Kosmidou 2008.
Methods | 6‐Week dietary lead‐in 12‐Week before‐and‐after study |
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Participants | 97 men and women with hyperlipidaemia with and without HTN; LDL‐C > 160 mg/dL (4.14 mmol/L), TG < 250 mg/dL (2.82 mmol/L) 60 participants received atorvastatin, 37 received no medication Exclusion criteria: renal dysfunction, liver disease, TSH > 5 mU/L, diabetes mellitus, childbearing potential, use of lipid‐altering drugs, antihypertensive therapy Atorvastatin baseline TC: 7.3 mmol/L (282 mg/dL) Atorvastatin baseline LDL‐C: 5.1 mmol/L (197 mg/dL) Atorvastatin baseline HDL‐C: 1.3 mmol/L (50 mg/dL) Atorvastatin baseline TG: 1.9 mmol/L (168 mg/dL) |
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Interventions | Atorvastatin 20 mg/d | |
Outcomes | Per cent change from baseline at 12 weeks of serum TC, LDL‐C, HDL‐C and TG | |
Notes | SDs were imputed | |
Risk of bias | ||
Bias | Authors' judgement | Support for judgement |
Random sequence generation (selection bias) | Unclear risk | Atorvastatin 20 mg/d; intervention was analysed, and as no placebo group was included for comparison, assessment of random sequence generation is not applicable |
Allocation concealment (selection bias) | Unclear risk | Atorvastatin 20 mg/d; intervention was analysed, and as no placebo group was included for comparison, assessment of allocation concealment is not applicable |
Blinding (performance bias and detection bias) All outcomes | Unclear risk | Atorvastatin 20 mg/d; intervention was analysed, and as no placebo group was included for comparison, blinding status is not applicable |
Incomplete outcome data (attrition bias) All outcomes | Low risk | Data on all participants were reported |
Selective reporting (reporting bias) | Low risk | All lipid parameters were measured |
Other bias | Unclear risk | The source of funding was not provided |