Elaine C. Payumo, M.D., F.P.C.P., F.P.C.C.

Danilo S. Santos, M.D., F.P.C.P., F.P.C.C.

Danilo S. Kuizon, M.D., F.P.C.P., F.P.C.C., F.A.C.C.
ABSTRACT
Background: Hypertriglyceridemia is a common form of
dyslipidemia that is usually correlated with cardiovascular dis-
eases including the occurrence of an acute coronary syndrome or
the need for a coronary intervention. Of all anti-lipidemic drugs,
fenofibrates exert the highest lowering of triglycerides by as
much as 40% to 50%. Likewise fibrates lower serum cholesterol as
much as 20% to 25%, increase by HDL 10-20% and decrease LDL by
5-25%. Fenogal is one such fibrate, that is uniquely formulated
in lidose technology, which combines the advantages of a capsule
and a liquid. At 37oC in-vivo, a very fine emulsion is formed coat-
ing the gastric mucosa thereby enhancing bioavalability of active
ingredients and reducing risks of gastrointestinal side effects.
In addition a good mass and drug content uniformity is formed.
Lidose protects the active ingredient against oxidation.
General Objective:
To determine the efficacy and safety of fenofibrates particularly
Fenogal (lidose technology) in dyslipidemic patients.
Specific Objective: (1.) To determine the efficacy of Fenogal
in decreasing triglycerides, total cholesterol, and LDL; while in-
creasing HDL. (2.) To determine the safety of the lidose tech-
nology using clinical parameters, biochemical profile, and side
effects
Methodology: This was an open labeled study of Fenogal
160 mg once daily involving adult out-patients of cardiologists
and internist in all over the Philippines who have hypertriglyceri-
demia, hypercholesterolemia, or both from August 2007 to May
2009. Previous medications for dyslipidemia of patients were
discontinued. Demographic data of patients were based upon
OPD charts. Assessment of lipid parameters (total cholesterol,
triglycerides, LDL, and HDL) were taken at baseline, week 4, and
week twelve. Blood pressure, heart rate, and biological markers
(SGOT, SGPT, alkaline phosphatase, and FBS) were also measured
at same interval.
Statistical Analysis: Continuous data such as age, weight,
and height were described using mean and SD. Categorical data
were presented in frequency and percent distribution. To deter-
mine the significance of change in the different outcome vari-
ables, paired t-test was applied to the data. A p-value ≤ 0.05 was
considered significant.
Results: There were 3,000 patients included in this open
1
label study with a mean age of 52 ± 11.60 years, and almost
equal number of males (50.6%) and females (49.0%). However,
there were 10 patients with gender not indicated. More than
half (50.2%) of the patients had both hypercholesterolemia and
hypertriglyceridemia. Fenogal significantly decreased total cho-
lesterol by 9.91% after 4 weeks of treatment and by 16.37% af-
ter 12 weeks (p=0.000). LDL likewise significantly decreased by
8.15% after 4 weeks of treatment and by 15.91% after 12 weeks
(p=0.000). HDL significantly increased by 15.64% after 4 weeks
and by 23.51% after 12 weeks (p=0.000). Trigylcerides decreased
significantly by 20.72% after 4 weeks and by 33.15% after 12
weeks (p=0.000). FBS decreased significantly by 10.12 mg/dl at
4 weeks of treatment (p=0.000) and by 13.34 mg/dl at 12 weeks
of treatment (p=0.000).
The systolic blood pressure decreased significantly by a mean
of 10-14 mmHg as well as the diastolic blood pressure by a mean
of 6-8 mmHg (p=0.000). There was a significant decrease in heart
rate by a mean of 1.3-1.8 bpm (p=0.000)
There was no significant change in the SGOT (p=0.30 at 4
weeks and p=0.326 at 12 weeks) and SGPT (p=0.817 at 4 weeks
and p=0.945 at 12 weeks).
The adverse event rate was 1.1% and was mostly gastrointes-
tinal related. Bloatedness was the most common complaint.
Conclusion: The authors conclude that Fenogal (lidose tech-
nology) is effective in improving the lipid profile of dyslipidemic
patients, and can be safely and effectively used among Filipino
patients. Increase in alkaline phosphatase needs further inves-
tigation. The improvement in blood pressure, FBS, and heart
rate may reflect the patient’s overall change in lifestyle brought
about by the physician’s recommendation for such a change.
Introduction:
Cardiovascular diseases are the main causes of mortality
and morbidity in the industrialized countries. The presence of
atherosclerosis is associated with 50% of myocardial infarctions,
and 70% of deaths due are to cardiovascular diseases. Major epi-
demiological studies showed that the modification of the plasma
lipoproteins profile has major beneficial effects on mortality and
morbidity related to cardiovascular diseases.1,2
It is therefore imperative to focus on risk factors modifica-
tion. Included among the most important modifiable risk factors
are dyslipidemia, diabetes mellitus, obesity, and hypertension.
In all of these risk factors, an important characteristic abnormal
level of plasma lipids is seen.
Various anti-lipidemic drugs are available. Among these,
statins are considered the first line of treatment for cholesterol
control. Side effects of statins are very well known.3 Hypertrig-
lyceridemia is a common form of dyslipidemia that is usually cor-
related with cardiovascular diseases, which is generally defined
by the occurrence of an acute coronary syndrome or the need for
a coronary intervention.
Fenofibrates can lower both triglycerides by 40% to 50%, and
serum cholesterol as much as 20% to 25%. Cholesterol reduction
is obtained by lowering low density atherogenic factors such as
VLDL and LDL. It is a known fact that the directly proportional
relationship between hypercholesterolemia and atherosclerosis
existed and has been well established. However, low level of HDL
is also associated with an increased coronary risk. Considering all
other factors, increased triglyceride level is also associated with
increased vascular risk.4,5,6
Fenogal in lidose technology combines the advantages of a
capsule and a liquid. When in contact with a physiological me-
dium at a temperature of 37oC, it forms a very fine emulsion
that coats the gastric mucosa (one dose produces approximately
50 micro micelles droplets). Lidose enhances bioavailability of
active ingredients and it reduces risks of gastrointestinal side
effects.
With its IUPAC name of: propan-2-yl 2-[4-(4-chlorobenzoyl)
phenoxy]-2-methylpropanoate.
It is a hard capsule with a semi-solid content in which fenofi-
brate 160mg is homogeneously dispersed within a mixture of lipid
excipients. A hydroxypropylcellulose type of polymer is present
to prevent any formation of fenofibrate crystal when exposed to
2
gastrointestinal fluids, and it is continuously released by a diffu-
sion-erosion process. This technology has enhanced bioavailabil-
ity as compared to the standard formulation.
Other advantages of lidose technology are: (1) a good mass
and drug content uniformity, the volumetric filling of a liquid is
not influenced by density of the product; (2) lidose protects the
active ingredient against oxidation; and (3) capability to use hard
gelatin capsules for: liquid substances, low dosing substances so
as to obtain a uniform blend of sensitive substances, and slightly
soluble drugs to obtain dispersion.
OBJECTIVES:
General Objective:
To determine the efficacy and safety of fenofibrates particularly
Fenogal (lidose technology) in dyslipidemic patients
Specific Objective:
1. To determine the efficacy of Fenogal in decreasing triglycer-
ides, total cholesterol, and LDL; and increasing HDL
2. To determine the safety of the lidose technology using clini-
cal parameters, biochemical profile and side effects
Significance of the Study:
Fenofibrates are mainly indicated in the treatment of hy-
pertriglyceridemia when diet and lifestyle changes are not suf-
ficient. Fibrates are known to lower total cholesterol, LDL, while
increasing HDL when statins are not tolerated.1
Mixed dyslipidemia is a common lipid disorder described
by the presence of an atherogenic lipoprotein phenotype due to
abnormalities in various atherogenic and anti-atherogenic lipo-
proteins. Fenofibrates are particularly useful in high residual risk
seen in statin trials which may be due to lipoprotein abnormali-
ties other than LDL. It exerts favorable effects on the atherogen-
ic lipid profile of mixed dyslipidemia and can effectively reduce
cardiovascular disease in patients with mixed dyslipidemia.1
The addition of fenofibrate to statins seems to be beneficial
in patients with acute coronary syndrome. According to Shah et.
al., statins decreased plasma fibrinogen significantly and the ad-
dition of fenofibrate further enhanced this reduction of the novel
risk factor fibrinogen.3
Methodology:

This was an open labeled study of Fenogal 160mg once scribed using mean and standard deviation. Categorical data

daily involving adult out-patients of cardiologists and internist were presented in frequency and percent distribution. To de-

all over the Philippines who have hypertriglyceridemia, hyper- termine the significance of change in the different outcome

cholesterolemia, or both, from August 2007 to May 2009. Pre- variables, paired t-test was applied to the data. A p-value ≤

vious medications for dyslipidemia (statins, fenofibrates, gemfi- 0.05 was considered significant.

brozil, ezetemibe) were discontinued prior to administration of Results:

Fenogal. Demographic data of patients were based upon OPD There were 3,000 patients included in this open labeled

charts. Assessment of lipid parameters (total cholesterol, trig- study with a mean age of 52 ± 11.60 years. There were almost

lycerides, LDL, and HDL) and were taken at baseline, week 4, equal number of males (50.6%) and females (49.0%). However,

and week twelve. Blood pressure, heart rate, and biological there were 10 patients with gender not indicated. More than

markers (SGOT, SGPT, alkaline phosphatase, and FBS) were also half (50.2%) of the patients were with both hypercholester-

measured at same interval. olemia and hypertriglyceridemia. Only 12.3% were with hyper-

Statistical Analysis: cholesterolemia, 33.4% with hypertriglyceridemia, and majority

Continuous data such as age, weight, and height were de- at 50.2% were with both, as shown in Table 1.

Table 1 Baseline Characteristics of Patients Included in the Study

CHARACTERISTICS Mean SD
Age (Years) 52 11.60
Weight (lbs.) 150.67 25.08
Height (cms.) 161.43 8.42
No. %
Gender:
Male 1519 50.6
Female 1471 49.0
Not Indicated 10 0.3
Total 3000 100
Type of Dyslipidemia:
Hypercholesterolemia 370 12.3
Hypertriglyceridemia 1002 33.4
Both 1506 50.2
Not Indicated 122 4.1
Total 3000 100

The most common medicines taken by patients before
entering the study were simvastatin, 19.60% followed by
atorvastatin, 3.47% and Lipanthyl, 2.07%. There were 3 pa-
tients (0.10%) who were already on Fenogal before the study
started, see Appendix A.
The total cholesterol decreased significantly as early as
week 4 of therapy with actual change of 28.12 mg/dl and per-
cent change from baseline of 9.91%. At week 12, the actual
mean decrease was 44.01 mg/dl with percent change from
baseline of 16.37%.
LDL likewise significantly decreased from baseline to
week 4 and week 12. The actual mean decrease at week 4
was 17.41 mg/dl with percent change of 8.15% while at week
12 the mean decrease was 29.86 mg/dl with percent change
of 15.91%.
HDL on the other hand increased significantly after 4
weeks and 12 weeks of treatment. The actual mean increase
was 4.27 mg/dl and percent increase from baseline of 15.64%.
At week 12, the actual increase was 6.80 mg/dl with percent
change from baseline of 23.51%.

3
 Triglycerides decreased significantly with actual mean of 60.30 mg/dl from baseline up to week 4 of therapy.
The percent decrease was 20.72%. At week 12, there was 90.61 mg/dl actual decrease and 33.15% change from
baseline. Table 2 shows the details of the effect of the treatment on lipid profile of the patients.

Table 2 Assessment of Lipid Profile of Patients by Observation Periods

Observation Period Lipid Profile
Mean SD
Total Cholesterol
Baseline (n=2489) 232.45 64.12
Week 4 204.33 48.18
Difference:
Actual 28.12 51.19
Percent from baseline 9.91 19.67
p-value 0.000*
Baseline (n=2909 229.84 62.00
Week 12 185.83 41.75
Difference:
Actual 44.01 56.33
Percent from baseline 16.31 20.88
p-value 0.000*
LDL
Baseline (n=2239) 140.47 51.11
Week 4 123.06 39.82
Difference:
Actual 17.41 34.32
Percent from baseline 8.15 26.39
p-value 0.000*
Baseline (n=2599) 139.01 51.91
Week 12 109.15 36.82
Difference:
Actual 29.86 45.19
Percent from baseline 15.91 31.76
p-value 0.000*
HDL
Baseline (n=2217) 49.88 27.97
Week 4 54.16 26.81
Difference:
Actual 4.27 19.26
Percent from baseline 15.64 42.60
p-value 0.000*
Baseline (n=2580) 49.46 26.13
Week 12 56.26 25.32
Difference:
Actual 6.80 22.18
Percent from baseline 23.51 48.38
p-value 0.000*

4


Triglyceride
Baseline (n=2532) 234.98 98.11
Week 4 174.68 64.66
Difference:
Actual 60.30 74.34
Percent from baseline 9.91 31.16
p-value 0.000*
Baseline (n=2944) 235.27 97.84
Week 12 144.66 54.99
Difference:
Actual 90.61 86.68
Percent from baseline 33.15 28.86
p-value 0.000*

A statistically significant favorable lipid lowering response based on NCEP-ATP III goals was
achieved as early as 4 weeks of treatment and was sustained up to 12 weeks of treatment, see
table 3.

Table 3 Assesment of LIPID Response by NCEP-ATPIII Guideline by

Observation Period
Baseline Follow-up
Lipid No. % No. %
p-value
Total Cholesterol
Week 4
≥ 200mg/dl 1806 72.6 1281 51.5 0.000*
< 200mg/dl 683 27.4 1208 48.5
Total 2489 100 2489 100
Week 12
≥ 200mg/dl 2061 70.8 944 32.5 0.000*
< 200mg/dl 848 29.2 1965 67.5
Total 2909 100 2909 100
HDL
Week 4
< 40mg/dl 852 38.4 531 24.0 0.000*
≥ 40mg/dl 1365 61.6 1686 76.0
Total 2217 100 2217 100
Week 12
< 40mg/dl 974 37.8 487 18.9 0.000*
≥ 40mg/dl 848 29.2 1965 81.1
Total 2580 100 2580 100
Triglyceride
Week 4
≥ 150mg/dl 2250 88.9 1706 67.4 0.000*
< 150mg/dl 282 11.1 826 32.6
Total 2532 100 2532 100
Week 12
≥ 150mg/dl 2625 89.2 1298 44.1 0.000*
< 150mg/dl 319 10.8 1646 55.9
Total 2944 100 2944 100
LDL
Week 4
≥ 100mg/dl 1758 78.5 1458 65.1 0.000*
< 100mg/dl 481 21.5 781 34.9
Total 2239 100 2239 100
Week 12
≥ 100mg/dl or ↓ < 30% 2035 78.3 1264 48.6 0.000*
< 100mg/dl or ↓ ≥ 30% 564 21.7 1335 51.4
Total 2599 100 2599 100

5
The systolic and diastolic blood pressures of patients decreased significantly from base-
line to week 4 and week 12 of therapy. Heart rate likewise decreased significantly, as
shown in Table 4.

Table 4 Assessment of Vital Signs of Patients by Observation Period

Observation Period Lipid Profile
Mean SD
Systole
Baseline (n=2624) 140 20.88
Week 4 129 13.51
Difference 10.67 13.66
p-value 0.000*

Baseline (n=2949) 138 20.89

Week 12 124 10.90
Difference 14.76 17.65
p-value 0.000*
Diastole
Baseline (n=2624) 84 11.80
Week 4 82 8.09
Difference 5.65 9.59
p-value 0.000*
Baseline (n=2949) 87 11.71
Week 12 79 7.22
Difference 7.95 11.05
p-value 0.000*

Heart Rate
Baseline (n=2498) 79 9.87
Week 4 78 8.18
Difference 1.53 6.99
p-value 0.000*
Baseline (n=2750) 79 9.57
Week 12 77 8.66
Difference 1.80 8.78
p-value 0.000*

6
 There were no significant changes in SGOT and SGPT of patients. Alkaline phosphatase
however showed significant increase in both 4th and 12th week observation periods.
FBS decreased significantly at week 4 and week 12 follow-up. Table 5 shows the results.

Table 5 Assessment of Laboratory Results by Observation Periods

Observation Period Lipid Profile
Mean SD
SGOT
Baseline (n=1604) 32.05 17.78
Week 4 31.64 14.22
Difference 0.41 15.74
p-value 0.300 ns

Baseline (n=2949) 33.13 18.47

Week 12 32.69 15.33
Difference 0.44 19.33
p-value 0.326 ns
SGPT
Baseline (n=1902) 35.03 19.54
Week 4 34.93 19.26
Difference 0.10 19.12
p-value 0.817 ns
Baseline (n=2239) 35.81 19.66
Week 12 35.85 25.15
Difference 0.04 26.63
p-value 0.945 ns
Alkaline phosphatase
Baseline (n=943) 69.93 35.23
Week 4 73.47 39.59
Difference 3.54 22.37
p-value 0.000*
Baseline (n=1061) 69.68 36.03
Week 12 71.85 38.22
Difference 2.18 27.13
p-value 0.009
Fasting Blood Sugar
Baseline (n=2076) 115.05 43.18
Week 4 104.94 24.92
Difference 10.12 27.89
p-value 0.000*
Baseline (n=2398) 113.62 41.74
Week 12 100.27 21.93
Difference 13.34 34.82
p-value 0.000*

7
There were 34 patients who experience adverse events with 1.1% event rate. Most of
the events were gastrointestinal related. Bloatedness was the most common. There
were also elevated laboratory results noted as shown in Table 6.

Table 6 Adverse Events Experienced by Patients

Adverse Events No. %

Present 34 1.1
Absent 2966 98.9
Total 3000 100
Specific Events
Bloatedness 11 0.37
Chest constriction 1 0.03
Constipation 2 0.07
Dyspepsia 1 0.03
Elevated transaminase 2 0.07
Elevated SGOT 2 0.07
Elevated SGPT 3 0.10
Elevated LDL 1 0.03
Epigastric pain 2 0.07
Epigastric discomfort 1 0.03
Flatulence 5 0.17
Abdominal fullness 1 0.03
Nausea 1 0.03
Gas pains 1 0.03
Muscle pain 2 0.07
Ringing of both ears 1 0.03

The compliance of patients was high, 95.3% as shown in Table 7

Table 7 Adverse Events Experienced by Patients

Compliance No. %
Yes 2860 95.3
No 97 3.2
Not Indicated 43 1.4
Total 3000 100

8
Discussion:
Results of this study revealed that Fenogal (lidose tech-
nology) can significantly decrease triglycerides, LDL, and to-
tal cholesterol, while significantly increasing the HDL. Based
on the ATP III study, fibric acids were able to lower LDL by
5-20%, TG by 20-50%, increase HDL by 10-20%.7,8 Comparing
with the present study, similar changes in the lipid profile was
achieved, namely a decrease in TG by 90.61 mg/dL (33.15%),
an increase in HDL by 6.80 mg/dL (23.51%), and a decrease in
LDL by 29.86 mg/dL (15.91%). In addition we report a total
cholesterol decrease by 44.01 mg/dL (16.37%).
The 3rd Report of the National Cholesterol Education
Program (NCEP) Expert Panel on Detection, Evaluation, and
Treatment of High Blood Cholesterol in Adults (Adult Treat-
ment Panel III) Final Report state that the recommended lev-
els of plasma lipids are as follows: total cholesterol <200mg/
dL, HDL ≥40mg/dl, and triglycerides <150mg/dL. For LDL the
goal is based on the risk level: CHD and CHD risk equivalent
with a target of <100mg/dL, multiple (>2) risk factors with
a target of <130mg/dL and with 0-1 risk factor with a target
of <160mg/dL.7,8 In this study, these targets were achieved
as early as 4 weeks of treatment and was sustained up to
12 weeks of treatment with Fenogal. Total cholesterol de-
creased to a mean of 185.83mg/dL and mean triglyceride
level was 144.66mg/dL. Average LDL of 109.15mg/dL at 12
weeks was close to the recommended value of <100mg/dL as
well as mean HDL of 56.26mg/dL at 12 weeks was greater
than the prescribed value of ≥40mg/dL.
Grundy et. al., reported that when LDL lowering drug
therapy is employed in high-risk or moderately high-risk per-
sons, it is advised that intensity of therapy be sufficient to
achieve at least a 30-40% reduction in LDL-C levels.9 In our
study, a mean LDL level of 109.15mg/dL corresponding to a
15.91% reduction was achieved from baseline up to the 12
weeks of study. The results may not have reached the target
of the NCEP guidelines however the mean LDL was close to
the target level of 100mg/dL. In addition, one reason for
not achieving the goal may be that the subjects may rep-
resent a mixed dyslipidemic population such as in patients
with combined hyperlipidemia wherein only slight changes in
LDL cholesterol are observed with fibrates. Furthermore LDL
levels may rise with fibrate therapy in patients with hyper-
triglyceridemia.8
According to the National Nutrition and Health Survey
(NNHeS) study10 in 2003-2004, the average lipid levels and
9
prevalence of dyslipidemia among adult Filipinos >20 years
old are as follows: total cholesterol 184.4mg/dL (8.5%), LDL
119.4mg/dL (3.7%), HDL 41.1mg/dL (54.2%), and triglycerides
118.0mg/dL (20/6%).10 In the present study, it was noted
a higher mean baseline total cholesterol (232.45mg/dL), LDL
(140.47mg/dL), triglycerides (235.98mg/dL) and a somewhat
similar HDL level (49.88mg/dL). This may mean that the pop-
ulation in this study represents a high risk population while
the NNHes study included the normal average adult Filipino.
The study affirmed the safety of Fenogal in the treat-
ment of dyslipidemic patients as evidenced by no significant
changes in the SGOT and SGPT levels. The adverse event rate
was 1.1% and was mostly gastrointestinal related. Bloated-
ness was the most common complaint. This was consistent
with the NCEP ATP III guidelines which reported that fibrates
are generally well tolerated and the most common adverse
effects were gastrointestinal.7,8
Similarly, in a study done by Keating et.al., micronised
fenofibrate was associated with significantly greater im-
provements from baseline in TC, LDL-C, HDL-C and TG lev-
els than placebo in patients with type 2 diabetes mellitus
and metabolic syndrome as well as with significantly less
progression of coronary atherosclerosis than placebo. It was
generally well tolerated in clinical trials, and indicated that
gastrointestinal disorders are the most frequent adverse
events. Elevations in serum transaminase and creatine phos-
phokinase levels have been reported rarely with micronised
fenofibrate.11, 12
The improvement in the blood pressure, FBS and heart
rate may reflect the patients’ overall change in lifestyle
brought about by the physicians’ recommendation for such a
change. Likewise such improvements may represent an over-
all progress in the cardiovascular status of the patients as a
consequence of the correction of the lipid levels.
A number of trials 13,14,15,16 have been done world-
wide to determine the effectiveness of fibrates in the preven-
tion of cardiovascular disease. These include: Helsinki Heart
Study, Veterans Affairs High Density Lipoprotein Cholesterol
Intervention Trial (VA-HIT), Bezafibrate Infarct Prevention
(BIP) trial, and Fenofibrate Intervention and Event Lowering
in Diabetes (FIELD) trial which focused on patients with dia-
betes and dyslipidemia. However, results have indicated a
general trend that fibrates can reduce cardiovascular events.
Some studies have also suggested that fibrates may have confirm the benefit of cholesterol-lowering therapy in high-
some significant non-cardiac side effects that other drugs do risk patients and support the ATP III treatment goal of LDL-C
not share. Fibrates may also be appropriate for use in pa- <100mg/dL. It supported the inclusion of patients with diabe-
tients at risk of acute pancreatitis due to high triglyceride tes in the high-risk category and confirms the benefits of LDL-
levels. lowering therapy in these patients. It further confirms that
older persons benefit from therapeutic lowering of LDL-C.
Based on the study done by Fiévet et.al.17, statin treat-
One of the major recommendations for modifications is that:
ment substantially reduces cardiovascular morbidity and
in high-risk persons, the recommended LDL-C goal is <100mg/
mortality. Statins lower LDL cholesterol (LDL-C), with limited
dL, but when risk is very high, an LDL-C goal of <70mg/dL is a
effects on other lipid parameters. Fibrates improve athero-
therapeutic option. This therapeutic option extends also to
genic dyslipidemia characterized by high triglyceride and/
patients at very high risk who have a baseline LDL-C <100mg/
or low HDL cholesterol levels and elevated concentrations of
dL. Moreover, when a high-risk patient has high triglycerides
small dense LDL particles, with or without high LDL-C levels.
or low HDL-C, consideration can be given to combining a fi-
Fibrates decrease cardiovascular morbidity, especially in pa-
brate or nicotinic acid with an LDL-lowering drug.7,8
tients with the metabolic syndrome. The purpose of this re-
view is to provide a rationale for the combined use of statins
and fibrates in the management of patients with high resid-
ual cardiovascular risk related to atherogenic dyslipidemia
Conclusion:
The authors conclude that Fenogal (lidose technology)
and persisting after single therapy. Reducing the residual
cardiovascular risk in patients treated with statins requires can be safely and effectively included in the armamentarium

addressing multiple lipid goals. In this context, future thera- of cardiovascular medications. Profiles of patients who had

peutic interventions based on combination therapy, such as
statins and fibrates, appears particularly promising.
According to Shek et.al.14, practical recommendations
for clinicians who care for patients with refractory mixed
hyperlipidemia are needed. Combination therapy with a sta-
tin and fibrates offers significant therapeutic advantage for
the treatment of severe or refractory mixed hyperlipidemia.
experienced rise in alkaline phosphatase needs further inves-
tigation. Even systolic and diastolic blood pressures, fasting
blood sugar, and heart rate were significantly lowered.
Recommendation:
The authors recommend the use of Fenogal (lidose
technology) to be included to optimize medical therapy in

Although such a combination does increase the risk of myo- patients with dyslipidemia.

pathy, with an incidence of approximately 0.12%, this small

risk of myopathy rarely outweighs the established morbidity Disclosure:
and mortality benefits of achieving lipid goals. Nevertheless, The study was performed as part of the PMS (Post
a higher incidence of myopathy has been reported with sta- Marketing Surveillance) required by the BFAD (Bureau of Food
tin monotherapy. When monotherapy with a statin fails to and Drug) for Fenogal brand of Fenofibrate.
control mixed hyperlipidemia; combination therapy may be
considered. Niacin may be added before a fibrate is consid-
ered, as it appears to have less risk of myopathy. Statin-
fibrate combination therapy must be undertaken cautiously
and only after careful risk-benefit analysis. Patient counsel-
ing on the risks and warning signs of myopathy is extremely
important.18,19,20,21,22

The Adult Treatment Panel III of the National Cholesterol

Education Program issued an evidence-based set of guidelines
on cholesterol management. Since its release, there were 5
major clinical trials of statin therapy with clinical end points
have been published. Therapeutic lifestyle changes remain
an essential modality in clinical management. The trials

10
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Trial (BECAIT) and Other Angiographic Trials. Cardiovascular Drugs and Therapy 1997;11:257-263
3. HD Shah, KH Parikh, MC Chag et al. Beneficial Effects of the Addition of Fenofibrate to Statin Therapy in Patients with Acute
Coronary Syndrome After Percutaneous Coronary Interventions. Exp Clin Cardiol 2007;12(2):91-96
4. Arca M, Montali A, Pigna G, Antonini R, Antonini TM, Luigi P, Fraioli A, Mastrantoni M, Maddaloni M, Letizia C. Comparison of Ator-
vastatin Versus Fenofibrate in Reaching Lipid Targets and Influencing Biomarkers and Endothelial Damage in Patients with
Familial Combined Hyperlipidemia. Metabolism 2007 Nov;56(11):1534-41
5. Goa KL, Barradell LB, Plosker GL. Bezafibrate. An Update of its Pharmacology and use in the Management of Dyslipidemia.
Drugs 1996 Nov;52(5):725-53
6. Spencer CM, Barradell LB. Gemfibrozil: A Reappraisal of its Pharmacological properties and Place in the Management of Dys-
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Appendix A. Previous Medication of Patients for Dyslipidemia
Medications No. %
Afordel 1 0.03
Atorvastatin 104 3.47
Cholestad 5 0.17
Ciprofibrate 1 0.03
Crestor 52 1.73
Ezetemibe 2 0.07
Ezetrol 1 0.03
Fenofibrate 49 1.63
Fenoflex 8 0.27
Fenogal 3 0.10
Fibrafen 5 0.17
Fibrate 3 0.10
Fluvastatin 3 0.10
Forcad 10 0.33
Gemfibrozil 58 1.93
Lescol 6 0.20
Lipanthyl 62 2.07
Lipigem 2 0.07
Lipitor 58 1.93
Lipway 5 0.17
Lopid 18 0.60
Niacin 9 0.30
Nubrex 21 0.70
Omacor 2 0.07
Orlistat 1 0.03
Pravastatin 4 0.13
Reducel 14 0.47
Rosuvastatin 31 1.03
Simvastatin 588 19.60
Vamstat 1 0.03
Vidastat 46 1.53
Vytorin 10 0.33
Ximvast 1 0.03
Zocor 22 0.73
Unrecalled 3 0.10
None indicated 1877 62.56