ReviewDrugs1996
Fluvastatin: a review of its pharmacology and use in the management of hypercholesterolaemia.
Review in Drugs, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 121 citations in OpenAlex.
- Lipid-lowering response of the HMG-CoA reductase inhibitor fluvastatin is influenced by polymorphisms in the low-density lipoprotein receptor gene in Brazilian patients with primary hypercholesterolemia.Journal of clinical laboratory analysis · 2000Trial
- Site-Selective Benzylic Dehydrogenation of Alkylindoles.JACS Au · 2025Article
- Indole-containing pharmaceuticals: targets, pharmacological activities, and SAR studies.RSC medicinal chemistry · 2024Review
- Diversity of Solid Forms Promoted by Ball Milling: Characterization and Intrinsic Dissolution Studies of Pioglitazone Hydrochloride and Fluvastatin Sodium Drug-Drug Systems.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Progress of Statin Therapy in the Treatment of Idiopathic Pulmonary Fibrosis.Oxidative medicine and cellular longevity · 2022Review
- Effects of Fluvastatin on the Pharmacokinetics of Repaglinide: Possible Role of CYP3A4 and P-glycoprotein Inhibition by Fluvastatin.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2013Article
- Targeting tumor cell metabolism with statins.Oncogene · 2012Review
- Overexpression of RhoA enhances peritoneal dissemination: RhoA suppression with Lovastatin may be useful for ovarian cancer.Cancer science · 2008Article
- Hmgcr in the corpus allatum controls sexual dimorphism of locomotor activity and body size via the insulin pathway in Drosophila.PloS one · 2007Article
- HMG-CoA reductase inhibitors and the malignant cell: the statin family of drugs as triggers of tumor-specific apoptosis.Leukemia · 2002Review
- Pharmacokinetic-pharmacodynamic drug interactions with HMG-CoA reductase inhibitors.Clinical pharmacokinetics · 2002Review
- How well tolerated are lipid-lowering drugs?Drugs & aging · 2001Review
- Clinical pharmacokinetics of fluvastatin.Clinical pharmacokinetics · 2001Review
- Clinical pharmacokinetics of pravastatin: mechanisms of pharmacokinetic events.Clinical pharmacokinetics · 2000Review
- Effects of liver disease on pharmacokinetics. An update.Clinical pharmacokinetics · 1999Review
- Review
- Impact of dyslipidaemia. Lessons from clinical trials.PharmacoEconomics · 1998Review
- Clinical positioning of HMG-CoA reductase inhibitors in lipid management protocols.PharmacoEconomics · 1998Review
- Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Similarities and differences.Clinical pharmacokinetics · 1997Review
- Atorvastatin. A review of its pharmacology and therapeutic potential in the management of hyperlipidaemias.Drugs · 1997Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fluvastatin, a member of the group of drugs known as HMG-CoA reductase inhibitors, is used in the treatment of patients with hypercholesterolaemia. In clinical trials in patients with primary hypercholesterolaemia, fluvastatin 20 or 40 mg/day achieved marked reductions from baseline in serum levels of low density lipoprotein (LDL)-cholesterol (19 to 31%) and total cholesterol (15 to 21%), along with modest declines in serum triglyceride levels (1 to 12%) and small increases in high density lipoprotein (HDL)-cholesterol levels (2 to 10%). These beneficial effects on the serum lipid profile were similar to those demonstrated with other HMG-CoA reductase inhibitors, although direct comparative trials are limited. Concomitant administration of fluvastatin plus another lipid-lowering agent, such as a bile acid sequestrant, a fibrate or nicotinic acid, usually reduced serum levels of total cholesterol and LDL-cholesterol by at least a further 5 to 10% from baseline compared with fluvastatin monotherapy. Fluvastatin has a similar tolerability profile to that of other HMG-CoA reductase inhibitors. Gastrointestinal disturbances, which are usually mild and transient, were the most frequently reported adverse events with fluvastatin in clinical trials. Persistent elevation of serum transaminase levels occurred in approximately 1% of fluvastatin recipients, which is similar to the rate for other HMG-CoA reductase inhibitors. Unlike other HMG-CoA reductase inhibitors, which have been infrequently associated with myopathy and rarely with rhabdomyolysis, these events have not been associated with fluvastatin to date, although fluvastatin has not been used as extensively as agents such as lovastatin. HMG-CoA reductase inhibitors other than fluvastatin, when given in combination with drugs such as fibrates, nicotinic acid, cyclosporin or erythromycin, can increase the risk of these potentially serious adverse events. Thus far, myopathy or rhabdomyolysis have not been reported among patients receiving fluvastatin concomitantly with any of these drugs. Therefore, fluvastatin can be given with caution in combination with fibrates, nicotinic acid, cyclosporin or erythromycin. In conclusion, fluvastatin has similar efficacy and tolerability profiles to other HMG-CoA reductase inhibitors, which are among the most effective agents available for treating patients with hypercholesterolaemia. Pharmacoeconomic studies performed to date suggest an advantage for fluvastatin over other HMG-CoA reductase inhibitors, predominantly because of its relatively low acquisition costs (at least in those countries in which the evaluations were conducted). Thus, fluvastatin is effective and well tolerated in patients with hypercholesterolaemia and appears to have an economic advantage over other HMG-CoA reductase inhibitors, primarily as a result of its relatively low acquisition costs.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.