CLINICAL PHARMACY & Chapter 24: Dyslipidaemia

PHARMCOTHERAPY 1 Ms. Neri Margaret Fabillo

AY 2022-2023 MM/DD/YYYY
2nd Semester

OUTLINE → For the disorders of ipoproteins the term “dyslipidemia” is be

Alternative Treatment beter than hyperlipidemia because it encompasses both high
Pathophysioloy and low leves of specific lipoproteins.
Strategies
→ This condition can result from diet, tobacco exposure, or
Clinical Manifestation Palliative Care
genetic and can lead to cardiovascular disease with severe
Differential Analysis Goal of Therapy complications.
Laboratory Tests Possible Drug Interactions
Drug of choice and Mode of
Patient Education Patient
Action
Alternative Drug Treatment &
Assessment and Monitoring
MOA
Other Drug Therapies &
MOA

KEY POINTS
• Elevated concentrations of total cholesterol (TC) and low-density
lipoprotein cholesterol (LDL-C) increase the risk of cardiovascular
disease (CVD), while high-density lipoprotein cholesterol (HDL-C)
confers protection.
• Two-thirds of the UK adult population have a serum TC above
5mmol/L. The average TC concentration is 5.6mmol/L.
• Dyslipidaemia may develop secondary to disorders such as diabetes
mellitus, hypothyroidism, chronic renal failure, nephrotic syndrome, A. EPIDEMIOLOGY
obesity, high alcohol intake and some drugs.
• Androgens, b-blockers, ciclosporin, oral contraceptives, diuretics, ● Lipid and lipoprotein concentrations vary among different
glucocorticoids and vitamin A derivatives are examples of drugs that populations. (Ex: US - diet high with TC and LDL-C lvls).
can have an adverse effect on the lipid profile.
• There are five main classes of lipid-lowering agents: statins, fibrates,
→ The death rate from CVD is threefold higher in males than
resins, nicotinic acid derivatives and absorption blockers.
• Statins are generally the drugs of choice in the treatment of primary females, but because women live longer and are at
prevention and secondary prevention of CVD. increased risk of stroke after the age of 75 years their lifetime
•The aim of treatment in primary prevention (>20% risk of risk of disease is great
cardiovascular disease over 10 years) is to reduce overall
cardiovascular risk by treatment with simvastatin 40mg/day or a suitable → Population-based approaches to vascular screening have
alternate generic agent. No target treatment levels for TC or LDL the potential to provide significant health gain for society as
cholesterol are recommended in primary prevention. • In secondary most deaths from CVD occur in individuals who are not yet
prevention, treatment should be started with simvastatin 40mg/day or a
suitable alternate generic agent. If serum TC remains above 4mmol/L or
identified as at increased risk.
LDL-C remains above 2mmol/L, the dose of statin can be increased, but
this may increase the likelihood of side effects → Moreover, a small reduction in average population levels of
TC and LDL-C can potentially prevent many deaths

I. PATHOPHYSIOLOGY

● DYSLIPIDEMIA
→ Dyslipidemia is the imbalance of lipids such as cholesterol,
low-density lipoprotein cholesterol, (LDL-C), triglycerides,
and high-density lipoprotein (HDL).
→ Simply, Dyslipidemia refers to unhealthy levels of one or
more kinds of lipid (fat) in your blood.

→ Causes of Atherosclerotic disease:

▪ Disorders of lipoprotein metabolism
▪ high fat diets
▪ obesity
▪ physical inactivity

★ Disorders of lipoprotein metabolism that result in

elevated serum concentrations of total cholesterol (TC)
and low-density lipoprotein cholesterol (LDL-C) increase
the risk of an individual developing cardiovascular
disease (CVD).

CLINPHARM Group 2 - 2A : Andres, Balando, Bucane, Canillas, Galangue,Gonzales, Llarenas, Mengote, Muncada, Pabia, Pazon, Rosales, Samante, Severino, Vierras, Yee 1 of 7
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 B. LIPID TRANSPORT AND LIPOPROTEIN
METABOLISM
➔ There are six main classes of lipoproteins:
1. Chylomicrons
2. Chylomicron remnants
3. Very low-density lipoproteins (VLDL-C)
4. Intermediate-density lipoproteins (IDL-C)
5. Low density lipoproteins (LDL-C)
6. High-density lipoproteins (HDL-C).
➔ The protein components of lipoproteins are known as
apoproteins (apo), of which apoproteins A-I, E, C and B
are perhaps the most important.
◆ Apoprotein B exists in two forms:
● B-48 - which is present in
chylomicrons and associated with the
transport of ingested lipids
● B-100 - found in secreted VLDL-C
and associated with the transport of
lipids from the liver.
PROCESS:
1. Chylomicrons carry dietary cholesterol and triglycerides
from the gut. The biggest lipoprotein particles contain
about 80% triglycerides.
2. Adipose tissue and skeletal muscle blood capillaries
include the endothelium-bound enzyme lipoprotein
lipase, where chylomicrons pass.
3. Chylomicron apoprotein C-II activates lipoprotein
lipase. Lipase breaks down chylomicron triglyceride to
free fatty acid and glycerol, which enter adipose tissue
and muscle.
4. Hepatocyte membrane receptors take up the
cholesterol-rich chylomicron remnant, delivering
dietary cholesterol to the liver and clearing it from
circulation.
5. VLDL-C delivers triglycerides, which make up 80% of
its lipid core, to the periphery from the liver.
6. Lipoprotein lipase removes VLDL-C triglycerides to
create IDL-C particles, comparable to chylomicrons.
7. Lecithin-cholesterol acyltransferase converts HDL-C
into IDL-C particles, which contain 50% triglyceride and
50% cholesterol esters (LCAT).
8. The liver removes 50% of serum IDL particles. 50% of
IDL-C is hydrolyzed and converted to produce LDL-C
particles.
9. LDL-C carries most serum cholesterol. LDL-C gives
cells that need cholesterol, bile acid, and steroid
hormone precursors.
10. After oxidation, LDL-C is the primary lipoprotein in
atherogenesis. (formation of fatty plaques in the
arteries)
11. Lipoprotein permeates the vascular endothelium for
unknown reasons. Monocytes travel through the porous
endothelium and ingest lipoprotein, forming lipid-laden
macrophages that cause atherosclerosis.
★ Hence why, Dyslipidemia treatment typically lowers
LDL-C and TC.
○ VLDL-C and LDL-C are "bad" lipoproteins,
○ HDL-C is "good" antiatherogenic lipoprotein.
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Edit: Refer to the book for a schematic diagram also. Tnx
High-Density Lipoprotein
● HDL-C is formed from the unesterified cholesterol and
phospholipid removed from peripheral tissues and the surface
of triglyceride-rich proteins.
o The major structural protein is apoA-I.
● HDL-C mediates the return of lipoprotein and cholesterol
from peripheral tissues to the liver for excretion in a process
known as reverse cholesterol transport
Reverse cholesterol transport pathway
● involves lipoprotein-mediated transport of cholesterol from
peripheral, extra-hepatic tissues and arterial tissue (potentially
including cholesterol-loaded foam cell macrophages of the
atherosclerotic plaque) to the liver for excretion, either in the
form of biliary cholesterol or bile acids.
→ HDL-C plays a major role in maintaining cholesterol
homeostasis in the body.
→ Low levels of HDL-C are found in 17% of men and 5% of
women and may be a risk factor for atherogenesis
→ Drugs that reduce HDL-C levels are considered to have an
undesirable effect on lipid metabolism and increase the risk
of developing CVD. (cardio vascular disease)
Triglycerides
● Triglyceride levels are confounded by low HDL-C, hypertension,
diabetes, obesity, and a synergistic impact with LDL-C and/or
low HDL-C, making hypertriglyceridemia an uncertain risk
factor for coronary heart disease (CHD).
→ Elevated lvls causes or consequence of the following:
▪ Lipid impared metabolism disease
▪ medication use
▪ metabolic syndrome
▪ type 2 diabetes mellitus.
C. AETIOLOGY
PRIMARY DYSLIPIDEMIA
● Up to 60% of the variability in cholesterol fasting lipids may be
genetically determined, although expression is often
influenced by interaction with environmental factors
→ familial (genetic) disorders can be classified as:
▪ the primary hypercholesterolaemias such as familial
hypercholesterolaemias in which LDL-C is raised
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 ▪ the primary mixed (combined) hyperlipidaemias in which ● not associated with an increased susceptibility to
both LDL-C and triglycerides are raised atherosclerosis; the major complication is acute pancreatitis
▪ the primary hypertriglyceridaemias such as type III
hyperlipoproteinaemia, familial lipoprotein lipase Familial apolipoprotein C-II deficiency
deficiency and familial apoC-II deficiency. ● reduced levels of apoC-II, the activator of lipoprotein lipase
→ may develop acute pancreatitis
Familial Hypercholesterolinemia → Premature atherosclerosis is unusual but has been
● Familial hypercholesterolaemia is caused by a range of described.
mutations (genes for the pathway that clears LDL-C from the
blood.) Liporpotein(a)
● The most common mutation affects the LDL receptor gene. ● a raised level of lipoprotein(a), otherwise known as Lp(a),
o Patients with FH may have serum levels of LDL-C appears to be a genetically inherited determinant of CVD.
two to three times higher than the general → A parental history of early-onset CVD is associated with
population. raised concentrations of Lp(a), and these appear to play a
● Familial hypercholesterolaemia is transmitted as a role in both atherogenesis and thrombosis.
dominant gene, with siblings and children of a parent with
FH having a 50% risk of inheriting it. SECONDARY DYSLIPIDEMIA
● caused by lifestyle factors or medical conditions that interfere
with blood lipid levels over time these may include unhealthy
Heterozygous FH Homozygous FH lifestyle factors and acquired medical conditions, including
underlying diseases and applied drugs.
exhibits the signs of: cholesterol associated with an absence of → Here are conditions that affect lipid profile
deposition such as LDL receptors ( inability to clear
● corneal arcus (crescentic LDL-C)
deposition of lipids in the ● involvement of the aorta is
cornea), evident by puberty and
● tendon xanthoma (yellow usually accompanied by
papules or nodules of lipids cutaneous and tendon
deposited in tendons) xanthomas.
● xanthelasma (yellow plaques ● Myocardial infarction early
or nodules of lipids deposited as 1.5–3 years of age
on eyelids) in their third decade

Familial combined hyperlipidemia

● excessive synthesis of VLDL-C.
● increases in triglyceride and LDL-C levels,
● raised levels of apoB and elevated levels of small, dense LDL
particles.
● It is associated with an increased risk of atherosclerosis and
occurs in approximately 15% of patients who present with CHD
before the age of 60 years.

Familial type III hyperlipoproteinemia Diabetes mellitus

● accumulation of chylomicron and VLDL remnants that fail to get ● The prevalence of CHD is up to four times higher among
cleared at a normal rate by hepatic receptors due to the diabetic patients with more than 80% likely to die from a
presence of less active polymorphic forms of apoE. cardiovascular event.
→ accompanied by ● LDL levels are a stronger predictor of CV risk in diabetic
o corneal arcus patients than blood glucose control or blood pressure
o xanthelasma
o tuberoeruptive xanthomas (groups of flat or
yellowish raised nodules on the skin over joints,
Type 1 DM Type 2 DM
especially the elbows and knees)
o palmar striae (yellow raised streaks across the
palms of the hand) ● HDL-C may appear high but for ● typically have increased
o predisposes to premature atherosclerosis.. reasons which are unclear triglycerides and decreased
● Patients with type 1 diabetes HDL-C.
have a two- to three-fold ● has increased levels of highly
increased risk of developing atherogenic small dense LDL
Familial lipoprotein lipase deficiency CVD particles.
● marked hypertriglyceridaemia and chylomicronaemia, and
usually presents in childhood.
● deficiency of the enzyme lipoprotein lipase, which results in
accumulation of chylomicrons in plasma.
→ patient presents with Hypothyroidism
o recurrent episodes of abdominal pain ● Abnormalities of serum lipid and lipoprotein levels are common
o eruptive xanthomas, → may elevate LDL-C because of reduced LDL receptor
o lipaemia retinalis (retinal deposition of lipid) activity and it frequently causes hypertriglyceridaemia and an
o enlarged spleen.

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 associated reduction in HDL-C as a result of reduced
lipoprotein lipase activity
o Solution:
= adequate thyroid replacement has been instituted
the dyslipidaemia should resolve
● Dyslipidemia is determined mainly by blood tests. Because
blood lipid levels are related to meals, the ideal time to do this is
when the patient has fasted for 12 hours, usually in the morning
after waking up.
III. DIFFERENTIAL ANALYSIS

Chronic renal failure ●

● associated with reduced lipoprotein lipase activity and often A. PRIMARY
persists despite starting chronic maintenance renal dialysis.

1. familial hypercholesterolemia
Nephrotic syndrome 2. familial combined hyperlipidemia
● dyslipidaemia appears to be caused by an increased 3. Dysbetalipoproteinemia
production of apoB-100 and associated VLDL-C along with 4. familial defective apo B-100
increased hepatic synthesis of LDL-C and a reduction in 5. PCSK9 gain of function mutations
HDL-C.
● The necessary use of glucocorticoids in patients with the
nephrotic syndrome may exacerbate underlying lipoprotein A. SECONDARY
abnormality

Obesity 1. obstructive liver disease or biliary obstruction

● Chronic, excessive intake of calories leads to increased 2. Hypothyroidism
concentrations of triglycerides and reduced HDL-C. 3. nephrotic syndrome
● Individuals with central obesity appear to be at particular risk of 4. chronic renal insufficiency
what has become known as the metabolic or DROP 5. anorexia
(dyslipidaemia, insulin resistance, obesity and high blood 6. obesity
pressure) 7. metabolic syndrome, and diabetes

Alcohol
● alcohol increases hepatic triglyceride synthesis, which in turn IV. LABORATORY TESTS
produces hypertriglyceridaemia.
→ Men should be advised to limit their alcohol intake to 3–4
units a day, and not exceed 21 units a week. For Primary Dyslipidemia For Secondary Dyslipidemia
→ For women, the equivalent recommendation is 2–3 units a
day with a maximum intake of 14 units a week ● *Lipid profile measurement ● Tests include measurements
★ EVERYONE SHOULD BE ADVISED NOT TO → Total cholesterol (TC) of
BINGE DRINK AND HAVE ONE OR TWO → Triglycerides (TGs) → Creatinine
ALCOHOL FREE DAYS A WEEK (edit: tak mga → High-density lipoprotein → Fasting glucose
parahubog dida na cms tsk tsk ayaw adlaw adlawan cholesterol (HDL-C) → Liver enzymes
intawon, charis) → Low-density lipoprotein → Thyroid-stimulating
cholesterol (LDL-C) hormones (TSH)
Drugs → Urinary Protein
● Antihypertensive agents (Diuretics, ß-Blockers) → Physical examination
▪ antihypertensive agent is required, that is, without adverse
effects on lipoproteins, many studies would suggest that
angiotensin converting enzyme (ACE) inhibitors,
● Most of the clinical manifestations of dyslipidemia are detected
angiotensin II receptor antagonists, calcium channel
only when high levels of blood lipid components persist or
blockers or α-adrenoceptor blockers could be used.
cause complic
● Oral contraceptives
● Corticosteroids
● Ciclosporin
● Hepatic microsomal enzyme inducers DRUG OF CHOICE AND MODE OF ACTION

II. CLINICAL MANIFESTATIONS

● Most of the clinical manifestations of dyslipidemia are detected

only when high levels of blood lipid components persist or
cause complications in organs such as atherosclerosis,
myocardial infarction, stroke. brain vessels, yellow rashes on
eyelids, elbows, knees.
● In addition, when triglyceride levels are too high in the blood,
the plasma becomes cloudy like milk and can cause acute
pancreatitis, affecting the lungs
● In most cases, dyslipidemia is often detected late in many
different pathologies of the cardiovascular - endocrine -
metabolic group of diseases.

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 ● Serum concentrations of triglycerides increase after the
ingestion of a meal and, therefore, patients must fast for 12–15
h before they can be measured.
● Patients must also be seated for at least 5 min prior to drawing
a blood sample.xOnce the TC, HDL-C and triglyceride values
are known it is usual to calculate the value for LDL-C using the
Friedewald equation:

● The Friedewald equation should not be used in non-fasting

individuals, it is less reliable in individuals with diabetes and is
ALTERNATIVE DRUG TREATMENT AND MODE OF not valid if the serum triglyceride concentration >4 mmol/L.
ACTION
Lifestyle
● When a decision is made to start treatment with a lipid- lowering
agent, other risk factors must also be tackled as appropriate,
such as smoking, obesity, high alcohol intake and lack of
exercise
● Underlying disorders such as diabetes mellitus and hypertension
should be treated as appropriate
● Body weight and waist measurement
→ The overweight patient is at increased risk of atherosclerotic
disease and typically has elevated levels of serum
triglycerides, raised LDL-C and a low HDL-C.
→ The BMI (kg/m2) in all but the most muscular individual gives
a clinical measure of adiposity.

▪ BMI 18.5: underweight

OTHER DRUG THERAPIES AND MODE OF ACTION ▪ BMI 18.6 to 24.9: ideal
▪ BMI 25 to 29.9: overweight (low health risk)
▪ BMI 30 to 40: obese (moderate health risk)
● Fish Oil - contains omega-3 fatty acids which reduce serum
▪ BMI >40: morbidly obese (high health risk)
triglyceride levels
● Soluble Fiber - reduce lipid levels by binding bile acids in the
→ Measurement of waist circumference is perhaps the easiest
gut
● Cholesterol Ester Transfer Protein Inhibitors and most practical indicator of central obesity and correlates
well with CVD risk.
➔ lowering of CETP increase levels of HDL-C
▪ Target waist circumference should be <102 cm in white
➔ prevent CETP from transferring cholesterol from HDL-C caucasian men, <88 cm in white caucasian females and in
to LDL-C
Asians <90 cm in men and <80 cm in females.
● Diet
ALTERNATIVE TREATMENT STRATEGIES → Diet modification should always be encouraged in a patient
with dyslipidaemia but is rarely successful alone in bringing
● Avoid smoking about a significant improvement in the lipid profile
● Regular exercise
● Diet rich in fiber
→ Fish.
● Diet low in saturated fat
▪ Regular consumption of the long chain omega-3 fatty
acids, principally ecosapentaenoic acid and
PALLIATIVE CARE
docosahexaenoic acid, typically found in fatty fish and fish
oils, has been linked to the low levels of CHD seen in
● prevention and relief of suffering of any kind – experienced by Inuits (Eskimos).
adults and children living with life – limiting health problems
→ Trans fats.
▪ Trans fats are unsaturated fatty acids with at least one
double bond in the trans configuration.
▪ They are formed when vegetable oils are hydrogenated to
convert them into semisolid fats that can be incorporated
into margarines or used in commercial manufacturing
processes.
▪ When the calorific equivalent of saturated fats, cis
unsaturated fats and trans fats are consumed, trans fats
TREATMENT: BOOK raise LDL-C, reduce HDL-C and increase the ratio of
TC:HDL-C.
Lipid profile ▪ trans fats also increase the blood levels of triglycerides,
● When a decision has been made to determine an individual's increase levels of Lp(a) and reduce the particle size of
lipid profile, a random serum TC and HDL-C will often suffice. LDL-C, all of which further increase the risk of CHD.

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→ Stanol esters and plant sterols
▪ The availability of margarines and other foods enriched
with plant sterols or stanol esters appears to increase the
likelihood that LDL-C can be reduced by dietary change.
→ Antioxidants.
▪ consumption is thought to be beneficial in reducing the
formation of atherogenic, oxidised LDL-C
→ Salt.
▪ As part of dietary advice the average adult intake of
sodium should be reduced from approximately 150 mmol
(9 g)–100 mmol (6 g) of salt or even lower.
▪ This intake can be reduced by consuming fewer
processed foods, avoiding many
→ ready meals and not adding salt to food at the table
● Exercise
→ Moderate amounts of aerobic exercise (brisk walking,
jogging, swimming, cycling) on a regular basis have a
desirable effect on the lipid profile
Drugs
Primary prevention
● treatment will normally include:
▪ lipid-lowering agent such as simvastatin 40 mg/day (or
alternative) but no treatment targets are set
▪ personalised information on modifiable risk factors
including physical activity, diet, alcohol intake, weight and
tight control of diabetes
▪ advice to stop smoking
▪ advice and treatment to achieve blood pressure below
140 mmHg systolic and 90 mmHg diastolic.
Secondary prevention
● In individuals diagnosed with CVD or other occlusive arterial
disease, treatment should include:
▪ a lipid-lowering agent to lower TC aiming towards a TC
<4 mmol/L and LDL-C <2 mmol/L
▪ advice to stop smoking
▪ personalised information on modifiable risk factors
including physical activity, diet, alcohol intake, weight and
diabetes
▪ advice and treatment to achieve blood pressure at least
below 140 mmHg systolic and 90 mmHg diastolic
▪ tight control of blood pressure and glucose in those with
diabetes
▪ low-dose aspirin (75 mg daily)
▪ ACE inhibitors especially for those with left ventricular
dysfunction, heart failure, diabetes, hypertension or
nephropathy
▪ b-blocker for those who have had a myocardial infarction
and in those with heart failure
▪ warfarin (or aspirin) for those with atrial fibrillation and
additional stroke risk factors.
LIPID LOWERING DRUGS
Statins
● Their primary site of action is the inhibition of HMG-CoA
reductase in the liver and the subsequent inhibition of the
formation of mevalonic acid, the rate-limiting step in the
biosynthesis of cholesterol.
● The overall effect is a reduction in TC, LDL-C, VLDL-C and
triglycerides with an increase in HDL-C.
● Simvastatin is currently the preferred agent because of its
relatively low cost, safety profile and evidence of efficacy
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● Rosuvastatin is the most potent of the statins with evidence of
impact on morbidity and mortality.
● It is normally reserved for those individuals that have had an
inadequate response to their first-line statin.
● Adverse effect of rosuvastatin: rhabdomyolysis
Fibrates
● Members of this group include bezafibrate, ciprofibrate,
fenofibrate and gemfibrozil.
● They are thought to act by binding to peroxisome
proliferator-activated receptor α (PPAR-α) on hepatocytes.
● fibrates reduce triglyceride and, to a lesser extent, LDL-C levels
while increasing HDL-C
● fibrates should not be used first line to reduce lipid levels in
either primary or secondary prevention.
● Fibrates can be used first line in patients with isolated severe
hypertriglyceridaemia.
Bile acid binding agents
● The three members of this group in current use are
colestyramine, colestipol and colesevelam.
● Each of the bile acid binding agents reduce TC and increase
triglyceride levels.
● With all three agents, side effects are more likely to occur with
high doses and in patients aged over 60 years.
Cholesterol absorption inhibitors
● Ezetimibe is a 2-azetidinone derivative that interacts with a
putative cholesterol transporter in the intestinal brush border
membrane and thereby blocks cholesterol re-absorption from
the gastro-intestinal tract
Nicotinic acid and derivatives
● Nicotinic acid in pharmacological doses (1.5–6 g) lowers serum
LDL-C, TC, VLDL-C, apolipoprotein B, triglycerides and Lp(a)
and increases levels of HDL-C (particularly the beneficial HDL3
subfraction).
● licensed for use in combination with a statin, or by itself if the
patient is statin intolerant or a statin is inappropriate
● The commonest side effect: flushing which is most prominent in
the head, neck and upper torso
Fish oils
● Fish oil preparations rich in omega-3 fatty acids have been
shown to markedly reduce serum triglyceride levels by
decreasing VLDL-C synthesis, although little change has been
observed in LDL-C or HDL-C levels.
Soluble fiber
● The fibre is thought to bind bile acids in the gut and increase the
conversion of cholesterol to bile acids in the liver
● Cholesterol ester transfer protein (CETP) inhibitors
● Low levels of CETP are associated with increased levels of
HDL-C and reduced cardiovascular risk
X. GOAL OF THERAPY
★ Reduce the risk of cardiovascular disease by:
Lower the LDL levels
Control Triglyceride Levels
Raise the HDL levels
XI. POSSIBLE DRUG INTERACTIONS
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 1. ORAL CONTRACEPTIVES

➢ Anti-HIV Drugs
➢ Anti-Fungal Medications
➢ Anti-Seizure Drugs

2. CICLOSPORIN

➢ Statins
➢ Antibiotics
➢ Antineoplastics
➢ Antifungals
➢ Anti-inflammatory drugs

3. CORTICOSTEROIDS

➢ Drugs that affect the levels of potassium in blood (e.g.

diuretics, certain laxatives)
➢ Drugs that have known side effects when potassium
levels drop in the bloodstream. (e.g. digitalis)
➢ Drugs resulting in decreased cortisone in the blood
(e.g. rifampicin, carbamazepine, phenobarbital,
phenytoin, primidone) or decrease the
gastrointestinal absorption of cortisone (e.g. gastric
dressing)
➢ Lithium (corticosteroids decrease blood levels of
lithium)

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