Patients with inflammatory bowel disease (IBD) have a 1.5-3.5-fold higher risk of thromboembolism when compared to the non-IBD population and the risk is much more prominent at the time of a flare. Arterial thromboembolism (ischemic stroke, focal white matter ischemia, cardiac ischemia, peripheral vascular disease and mesenteric ischemia) and venous thromboembolism (deep vein thrombosis and pulmonary embolism, cerebral venous sinus thrombosis, retinal, hepatic, portal and mesenteric vein thromboses) belong to the group of underestimated extraintestinal complications in IBD patients, which are associated with a high morbidity and mortality rate (the overall mortality is as high as 25 % per episode). Thromboembolism occurs in younger patients compared to the non-IBD population and has a high recurrence rate. Multiple risk factors are involved in the etiopathogenesis, but the acquired ones play the key role. Congenital alterations do not occur more frequently in IBD patients when compared to the non-IBD population. Standardized guidelines for the prophylaxis of thromboembolism in IBD patients are urgently needed and these should be respected in clinical practice to avoid preventable morbidity and mortality.

• MeSH
• idiopatické střevní záněty * komplikace   mortalita   patologie   terapie   MeSH
• lidé MeSH
• recidiva MeSH
• směrnice pro lékařskou praxi jako téma MeSH
• tromboembolie * etiologie   mortalita   patologie   prevence a kontrola   MeSH
• věkové faktory MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH

Major controversy exists as to whether increased C-reactive protein (CRP) contributes to individual components of the metabolic syndrome or is just a secondary response to inflammatory disease processes. We measured blood pressure and metabolic phenotypes in spontaneously hypertensive rats (SHRs) in which we transgenically expressed human CRP in the liver under control of the apolipoprotein E promoter. In transgenic SHRs, serum levels of human CRP approximated the endogenous levels of CRP normally found in the rat. Systolic and diastolic blood pressures measured by telemetry were 10 to 15 mm Hg greater in transgenic SHRs expressing human CRP than in SHR controls (P<0.01). During oral glucose tolerance testing, transgenic SHRs exhibited hyperinsulinemia compared with controls (insulin area under the curve: 36±7 versus 8±2 nmol/L per 2 hours, respectively; P<0.05). Transgenic SHRs also exhibited resistance to insulin stimulated glycogenesis in skeletal muscle (174±18 versus 278±32 nmol of glucose per gram per 2 hours; P<0.05), hypertriglyceridemia (0.84±0.05 versus 0.64±0.03 mmol/L; P<0.05), reduced serum adiponectin (2.4±0.3 versus 4.3±0.6 mmol/L; P<0.05), and microalbuminuria (200±35 versus 26±5 mg of albumin per gram of creatinine, respectively; P<0.001). Transgenic SHRs had evidence of inflammation and oxidative tissue damage with increased serum levels of interleukin 6 (36.4±5.2 versus 18±1.7 pg/mL; P<0.005) and increased hepatic and renal thiobarbituric acid reactive substances (1.2±0.09 versus 0.8±0.07 and 1.5±0.1 versus 1.1±0.05 nmol/L per milligram of protein, respectively; P<0.01), suggesting that oxidative stress may be mediating adverse effects of increased human CRP. These findings are consistent with the hypothesis that increased CRP is more than just a marker of inflammation and can directly promote multiple features of the metabolic syndrome.

• MeSH
• adiponektin metabolismus   MeSH
• analýza rozptylu MeSH
• C-reaktivní protein genetika   metabolismus   MeSH
• glukózový toleranční test MeSH
• inzulin metabolismus   MeSH
• krevní glukóza metabolismus   MeSH
• krevní tlak genetika   MeSH
• krysa rodu Rattus MeSH
• lidé MeSH
• metabolický syndrom etiologie   genetika   metabolismus   MeSH
• oxidační stres genetika   MeSH
• potkani inbrední SHR MeSH
• potkani transgenní MeSH
• telemetrie MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adiponektin MeSH
• C-reaktivní protein MeSH
• inzulin MeSH
• krevní glukóza MeSH