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‫[سورة طه ‪ -‬اآلية‪]114 :‬‬
‫‪1‬‬
 Diabetic dyslipidaemia (DD)
Dr. Ghazala Othman Elfeitouri

2
Diabetic dyslipidaemia (DD)
• Epidemiologic studies have demonstrated that people with
diabetes have a 3- to 4-fold increase in developing cardiovascular
diseases than those without diabetes .
• Dyslipidaemia is very common in type 2 diabetes mellitus
(T2DM), affecting around 72% to 85% of patients, with a more
atherogenic lipid profile.

3
Diabetic dyslipidaemia (DD) comprises a complex group of
potentially atherogenic lipid and lipoprotein abnormalities,
including both quantitative and qualitative changes. It is
characterized by:
1. Low high-density lipoprotein cholesterol.
2. Elevated low-density lipoprotein cholesterol (LDL-C).
3. Higher prevalence of small, dense LDL particles.
4. Elevated fasting and postprandial triglycerides.
5. High levels of apolipoprotein B (ApoB), non-high-density
lipoprotein (HDL).

4
• Controlling of dyslipidaemia in patients with Type 2 diabetes
mellitus has a big impact on morbidity and mortality.

5
Pathophysiology diabetic dyslipidemia

1. Increase plasma Triglycerides

•Metabolism of lipids in diabetes, particularly Type 2 diabetes
mellitus (T2DM), is influenced by a series of factors, including
the degree of glycemic control and the presence of insulin
resistance, which are the most prominent elements.
•Insulin resistance is the basis of the pathophysiological
mechanisms of DD and is closely related to hypertriglyceridemia
and postprandial lipaemia.
•Insulin reduces VLDL production by decreasing circulating
levels of FFA, which are substrates of VLDL, and by exerting a
direct inhibitory effect on VLDL production in hepatocytes.

6
7
• Insulin inhibits the maturation phase of VLDL assembly through
the phosphatidylinositol 3-kinase pathway, preventing the transfer
of bulk lipids to VLDL precursors. This mechanism is involved in
the inhibitory effect of insulin related to the secretion of VLDL.
• An important consequence of insulin resistance, with respect to
lipid metabolism, is the loss of the suppressive effect of insulin on
the mobilization of adipose tissue fat. As a result, there is an
increase in FFA due to a reduction in the suppression of lipolysis.
• The lack of suppression of FFA in the postprandial period results
as a consequence of the decrease in lipoprotein lipase activity, and
the increase in plasma FFA is due to an increase in lipolysis in
adipocytes. These form the key mechanisms that underlie the
increase in hepatic TG secretion of VLDL.

8
 The pathogenesis of diabetic dyslipidaemia
9
• In healthy individuals, insulin inhibits the assembly and secretion
of VLDL particles through an increase in the degradation of
apolipoprotein B (ApoB) and a decrease in the expression of
microsomal transfer protein in the hepatocytes. As a consequence,
insulin inhibits hepatic secretion of TG-VLDL and ApoB-100.
• In T2DM patients and those with other states of insulin
resistance, an increase in microsomal transfer protein expression
occurs in the liver, along with an increase in lipid bioavailability
(i.e., the flow of FFA), and this leads to an overproduction of TG-
VLDL and VLDL-ApoB.
• The overproduction of hepatic VLDL corresponds to large,
floating VLDL particles, which are a predominant feature of DD.
Most of the increase in TRL observed in DD is due to VLDL
particles.

10
• In fact, the long residence time of VLDL in the plasma, due to the
reduction of lipolysis, is a prerequisite for the formation of small,
dense LDL since it favours the excess lipid exchange of TG and
cholesterol esters between TRL and LDL. When the LDL have
depleted cholesterol esters and an enrichment of TG, an increase
in the action of hepatic lipase results in the formation of the
subclass of small, dense particles.
• Since each particle of LDL contains a molecule of ApoB-100, the
number of small, dense LDL is increased and, similarly, the
concentration of ApoB-100 increases in direct relation.
Consequently, ApoB concentrations are a marker of the number of
atherogenic particles and hypertriglyceridaemia with hyper-ApoB-
100 is a well-known feature of DD and other conditions.

11
2. Low Concentrations of High-Density Lipoprotein
Cholesterol
• The increase in plasma TG presents a central lipid exchange
between TRL and HDL particles. There is an increase in the
transfer of esterified cholesterol to the TRL, facilitated by the
cholesterol ester transfer protein, and the transfer of TG to the
HDL particles, which leads to an enrichment of TG in these
particles.
• HDL TG are a suitable substrate for hepatic lipase and
hydrolysis produces smaller HDL particles and free ApoA-I
that are excreted by the kidneys.
• The catabolism of small HDL is faster than that of normal
HDL, and this results in a reduction in the amount of
circulating HDL particles.

12
Main compositional differences between the HDL of healthy individuals
and the HDL of patients with type 2 diabetes. Apo: apolipoprotein; CE:
cholesteryl ester; PON-1: paraoxonase-1; S1P: sphingosine 1-phosphate; SAA:
serum amyloid A; TG: triglyceride; 🡫: decreased; 🡩: increased.

13
 3. Predominance of Small, Dense Low-Density Lipoproteins
and Excessive Post prandial Lipaemia
• Small dense LDL particles (Phenotype B) are a prominent
feature of DD and the number of these atherogenic particles is
increased.
• It has been repeatedly confirmed that the concentration of
plasma TG is the most important determinant of the size of
LDL.
• On the other hand, the size of LDL decrease progressively as
glucose tolerance worsens, until overt diabetes is achieved.
This decrease is greater in women than in men.
• TG of VLDL are the main predictors of LDL size in
individuals with T2DM, and kinetic data indicate that VLDL
are the precursors of small, dense LDL particles.

14
 LDL particles can be separated on the basis of size and density into several
different subclasses, as illustrated here. Small dense, triglyceride-rich LDL
are believed to be more atherogenic than the large buoyant variety.
A predominance of small LDL is referred to as the pattern B phenotype.
Pattern B phenotype is one manifestation of what has been termed the
Atherogenic Lipid Profile, a Mendelian-dominant inherited condition which
also includes low levels of HDL-C, raised triglycerides, and insulin
resistance. The presence of the pattern B phenotype increases the risk for
clinical coronary heart disease by several fold. Niacin, fibrates, and bile-acid
binding resins (but not statins) can cause favorable shifts in the LDL
15 particle size subclass distribution from small towards large.
 A schematic image of the low density lipoprotein (LDL) subtype
patterns. Low density lipoprotein particles vary in size and
density, and studies have shown that small dense LDL particles,
called Pattern B , equates to a higher risk factor for CVD than
does a pattern with more of the larger and less-dense LDL
particles ( Pattern A ).
16
 LDL levels may remain within the normal range, the lipid measures
used in clinical practice do not always reveal the malignant nature
of diabetic dyslipidaemia. It may be better revealed by non-HDL
levels.

17
 Major changes in lipoprotein metabolism in T2DM
Quantitative Kinetic/metabolic
Lipoprotein Qualitative changes
changes changes

Higher proportion of
No change or small dense particles
LDL Decreased catabolism
slight increase Increased oxidation
Glycation

Decreased
HDL plasma Glycation Increased catabolism
concentration

Higher proportion of
Increased
larger particles Increased production
VLDL plasma
(VLDL1) Decreased catabolism
concentration
Glycation

18
19
20
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22
Management of diabetic dyslipidemia
Non-Pharmacological Therapy
• Lifestyle changes remain the pillar of treatment, not only for
DD but for diabetes in general, and are strongly advised for
diabetic patients.
• Nutritional therapy should be adapted to each patient and
there is no enough evidence to recommend an ideal
distribution of principal macronutrients.
• In terms of cardiovascular risk, the total amount of fat
consumed is less important than the type of fat. In general,
recommendations must focus on reducing cholesterol and
saturated and trans-fat intake, and increasing fibre, n-3 fatty
acids, and plant stanols/sterols intake.

23
• A Mediterranean-style diet (rich in monounsaturated and
polyunsaturated fats) has been shown to be effective at
improving lipid profile and glycaemic control.
• In addition, the loss and maintenance of weight (of at least 5%),
if indicated, is associated with improvements in lipid levels.

• Dietary fats and processed foods are rich in advanced glycation

end-products, which are primarily elevated in diabetic patients,
and an excessive consumption of these can increase the total
pool in the body.

• Advanced glycation end-products can raise oxidative stress and

increase arterial endothelial dysfunction.

24
25
26
 Commonalities and unique features of the DASH diet, USDA food
27 patterns, and Mediterranean diet.
Physical activity

• Fundamentally aerobic exercise alone and in combination with

resistance exercise, improves certain cardiovascular risk factors,
including blood pressure, glucose metabolism, BMI, and waist
circumference, but the effects on lipid parameters are
inconsistent and sometimes contrasting. Combined exercise has
shown better outcomes than each exercise separately.

• The ADA recommends ≥150 minutes of moderate-to-vigorous

aerobic activity weekly, divided between at least 3 days,
combined with two or three sessions per week of resistance
exercise on non-consecutive days.

28
• A combination of exercise and diet obtains better weight loss than
diet alone and shows better improvements in lipid profile than
exercise alone.

• Smoking cessation is associated with elevation of HDL-C levels,

but there are no specific data in diabetic patients.

29
• Weight loss has been shown to improve multiple risk factors,
such as haemoglobin A1C and blood pressure; however, the
“Look AHEAD” study did not show improvement in CV events
after long-term weight loss with intensive lifestyle change,
indicating the need for pharmacotherapy to reduce
atherosclerotic cardiovascular disease (ASCVD).

30
Pharmacotherapy
• The old drugs used to treat diabetic dyslipidaemia include statins,
cholesterol absorption inhibitors, niacin, fibrates, bile acid
sequestrants (BAS), and omega-3 free fatty acids.
• A relatively novel agent proprotein convertase subtilisin/kexin
type 9 (PCSK9) inhibitor and other agents still on the horizon
(such as icosapent ethyl [IPE], bempedoic acid [BA], and
inclisiran) are options to manage this important risk factor.
• Diabetic dyslipidaemia should be treated with statins. However,
some patients do not reach the established therapeutic target for
LDL and are candidates for potential combination therapy.

31
Drugs targeting LDL cholesterol
1. Statins
2. Ezetimibe
3. Bile acid sequestrants
4. Proprotein convertase subtilisin-kexin 9 (PCSK9) inhibitors
5. Bempedoic acid
Drugs targeting TG-rich and other lipoproteins
1.Fibrates
2.Omega-3 fatty acids
3.Apo C-III and ANGPLT3 inhibitors
oApo C-III gene inhibition
oANGPTL3 inhibition
4. CETP inhibitors
32
TREATMENT OF DIABETIC DYSLIPIDAEMIA
Treatment Targets
 The American Diabetes Association (ADA) guidelines recommend
the following treatment for DD:
1. People <40 years:
• No ASCVD: no statin.
• With ASCVD: high-intensity statin.
2. People ≥40 years:
• No ASCVD: moderate-intensity statin.
• With ASCVD: high-intensity statin.
With ASCVD, if LDL-C is ≥70 mg/dL, despite a maximally tolerated
statin dose, consider an additional LDL-lowering therapy (e.g.,
ezetimibe, PCSK9 inhibitor).

33
 The Joint European Society of Cardiology (ESC) guidelines also
recommend lipid-lowering agents (principally statins) in patients
with diabetes (Type 1 or Type 2) >40 years of age.
They use LDL targets to guide therapy:
o In patients with diabetes at a very high risk (diabetes with target
organ damage such as proteinuria or with a major risk factor, such
as smoking or marked hypercholesterolaemia or marked
hypertension), the LDL-C target is <1.8 mmol/L (<70 mg/dL) or a
reduction of at least 50% if the baseline LDL-C is between 1.8 and
3.5 mmol/L (70 and 135 mg/dL).

34
o In patients with diabetes at a high-risk (most other people with
diabetes, with the exception of young people with Type 1 diabetes
mellitus and without major risk factors that may be at low or
moderate risk), the LDL-C target is <2.6 mmol/L (<100 mg/dL)
or a reduction of at least 50% if the baseline LDL-C is between
2.6 and 5.1 mmol/L (100 and 200 mg/dL).

 ESC guidelines also highlight that non-HDL-C is a reasonable

and practical alternative target because it does not require fasting.
• Non-HDL-C secondary targets include:
o 2.6 mmol/L (100 mg/dL) for very high-risk subjects.
o 3.3 mmol/L (130 mg/dL) for high-risk subjects. There is
increasing evidence of a very high relative risk in younger
individuals with T2DM so additional studies and guidance are
needed in this group.
35
 Treatment algorithm for diabetic dyslipidaemia. Statins are the
cornerstone of the treatment. Combination therapies may be considered
in patients at very high risk.

BAS: bile acid sequestrant; LDL: low-density lipoprotein; ω3FA: omega-3 fatty
acids
36
Pharmacotherapy
1. Statins are the first line treatment for dyslipidaemia, unless
contraindicated. In general, statins can be administered to all
diabetic patients when LDL is above 100 mg/dL, starting with a
moderately potent statin and continuous monitoring of LDL.

37
Statins
o Statins competitively inhibit 3-hydroxymethylglutaryl
coenzyme A, which is a rate-limiting step in the synthesis of
cholesterol in the liver.
o They are considered first-line treatments for patients with
T2DM, even at diagnosis. For these reasons, statins have
been associated with significant reductions in LDL
concentration as well as CVD risk reduction in both primary
and secondary prevention in patients with DM. This notion
is supported by many randomized controlled trials.
o It should be considered that individuals with T2DM with
additional CV risk factors receive statin therapy regardless
of their baseline LDL levels.

38
o According to guidelines, all DM patients should be treated with
statins, if tolerated, with different LDL goals based on the type
of DM, CV risk factors, and complications.
o Statins reduce cholesterol deposits, increase expression of LDL
receptors in the liver and enhance endocytosis of the circulating
LDL.
o Statins have pleiotropic effects - reduction of high-sensitivity C-
reactive protein (hsCRP) and other markers of inflammation
that help to stabilize plaque, improve endothelial function, and
decrease vascular inflammation and oxidative stress.

39
Statins are divided into:
1. High-intensity – these statins decrease LDL by 50% or more
(atorvastatin 40-80 mg, rosuvastatin 20-40 mg).
2. Moderate-intensity – these statins decrease LDL by
approximately 30-50% (atorvastatin 10-20 mg, rosuvastatin 5-10
mg, simvastatin 20-40 mg, pravastatin 40 mg, lovastatin 40 mg,
fluvastatin 80 mg, pitavastatin 2-4 mg).
3. Low-intensity – these statins decrease LDL by <30%
(simvastatin 10 mg, pravastatin 10-20 mg, lovastatin 20 mg,
fluvastatin 20-40 mg, pitavastatin 1 mg).

40
41
 Many trials have shown a reduction in CV events with statin
use. The Heart Protection Study reported a 22% reduction of
events including stroke.

 A meta-analysis of 14 randomised clinical trials including over

18,000 patients with T2DM demonstrated, during an average
follow up of 4.3 years, that statin therapy reduced CVE by 21%
and vascular mortality by 13% for every 39 mg/dL reduction in
LDL . It is important to note that the benefits of using statins in
diabetic patients were independent of LDL and lipid values.

42
Side effects of statins
Statins are generally well tolerated.
o The most common side effect is myalgia.
o Necrotising autoimmune myopathy and rhabdomyolysis are rare.
However, caution is needed in elderly patients, especially those
with chronic kidney disease or patients with untreated clinical or
subclinical hypothyroidism, and those receiving drugs that
interact with statins.
o Statins can also cause new-onset diabetes, but the risk is very
low compared with the statin-induced decrease in CVD events. It
is important to certify that intolerance to statins is true to avoid
unnecessary suspension of the drug.

43
2. Cholesterol absorption inhibitors – ezetimibe
o Ezetimibe acts by inhibiting intestinal absorption of cholesterol
binding to sterol transporter Niemann-Pick C1-Like 1 (NPC1L1),
ultimately causing a reduction in LDL.
o Ezetimibe appears to increase insulin sensitivity in patients with
insulin resistance. It is particularly efficacious in patients with
DM, reducing LDL by 24%. There is an intensification of LDL
reduction when ezetimibe is added to statin therapy.
o The IMPROVE-IT trial showed that ezetimibe add-on therapy to
simvastatin is particularly beneficial for diabetic patients, with a
relative risk reduction in CVE of 15% and an absolute risk
reduction of 5.5%.

44
o A meta-analysis (n=109,244) showed that an ezetimibe/statin
combination leads to a significant reduction of CV events in
patients with high CVD risk.
o Ezetimibe associated with statins is indicated for diabetic
patients with suboptimal lipid levels despite maximal dose of
statin therapy, individuals unable to tolerate maximum statin
doses or as monotherapy in patients who are statin intolerant.

45
3. Niacin
o Niacin is a potent drug to increase HDL and to reduce LDL and
TRG moderately.
o In addition, it can lower lipoprotein(a) levels by 25%.
o However, its benefits have not been proven effective in
reducing CV events.
o In practice, the use of niacin is limited by its side effects: at the
standard dose, 80% of users describe flushing, and another
20% complain of pruritus, paraesthesia, and nausea.
o The AIM-HIGH trial showed no clinical benefit despite
significant improvements in HDL and TRG levels.
o Thus, the combination of statin with niacin in diabetic subjects
has no clinical benefit and should be avoided.

46
4. Fibrates
o Fibrates reduce serum TRG levels and increase HDL levels by
means of activation of peroxisome proliferator-activated receptor α
(PPAR-α) and promote a moderate reduction in LDL.
o Fenofibrate reduces TRG concentration by 30-50%. Its effects are
seen in high-risk diabetic patients with high triglyceride levels.
o The FIELD study showed that fenofibrate should be considered in
individuals with hypertriglyceridaemia and low HDL and high CV
risk but should not be considered a substitute for statins.
o A meta-analysis with 45,058 participants showed that fibrates
reduce the relative risk of major events by 10% and the risk of
coronary events by 13%.

47
o Fibrates are metabolized in the kidney and should be
avoided or used with caution in patients with kidney disease.
o Pemafibrate is a selective PPAR-α modulator (SPPARM-α),
a newer, more potent fibrate. It is metabolized in the liver
and excreted into the bile, so it can be used in patients with
kidney dysfunction.
o The PROMINENT trial failed to show that
pemafibrate improved cardiovascular outcomes
among patients with diabetes and
hypertriglyceridemia.

48
5. Bile acid sequestrants (BAS)
o BAS bind to bile acids in the intestinal lumen interrupting the
enterohepatic circulation of bile acids, reducing the level of LDL
by up to 30%.
o Cholestyramine, colestipol, and colesevelam are commonly used
BAS.
o Historically, they have been used when statins are not tolerated, in
women of childbearing age and in children
o Their side effects such as constipation, cholelithiasis, and
hypertriglyceridaemia limit their use.
o Colesevelam has a lower incidence of these side effects and the
benefit of improving HbA1c in patients with inadequately
controlled diabetes.
o BAS are considered second-line therapy for lowering LDL and
are used in combination therapy.
49
6. Icosapent ethyl (IPE)
o Omega-3 free fatty acids are used as a complementary therapy to
reduce the level of triglycerides, but their effects on other
lipoproteins are trivial.
o High doses (3-5 g) of the formulation eicosapentaenoic acid (EPA) +
docosahexaenoic acid are necessary to show any CV benefit.
o Icosapent ethyl is a highly purified EPA ethyl ester. It acts on PPAR
expressed on adipocytes and inflammatory cells to reduce levels of
TRG, increase insulin sensitivity, and regulate the inflammatory
cascade.

50
o Recently, the REDUCE IT trial showed that the primary
endpoint of major adverse CV events (MACE) was significantly
lower in the group treated with IPE versus placebo, p<0.001,
but an increase in hospitalization for atrial fibrillation or flutter
was observed.
o IPE emerges as an option adjunct to statins to treat patients with
ASCVD and high TRG levels.

51
7. Bempedoic acid (BA)
o Bempedoic acid decreases LDL level through competitive
inhibition of adenosine triphosphate citrate lyase (ACL), an
enzyme responsible for catalyzing the production of acetyl
coenzyme A, an integral substrate in the cholesterol synthesis
pathway in the liver.
o It acts in a similar way to statins, up regulating the expression
of the hepatic LDL receptor, increasing the clearance of
circulating.
o Randomized trials have shown an LDL decrease from 18% to
28% when BA can be used as monotherapy or added to statin.
It requires activation by an enzyme present in the liver, not in
the muscles, decreasing the risks of muscle-related adverse
effects, but there is an increase in uric acid and gout can occur.

52
o A meta-analysis of 7 randomized trials concluded that BA is a
valuable option for patients with statin intolerance and a high
CV risk, not reaching the LDL target, despite a maximally
tolerated lipid-lowering treatment, including both statin and
ezetimibe.

53
8. PCSK9 inhibitors (Proprotein convertase subtilisin-kexin 9
inhibitors)
• The currently available fully human monoclonal antibodies,
evolocumab and alirocumab.
o Inclisiran is a synthetic small interfering ribonucleic acid
(RNA) that leads to the degradation of PCSK9-specific
messenger RNA (mRNA) in the liver. It is a long-acting agent
(1 to 2 times a year) that decreases PCSK9 production by the
liver. It results in a reduction of LDL levels of >50%.
o Inclisiran differs from other PCSK9 inhibitors due to its
longer duration of action and acts at an intracellular level
within hepatocytes, as opposed to the plasma level. It yields a
rapid, significant and prolonged reduction in LDL levels,
improves atherogenic lipids and lipoprotein profiles, and is
safe and well tolerated. Like other PCSK9 inhibitors, the cost
limits its use.
o The use of twice a year therapy has the potential to improve
adherence and achieve the most complete LDL goal

55
 Effects of antidiabetic drugs on diabetic hyslipidemia
• Clinical studies have highlighted the effect of novel antidiabetic
drugs beyond glucose lowering - reduction in body weight,
blood pressure, lipids, inflammatory markers, oxidative stress,
endothelial dysfunction and subclinical atherosclerosis.
• Incretin-based therapies (IBTs), including glucagon-like
peptide-1 receptor agonists (GLP-1RA), sodium/glucose
cotransporter 2 inhibitors (SGLT2is), have beneficial effects,
reducing CV events.

56
 DRUG
TOTAL LDL HDL TRG
CHOLESTEROL

Metformin - /0 - 0/+ - /0

DPP-4 inhibitors
Sitagliptin 0 0 0/+ 0

Vildagliptin 0 0 0/+ 0

Saxagliptin 0 0 0 0

Linagliptin 0 0 0 0

57
 GLP1 analogues
Liraglutide 0 0 0 -

Exenatide 0/- +/0 +/0 -

SGLT2 inhibitors
Empaglifozin +/0 +/0 +/0 -

Dapaglifozin +/0 +/0 +/0 0/-

Canaglifozin + + + +

Insulin 0/- - +/0 -

DPP-4: dipeptidyl peptidase-4; GLP1: glucagon-like peptide-1; SGLT2:

sodium/glucose cotransporter 2; LDL: low-density lipoprotein; HDL: high-density
lipoprotein; TRG: triglyceride
0: no effect +: increase -: decrease
58
0/+: no effect or increase -/0: no effect or decrease
 Type 1 diabetes mellitus (T1DM)
• The exposure of patients with DM1 to hyperglycaemia is of
paramount importance in the development of CVD. Duration of
diabetes is important.
• These patients develop the disease early in their lives, during
childhood. The pattern the disease shows is more
atherosclerotic, driven by hyperglycaemia and ensuing early
renal damage.
• Furthermore, even minimal evidence of nephropathy greatly
increases the risk of CVD in T1DM. It may be prudent to
consider statins for the majority of patients with T1DM above
the age of 30.

59
Conclusion
• Diabetes mellitus is a high-risk factor for atherosclerotic disease.
• Dyslipidaemia has a high prevalence among diabetics and behaves
in a more atherogenic manner with high levels of triglycerides and
small dense LDL particles in addition to low HDL.
• An early approach is imperative.
• Statins are the first choice and are highly effective.
• When association is necessary or in cases of intolerance ezetimibe
is the first option and/or PCSK9 inhibitors, in addition to fibrates
for hypertriglyceridaemia.

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• Emerging evidence suggests the need to consider lipid-lowering
therapies more frequently in younger patients with T1DM and
T2DM.
• Statins should always be considered first-line therapy. In general,
statins can be administered to all diabetic patients when LDL is above
100 mg/dL, starting with a moderately potent statin and continuous
monitoring of LDL.
• Ezetimibe in combination with statins can result in an incremental
reduction in LDL levels and improve cardiovascular outcomes
further.
• Fibrates have a role in patients with high TRG and low HDL, and
fenofibrate should also be considered in patients with T2DM and
retinopathy.

61
• Finally, PCSK9 inhibitors are a new class of lipid-lowering
drugs that can be integrated into the treatment of individuals
with diabetes and dyslipidaemia. They can be used in
addition to statins, ezetimibe, and fibrates.
• It is important to know that treating lipid abnormalities has
the potential to reduce CV events by more than 50%.

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63