Orlistat  reduced body weight ( weighted mean difference : −2.12 , p < 0.001 ) , total‐cholesterol ( weighted mean difference : −0.30 mmol/L , p < 0.001 ) , low‐density lipoprotein cholesterol ( weighted mean difference : −0.27 mmol/L , p < 0.001 ) , high‐density lipoprotein cholesterol ( weighted mean difference : −0.034 mmol/L , p < 0.001 ) and triglyceride ( weighted mean difference : −0.09 mmol/L , p < 0.001 ) concentrations , while no effect on lipoprotein(a ) was observed .
Total‐ and low‐density lipoprotein cholesterol‐lowering were associated negatively with duration of orlistat treatment and positively with body weight changes .
In conclusion , Orlistat treatment slightly reduces cholesterol and triglyceride levels , but not lipoprotein(a ) levels .
Total‐ and low‐density lipoprotein cholesterol levels reductions are more consistent in patients with greater body weight reduction and shorter duration of orlistat treatment .
We investigated the efficacy of orlistat on plasma lipids and body weight in a meta‐ analysis of 33 studies including 9732  participants .Orlistat  was associated with a slight but significant decrease in body weight , plasma cholesterol and triglyceride concentrations , whereas plasma Lp(a ) levels were not affected by orlistat treatment .
Greater body weight reduction and lower duration of orlistat treatment promoted more consistent plasma total‐ and LDL‐cholesterol lowering
& NA ; Orlistat , an inhibitor of intestinal lipase , promotes body weight reduction .
The lipid‐lowering efficacy of orlistat is controversial and the effect of orlistat‐induced body weight reduction on lipid changes has not been explored in meta‐regression analyses .
HighlightsOrlistat is an inhibitor of intestinal lipase promoting body weight reduction , but whose lipid‐lowering efficacy is controversial .
Lipoprotein(a) as a cardiovascular risk factor: current status
Aims The aims of the study were , first , to critically evaluate lipoprotein(a ) [ Lp(a ) ] as a cardiovascular risk factor and , second , to advise on screening for elevated plasma Lp(a ) , on desirable levels , and on therapeutic strategies . Methods and results The robust and specific association between elevated Lp(a ) levels and increased cardiovascular disease (CVD)/coronary heart disease ( CHD ) risk , together with recent genetic findings , indicates that elevated Lp(a ) , like elevated LDL-cholesterol , is causally related to premature CVD/CHD . The association is continuous without a threshold or dependence on LDL- or non-HDL-cholesterol levels . Mechanistically , elevated Lp(a ) levels may either induce a prothrombotic/anti-fibrinolytic effect as apolipoprotein(a ) resembles both plasminogen and plasmin but has no fibrinolytic activity , or may accelerate atherosclerosis because , like LDL , the Lp(a ) particle is cholesterol-rich , or both . We advise that Lp(a ) be measured once , using an isoform-insensitive assay , in subjects at intermediate or high CVD/CHD risk with premature CVD , familial hypercholesterolaemia , a family history of premature CVD and /or elevated Lp(a ) , recurrent CVD despite statin treatment , ≥3 % 10-year risk of fatal CVD according to European guidelines , and /or ≥10 % 10-year risk of fatal + non-fatal CHD according to US guidelines . As a secondary priority after LDL-cholesterol reduction , we recommend a desirable level for Lp(a ) < 80th percentile ( less than ∼50 mg/dL ) . Treatment should primarily be niacin 1–3 g/day , as a meta- analysis of r and omized , controlled intervention trials demonstrates reduced CVD  by niacin treatment . In extreme cases , LDL-apheresis is efficacious in removing Lp(a ) . Conclusion We recommend screening for elevated Lp(a ) in those at intermediate or high CVD/CHD risk , a desirable level < 50 mg/dL as a function of global cardiovascular risk , and use of niacin for Lp(a ) and CVD/CHD risk reduction
Orlistat  reduced body weight ( weighted mean difference : −2.12 , p < 0.001 ) , total‐cholesterol ( weighted mean difference : −0.30 mmol/L , p < 0.001 ) , low‐density lipoprotein cholesterol ( weighted mean difference : −0.27 mmol/L , p < 0.001 ) , high‐density lipoprotein cholesterol ( weighted mean difference : −0.034 mmol/L , p < 0.001 ) and triglyceride ( weighted mean difference : −0.09 mmol/L , p < 0.001 ) concentrations , while no effect on lipoprotein(a ) was observed .
Total‐ and low‐density lipoprotein cholesterol‐lowering were associated negatively with duration of orlistat treatment and positively with body weight changes .
In conclusion , Orlistat treatment slightly reduces cholesterol and triglyceride levels , but not lipoprotein(a ) levels .
Total‐ and low‐density lipoprotein cholesterol levels reductions are more consistent in patients with greater body weight reduction and shorter duration of orlistat treatment .
We investigated the efficacy of orlistat on plasma lipids and body weight in a meta‐ analysis of 33 studies including 9732  participants .Orlistat  was associated with a slight but significant decrease in body weight , plasma cholesterol and triglyceride concentrations , whereas plasma Lp(a ) levels were not affected by orlistat treatment .
Greater body weight reduction and lower duration of orlistat treatment promoted more consistent plasma total‐ and LDL‐cholesterol lowering
& NA ; Orlistat , an inhibitor of intestinal lipase , promotes body weight reduction .
The lipid‐lowering efficacy of orlistat is controversial and the effect of orlistat‐induced body weight reduction on lipid changes has not been explored in meta‐regression analyses .
HighlightsOrlistat is an inhibitor of intestinal lipase promoting body weight reduction , but whose lipid‐lowering efficacy is controversial .