Liv.52 DS Tablets
Evaluation of Liv.52 DS tablet as a hepatoprotective agent in prophylaxis with statin therapy
Dr. JKL Das Associate Professor, Department of Medicine, Patna Medical College, Patna, India. Dr. S.R. Prasad*, Medical Advisor, Dr. S.K. Mitra, Executive Director, R&D Center, The Himalaya Drug Company, Bangalore-562 123, India. *Corresponding author: Dr. S.R. Prasad, M.D, Medical Advisor, R&D Center, The Himalaya Drug Company, Bangalore, India. Phone : 91 080-2371 4444 Fax : 91 080-2371 4471 E-mail : dr.prasad@himalayahealthcare.com
ABSTRACT
The present study was planned to evaluate Liv.52 DS tablet as a hepatoprotective agent in prophylaxis with statin therapy. HMG-CoA reductase inhibitors (statins) are the most commonly prescribed classes of medications for dyslipidemia, which is a risk factor for chronic heart disease. Statin can cause liver damage in the form of increasing transaminase levels.
The present study was an open clinical trial, conducted as per the ethical guidelines of Declaration of Helsinki. All patients on antihyperlipidemic therapy with statins were included in the study; patients having evidence of extensive disease that requires hospitalization, and pregnant women were excluded from the study.
A total of 50 patients were enrolled into the trial and all patients completed the study. Patients were divided into two equal groups of 25 each; one group received Liv.52 DS tablet + Atorvastatin tablet, while the second group received Atorvastatin tablet alone. Patients were advised to take Liv.52 DS tablet at a dose of 1 tablet twice a day and Atorvastatin 10 mg, 1 tablet twice a day for a period of three months.
A thorough history, symptomatic evaluation and clinical examination were done for all patients before treatment and during follow-up visits every week till the end of treatment after three months. Liver function tests, hemogram and other biochemical tests were done at the end of 1st, 2nd and 3rd month of treatment. The predefined primary endpoints were clinical and laboratory evidence of normal functioning of liver.
In the Atorvastatin alone group, there was a significant increase (p < 0.01) in the mean values of SGPT from 45.87 ± 4.98 to 102.70 ± 12.05, SGOT from 42.70 ± 4.74 to 98.87 ± 12.35, and total bilirubin from 0.800 ±
0.026 to 1.022 ± 0.077 after 3 months, whereas no such increase in SGPT, SGOT and total bilirubin was observed in the group receiving Liv.52 DS tablet + Atorvastatin, after 3 months.
There were no significant differences between the groups in terms of physical examination and subjective signs after 3 months of treatment. Therefore, it may be concluded that Liv.52 DS tablet has hepatoprotective effect against statininduced liver damage.
INTRODUCTION
Lipids are important biomolecules. Cholesterol, for example, is an essential component of the human cell membrane and a precursor for steroid hormones and bile acids. Triglycerides also play an important role in transferring energy from food into body cells. Elevation of different forms of lipids in the bloodstream, a condition generally termed hyperlipidemia, causes a constant health problem. Because lipids are carried in the bloodstream,
| Dunnett's Multiple Comparison Test | |||||||
|---|---|---|---|---|---|---|---|
| Parameters | Group | 1st month | 2nd month | 3rd month | 1st Month vs 2nd Month | 1st Month vs 3rd Month | Overall Significance |
| SGPT (IU/L) | Liv.52 DS + Atorvastatin | 49.95 ± 12.26 | 52.05 ± 14.54 | 62.50 ± 12.01 | NS | NS | p=0.4547; F=0.8030; R2=0.03683; NS |
| Atorvastatin alone | 45.87 ± 4.98 | 76.09 ± 8.66 | 102.70 ± 12.05 | p<0.01 | p<0.01 | p<0.0001; F=35.17; R2=8.654; S | |
| SGOT (IU/L) | Liv.52 DS + Atorvastatin | 42.77 ± 7.90 | 45.77 ± 7.21 | 50.50 ± 8.55 | NS | NS | p=0.4884; F=0.7289; R2=0.03355; NS |
| Atorvastatin alone | 42.70 ± 4.74 | 70.35 ± 8.15 | 98.87 ± 12.35 | p<0.01 | p<0.01 | p<0.0001; F=35.64; R2=0.6183; S | |
| Total bilirubin (g/dl) | Liv.52 DS + Atorvastatin | 1.073 ± 0.205 | 1.036 ± 0.161 | 0.959 ± 0.081 | NS | NS | p=0.5800; F=0.5519; R2=0.02561; NS |
| Atorvastatin alone | 0.800 ± 0.026 | 0.870 ± 0.029 | 1.022 ± 0.077 | NS | p<0.01 | p<0.0009; F=8.194; R2=0.2714; S | |
hyperlipidemia is always a threat to coronary arteries and the most important risk factor for coronary heart disease (CHD).
However, to fight these problems, human wit has acquired several drugs, commonly known as lipid-lowering drugs. One group of drugs (statins) lowers cholesterol by interfering with the cholesterol biosynthetic pathway.1,2
3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase is the key rate-limiting enzyme of cholesterol biosynthetic pathway. Statins are structural analogues of HMG-CoA and thereby inhibit HMG-CoA reductase competitively with an affinity about 1000-10,000 times greater than that of the natural substrate. In addition to direct inhibition of cholesterol synthesis, statins have also been shown to lower plasma cholesterol levels indirectly due to up-regulation of the low-density lipoprotein (LDL) receptor.3
There are currently seven statins available in pharmaceutical form lovastatin, simvastatin, pravastatin, fluvastatin, atorvastatin, rosuvastatin, and pitavastatin.4,5 Statins have become the mainstay of therapy for controlling lipid disorders. The future promises more patients to be taking these medications as goals for cholesterol therapy are dropped and new indications for statin therapy are introduced. While serious adverse events are rare with statin therapy, less serious side effects and minor laboratory abnormalities are relatively common.
Based on data from clinical trials and from review of primary care medical records, elevations in transaminases on liver function tests (LFTs) to clinically significant levels (usually defined as three times the upper limit of normal) are seen in about 0.5% to 2% of patients taking statins, and this abnormality is dose dependent.6-8 The majority of liver abnormalities, if they are to occur, appear within the first 3 months of therapy.9 Therefore, the challenge is to maintain cholesterol or lipid homeostasis in lipid-independent disorders after the use of lipid-lowering drugs in order to minimize side effects.
Liv.52 DS tablet is a polyherbal formulation that consists of powders of Capparis spinosa, Cichorium intybus, Solanum nigrum, Cassia occidentalis, Terminalia arjuna, Achillea millefolium, Tamarix gallica, and Mandura bhasma. It is a hepatotonic and has been used traditionally in the treatment of various liver disorders. This study was planned to evaluate Liv.52 DS tablet as a hepatoprotective agent in prophylaxis with statins.
Refference: http://www.himalayahealthcare.com/pdf_files/liv263.pdf
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