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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the metabolic syndrome together with insulin resistance and their consequences are probably basic factors in pathogenesis of atherosclerosis, inflammatory and infectious aspects of this process are unquestionable only in some of the patients. Endothelial dysfunction was identified both in the experiment and in patients after herpes virus simplex 1 infection, cytomegaloviral infection, Chlamydia pneumoniae infection, or Helicobacter pylori infection. However, it is not clear whether it is always caused by direct specific activity of a given pathogen or whether it is a result of inflammatory cytokines activity, heat shock protein activity, or CRP activity. In recent years secondary antibiotic prevention in patients after myocardial infarction has been discussed. Lower mortality rate from acute myocardial infarction and cerebral vascular accidents were found in several observations of patients vaccinated against influenza. In patients with non-stable angina pectoris we have found significantly more frequent occurrence of IgG antibodies against Chlamydia pneumoniae. This occurrence was more frequent in diabetics compared to non-diabetics. Endothelia exposed to cyto-megaloviral infection exprimed adhesive molecules on their surfaces. After an increase of the concentration of glucose in medium to 11.0 mmol/l and 16.5 mmol/l the expression of adhesive molecules after cyto-megaloviral infection increased. Relationship of infection, inflammation, and atherosclerosis has been a subject of intensive investigation in recent years. Discussion of possible consequences of these findings, especially from viewpoint of atherosclerosis prevention and its organ complications, is of the same intensity. Hypothesis about participation of infection and inflammation in pathogenesis of atherosclerosis seems to be very attractive. In spite of the fact that findings supporting this hypothesis cumulate final conclusion can't be made yet.
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PMID:[Infectious and inflammatory factors in the etiology and pathogenesis of atherosclerosis]. 1504 Jan 64

Genetic factors, Helicobacter pylori infection, salt over-uptake, decreased vegetable/fruit consumption, smoking, and metabolic syndrome are risk factors of human gastric cancer. Germline mutations of CDH1 gene, and SNPs of PTPN11 (SHP2), TLR4, IL1B, TNFA, BMP6, GDF15 and RUNX3 genes are associated with gastric cancer. Helicobacter pylori activates CagA-SHP2-ERK and peptidoglycan-NOD1-NFkappaB signaling cascades in gastric epithelial cells using type IV secretion system, and also TRAF6-MAP3K7-NFkappaB and TRAF6-MAP3K7-AP-1 signaling cascades in epithelial and immune cells through lipopolysaccharide recognition by TLR2 or TLR4. IL-1beta, IL-6, IL-8, TNFalpha and IFNgamma are elevated in gastric mucosa with Helicobacter pylori infection. IL-6 and TNFalpha induce upregulation of WNT5A and WNT10B, respectively. WNT signals are transduced to beta-catenin-TCF/LEF, RhoA, JNK, PKC, NFAT, and NLK signaling cascades. WNT-beta-catenin-TCF/LEF signaling induces upregulation of MYC, CCND1, WISP1, FGF20, JAG1 and DKK1 genes. Notch signals are transduced to CSL-NICD-MAML and NFkappaB signaling cascades. FGF signals are transduced to ERK, PI3K-AKT, PKC, and NFAT signaling cascades. Helicobacter pylori infection induces SHH upregulation in parietal cell lineage, while BMP signals induce IHH upregulation in pit cell lineage. Hedgehog signals induce upregulation of GLI1, PTCH1, CCND2, FOXL1, JAG2 and SFRP1 genes. JAG1 and JAG2 activate Notch signaling, while DKK1 and SFRP1 inhibit WNT signaling. Stem cell signaling network, consisting of WNT, Notch, FGF, Hedgehog and BMP signaling pathways, is activated during chronic Helicobacter pylori infection. Epigenetic silencing of SFRP1 gene occurs in the earlier stage of carcinogenesis in the stomach, while amplification and overexpression of FGFR2 gene in the later stage. Dysregulation of the stem cell signaling network due to the accumulation of germline mutation, SNP, Helicobacter pylori infection, epigenetic change and genetic alteration gives rise to gastric cancer. SNP typing and custom-made microarray analyses on genes encoding stem cell signaling molecules could be utilized for the personalized medicine.
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PMID:Dysregulation of stem cell signaling network due to germline mutation, SNP, Helicobacter pylori infection, epigenetic change and genetic alteration in gastric cancer. 1756 83

The prevalence of reflux esophagitis is increasing in Korea. To estimate the prevalence and clinical characteristics of reflux esophagitis in healthy subjects, we retrospectively examined the medical records of healthy subjects undergoing a routine check-up from October 2004 to September 2005. A total of 6,082 (3,590 men, mean age 44+/-10 yr) subjects were enrolled in this study. The prevalence of reflux esophagitis in healthy subjects was 10.5%. According to the univariate analysis, male sex (odds ratio [OR] 3.49, 95% confidence interval [CI] 2.84-4.30), smoking history (OR 1.91, 95% CI 1.60-2.28), body mass index (BMI) >30 kg/m(2) (OR 2.13, 95% CI 1.37-3.33), total cholesterol >250 mg/dL (OR 1.50, 95% CI 1.05-2.14), low-density lipoprotein (LDL) cholesterol >/=160 mg/dL (OR 1.52, 95% CI 1.08-2.14), triglyceride >/=150 mg/dL (OR 1.92, 95% CI 1.61-2.30), high blood pressure (BP) (OR 1.46, 95% CI 1.20-1.76), and fasting glucose >/=110 mg/dL (OR 1.45, 95% CI 1.13-1.86) were significantly associated with reflux esophagitis (all p<0.05). However, age, alcohol drinking and Helicobacter pylori infection were not associated with reflux esophagitis. In conclusion, significant relationships of reflux esophagitis with obesity, low high-density lipoprotein (HDL) cholesterol, high triglyceride, high BP, and elevated fasting glucose suggested that reflux esophagitis might represent the disease spectrum of the metabolic syndrome.
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PMID:The prevalence and clinical characteristics of reflux esophagitis in koreans and its possible relation to metabolic syndrome. 1939 58

Gastroesophageal reflux disease (GERD), previously uncommon in Asia, has now become an important disease in the region. Although much variability exists between studies, most endoscopy-based studies show a prevalence of erosive esophagitis of more than 10%. Symptom-based studies also show a prevalence of 6-10%. Two longitudinal follow-up studies on GERD symptoms have shown an increase with time, and several endoscopy-based time trend studies have also shown a significant increase in erosive reflux esophagitis. Studies on Barrett's esophagus have been confounded by the description of short (SSBE) and long segment (LSBE) Barrett's esophagus. Great variation in prevalence rates has been reported. SSBE vary from 0.1% to more than 20% while LSBE vary from 1-2%. Of the putative causative factors, obesity has been the most important. Many studies have linked GERD-esophagitis as well as occurrence of reflux symptoms with an increase in body mass index (BMI), obesity, especially visceral or central obesity, and metabolic syndrome. A decline in Helicobacter pylori infection with growing affluence in Asia has been broadly thought to result in healthier stomachs and a higher gastric acid output resulting in reflux disease. However, variable results have been obtained from association and H. pylori eradication studies.
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PMID:Gastroesophageal reflux disease in Asia: A historical perspective and present challenges. 2119 9

Metabolic syndrome is one of the most prevalent global health problems that predisposes to Type 2 diabetes. It is strongly linked to insulin resistance, which results in hyperglycemia. Over the past few years, lot of studies have been carried out on Helicobacter pylori infection and found a possible causal relationship through releasing some of the interleukins factors, which result in endothelial dysfunction. However, some studies attributed that due to coincidence were not able to establish any causal relationship. In this review, the literature has been reviewed to check this possible association.
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PMID:Helicobacter pylori infection and its relationship to metabolic syndrome: is it a myth or fact? 2206 47

Ethnic differences in the prevalence of gastro-oesophageal reflux disease (GORD) and its complications, including Barrett's oesophagus (BO), are well described in multiracial Asian patient populations. These findings together with familial aggregation of GORD symptoms and twin studies suggest the possibility of a genetic component to GORD. Nevertheless, environmental factors, e.g. Helicobacter pylori infection, abdominal adiposity and metabolic syndrome, could equally account for these differences. Indian (South Asian) race is a risk factor for Barrett' oesophagus. This may be related to the Caucasian genetic make-up of Indians as opposed to an Oriental one as is the case of most other Asians. The HLA-B07 gene commonly found in South Asian and Caucasian populations, but not Orientals, may confer an increased risk for BO. Nevertheless, the high prevalence of H. pylori in South Asians and the consequent atrophic gastritis and hypochlorhydria may partially ameliorate this genetic predisposition to BO. The higher prevalence of obesity and the metabolic syndrome amongst certain Asiatic races may also contribute to the observed increased risk for BO. Future research should target the search for GORD/BO genes, ethnic differences in parietal cell mass and hiatal hernia, H. pylori colonization factors (e.g. MUC1 and MUC2) and adhesion molecules (BabA). Racial differences in lifestyle factors, i.e. abdominal adiposity, consumption of fruit and vegetables as well as smoking, should all be investigated as potential causes for this interethnic variation in GORD and BO. Nature or nurture, the clues are teasing and tantalizing and illustrate the complex relationship between the genetic make-up of man and the environment.
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PMID:Barrett's oesophagus in Asians--are ethnic differences due to genes or the environment? 2181 67

Extragastric or extraintestinal manifestations of Helicobacter pylori infection attract a lot of attention, and recently this microorganism has also been linked with insulin resistance (IR). The metabolic syndrome consists of several known factors which include IR, abnormal fat metabolism, hypertension, abdominal obesity, proinflammatory and prothrombotic state. H. pylori infection and metabolic syndrome both show increase in prevalence with age, and since IR is a key factor in the pathogenesis of metabolic syndrome, research of a possible correlation between H. pylori infection and IR has intensified in the last decade. A few studies demonstrated a direct link between H. pylori infection and IR, and research studies on the influence of eradication therapy on IR and other metabolic parameters were also conducted. It is necessary to carry out additional prospective studies controlling all the confounding factors that could influence the end result so that the association between H. pylori infection and IR development could be elucidated. So far it is premature to advocate intervention measures in high-risk communities, but if this particular association is confirmed, it could drastically change our understanding of pathophysiology and treatment of IR, type 2 diabetes and metabolic syndrome.
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PMID:[Helicobacter pylori and insulin resistance]. 2329 15

The incidence of oesophageal adenocarcinoma has increased dramatically in the developed world in the last half century. Over approximately the same period there has been an increase in the prevalence of obesity. Multiple epidemiological studies and meta-analyses have confirmed that obesity, especially abdominal, visceral obesity, is a risk factor for gastro-oesophageal reflux, Barrett's oesophagus and oesophageal adenocarcinoma. Although visceral obesity enhances gastro-oesophageal reflux, the available data also show that visceral obesity increases the risk of Barrett's oesophagus and adenocarcinoma via reflux-independent mechanisms. Several possible mechanisms could link obesity with the risk of oesophageal adenocarcinoma in addition to mechanical effects increasing reflux. These include reduced gastric Helicobacter pylori infection, altered intestinal microbiome, factors related to lifestyle, the metabolic syndrome and associated low-grade inflammation induced by obesity and the secretion of mediators by adipocytes which may directly influence the oesophageal epithelium. Of these adipocyte-derived mediators, increased leptin levels have been independently associated with progression to oesophageal adenocarcinoma and in laboratory studies leptin enhances malignant behaviours in cell lines. Adiponectin is also secreted by adipocytes and levels decline with obesity: decreased serum adiponectin levels are associated with malignant progression in Barrett's oesophagus and experimentally adiponectin exerts anticancer effects in Barrett's cell lines and inhibits growth factor signalling. At present there are no proven chemopreventative interventions that may reduce the incidence of obesity-associated oesophageal cancer: observational studies suggest that the combined use of a statin and aspirin or another cyclo-oxygenase inhibitor is associated with a significantly reduced cancer incidence in patients with Barrett's oesophagus.
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PMID:The role of obesity in oesophageal cancer development. 2536 84

In recent decades there has been a dramatic rise in the incidence of esophageal adenocarcinoma (EAC) in the developed world. Over approximately the same period there has also been an increase in the prevalence of obesity. Obesity, especially visceral obesity, is an important independent risk factor for the development of gastro-esophageal reflux disease, Barrett's esophagus and EAC. Although the simplest explanation is that this mediated by the mechanical effects of abdominal obesity promoting gastro-esophageal reflux, the epidemiological data suggest that the EAC-promoting effects are independent of reflux. Several, not mutually exclusive, mechanisms have been implicated, which may have different effects at various points along the reflux-Barrett's-cancer pathway. These mechanisms include a reduction in the prevalence of Helicobacter pylori infection enhancing gastric acidity and possibly appetite by increasing gastric ghrelin secretion, induction of both low-grade systemic inflammation by factors secreted by adipose tissue and the metabolic syndrome with insulin-resistance. Obesity is associated with enhanced secretion of leptin and decreased secretion of adiponectin from adipose tissue and both increased leptin and decreased adiponectin have been shown to be independent risk factors for progression to EAC. Leptin and adiponectin have a set of mutually antagonistic actions on Barrett's cells which appear to influence the progression of malignant behaviour. At present no drugs are of proven benefit to prevent obesity associated EAC. Roux-en-Y reconstruction is the preferred bariatric surgical option for weight loss in patients with reflux. Statins and aspirin may have chemopreventative effects and are indicated for their circulatory benefits.
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PMID:Pathophysiological mechanisms linking obesity and esophageal adenocarcinoma. 2540 Sep 97

The article presents the results of a study that describes the impact of successful Helicobacter pylori infection eradication on the main biochemical markers of metabolic syndrome. It was found that successful anti-helicobacter therapy in patients with MS was accompanied by statistically significant improvement in carbohydrates and lipid metabolism, the liver functional state, lowering hsCRP levels.
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PMID:[Influence of Helicobacter pylori eradication on the metabolic syndrome components]. 2579 32


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