[Rehabilitation of the population living in poor environmental areas in the Sverdlovsk Region].

Medical rehabilitation of the population living in poor environmental areas has been realized since 1999 and is the basis for environmental safety policy in the Sverdlovsk Region, along with the prevention and reduction of environmental pollution, the rational use, conservation, and replenishment of natural complexes. Medical rehabilitation activities for the population's health are aimed at managing the risks associated with human environmental factors, managing address medical prophylactic services, individual behavioral factors, habits, and awareness of the population. Interaction of the participants of the medical rehabilitation system provides for tackling the set health promotion tasks in the Sverdlovsk Region.

Ezetimibe-induced hyperlipidaemia.

Ezetimibe is intestinally active cholesterol absorption inhibitor used to reduce low-density lipoprotein-cholesterol levels. This case report describes a novel side effect with this agent: ezetimibe-induced hyperlipidaemia in a patient with statin intolerance and familial combined hyperlipidaemia. Ezetimibe therapy induced an asymptomatic 770% increase in triglycerides (TGs) (3.51-27.1 mmol/l) and a 190% increase in total cholesterol (9.8-18.5 mmol/ 1) secondary to an increase (4.6-25.9 micromol/l; 560%) in hepatic cholesterol (lathosterol) synthesis. This lipid profile resolved 9 months after cessation of ezetimibe therapy. This report shows that ezetimibe may have long-lasting effects in man far exceeding its plasma half-life and that ezetimibe monotherapy can induce a large increase in hepatocyte very-low-density lipoprotein synthesis in rare individuals with a consequent mixed hyperlipidaemia or possibly hypercholesterolaemia depending on the metabolism and clearance of TG-rich lipoproteins.

The response of serum apolipoprotein H to an oral fat load.

BACKGROUND: We tested the hypothesis that serum apolipoprotein H (apo H) concentration increases after an oral fat load. Such a study would give valuable insight into whether apo H was influenced by the postprandial state. METHODS: Ten male subjects aged 24-48 years were fed 62.5 g of total fat (saturates 12 g, monounsaturates 35.3 g, polyunsaturates 12.5 g). Venous blood was sampled hourly for 5 h post-oral fat load. RESULTS: No significant change in serum apo H concentration occurred following the oral fat load. However, serum apo H in the baseline samples correlated significantly with subject body mass index (r = 0.683, P < 0.05), body fat mass (r = 0.778, P < 0.01), lean body mass (r = 0.693, P < 0.05), serum triglyceride (r = 0.732, P < 0.02), serum insulin (r = 0.808, P < 0.01) and insulin resistance index (r = 0.794, P < 0.01). In stepwise multiple linear regression model, with serum apo A1, apo B, lipoprotein(a), total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol, plasma glucose and insulin and apo H as the dependent variable, insulin remained in the model (r = 0.81, P < 0.01). Conversely, with body mass index, body fat mass, lean body mass and waist/hip ratio in the model and apo H as dependent variable, only body fat mass remained in the model (r = 0.78, P < 0.01). CONCLUSIONS: Serum apo H may be involved in insulin resistance and relates to various indices of adipose tissue, including body fat mass. However, serum apo H concentrations do not significantly change postprandially.

Effect of moxonidine on lipid subfractions in patients with hypertension.

Moxonidine is centrally acting imidazoline type-1 receptor agonist that significantly lowers blood pressure and has some insulin-sensitising actions. Its effects on plasma lipid profiles are uncertain. This study examined the effects of moxonidine on detailed lipid and lipoprotein profiles in 12 patients with hypertension and type 2b Fredricksen hyperlipidaemia. Treatment with moxonidine in six patients who completed the study resulted in a 10/5 mmHg reduction in 24-h ambulatory blood pressure (p = 0.01). A significant reduction in total and low-density-lipoprotein cholesterol (LDL-C) of 10% (p = 0.04) and 18% (p = 0.03), respectively, was seen. Triglycerides were reduced non-significantly by 23%, and high-density-lipoprotein cholesterol (HDL-C) was increased by 16%. There were no significant changes in apolipoprotein (apo) A-1 and B concentrations. No significant shifts were seen in HDL-C, LDL-C, very-low-density-lipoprotein cholesterol (VLDL-C) or apolipoprotein peak positions with therapy. Analysis of area under curve for each subfraction showed that moxonidine therapy resulted in a redistribution within the apoB profile. A slight non-significant reduction in VLDL apoB was seen. There was a reduction in the dense LDL apoB peak (p = 0.02) but less in the buoyant LDL apoB peak (p = 0.17) with a countervailing increase in LDL-C in the buoyant fraction (p = 0.01). The HDL-C and apoA-1 profile showed a shift from dense HDL apoA-1 (p = 0.01) to a buoyant HDL apoA-1sub-species (p = 0.01). These changes are consistent with a tendency for moxonidine to improve atherogenic lipid and lipoprotein profiles by actions on insulin-sensitisation and possibly through a direct cholesterol-reducing effect as seen with other imidazoles.

The response of serum sialic acid and other acute phase reactants to an oral fat load in healthy humans.

BACKGROUND: Elevated serum total sialic acid (TSA) has been shown to be associated with increased cardiovascular mortality. It has been postulated that atherogenesis is a postprandial phenomenon. We tested the hypothesis that serum TSA and other acute phase proteins, namely C-reactive protein (CRP) and fibrinogen, may be related to the postprandial state. METHODS: Ten healthy male subjects, aged 24-48 years, were fed 62.5 g of total fat (saturates 12 g, monounsaturates 35.3 g and polyunsaturates 12.5 g) in the form of strawberry flavoured Calogen. Venous blood was sampled hourly for 5 h. Concentrations of serum triglyceride, TSA and acute phase proteins were measured. RESULTS: Serum triglyceride concentration increased postprandially, peaking at 240 min. Serum CRP and plasma fibrinogen did not significantly increase after the oral fat load. However, serum TSA did increase from baseline (0.599+/-0.051 g/l) in response to the oral fat load, peaking at 120 min post-oral fat load (0.633+/-0.066 g/l, P<0.02). There was a significant correlation between serum TSA and plasma fibrinogen at baseline (rho=0.62, P=0.05) but not for serum CRP (rho=-0.22) or triglyceride (rho=0.21). CONCLUSIONS: We conclude that serum TSA increases postprandially and this finding gives further insight as to why the former is considered to be a cardiovascular risk factor.

Fibrinogen response with simvastatin versus atorvastatin in familial hypercholesterolemia.

The clinical and biochemical determinants of the fibrinogen response to simvastatin or atorvastatin therapy were assessed in 130 patients with severe polygenic or familial hypercholesterolemia treated in a randomized open-trial format design. Hyperfibrinogenemia was associated with atorvastatin, baseline fibrinogen, and initial concentration and change in concentration of apolipoprotein B or low-density lipoprotein cholesterol.

Comparison of therapy with simvastatin 80 mg and 120 mg in patients with familial hypercholesterolaemia.

High-dose preparations of simvastatin and atorvastatin have recently become available to treat resistant hypercholesterolaemia aggressively, but few studies have compared these two agents. This study compared the efficacy of simvastatin 80 mg and 120 mg in 22 patients with severe familial hypercholesterolaemia over a three-month period using an open label format. Simvastatin 120 mg was reasonably well tolerated and delivered a further 8% reduction in LDL over 80 mg, giving a total reduction of 55 +/- 13%, while further decreasing triglycerides (18%) and continuing to raise HDL (13%) further than the 80 mg dose. However, transient adverse changes were noted in both lipoprotein (a) and fibrinogen and 20% of patients were unable to tolerate the higher dose. One late case of rhabdomyolysis was observed, suggesting patients on the 120 mg dose require continued regular review.

High-density lipoprotein cholesterol and triglyceride response with simvastatin versus atorvastatin in familial hypercholesterolemia.

The clinical and biochemical determinants of high-density lipoprotein (HDL) and triglyceride response to simvastatin and atorvastatin were assessed in 150 patients with severe hyperlipidemia treated in a randomized open-trial format design. Triglyceride reduction was only dependent on HDL:apolipoprotein A1, change in apolipoprotein B, and dose response, whereas an increase in HDL was dependent on initial LDL, change in LDL or dose response, and therapy with simvastatin.

Atorvastatin compared with simvastatin-based therapies in the management of severe familial hyperlipidaemias.

We compared atorvastatin with simvastatin-based therapies in a prospective observational study of 201 patients with severe hyperlipidaemia. Atorvastatin 10 mg therapy was substituted for simvastatin 20 mg, 20 mg for 40 mg, 40 mg for simvastatin 40 mg plus resin, and 80 mg for simvastatin-fibrate-resin therapy. Lipid and safety profiles were assessed. Atorvastatin reduced total cholesterol by 31 +/- 11-40 +/- 14% vs. 25 +/- 12-31 +/- 11%; LDL by 38 +/- 16-45 +/- 18% vs. 31 +/- 18-39 +/- 18% and geometric mean triglycerides by 29.3-37.3% vs. 16.6-24.8%, but reduced HDL 11% +/- 47% at 80 mg compared with a 16% +/- 34% increase with simvastatin-based therapy. Target LDL < 3.5 mmol/l was achieved more often with atorvastatin (63% vs. 50%; p < 0.001). Atorvastatin increased geometric mean fibrinogen by 12-20% vs. a 0-6% fall with simvastatin (p << 0.001). Side effects were noted in 10-36% of patients, including one case of rhabdomyolysis, and 36% discontinued therapy. These data suggest that atorvastatin is more effective than current simvastatin-based therapies in achieving treatment targets in patients with familial hypercholesterolaemia but at the expense of a possible increase in side-effects. This issue needs further study in randomized controlled trials.

Comparison of therapy with simvastatin 80 mg and atorvastatin 80 mg in patients with familial hypercholesterolaemia.

This study compared the efficacy of simvastatin 80 mg and atorvastatin 80 mg in the treatment of 26 patients with familial hypercholesterolaemia over 12 weeks using an open crossover trial format. Both, similarly, reduced LDL by 47 +/- 13% and 43 +/- 16% and median triglycerides by 22% and 27% respectively. However, atorvastatin reduced HDL by 2 +/- 24% compared with 8 +/- 30% increase with simvastatin (p = 0.05) affecting the LDL:HDL ratio achieved (4.478 +/- 1.56 vs 3.74 +/- 0.93, p = 0.001). Atorvastatin raised median fibrinogen by 15% compared with a non-significant 5% increase with simvastatin (p = 0.05). Simvastatin reduced lipoprotein (a) by a median 20% compared with baseline (p = 0.05) compared with 5% for atorvastatin. Side-effects, mostly gastrointestinal, were seen in four patients (16%) with atorvastatin compared with one case of myalgia with simvastatin (4%). We conclude both drugs are equally effective in LDL reduction but that simvastatin is superior in raising HDL and causes fewer side-effects. These results require confirmation in larger studies.

Normal values for plasma creatinine concentration related to maturity in normal term and preterm infants.

Creatinine concentration was measured by a kinetic method in 475 plasma samples obtained from 260 term and preterm infants during the first 2 months post-natal age. In term infants plasma creatinine fell from 88 +/- 4.4 mumol/L (mean + SEM) at birth, to 60 +/- 1.9 mumol/L by the fourth day remaining stable thereafter; in preterm infants creatinine fell to 86 +/- 7 mumol/L by the fourth day. Analysis of pooled data from all infants of more than 4 days post natal age revealed a progressive fall in creatinine with increasing post conceptual age. The normal range of values varies with post conceptual age and was not influenced by gestational age at the time of birth.