Plant Sterols/Stanols: Do they have a Role in Current Cardiovascular Disease Prevention?

Plant sterols/stanols inhibit cholesterol absorption in the gastrointestinal tract. The daily consumption of 2 g/day of plant sterols/stanols decreases low-density lipoprotein cholesterol (LDL-C) levels by approximately 10%. Plant sterols/stanols also reduce LDL-C levels when co-administered with statins, a fact useful for patients intolerable to high-dose statins. However, no randomized, controlled clinical trials have examined the clinical benefit of daily consumption of plant sterols/stanols. Furthermore, concerns regarding a possible atherogenic effect of plant sterols have been expressed. The use of plant sterols/stanols-enriched foods is a useful adjunct for hypercholesterolemic patients to achieve their LDL-C target, but we need more data to establish if this hypolipidemic effect results to reduced cardiovascular risk

Life-threatening hypophosphataemia in a cirrhotic patient with jaundice

We report the case of a 51-year-old patient with a history of liver cirrhosis, who presented with jaundice (total bilirubin 50 mg/dl [855 µmol/l], direct bilirubin 20 mg/dl [342 µmol/l]) and life-threatening hypophosphataemia (serum phosphate 0.5 mg/dl [0.16 mmol/l]), accompanied by inappropriate phosphaturia. The patient also manifested hypouricaemia (serum uric acid 1.7 mg/dl [101 µmol/l]) with renal uric acid wasting and renal glycosuria. This generalized proximal tubular defect may occasionally be seen in deeply jaundiced patients. Therefore, serum phosphate levels should be closely monitored in these patients

Dyslipidemia Associated with Chronic Kidney Disease

Cardiovascular disease is a major cause of morbidity and mortality in patients with impaired renal function. Dyslipidemia has been established as a well-known traditional risk factor for cardiovascular disease (CVD) in the general population and it is well known that patients with chronic kidney disease (CKD) exhibit significant alterations in lipoprotein metabolism. In this review, the pathogenesis and treatment of CKD-induced dyslipidemia are discussed. Studies on lipid abnormalities in predialysis, hemodialysis and peritoneal dialysis patients are analyzed. In addition, the results of the studies that tested the effects of the hypolipidemic drugs on cardiovascular morbidity and mortality in patients with CKD are reported

Add-on-Statin Extended Release Nicotinic Acid/Laropiprant but Not the Switch to High-Dose Rosuvastatin Lowers Blood Pressure: An Open-Label Randomized Study

Introduction. Nicotinic acid (NA) and statins have been associated with reductions in blood pressure (BP). Patients and Methods. We recruited 68 normotensive and hypertensive dyslipidemic patients who were treated with a conventional statin dose and had not achieved lipid targets. Patients were randomized to switch to high-dose rosuvastatin (40 mg/day) or to add-on current statin treatment with extended release (ER) NA/laropiprant (1000/20 mg/day for the first 4 weeks followed by 2000/40 mg/day for the next 8 weeks) for 3 months. Results. Switching to rosuvastatin 40 mg/day was not associated with significant BP alterations. In contrast, the addition of ER-NA/laropiprant to current statin treatment resulted in a 7% reduction of systolic BP (from 134 ± 12 to 125 ± 10 mmHg, P < .001 versus baseline and P = .01 versus rosuvastatin group) and a 5% reduction of diastolic BP (from 81 ± 9 to 77 ± 6 mmHg, P = .009 versus baseline and P = .01 versus rosuvastatin group). These reductions were significant only in the subgroup of hypertensives and were independent of the hypolipidemic effects of ER-NA/laropiprant. Conclusions. Contrary to the switch to high-dose rosuvastatin, the addition of ER-NA/laropiprant to statin treatment was associated with significant reductions in both systolic and diastolic BP

Management of dyslipidemias with fibrates, alone and in combination with statins: role of delayed-release fenofibric acid

Cardiovascular disease (CVD) represents the leading cause of mortality worldwide. Lifestyle modifications, along with low-density lipoprotein cholesterol (LDL-C) reduction, remain the highest priorities in CVD risk management. Among lipid-lowering agents, statins are most effective in LDL-C reduction and have demonstrated incremental benefits in CVD risk reduction. However, in light of the residual CVD risk, even after LDL-C targets are achieved, there is an unmet clinical need for additional measures. Fibrates are well known for their beneficial effects in triglycerides, high-density lipoprotein cholesterol (HDL-C), and LDL-C subspecies modulation. Fenofibrate is the most commonly used fibric acid derivative, exerts beneficial effects in several lipid and nonlipid parameters, and is considered the most suitable fibrate to combine with a statin. However, in clinical practice this combination raises concerns about safety. ABT-335 (fenofibric acid, Trilipix®) is the newest formulation designed to overcome the drawbacks of older fibrates, particularly in terms of pharmacokinetic properties. It has been extensively evaluated both as monotherapy and in combination with atorvastatin, rosuvastatin, and simvastatin in a large number of patients with mixed dyslipidemia for up to 2 years and appears to be a safe and effective option in the management of dyslipidemia

Native valve endocarditis due to Micrococcus luteus: a case report and review of the literature

<p>Abstract</p> <p>Introduction</p> <p><it>Micrococcus luteus </it>endocarditis is a rare case of infective endocarditis. A total of 17 cases of infective endocarditis due to <it>M luteus </it>have been reported in the literature to date, all involving prosthetic valves. To the best of our knowledge, we describe the first case of native aortic valve <it>M luteus </it>endocarditis in an immunosuppressed patient in this report.</p> <p>Case report</p> <p>A 74-year-old Greek-Cypriot woman was admitted to our Internal Medicine Clinic due to fever and malaise and the diagnosis of aortic valve <it>M luteus </it>endocarditis was made. She was immunosuppressed due to methotrexate and steroid treatment. Our patient was unsuccessfully treated with vancomycin, gentamicin and rifampicin for four weeks. The aortic valve was replaced and she was discharged in good condition.</p> <p>Conclusions</p> <p>Prosthetic infective endocarditis due to <it>M luteus </it>is rare. To the best of our knowledge, we report the first case in the literature involving a native valve.</p

LDL cholesterol estimation in patients with the metabolic syndrome

BACKGROUND: The Friedewald formula (LDL-F) for the estimation of low-density lipoprotein (LDL) cholesterol concentrations is the most often used formula in clinical trials and clinical practice. However, much concern has been raised as to whether this formula is applicable in all patient populations such as the presence of chylomicronaemia and/or hypertriglyceridaemia. The aim of the present study was to evaluate various LDL cholesterol calculation formulas as well as LDL cholesterol levels provided by the Lipoprint LDL System (LDL-L) in patients with the metabolic syndrome (MetSyn). RESULTS: LDL-F showed significant differences from other formulas in the total cohort, as well as in MetSyn individuals. This was not the case in nonMetSyn subjects, where LDL-F did not differ with other formulas, with the exception of one formula (LDL by Planella, LDL-P). The bias between LDL-F and other LDL estimation formulas were significantly higher in MetSyn subjects compared to nonMetSyn individuals, except for LDL-L which produced similar bias with LDL-F in both study groups. CONCLUSION: LDL-F seems to exhibit some limitations as far as the calculation of LDL-C levels in patients with the MetSyn is concerned. LDL-L might be more accurate in MetSyn subjects, but so far its use is limited for the estimation of small, dense LDL (sdLDL) cholesterol levels and mean LDL particle size for research purposes only

Acid-Base and Electrolyte Abnormalities in Patients With Acute Leukemia

Disturbances of acid-base balance and electrolyte abnormalities are commonly seen in patients with acute leukemia. Our study aimed at illuminating the probable pathogenetic mechanisms responsible for these disturbances in patients with acute leukemia admitted to our hospital. We studied 66 patients (24 men and 44 women) aged between 17 and 87 years old on their admission and prior to any therapeutic intervention. Patients with diabetes mellitus, acute or chronic renal failure, hepatic failure, patients receiving drugs that influence acid-base status and electrolyte parameters during the last month, such as corticosteroids, cisplatin, diuretics, antacids, aminoglycosides, amphotericin, penicillin, and K + , PO 4 3− , or Mg 2+ supplements were excluded. Forty-one patients had at least one acid-base or electrolyte disturbance. There were no significant differences in the incidence of acid-base balance and electrolyte abnormalities between patients with acute myeloid leukemia (AML) and patients with acute lymphoblastic leukemia (ALL). The most frequent electrolyte abnormality was hypokalemia, observed in 41 patients (63%), namely in 34 patients with AML, and 7 with ALL; the main underlying pathophysiologic mechanism was inappropriate kaliuresis. Furthermore, hypokalemic patients more frequently experienced concurrent electrolyte disturbances (i.e., hyponatremia, hypocalcemia, hypophosphatemia, and hypomagnesemia), as well as various acid-base abnormalities compared to normokalemic patients. Hypokalemia in patients with acute leukemia may serve as an indicator of multiple concurrent, interrelated electrolyte disturbances, especially in patients with AML. Am

Effect of Plant Polyphenols on Adipokine Secretion from Human SGBS Adipocytes

Introduction. Adipose tissue contributes to atherosclerosis with mechanisms related to adipokine secretion. Polyphenols may exhibit antiatherogenic properties. The aim of the study was to investigate the effects of three polyphenols, namely, quercetin, epigallocatechin gallate (EGCG), and resveratrol on adipokine secretion from cultured human adipocytes. Methods. Human SGBS adipocytes were treated with quercetin, EGCG, and resveratrol for 24 and 48 hours. Visfatin, leptin, and adiponectin were measured in the supernatant. Results. Visfatin secretion was inhibited by quercetin 10 μM by 16% and 24% at 24 and 48 hours respectively. The corresponding changes for quercetin 25 μM were 47% and 48%. Resveratrol 25 μM reduced visfatin by 28% and 38% at 24 and 48 hours. EGCG did not have an effect on visfatin. None of tested polyphenols influenced leptin and adiponectin secretion. Conclusion. Quercetin and resveratrol significantly decreased visfatin secretion from SGBS adipocytes. This effect may contribute to their overall antiatherogenic properties