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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stroke (Ischemic) initiates numerous pathophysiological processes and each of them can be dangerous. When evaluating patient's state and choosing therapeutical strategy, a complexity of the followed-up parameters should be taken into account as well as a complexity of a given therapeutical approach. On the basis of literary data and acquired clinical experience, we developed our own algorithm for diagnosis of the nutritional state and it was implemented into a semi-expert computing system SOFT. Using SOFT program, the group of 23 patients with ischemic CMP was examined within 40 hrs after its origin. These patients were found to show a slight protein catabolism and nutritional stress (aminograms, stress index, nutritional percentage of complications, nitrogen balance, CRP, prealbumin). necessity of an early diagnosis of nutritional deficiency and disorders of protein metabolism in STROKE patients is discussed. The paper reports on means of enteral nutrition prepared in the Hospital in Sternberk which appeared to be highly favorable. The aspects of administration of parenteral nutrition are discussed.
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PMID:[Nutritional status in patients with stroke. Diagnosis, therapy and its monitoring]. 897 56

Numerous reports have established the association of inflammation with acute coronary events. Data have been presented that suggest that elevated levels of CRP indicate heightened risk of future MI and stroke. Thus CRP measurement is both predictive and prognostic of cardiovascular and cerebrovascular events. Is inflammation merely a marker, an invited guest so to speak, or is inflammation an active participant that influences the process of plaque rupture and thrombus formation? The beneficial effects of aspirin in reducing the risks of a first MI and stroke are directly related to high plasma concentrations of CRP, whereas small, nonsignificant reductions in risk occurred among patients with low or normal CRP levels. Thus inflammation is not only an uninvited guest but is actually an aggressive participant in the destabilization of the atheromatous endothelial plaque.
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PMID:Inflammation in plaque rupture: an active participant or an invited guest? 950 30

The causes of pituitary apoplexy are unclear. We report a case of pituitary apoplexy presenting with headache and nausea. On June 17th, 1997 a 74-year-old woman had complained of retro-orbital headache, fever and vomiting. A cold was diagnosed for which she recurred medication. In addition to the previous symptoms she was getting to lose appetite. She was admitted to our hospital for further examination and treatment on June 21. On admission neurological examination showed left pupil mydriasis, the left eye had no light reflex and the right eye had only a slight response to the light. She could hardly move both eyeballs up. Laboratory data showed a normal white blood cell count and the CRP was 16.2 mg/dl. Lumbar puncture showed 97 mg/dl total protein and 82 cells per microliter, most of which were lymphocytes. We diagnosed viral infection based on the evidence of clinical symptoms and lumbar puncture data. The patient was treated with gamma-globulin and improved. From the 16th day of sickness we recognized symptoms of oculomotor paralysis and the syndrome of inappropriate antidiuretic hormone. On the 23rd day of sickness we strongly suspected pituitary apoplexy based on transaxial MR images. After absorption of intra-tumor hemorrhage, the oculomotor symptoms recurred. We finally reached a diagnosis of pituitary apoplexy based on pathological material, MR images, symptoms and laboratory data. We must think of pituitary apoplexy when we see an aged out-patient with severe headache, nausea, vomiting and oculomotor paralysis. It was difficult to diagnose this disease in the early time course of the disease.
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PMID:[A case of pituitary apoplexy approving as severe headache and nausea]. 1065 40

Atherosclerotic plaques were likened histologically to healing inflammatory lesions by Russell Ross, who proposed a "response to injury" hypothesis for their formation. More recently, intraplaque inflammation has been postulated to play a role in thinning of the fibrous cap, plaque rupture, and superadded thrombosis. Potential causes for vascular injury include mechanical stress, smoke exposure, hypercholesterolemia, hyperhomocysteinemia, and chronic infection (direct, or indirect). Blood levels of inflammatory markers (e.g., C-reactive protein [CRP]; serum amyloid A [SAA]; fibrinogen; plasma viscosity; erythrocyte sedimentation rate [ESR]; leukocyte count, low serum albumin) have been associated with vascular risk factors and with prevalent and incident atherothrombotic cardiovascular disease (CVD) (coronary heart disease, [CHD]; stroke; and peripheral arterial disease). More recently, cytokines (e.g., interleukin-6 [IL-6]) and soluble adhesion molecules (e.g., intercellular adhesion molecule-1, vascular cell adhesion molecule-1) have been associated with both risk factors and disease; and offer potential therapeutic targets for nonspecific "anti-inflammatory" treatment of arterial disease. Infections associated with arterial disease include specific infections (Chlamydia pneumoniae, Helicobacter pylori) and nonspecific infections (periodontal infections, respiratory tract infections). Recent meta-analyses have shown that associations of serum markers of C. pneumoniae and H. pylori with arterial disease, risk factors, or potential intermediary mechanisms for disease are weaker than was first suggested by early reports. Likewise, further studies and meta-analyses are required to evaluate the epidemiologic relationships of CVD to periodontal infection and disease and to chronic pulmonary infections and disease. The weaker the associations between chronic infections and CVD, the larger is the size of randomized controlled trials required to establish (or exclude) a preventive effect of infection treatment. While control of chronic infection in the mouth, stomach or lungs is appropriate for its local effects, proving its efficacy in prevention of CVD presents a continuing challenge to medical science.
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PMID:The relationship between infection, inflammation, and cardiovascular disease: an overview. 1188 52

Sero-epidemiological case control studies have observed positive relations between infections with Chlamydia pneumoniae, Helicobacter pylori or cytomegalovirus (CMV) and the occurrence of coronary artery disease (CAD) and stroke. Moreover, positive relations between 'infection burden' and CAD and the role of inflammation have recently been described. However, the relations between infection, inflammation and the occurrence of peripheral arterial disease (PAD) have not been reported so far. We performed a multi-centre population-based case-control study, using serum samples of 228 young female PAD patients and 643 control women to determine IgG antibody titres and C-reactive protein. The odds ratios for PAD in women with serological evidence for infection with C. pneumoniae, H. pylori or CMV were 2.0 (95% CI; 1.3-3.1), 1.6 (95% CI; 1.1-2.2) and 1.6 (95% CI; 1.1-2.3), respectively. The cumulative number of infections was positively related to the risk of PAD; the odds ratio was 1.5 (95% CI; 1.0-2.4), 2.7 (95% CI; 1.6-4.4) and 3.5 (95% CI; 1.5-8.1) for women with one, two or three infections, respectively. This increased risk, related to the 'infection burden', was found again in the subgroup of women with a high CRP level, but not in the subgroup with a low CRP level. Infections might be a causal component in the development of PAD. The risk of PAD is not only related to a single pathogen in particular, but also to the cumulative number of infections. The positive relation between 'infection burden' and PAD was only found in women with a high CRP level, which indicates that inflammation might be involved in the process that leads to PAD.
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PMID:Chlamydia pneumoniae, Helicobacter pylori and cytomegalovirus infections and the risk of peripheral arterial disease in young women. 1204 33

The bulk of the experimental data suggest beneficial effects of estrogen (both premenopausal use of OCs and postmenopausal use of ERT-HRT). An intriguing finding from the monkey studies is that social subordination, which induces estrogen deficiency in female monkeys, accelerates atherosclerosis premenopausally and predicts extent of postmenopausal atherosclerosis. This effect can be inhibited by exogenous estrogen, premenopausally. The results suggest that more effort on detecting and regulating premenopausal ovarian dysfunction may be justified. A complication in understanding estrogen action may be the result of varying extents of arterial damage. For example, primary prevention studies in both postmenopausal animals and women have provided strong evidence of atheroprotection with a variety of estrogens. In contrast, the results of secondary prevention studies [10,12] have in general suggested little cardioprotection with either ERT or HRT. Studies in rabbits suggest the antiatherogenic effect of estrogen may not be present when the endothelium is damaged [64]. The state of the endothelium may be critical for some estrogen actions. For those effects of estrogen that require the ER, be it ERalpha or ERbeta, the presence of the receptor may vary with age, disease state, or type of hormone therapy. If continuous combined HRT therapy decreases ER in the artery as it does in the uterus, this may eliminate those estrogen actions requiring the ER, but not others. Older women who have not been exposed to estrogens for many years may be more sensitive to some estrogen effects, and may need lower doses of ERT-HRT. Recent reports suggest that lower doses of estrogens maintain beneficial effects on lipoproteins and coagulation factors [95], while also requiring lower doses of progestogens to protect the uterus [96]. These beneficial findings are very promising in light of the improvements in CHD risk and decreased stroke risk reported with low-dose estrogens [5]. It ill be interesting to see if CRP is increased with lower doses of estrogens and whether these changes are associated with increased early risk of CHD. Perhaps older women with CHD are also more obese, may have diabetes, and may be more susceptible to inflammatory and thrombotic effects of higher doses of estrogens. There are many questions left unanswered. It is hoped that some of the answers may come from the WHI, which is a large prospective trial assessing ERT and HRT. The age range is also relatively large and may be able to determine if older women respond differently than younger women. Some initial data from the WHI have been made available suggesting a small increased risk in the first 2 years and a trend for decreasing risk in the last months of the first 2 years [34]. Just recently, the CEE + MPA arm of the study was stopped early by the data and-safety monitoring board as the overall health risks exceeded benefits with increases in both breast cancer and CVD [97]. The remainder of the study groups including an estrogen-only arm, are expected to continue until 2005.
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PMID:Reproductive hormones and cardiovascular disease mechanism of action and clinical implications. 1235 69

The prevalence of marked obesity is increasing rapidly among adults and has more than doubled in 10 years. Sixty-one percent of the adult population of the United States is overweight or obese. Americans are the fattest people on earth. Paradoxically these increases in the numbers of persons who are obese or overweight have occurred during recent years when Americans have been preoccupied with numerous dietary programs, diet products, weight control, health clubs, home exercise equipment, and physical fitness videos, each "guaranteed" to bring rapid results. Overweight and obesity are also world problems. The World Health Organization estimates that 1 billion people around the world are now overweight or obese. Westernization of diets has been part of the problem. Fruits, vegetables, and whole grains are being replaced by readily accessible foods high in saturated fat, sugar, and refined carbohydrates. Since class 3 obesity (morbid or extreme obesity) is associated with the most severe health complications, the incidence of hypertension, stroke, heart disease, diabetes, and peripheral vascular disease will increase substantially in the future. Recently, obesity alone has been implicated in the development of cardiac hypertrophy and CHF. The metabolic syndrome associated with abdominal obesity, which includes insulin resistance, dyslipidemia, and elevated CRP levels, identifies subjects who have an increase in cardiovascular morbidity and mortality. Twenty to 25% of the adult population in the United States have the metabolic syndrome, and in some older groups this prevalence approaches 50%. The prevalence of overweight children in the United States has also been increasing dramatically, especially among non-Hispanic blacks and Mexican-American adolescents. Overweight children usually become overweight adults. Atherosclerosis begins in childhood. The degree of atherosclerotic changes in children and young adults can be correlated with the presence of the same risk factors seen in adults. As health providers, our direction is obvious!
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PMID:Obesity and the metabolic syndrome. 1262 76

Current topics and new developments in risk factors for ischemic stroke were reviewed. Hypertension, diabetes mellitus, hyperlipidemia, atrial fibrillation, cigarrette smoking, and heavy alcohol drinking have been established as being common treatable risk factors for stroke. Recent studies have clarified that homocysteine, various cardiac sources of embolism such as patent foramen ovale, antiphopholipid antibodies, lipoprotein (Lp) abnormalities including Lp(a) and remnant-like particle, insulin resistance or hyperinsulinemia, infectious diseases such as Chlamydia Pneumoniae, and CRP are additional risk factors for stroke. In addition, genetic studies using single nucleotide polymorphisms have suggested that many gene polymorphisms are significant risk factors for certain subpopulations of stroke, which is recognized to be a polygenic disease. Management of these risk factors is crucial for primary prevention of stroke, which is the leading cause of death or disability all over the developed countries.
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PMID:[Risk factors for cerebral infarction: current topics and new developments]. 1278 67

The concept of the vulnerable patient has arrived. Enhanced diagnostic methods will eventually permit accurately finding and treating these patients and their disease. Clinical Cardiologists now recognize that coronary atherosclerosis is two pathophysiologically distinct syndromes: stable and unstable. Stable coronary syndromes result from fixed, severe stenoses limiting blood flow and causing secondary myocardial ischemia. The unstable acute coronary syndromes are frequently catastrophic and are pathophysiologically distinct. They result from different cell subsets causing vascular inflammatory syndromes rather than gradual lumen constriction by plaque. Though pathophysiologically distinct, they may show common pathophysiology when a ruptured plaque heals and progressively becomes a critical stenosis. For the present hs-CRP measurement is the strongest correlative factor for future clinical events due to arterial inflammation: myocardial infarction, unstable angina, stroke, and peripheral vascular disease in both diseased and apparently healthy, asymptomatic patients. The CRP plasma level also is the best risk assessment in patients with either stable or unstable angina, long term after myocardial infarction, and in patients undergoing revascularization therapies. One study showed the only independent cardiovascular risk indicators using multivariate, age adjusted and traditional risk analysis were CRP and Total/HDL cholesterol ratio. If CRP, IL-6, and ICAM-1 levels are added to lipid levels, risk assessment can be improved over lipids alone. The prevalence of high-risk subjects in the general population is low, amplifying diagnostic problems for vulnerable plaque. Since no test yet has high sensitivity or specificity, diagnostic errors are high, with many false positives and negatives. Sensitivity or specificity must be increased by developing a risk marker panel, or by simultaneously finding other markers that themselves are highly sensitive and specific for vulnerable plaque.
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PMID:Detecting vulnerable plaque using peripheral blood: inflammatory and cellular markers. 1280 Apr 2

Insulin resistance (IR)/hyperinsulinemia and low-grade inflammation (high-sensitivity C-reactive protein [hs-CRP]) can predict cardiovascular disease. However, because IR and inflammation (IF) have not been evaluated simultaneously, it is not known whether IR and IF are independently related to cardiovascular disease. Furthermore, the combined effect of IR and IF on the prediction of cardiovascular disease is presently unknown. Thus, we measured insulin sensitivity (K index of the insulin tolerance test; KITT) and hs-CRP in 350 Japanese patients with type 2 diabetes, and followed them for 1-7 years (mean, 4.5 years). During the follow-up, 33 patients died and 53 patients developed non-fatal coronary artery disease or stroke (endpoint). Age, systolic blood pressure, current smoking, past history of cardiovascular disease, KITT, and hs-CRP independently and significantly correlated with endpoint. One-S.D. difference was associated with a significant increase of relative risk in KITT (1.45; 95% CI 1.09-1.91) and hs-CRP (1.30; 1.04-1.67). When patients were subdivided to tertile, the relative risk in the highest tertile of KITT was 1.76 (95% CI 1.01-3.11) and hs-CRP was 2.00 (1.03-3.85) compared with the patients with lowest tertile. The relative risk in the highest tertile of both KITT and hs-CRP was 5.32 (1.18-24.0) compared with the lowest tertile of both values. In conclusion, low-grade IF and IR are independently related to all-cause of death and cardiovascular disease in Japanese patients with type 2 diabetes. Coexistence of low-grade IF and IR amplify this effect.
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PMID:Inflammation and insulin resistance are independently related to all-cause of death and cardiovascular events in Japanese patients with type 2 diabetes mellitus. 1292 84


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