helicobacter pylori infection and coronary artery disease. 1804 85

Patients with diabetes mellitus (DM) are at risk for Helicobacter pylori infection. This infection has been linked to atherosclerosis and its vascular complications. The aim of this study was to evaluate the: (1) prevalence of H pylori infection in patients with DM; (2) association between diabetic vascular complications and H pylori infection; and (3) influence of H pylori infection on atherosclerosis and inflammatory biomarkers. In this study, we evaluated 80 patients with DM for atherosclerosis; cardiac, cerebral, and peripheral vascular diseases; retinopathy; neuropathy; and nephropathy. We estimated the blood levels of glucose, glycosylated hemoglobin, complete blood cell count, erythrocytic sedimentation rate, lipid profile, tumor necrosis factor-alpha, interleukin (IL)-6, and anti-H pylori IgG antibodies. H pylori infection was detected in 85% of patients versus 76.7% for control subjects. Carotid artery intima-media thickness was significant in H pylori-infected patients. IL-6 and tumor necrosis factor-alpha were significantly associated with H pylori infection. In multivariate analysis, blood glucose, triglycerides, erythrocytic sedimentation rate, IL-6, and tumor necrosis factor-alpha increased the odds for atherothrombotic cause of cerebral ischemia in H pylori infection. We concluded that H pylori infection is common in DM and seems to be linked to the presence of atherosclerosis and ischemic cerebrovascular stroke. This effect could be mediated by increasing cytokine levels.
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PMID:Vascular risks and complications in diabetes mellitus: the role of helicobacter pylori infection. 1834 51


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