Home About us Contact | |||
Syndrome Components (syndrome + component)
Kinds of Syndrome Components Selected AbstractsPredictive Factors for Pure Steatosis in Alcoholic PatientsALCOHOLISM, Issue 6 2009Sylvie Naveau Background:, Bearing in mind the mechanisms involved in nonalcoholic fatty liver disease, this study aims to verify whether metabolic syndrome or its various individual components are independent predictive factors for steatosis ,10% in alcoholic patients. Methods:, This study included 281 consecutive alcoholic patients with abnormal liver tests and either normal liver histology or steatosis <10% (n = 119) or steatosis ,10% (n = 162). Logistic regression analysis was used to study the relationship between metabolic syndrome components and various risk factors and the presence of steatosis ,10%. We assessed apolipoprotein A1 (ApoA-1) levels, a major protein component of plasma high-density lipoprotein (HDL), rather than HDL-cholesterol levels. Results:, Plasma ApoA-1 levels (p < 0.01), body mass index (BMI) (p < 0.01), and waist circumference (p < 0.05) were significantly higher in patients with steatosis ,10% than in patients with normal liver histology or steatosis <10%. A higher percentage of patients with steatosis ,10% had high blood pressure (p = 0.003) than patients with normal liver histology or steatosis <10%. In the logistic regression, ApoA-1 [odds ratio (OR) = 1.57 (1.10,2.22)], BMI [OR = 1.10 (1.01,1.23)], and high blood pressure [OR = 1.84 (1.10,3.06)] were positively and independently correlated with the presence of steatosis ,10%. In the multivariate regression high blood pressure was independently and positively correlated with steatosis score (r = 0.55 ± 0.26; p < 0.05). On the other hand, when the presence of high blood pressure was the dependent variable, the presence of steatosis ,10% positively and independently correlated with it [OR = 1.82 (1.05,3.15)]. Conclusion:, In alcoholic patients without fibrosis, ApoA-1, BMI, and high blood pressure on the next morning after the admission were predictive of steatosis ,10%. High blood pressure was the only metabolic syndrome component associated with the presence of alcoholic steatosis ,10% and was not correlated with other metabolic syndrome components. These findings suggest that steatosis mechanisms are different in alcoholic and nonalcoholic fatty liver. [source] Uric Acid as a Marker for Renal Dysfunction in Hypertensive Women on Diuretic and Nondiuretic TherapyJOURNAL OF CLINICAL HYPERTENSION, Issue 5 2009Rodolfo. Hyperuricemia is a common finding in hypertensive patients, especially among those who are on diuretic therapy. However, its clinical relevance regarding cardiovascular and chronic kidney disease (CKD) has not clearly been established. The authors assessed whether, in a population of 385 hypertensive women categorized according to diuretic therapy, the stratification in quartiles by uric acid levels would identify a gradient of changes in renal function and in risk factors for cardiovascular disease. The following were evaluated: serum uric acid, glycemia, total and fractional cholesterol, triglycerides, apolipoprotein (Apo) B, Apo A-I, and C-reactive protein. Renal function was assessed by serum creatinine, albuminuria, and estimated glomerular filtration rate (eGFR) by the Modification of Diet in Renal Disease equation, whereas cardiovascular risk was estimated through the Framingham score. A total of 246 women were on diuretic therapy; 139 were taking other antihypertensive medications. There was a reduction in eGFR parallel to the increase in uric acid levels, regardless of diuretic use and without a concomitant increase in albuminuria. In both groups, higher uric acid levels translated into an increase in metabolic syndrome components, in markers of insulin resistance, triglyceride/high-density lipoprotein levels, and Apo B/Apo A-I ratios, as well as in Framingham scores. Hyperuricemia was associated with an increase in inflammatory markers only in patients on diuretic therapy. In a binary logistic regression, hyperuricemia (uric acid >6.0 mg/dL) was independently associated with CKD (eGFR <60 mL/min/1.73 m²) (odds ratio, 2.63; 95% confidence interval, 1.61,4.3; P<.001). In hypertensive women, the presence of hyperuricemia indicated a substantial degree of kidney dysfunction as well as a greater cardiovascular risk profile. [source] Predictive Factors for Pure Steatosis in Alcoholic PatientsALCOHOLISM, Issue 6 2009Sylvie Naveau Background:, Bearing in mind the mechanisms involved in nonalcoholic fatty liver disease, this study aims to verify whether metabolic syndrome or its various individual components are independent predictive factors for steatosis ,10% in alcoholic patients. Methods:, This study included 281 consecutive alcoholic patients with abnormal liver tests and either normal liver histology or steatosis <10% (n = 119) or steatosis ,10% (n = 162). Logistic regression analysis was used to study the relationship between metabolic syndrome components and various risk factors and the presence of steatosis ,10%. We assessed apolipoprotein A1 (ApoA-1) levels, a major protein component of plasma high-density lipoprotein (HDL), rather than HDL-cholesterol levels. Results:, Plasma ApoA-1 levels (p < 0.01), body mass index (BMI) (p < 0.01), and waist circumference (p < 0.05) were significantly higher in patients with steatosis ,10% than in patients with normal liver histology or steatosis <10%. A higher percentage of patients with steatosis ,10% had high blood pressure (p = 0.003) than patients with normal liver histology or steatosis <10%. In the logistic regression, ApoA-1 [odds ratio (OR) = 1.57 (1.10,2.22)], BMI [OR = 1.10 (1.01,1.23)], and high blood pressure [OR = 1.84 (1.10,3.06)] were positively and independently correlated with the presence of steatosis ,10%. In the multivariate regression high blood pressure was independently and positively correlated with steatosis score (r = 0.55 ± 0.26; p < 0.05). On the other hand, when the presence of high blood pressure was the dependent variable, the presence of steatosis ,10% positively and independently correlated with it [OR = 1.82 (1.05,3.15)]. Conclusion:, In alcoholic patients without fibrosis, ApoA-1, BMI, and high blood pressure on the next morning after the admission were predictive of steatosis ,10%. High blood pressure was the only metabolic syndrome component associated with the presence of alcoholic steatosis ,10% and was not correlated with other metabolic syndrome components. These findings suggest that steatosis mechanisms are different in alcoholic and nonalcoholic fatty liver. [source] Glucocorticoid replacement is associated with hypertriglyceridaemia, elevated glucose and higher non-HDL cholesterol and may diminish the association of HDL cholesterol with the ,629C>A CETP promoter polymorphism in GH-receiving hypopituitary patientsCLINICAL ENDOCRINOLOGY, Issue 3 2008Robin P. F. Dullaart Summary Objectives, The effect of glucocorticoid substitution on the prevalence of metabolic syndrome components (NCEP ATP III criteria) and serum lipid levels was determined in GH-replaced hypopituitary patients. As glucocorticoid replacement is associated with a pronounced decrease in plasma cholesteryl ester transfer protein (CETP) activity, we also tested associations of HDL cholesterol with the ,629C>A CETP promoter polymorphism in subjects with and without ACTH deficiency. Design and patients, In a university setting, we retrieved protocolized clinical and laboratory data from 165 adult hypopituitary patients, who had received GH for 1 year. Results, After adjustment for age, sex and smoking, non-HDL cholesterol (P = 0·05) and triglycerides (P = 0·004) were higher, but HDL cholesterol was not decreased in 117 glucocorticoid (mainly cortisone acetate in two divided doses) receiving subjects compared to 48 ACTH-sufficient subjects. The prevalence of elevated plasma glucose and/or diabetes (P = 0·04) and hypertriglyceridaemia (P = 0·005), but not of other metabolic syndrome components, was higher in glucocorticoid-replaced subjects. HDL cholesterol was higher in ,629 A allele carriers compared to ,629CC homozygotes in ACTH-sufficient subjects (P = 0·04), but not in glucocorticoid-treated subjects (P = 0·13). Multiple linear regression analysis demonstrated that only in ACTH-sufficient subjects, HDL cholesterol was independently related to this CETP gene variation (P = 0·03). Conclusions, In GH- and glucocorticoid-replaced hypopituitary patients, serum non-HDL cholesterol and triglycerides are higher and the prevalence of hyperglycaemia is increased, but HDL cholesterol is not decreased. Conventional glucocorticoid replacement appears to diminish the association of HDL cholesterol with a common CETP gene variation. [source] |