Acne and Rosacea Charity Training Manual

A R A U K
Acne and Rosacea Association UK

Module - 1
Acne Pathogenesis

Acne - Pathogenesis
The pathogenesis of acne is really very simple but new discoveries have demonstrated novel mechanisms that may improve our understanding of the disease
and lead to better treatments.
Acne is frequently a familial condition and severe or persistent acne may be seen in successive generations. It is a very common condition presenting a
spectrum from very mild disease with a few comedones to fulminant nodulocystic acne. As it is so common, it is deemed by some to be almost physiological.
Acne occurs in the pilosebaceous follicles which are present over the whole surface of the skin, apart from the palms and soles. It is a specific disease and is the
commonest disease within the spectrum of the follicular occlusion syndrome which includes hidradenitis suppurativa and dissecting folliculitis.
It is essential to understand the pathogenesis of acne to be able to treat it properly. There are essentially 4 main steps in the pathway to inflammatory acne
(Figure 1):
1. Increased sebum secretion
2. Follicular hypercornification with the development of the primary
lesion of acne, the microcomedone
3. Proliferation of the commensal anaerobic bacterium,
Propioibacterium acnes
4. Inflammation that is mediated by a T cell immunological
mechanism
Acne eventually resolves with the advent of development of immune
tolerance to the agents that are inducing the inflammatory response.
Glossary
• Pilosebaceous unit – Anatomical structure comprising the hair follicle and attached sebaceous gland with its exit onto the surface of the skin as the skin pore.
• Hidradenitis suppurativa – An inflammatory condition affecting specific sites of the body – mainly axillae, groins and under the breasts in women - where the apocrine
sweat gland arises from the hair follicle above the sebaceous gland. Occlusion of the follicle leads to buildup of apocrine secretions which lead to deep inflammation and
scarring.
• Dissecting folliculitis – Inflammatory condition of the pilosebceous unit in the scalp with multiple adjacent units becoming inflamed and the follicles rupture together to
form deep inflamed lesions with sinuses onto the scalp
• Hypercornifiaction – buildup of dead skin cells forming a partial blockage of the hair follicle
• Anaerobic – an organism that grows in the absence of oxygen

Sebum excretion
The sebaceous gland is one of the first glands to become active in foetal development. It is mainly controlled by androgens (male hormones) that after puberty are
produced by the gonads and the adrenal glands. In foetal life, androgens are derived from the maternal bloods supply and sebum produced solidifies as vernix
caseosum in the newborn.
Sebaceous glands gradually atrophy during infancy but in the infant sebum production is responsible for seborrheic dermatitis (cradle cap in the infant) and
neonatal acne. This stops in the second or third year of life.
Sebaceous glands are stimulated with the onset of adrenarche which may occur as early as 9 years in girls. This is heralded by the onset of oily skin and the
development of open comedones, particularly on the nose. With puberty, oil production increases and may lead to the onset of inflammatory acne. Ambient
temperature may have an effect on sebum production and most people with acne notice that their skin is oilier when they go on a sunny holiday.
With advancing age the oil gland become less active and sebum production reduces. As sebaceous glands are holacrine glands – i.e. the sebaceous cells accumulate
oil and the rupture and disgorge their contents into the hair follicle – as sebum production reduces, the cells accumulate and the glands get bigger. From being
microscopic and not visible, they enlarge to become pale or slightly yellowish papules, often with a central dip – at this stage they are called sebaceous gland
hyperplasia.
In acne, sebum production is increased leading to an oily skin. This is generally the hallmark of acne. Some patients, however, have a combination skin, with areas of
dryness and areas of oiliness.
Oil production is controlled by androgens but it is important to realize that in the majority of patients with acne, androgen levels are normal. Increase oil production
is due to an end organ response to the normal androgen levels and is an integral part of the disease. In men, androgen levels are always normal. In women, 30% may
have elevated levels of free testosterone as part of the polycystic ovary syndrome.
In addition to sebum levels being increased, the excess oil changes its normal constituents. Acne sebum is deficient in linoleic acid, an essential fatty acid, which may
be responsible for some of the morphological changes seen in acne (see section 2).
Glossary
• Androgen – male hormone, initially produced as testosterone by the gonads and adrenal glands but this the converted to its more active form in the sebaceous gland by the
enzyme 5-α-reductase. Testosterone is held in an inactive form in the blood by a protein called sex hormone binding globulin
• Adrenache – maturation of the adrenal glands which occurs before puberty
• Polycystic ovary syndrome – ovaries develop multiple cysts and generate increased levels of testosterone or low levels of sex hormone binding globulin which means that
more free/active testosterone is circulating. This syndrome may be manifest by increased weight gain, facial hirsutism and irregular periods.
• Essential fatty acid – this is a fatty acid that the body cannot manufacture and must be acquired from dietary sources.

Follicular Hypercornification
The ostium of the hair follicle or skin pore is lined with keratinocytes.
Keratinocytes are the major cell of the epidermis and continually divide and as
they push to the surface of the skin they mature to squames or dead skin cells
(Figure 1), which are then shed and removed by the flow of oil. The hair follicle
thus remains open allowing sebum to freely escape onto the surface of the
skin.
In acne, this changes with the cells growing abnormally and accumulating
within the follicle leading to the formation of a partial blockage – the
microcomedone. This is the primary lesion of acne and for successful
treatment it is essential to target this lesion.
Figure 1- Maturation of keratinocytes from pluripotent stem cells to
dead squames which are shed.
The development of the microcomedone has been extensively studied and two possible mechanisms have been suggested:
1. The change in the growth of the keratinocyte is due to an immunological reaction, possibly due to the local production of interleukin (IL)1. Studies looking at
isolated human pilosebaceous follicles stimulated with IL1. develop follicular hypercornification.
2. The growth change in keratinocytes is the result of alteration in the constituents of sebum. In rats made deficient in linoleic acid, they develop follicular
hypercornification. As stated before, the oil in sebum from acne sufferers is deficient in linoleic acid.
The microcomedone is a time bomb, waiting to go off, and when it does the inflammatory lesion of acne develops. They are microscopic which means that when you
target them, you need to treat the whole area of affected skin not just spots that you can see. With time, the blockages become bigger and visible. If they are close to the
surface, oxidation of surface lipids leads to pigmentation – the black of the blackhead. If deeper in the follicle they bulge giving rise to the closed comedone.
Glossary
• Interleukin (IL)1. – Interleukins are chemical produced by a variety of cells, particularly those involved in immunological reactions. IL1 is produced by a number of cells
including keratinocytes when they are stimulated by an immunological reaction.

Proliferation of P acnes
P acnes is a normal commensal bacterium in the skin which resides in active pilosebaceous follicles. Everyone has this bacterium in the skin, whether you have
spots or not. What causes the body’s immune system to react to it is not fully understood although there are a number of theories that have been proposed:
1. It has been shown that T lymphocytes isolated from early acne lesions are reactive to P acnes. Why the immune system should react to P acnes in
some people and not others have been a matter of debate. One possibility is that the milieu of the acne follicle with altered sebum constituents leads
to a change in the surface antigens on the bacteria and induce the immunological reactivity.
2. Keratinocytes express specific receptors called Toll-like receptors. These are analogous to the Toll receptor first identified in fruit flies or Drosophila.
These receptors recognize highly conserved antigens on the surface of certain bacteria and this triggers an immunological response as part of the
innate immune response to prevent infection. It has been shown that P acnes is recognized by Toll-like receptors in the skin and it has been suggested
that this can lead to the inflammation seen in acne. Why this does not occur in everyone, as we all carry the bacterium, is up for further investigation.
P acnes is an anaerobe, meaning that it grows in the absence of oxygen and is inhibited or killed by oxygen. The bacterium produces a protoporphyrin which
fluoresces in polarized black light and can be used as a target with forms of light therapy (see Module 5)
P acnes forms a biofilm, an amorphous goo that protects it from antibiotics and may contribute to follicular obstruction, contributing to the formation of the
microcomedone.
Glossary
• Milieu – environment
• Innate immune response – an ancient part of the immune system that reacts to infection and injury in a nonspecific manner and helps the body to prevent infection
• Protoporphyrin – a complex chemical related to the protein involved in Haem synthesis. It is a potent photosensitizer and when excited with light of specific
wavelengths, will lead to the production of free radicals and singlet oxygen, which are destructive

Inflammation
The inflammatory response in acne is very specific. The initial inflammatory response leads to recruitment of neutrophils within the follicle which leads to pus
formation.
Studies, as discussed in section 3, have shown that T cells in early acne lesions are reactive to P acnes. A typical type 4 immunological response would lead to an
eczematous reaction if on the surface of the skin or an itchy papule if deep in the skin, so the response in acne must lead to a specific cascade which induces the
infiltration of neutrophils, possibly due to local production of cytokines.
Stimulation of Toll-like receptors by P acnes could result in a pustular reaction but the unanswered question is why do people with acne respond in this way
while people without acne who are still exposed to the bacterium do not?
A number of early studies suggested that the breakdown of sebum into free fatty acids by P acnes could trigger an inflammatory response. But studies in which
free fatty acids are injected into the skin have failed to demonstrate an inflammatory response.
Morphological studies have shown rupture of follicles which would allow highly inflammatory constituents of the follicle to escape into the dermis where they
could induce an acute inflammatory response.
Summary
Simplistically, in the acne sufferer, sebum production is abnormally high. Follicular hyperkeratosis restricts oil flow onto the surface of the skin with oil retained in
the follicle which solidifies. This is the cheesy material that you squeeze out when you squeeze blackheads. Follicular occlusion leads to pooling of oil in the
follicle which stimulates proliferation of P acnes and this leads to an inflammatory response with ultimate pus formation. The pus takes the path of least
resistance and in most will point to the surface and bust onto the surface of the skin. If the inflammation is deeper in the follicle it may be retained within the
follicle and slowly resolve leading to clinical nodules, or may rupture into the dermis with damage to collagen and eventual scarring. Cystic lesion result from
fusion of adjacent inflamed follicles leading to lakes of pus with multiple heads.
Glossary
• Neutrophils – also known as polymorphs are white blood cells that will be induced to migrate into areas of inflammation or infection and lead to pus formation
• Type 4 response – immunological reactions have been classified into 4 types – type 4 is where the immune system reacts to a local antigen with a response of T
lymphocytes which leads to an eczema if it is on the surface of the skin or an itchy lump in the skin if it is deep in the skin.

Acne – Exacerbating factors
A number of factors can lead to an exacerbation of acne or may induce the development of acne in a susceptible person:
Hormonal changes
The onset of acne frequently coincides with the onset of puberty, with the first bursts of androgens comings from the gonads.
In women, exacerbations are often seen premenstrually. As a woman comes up to the period, oestrogen levels fall. Oestrogen induces sex hormone binding
globulin, which inactivates testosterone and has a direct anti-androgen effect. The fall of oestrogen can thus lead to a flare of acne.
Contraceptives
All contraceptive drugs are based on progesterones with or without oestrogens. Second generation progesterones are the commonest used in contraceptives
including oral and depot contraceptives and also present in the Mirena coil. Unfortunately, these progesterones have androgenic properties and can
exacerbate acne.
In the acne prone woman, contraceptive containing third generation progesterones should be used. The third generation progesterones include desogestrel
(contained in Marvalon) and norgestimate (present in Cliest).
Two contraceptive pills contain progesterones that have anti-androgenic effects. These contain cyproterone acetate (contained in Dianette) and drospirenone
(contained in Yasmin). Drospirenone is less effective as an anti-androgen than cyproterone acetate having only about 33% of the activity of cyproterone
acetate. In the UK Dianette is not licensed as an oral contraceptive but only as an anti-acne treatment.

High humidity
The comedone is formed in part by follicular hyper-cornification. The dead skin cells are a bit like dried
leaves and with sweat retention against the skin, or high humidity, the cells can swell and lead to an
acute blockage of the follicle and an intense inflammatory response. A major medical problem during
the Vietnam War was fulminant, tropical acne. High humidity in Vietnam led to acute follicular
occlusion in the young American GIs. Patients with acne should avoid saunas and steam rooms and
should be warned of the possibility of an exacerbation if they travel to the tropics.
Stress
Stress, whether physical or mental will stimulate the adrenal gland, leading to production of
adrenaline and steroids but also androgens. This will lead to exacerbation of acne. This is frequently
seen in students coming up to exams. Stress in the workplace has also been implicated in the
development of acne in older women who have high powered stressful jobs.
Unrecognized stress to the body may be responsible for exacerbation of acne in people who have a low
level, non-clinical sensitivity to certain foods including gluten and lactose. It is not unusual for patients
to report that when they go on a gluten or milk free diet their acne improves.
Stress in modern life may also be responsible for the persistence of acne in older age groups.

Drugs
A number of drugs may exacerbate acne. In some the mechanism of action is obvious, in others it is unknown.
• Corticosteroids – steroids are widely used in medicine to reduce inflammation. In the
non-acne individual, steroids can induce a follicular reaction called steroid acne (Figure
2). This is not true acne as comedones are not present and the inflamed papules are
fairly monomorphous. In the acne patient, steroids will exacerbate existing acne.
• Anabolic steroids – these drugs are used by bodybuilders and athletes and have
androgenic properties. These can cause and exacerbate acne.
• Second generation progesterones – see above section on oral contraceptives
• Lithium – this drug used for bi-polar disease can cause a very severe exacerbation of
acne leading to nodulocystic acne developing. The mechanism underlying thus is
unknown.
Figure 2 - Steroid acne due to oral prednisolone
Figure 3 - Chloracne caused by Dioxin poisoning
• Anti-convulsant drugs – all anti-epilepsy drugs can exacerbate acne which can be
very difficult to manage. Mechanism behind this is unknown
• Historically, bromides, iodides and other halogens have been associated with
exacerbation of acne, partly by stimulating aggressive comedogenesis.
• Halogenated hydrocarbons - In well documented industrial disasters, halogenated
hydrocarbons such as chlorinated dioxins and dibenzofurans used in the
manufacture of herbicides such as Agent Orange have been released into the
atmosphere causing a severe form of acne called Chloracne. In 1949, 226 workers
became ill after a container of herbicide exploded at a Monsanto Company plant
in Nitro, West Virginia. [5] Many were diagnosed with chloracne (Figure 3).

Psychological impact of acne
Acne is generally a very visible disease affecting the face and causing considerable psychological problems for the sufferer. The acne sufferer is often made to feel
guilty about their skin and made to feel that it is their fault that they have the condition. This is perpetuated by a number of myths that surround acne:
1. It is a teenage disease - clinical experience and recent publications have demonstrated that acne can persist throughout adult life and may occur for the first
time in adult life, induced by stress. A recent publication of a population in the USA showed that the incidence of acne over 50 years of age was 15% in women
and 7% in men (Figure 4). Adults with acne are often misdiagnosed as a skin infection or folliculitis and are embarrassed to have a ‘childhood’ disease.
Figure 4
J Am Acad Dermatol. 2008 Jan;58(1):56-9..
The prevalence of acne in adults 20 years and older.
Collier CN 1 , Harper JC, Cafardi JA, Cantrell WC, Wang W, Foster KW, Elewski BE

2 Acne is caused by poor diet, too much fried food and sweets - extensive studies in USA in children with acne have shown that the severity of acne
correlated with only 2 dietary factors – high dairy and high sugar. Such diets induce the formation of a hormone called insulin like growth factor which
has male hormone effects. Most people can eat a good balanced diet without problem. An occasional patient will report that giving up wheat or other
food stuffs led to an improvement of their acne. In such individuals, a low-grade sensitivity to those food stuffs could induce a degree of stress which
in turn will stimulate the adrenal gland and lead to higher androgen production (see section on stress)
3 Acne is due to poor cleanliness - patients with acne often have oily skin and will wash excessively to get rid of this. This will often make the skin too
sensitive for the use of the topical treatments they need to use. Acne sufferers should wash only twice a day. Blackheads are not caused by poor
cleanliness or dirt.
Acne can cause anxiety, depression, reclusiveness and suicidal ideation. It may be the cause of failure to achieve at school or university and has been
shown to increase the risk of unemployment.
Some patients with acne develop dysmorphophobia – an abnormal image of their body and the severity of their acne and even very mild acne will result
in them not going to school or work and staying hidden at home.
An unusual form of acne has been termed –‘acne excoriee des jeune filles’.
This is predominantly seen in young women who are convinced that the
cause of their acne is an abnormality deep in the skin and will pick and
excoriate the skin in an attempt to get rid of this abnormality and this leads
to severe scarring of the skin (Figure 5). This can be very difficult to manage.
All physicians treating acne should be aware and sensitive to the
psychological impact that this disease can have on the sufferer. Referral for
psychiatric evaluation should always be considered.
Figure 5 – Acne excoriee des jeune filles

Module - 2
Acne - Clinical

Acne – Clinical
The clinical lesions of acne can be divided into non-inflammatory and inflammatory. All clinical lesions arise from the micro-comedone, which is the primary
lesion of acne (see Module 1).
Non-inflammatory lesions of acne
Micro-comedones, as the name suggests are microscopic and are not clinically visible. These develop into open comedones – blackheads (Figure 1a), and
closed comedones – white heads (Figure 1b). In these lesions, the follicular cornification restricts oil flow to the surface with accumulation of sebum in the
follicle solidifies and gives rise to the toothpaste like substance that you squeeze out with blackheads. Blockage of the skin pore is compounded by the
formation of biofilm by P acnes.
Figure 1a - Open Comedones
Figure 1b - Mainly Closed Comedones and Papules
Glossary
• Biofilm – a matrix of extracellular polymeric substance produced by P acnes which sticks the bacteria together and to the follicular wall.

In some patients, comedones can be deep and so large that they totally
obliterate the skin pore. These are called macro-comedones (Figure 2).
These lesions do not respond to medical treatment and are often
responsible for the deeper nodular inflammatory lesions of acne.
Topical retinoids can loosen the blockage but the plug cannot get to
the surface. The only way of getting rid of them is to lightly cauterize the
surface of the skin which allows them to escape (see Module 4). Macrocomedones
are a contraindication to oral isotretinoin as they have the
potential to generate severe inflammatory lesions with the drug leading
to scarring.
Figure 2 – Macro-comedones
On the nose, the follicles are different to the follicles on general
glabrous skin often containing multiple hairs. With follicular hyper
cornification, the multiple hairs compound the follicular blockage
and blackheads are generally larger. This leads to a condition known
as Trichostasis spinulosa (Figure 3). Cosmetically this causes
problems and is more difficult to treat than normal comedones and
requires longer treatment with topical retinoids.
Figure 3 Trichostasis spinulosa

Inflammatory Acne
The clinical lesions of inflammatory acne are analogous to the Staphylococcus aureus infection of the hair follicle. Superficial infections of the hair follicle with S
aureus give rise to folliculitis with a superficial pustule developing which ruptures easily. In acne, superficial inflammatory lesions lead to papules and pustules
(Figure 4). These are normally painless and resolve quickly. Comedones are always present (Figure 5).
Figure 5 – Superficial Inflammatory Acne with Obvious
Comedones
Figure 4 – superficial inflammatory acne

With deeper lesion developing the deeper inflammatory lesions of acne
are analogous to furuncles in S aureus infections. These nodular lesions
are often painful and may last weeks before resolving. Some may not
come to a head and the pus takes time to be absorbed by the immune
system. Rupture of the follicle could lead to damage to collagen and
scarring (Figure 6)
Figure 6 – Deeper inflammatory acne with some
scarring
Cystic acne develops when adjacent nodules rupture together
analogous to a S aureus carbuncle. This leads to a large cavity
under the skin that is full of pus with multiple heads representing
the follicular openings. These are often persistent or recurrent
and generally lead to scarring (Figure 7).
Figure 7 – Multiple cysts with evidence of deep scarring

Skin changes depending of skin type
In skin Phototype 2 and 3, acne will resolve to leave normal skin or scarring.
However, in Phototype 1 skin, acne lesions may result in persistent
erythematous macules which look like active disease. In the inflammatory
process, cytokine cause vascular proliferation. In most individuals, the
vessels are remodeled and cleared fairly quickly. However, in Phototype 1
skin, the vessels may persist for many months. (Figure 8)
Figure 8. Persistent erythematous macules with active
papules and pustules making the acne look more severe
In Phototype 5 and 6 skin, post-inflammatory hyperpigmentation may
follow an inflammatory spot. These hyper-pigmented macules can last
for months or even years are some patients feel they are as bad as the
active acne (Figure 9)
Glossary
Figure 9 – Postinflammatory hyperpigmentation in a patient with
Phototype 6 skin with mild active acne
• Phototype – this is a classification of human skin developed by an American Dermatologist called Fitzpatrick which describes the skin response to ultraviolet light. There
are 6 Phototypes, Type 1 is the blond or redheaded Celt with freckles who burns in the sun; Type 6 is Afrocaribean skin.

Module - 3
Conventional Treatments of Acne

Conventional treatment of acne
As you will have learnt from module 1, acne can be divided into two parts:
1. Follicular hypercornification leading to the formation of the micro-comedone and the non-inflammatory lesions of acne
2. Inflammatory lesion of acne resulting from a type VI immunological reaction to proliferating P acnes
In patients with predominantly non-inflammatory acne the main target is the follicular hypercornification. In the majority of patients, however, there is a mix of
lesions and it is important to target both types of lesion.
Non-inflammatory acne
Follicular hypercornification is due to an abnormal growth of follicular keratinocytes leading to a partial blockage of the skin pore. The two main ways in which
this can be treated are to correct the keratinocytes growth or to dissolve the blockage.

Topical retinoids
Retinoids work by normalizing keratinocyte growth and are therefore used in conditions in which keratinocyte growth is abnormal. Systemic retinoids are use in
psoriasis, the ichthyoses and acne. Topical retinoids are the agents generally used in acne.
In the UK we have a limited number of topical retinoids and the majority of them are only available on prescription:
0.1% isotretinoin – marketed as Isotrex gel or in combination with 2%erythromycin as Isotrexin
gel.
0.025% tretinoin – marketed with 4% erythromycin as Aknemycin plus lotion or with 1%
clindamycin as Treclin gel. Retin A was discontinued some years ago but still can be
purchased online.
0.1%adapelene – marketed as Differin gel or cream or with 3% benzoyl peroxide marketed as
Epiduo
0.05% tretinoin is available on private prescriptions marketed Airol cream or Ketrel cream. Beware of on line products which may not have the same effect.

Topical Retinoids
A topical retinoid should be an essential part of any anti-acne regime. They are potentially photosenistisers so should only be used at night and washed off in
the morning. They may cause dryness and irritation of the skin – part of hyper-vitaminosis syndrome and must be used cautiously. A dollop the size of a pea is
enough to cover the whole face. It is very important to instruct your patient how to use the retinoid properly and to use it to all parts of the body affected. It is
really common to find a patient has been using the retinoid to the face but not chest, back, arms etc.
Some patients have very sensitive skin and may not tolerate the topical retinoid, even when used properly. In such patients, try using it short contact. Apply for
3 hours in the evening and wash off and moisturize.
The worst skin type for topical retinoids tends to be Indian Asian skin and many patients in this ethnic group are unable to tolerate the retinoid even when used
short contact.
Topical retinoids should not be used in women who are trying to conceive or are pregnant. Vitamin A is teratogenic and could affect a developing foetus.
Absorption of topical retinoids is minimal and the risk to the foetus is very small but women of child bearing age should be warned of this potential risk.
Glossary
• Photosensitiser – an agent that increases the sensitivity of the skin to sunlight leading to an exaggerated sunburn reaction
• Teratogenic – causing birth defects in a developing foetus

Alternative agents for non-inflammatory lesions of acne
Salicylic acid
Salicylic acid is keratolytic i.e. it dissolves keratin and can help to clear follicular blockage. It is usually available as a 2% product in washes
and gels. Always warn patients to try it in a test area first as salicylic acid is a sensitizer and allergy to salicylic acid is not uncommon.
Azeleic acid
Azeleic acid is available as a 20% cream (Skinoren cream) marketed for the
treatment of acne or as a 15% cream (Finacea cream) marketed for the treatment
of rosacea. Azeleic acid is comedolytic so can help to unseat comedones but is
not as effective as a topical retinoid. It does have some anti-inflammatory activity
so will treat inflammatory lesions of acne as well. It can be irritant so patients
should be warned to use it with caution.
Benzoyl Peroxide
Benzoyl peroxide has very mild comedolytic activity which is not sufficient on its own to treat non-inflammatory acne.

Tebiskin OSK and UV OSK (clinic version of retail and prescription Aknicare Lotion and Cream)
These products contains triethyl citrate and ethyl linoleate in a formulation that contains a number of other active ingredients including 0.5% salicylic acid. Aknicare is
available on prescription and can also be purchased over the counter or on line. Tebiskin OSK is the stronger private clinic only medical device range with greater antiinflammatory
activity and a higher concentration of the key active ingredients
It works in two ways, the first activity is on hyper-cornification and secondly it has a an antimicrobial action on P acnes without using antibiotics
1. As you will have learnt from Module 1, one possible mechanism for the development of the follicular hyper-cornification is a relative deficiency of acne sebum of
linoleic acid. OSK/Aknicare preparations increase linoleic acid concentrations in the follicle and thus suppress follicular hyper-cornification. Ethyl lineolate which
is digested by follicular bacteria and cutaneous enzymes into linoleic acid which can influence skin sensitivity to di-hydro-testosterone a key trigger of the acne
process.
2. Antimicrobial effect. Bacteria in the blocked follicle release enzymes to break down sebum to glycerol which they absorb as nutrient and the remaining free fatty
acids left from the enzyme breakdown exacerbate the immune response and inflammation. Also the bacteria congregate together for protection into a biofilm
which makes them more resistant to the body’s defense mechanisms and also to antibiotics designed to reduce or eradicate them. OSK/Aknicare utilises triethyl
citrate which is a preferential substrate for the bacterial enzyme (lipase). This means the bacterial enzyme (lipase) has a greater affinity to triethyl citrate hydrolysis
than for sebum hydrolysis. This has three effects
a. Glycerol availability is reduced (bacteria receive no nutrients) and sebum triglycerides remain intact.
b. Free fatty acid levels are reduced helping to control inflammation
c. The bacterial enzyme breaks down triethyl citrate sequentially into three molecules of citric acid. This lowers the pH in a sustained way in the follicle to a
level which kills the bacteria. The bacteria are more protected when enclosed in a biofilm, but OSK/Aknicare also contains a special peptide (GT Peptide)
which opens channels into the biofilm allowing the citric acid to also
kill the bacteria effectively within the biofilm and rapidly.
OSK/Aknicare products can be used in patients who are unable to tolerate topical retinoids or can be
used with topical retinoids – using the retinoid at night and OSK/Aknicare in the morning. It is safe to
use during conception and pregnancy.

Inflammatory acne
In mild to moderate acne, start with topical agents which can be very effective. In all patients apart from those with mild acne, always combine treatment
with a topical retinoid or other anti-comedonal treatment.
Topical treatment for inflammatory acne
Benzoyl peroxide
Benzoyl peroxide is used commercially to bleach flour. When applied to the skin it will enter the hair follicle and release oxygen. This is toxic
to the anaerobic bacteria living in the follicle including P acnes and kills them. It is a very effective treatment for inflammatory acne and the
bacteria cannot develop resistance to it.
Benzoyl peroxide is available in a number of different formulations from 2.5% to 10% in creams, gels and washes. It can be applied in the
morning to affected areas. It is very effective but does have a number of problems:
1. It is a bleaching agent and will bleach clothes, towels and bedding. Warn patients of this and advise to use white towels and white
pillowcases. If used on the trunk, white T-shirts
2. Benzoyl peroxide can be very drying and irritating. Some patients can only tolerate the lower concentrations. Advise care when using
benzoyl peroxide washes as they may make the skin too sensitive to use topical retinoids or other topical products.
3. Benzoyl peroxide is a sensitizer and patients may become allergic to it. Tell patients to use to a test area for a few days before using it
all over.
Benzoyl peroxide is also available in combination with adaplene (marketed as Epiduo, 0.1% adapalene with 3% benzoyl peroxide), targeting
inflammatory and non-inflammatory lesions at the same time.
A number of the benzoyl peroxide products came off the shelves due to manufacturing problems. Thankfully, they are now available on
prescription and over the counter.

Topical antibiotics
The main topical antibiotics used in acne are erythromycin and clindamycin. Both are very effective in treating inflammatory acne but the development of
antibiotic drug resistance may limit their usefulness.
Clindamycin
Clindamycin is available in a number of preparations:
1% alcoholic solution or lotion (marketed as Dalacin T) was the first topical antibiotic used in
acne. Usefulness is now limited by high antibiotic drug resistance.
1% clindamycin available as a gel with 3% or 5% benzoyl peroxide (marketed as Duac 3% or
5%). The benzoyl peroxide limits antibiotic drug resistance and will kill resistant bacteria.
Problems may occur with benzoyl peroxide as detailed on section of benzoyl peroxide
1% clindamycin with 1.2% zinc gel (marketed as Zindaclin gel). Zinc is supposed to reduce
drug resistance .Useful for treatment of the trunk or in patients where benzoyl peroxide needs
to be avoided.
1% clindamycin with 0.025% tretinoin (marketed as Treclin gel), this is a useful combination targeting inflammatory and non-inflammatory
lesions.

Erythromycin
Erythromycin is available in a number of preparations:
2% alcoholic solution (marketed as Steimycin), there are now issue with this solution due to antibiotic drug resistance.
4% alcoholic solution with 1.2% zinc (marketed as Zineryt lotion). The high concentration of erythromycin gives
good results in inflammatory lesions.
2% erythromycin is also available with 0.1% isotretinoin (marketed as Isotrexin) where the antibiotic reduces the irritancy of the retinoid and
targets inflammatory and non-inflammatory lesions at the same time.

Alternative topical therapy
Tebiskin OSK and UV OSK (clinic version of retail and prescription Aknicare Lotion and Cream) are also indicated in the
treatment of inflammatory acne
This preparation contains triethyl citrate and ethyl linolate in a carrier base that has a number of additional active ingredients. The triethyl citrate is
digested by follicular bacteria to diethyl citrate, monoethyl citrate and then to citric acid. This lowers the pH in the follicle which inhibits bacterial growth
and inhibits 5a-reductase, which in turn reduced sebum secretion.
The ethyl linolate is digested to linoleic acid which reduces follicular hypercornification and also has potent anti-inflammatory properties.
This product thus has anti-bacterial and anti-inflammatory effects and can reduce sebum production. It is well tolerated and a spray preparation is
available for use on back and chest.
See previous information in this section for more detail
Nicotinamide
This product was initially marketed as Papulex gel, then relaunched as Nicam gel and an OTC product is now
available as Freederm gel. It is anti-inflammatory and has its main effect on inflammatory lesions. Initial studies
showed that its efficacy was similar to benzoyl peroxide.

Systemic Antibiotics
Tetracyclines
The tetracyclines are the most commonly used antibiotics in acne. They have good activity against P acnes and have
potent ant-inflammatory activity. All tetracyclines can photosenitise but in practice, this is only a problem with
doxycycline, where 25% of patients can develop a significant photosensitization. A rare side effect of tetracyclines is
benign intracranial hypertension – this presents with severe headaches and the drug should be stopped immediately.
Tetracycline will colour developing secondary dentition and should be avoided in children under the age of 13 years.
Oxytetracycline –dose 250mg QDS. This is the most commonly used tetracycline as it is the cheapest. It has a half-life of 8 hours and thus should be used
QDS and it is inhibited by food in the stomach, so should be taken on an empty stomach and the patient instructed not to eat for 1 hours after taking it. In
my experience, this makes it almost impossible to take properly.
Lymecycline – dose 408mg OD or BD. This tetracycline is has a long half-life and is not affected by food in the stomach. The manufacturer suggests a once
daily dose but I find a BD dose more effective. Once clearance has been achieved, the dose can be reduced.
Doxycycline – dose 100mg OD. This drug has a long half-life and is not affected by food in the stomach. 25% of patients may develop significant
photosensitivity. The capsule of Doxycycline is very sticky and patients must be warned to take it with food and not just with a swallow of water. It can
adhere to the lining of the esophagus and cause a painful burn. One of my patients was hospitalized for 3 days following esophageal ulceration caused by
doxycycline.
Minocycline – dose 100mg OD. Minocycline was a very popular drug in acne as it had a long half-life and was not
inhibited by food in the stomach. There have been reports of a rare side effect – lupus like syndrome with severe
arthropathy and hepatotoxicity has now limited its use. It is still a very effective drug but if used long term, patients
should be tested for ANA. If used long term, minocycline can be deposited as a complex with melanin in scarred areas
leaving a bluish pigmentation. If this occurs the drug should be stopped immediately otherwise the pigmentation may
become permanent.
Minocycline pigmentation

Macrolide antibiotics
Erythromycin – dose 250mg QDS. This is possibly the second most commonly prescribed antibiotic in acne. It has a very short half-life of 2.5 hours and
should be taken QDS and it is inhibited by carbohydrate in the stomach so should be taken on an empty stomach. It is, however, a gastric irritant and may
not be tolerated if taken properly. It is the only antibiotic that can safely be taken in a woman who is trying to conceive or who is pregnant.
Clarithromycin – dose 250 – 500mg BD. This is a much better macrolide with a longer half-life than erythromycin and causes less gastric irritation
Trimethoprim
Trimethoprim – dose 200 – 300mg BD. This is a very good second line antibiotics for acne and has the advantage of working very quickly. It can be taken
with food and is generally well tolerated. A drug rash may occasionally occur – starts about 10 days after starting the drug and presents as an itchy
exanthema. The drug should be stopped immediately and the rash treated with mild topical steroids or calamine lotion. It settles after a few days.
Occasionally, dermatologist will use clindamycin (dose 150mg BD) or rifampicin (does 150mg BD) in severe acne,
not responsive to conventional antibiotics.
Trimethoprim induced drug rash
Other systemic antibiotics

Hormonal therapy in women
In women with severe acne, not responding to conventional antibiotics with a topical retinoid, hormonal therapy may be indicated. This may be due to
polycystic ovarian syndrome where women produce excess free testosterone which may lead to severe and or persistent acne.
Dianette
Dianette is licensed for the treatment of acne but is also an effective oral contraceptive agent. The oestrogen, ethyl-oestradiol will increase sex hormone
binding globulin which will bind to and inactivate testosterone. The progesterone, cyproterone acetate, inhibits 5-reductase and inhibits the activation
of testosterone to di-hydro-testosterone in the sebaceous gland. It is successful in treating acne in about 40% of women but due to increased risk of
thromboembolic phenomenon, should be used only short term i.e. 6 months. It has a number of side effects and is not well tolerated by some women.
In practice, Dianette is poorly used and is often given as a contraceptive agent in women who have acne of any severity and often continued for years. A
major problem is that acne will often flare significantly 2-3 months after the drug is stopped.
Yasmin
Yasmin is marketed as an oral contraceptive but is often given to women who have acne. The oestrogen is the same as Dianette but the progesterone is
drospirenone, an analogue of spironolactone, which amongst other anti-androgenic effects, inhibits 5-reductase. In practice, it is not as effective in
treating acne as Dianette and may have the same problem of rebound of acne after treatment is stopped.

Spironolactone
Spironolactone is a loop diuretic. It antagonizes the androgen receptor, inhibits 5a-reductase and has anti-androgen effects. Prior to the
advent of antibiotics it was commonly used to treat acne in women.
In the older woman it can be a very effective drug, reducing sebum production and controlling acne. It should be used at 100 to 200mg daily. I
find it very useful in younger women who have significant premenstrual exacerbations of their acne. 100mg daily for the 7 days before their
period can be effective in preventing this flare.
Spironolactone can affect the menstrual cycle giving very short cycles, spotting between periods and even amenorrhea. It should not be used
in women who are trying to conceive as they could affect a developing male foetus.
Dapsone
Dapsone is a suphone antibiotic which has potent anti-inflammatory action against polymorphs and thus inhibit pus formation. It is commonly use for the
treatment of leprosy in combination with other antibiotics. In dermatology, it is generally use in condition in which activated polymorphs play an
important role – dermatitis herpetiformis and vasculitis.
It can be very useful in acne, used at 50mg/day, suppressing inflammation, particularly deep seated nodules and cysts. I generally use it in combination
with other antibiotics.
In patients with glucose-6 -phosphate dehydrogenase deficiency, it may cause haemolysis and anaemia and patients should be tested for this before
given the drug.

Oral Isotretinoin
Oral isotretinoin is the most powerful drug we have for the treatment of acne. It reduces sebum production by up to 90%, normalizes keratinocyte growth so clears
follicular hyper-cornification, kills P acnes and has powerful anti-inflammatory effects. It thus is the only drug that targets the 4 principal pathological changes in
acne.
It is generally started at a dose of 0.5mg/kg/day for the first month and then increased to 1mg/kg/day until the skin is clear. Early studies showed that a cumulative
dose of 120mg/kg i.e. 1mg/kg/day for 4 months, reduced the risk of recurrence after stopping the drug. This had led to the misconception that the drug should only
be used for 4 months which is wrong. It should be used for at least 4 months even if the skin is clear, but should be used until the skin is totally clear of spots, which
in some patients may be 9 months or more.
In some patients, there can be a flare of acne in the first month of treatment, and if patients have particularly inflammatory acne, it is often started with a course of
systemic prednisolone or systemic antibiotics for the first month.
Isotretinoin is potentially hepatotoxic and can elevated serum triglycerides. It is also diabetogenic. Baseline blood tests must be performed on all patients and
repeated every month – these include:
• Full blood count
• Electrolytes and urea
• Liver function tests
• Fasting lipids and glucose
If liver functions are abnormal, the drug should be avoided. If lipids are high, patients should be put onto a low-fat diet and the fasting lipids carefully monitored.
Oral isotretinoin is a potent teratogen and women of childbearing age should be warned that they cannot get pregnant while on the drug or for 1 month after
stopping. An EU directive means that women of childbearing age can only be prescribed 4 weeks treatment at a time and must have a negative pregnancy test
before a further prescription can be given.
Symptomatic side effects are universal and all patients should be warned about them:
1. Cheilitis which may be severe- lip balms and Vaseline
2. Dry skin which may become eczematised – lots of moisturisers
3. Dry eyes may occur – avoid the use of contact lenses and use artificial tears
4. Myalgia and arthropathy –if these occur reduce exercise
5. Nose bleeds – apply Vaseline to nares
6. Photosenisitivity – occurs in about 25% of patients and can be severe and SPF 50+
sunblocks should be used
Severe cheilitis in a patient on Roaccutane
Rare or unusual side effects

Glossary
Other side effects
Concentration
Oral isotretinoin can impair concentration so should be avoided in patients studying for exams
Night blindness
This may be of major importance in patients who are pilots as they may not be able to fly while on the drug and there is legislation in the USA
that if you have ever had oral isotretinoin that you are prohibited from flying
Severe depression and suicide
This is a rare side effect but is now well documented. The effects start after about 4 week of treatment and will occur in patients with no past
history of depression. Suicides have been documented in these patients and the depression seems to persist even when the drug is
withdrawn.
Fatigue syndrome
Is a very rare side effect which seems to start about 4 weeks after starting the drug. It mimics ME and may well be ME that is in some way
precipitated by the isotretinoin. It does not improve when the drug is stopped.
Acute schizophrenia
This is a very rare side effect of isotretinoin and comes on fairly quickly after the drug has started. It generally affects young men and there has
been an argument that the occurrence is only coincidental.
Persistent symptomatic side effects
An early paper suggested that persistent, symptomatic side effects affected up to 10% of patients treated with oral isotretinoin and were mild.
This may present with generally dry skin which needs regular moisturizing or persistently dry lips or eyes. I have certainly treated patients who
have suffered severe chronic cheilitis for 7-8 years after oral isotretinoin. In such patients, normal oil production on the skin does not turn
back on.
• Myalgia – muscle pains • Cheilitis – inflammation of the lips

Module - 4
Additional Treatments of Acne

Peels
A number of peels are available for use in the acne patient. Most have their effect by their keratolytic action, removing the
top dead skin layers of the skin and unseating comedones and freeing the flow of sebum and reducing the occurrence of
inflammatory lesions.
The Enerpeel range is very useful as these peels are very easy to use and have been shown to be effective.

Salicylic Acid Peel (Enerpeel SA)
Enerpeel is a carrier system whereby carrier molecules attach to the acid molecules rendering them inactive and there is no water in the Enerpeel vials.
This allows the addition of acne treatment ingredients in this case, but other ingredients can be added to the other peels depending on their focus.
This particular peel delivers a 30% salicylic acid and the carrier releases the acid in and on the
stratum corneum. The skin if first cleaned with surface lipid dissolving wipe which allows the peel
to better ‘engage’ with the skin when the peel is applied with an applicator brush which attaches
directly to the end of the Enerpeel vial. There is usually some stinging which is noticed about 30
seconds post application. This continues for up to 2 minutes and then fades away as the salicylic
acid converts to an analgesic powder. The peel is left for 5 minutes and then removed using a
remover wipe.
Skin following Enerpeel SA application
powder present on the skin
The other key ingredients are carried into the blocked sebaceous duct where the P acnes bacteria have colonised. These ingredients are the same as
found in OSK/Aknicare and therefore the peel acts like a loading dose of the key antibacterial and anti-inflammatory properties of the creams. The creams
are used b.d. between the peels, which are normally repeated four times with a gap between peels of between two to four weeks
Elegant studies have shown that after treatment there is a significant reduction of the stratum corneum and removal of comedones. There is no real down
time - some dryness the next day although the associated Tebiskin OSK UV or Aknicare Cream are designed to counter that. If there is a significant build-up
of dead skin on the surface, some area may become white and this will persist for an hour or so.
Always take a history of salicylic acid sensitivity and avoid use in these patients.

Pyruvic Acid Peel (Enerpeel PA)
Pyruvic acid is an alpha keto acid and so has different properties to alpha and beta hydroxyl acids. It interacts with the skin and causes less irritation
compared with say a comparable strength glycolic acid. Also as it is lipophilic like salicylic and also has a sebum slowing effect again like salicylic and so
will penetrate into blocked pilo-sebaceous ducts. It is also the alternative acne treatment for those allergic to salicylic acid - aspirin. Last but not least it is
more skin penetrating than salicylic and so is more skin remodelling and is very useful for post acne oiliness and superficial post acne damage and scars.
This peel is very useful if the patient has very oily skin with a lot of congestion. After application it is left for 3 minutes for one layer. The clinician can apply
another layer for a further 2 minutes taking the total exposure time to 5 minutes, but this will also increase discomfort and for many one three minute layer
is adequate. This peel should always be neutralised and because of the Enerpeel carriers taking the peel deeper into the skin than with a normal peel it is
recommended that the skin is quenched with an Enerpeel neutralizer wipe which contains a 12% arginine solution (amino acid) which leads to a chemical
reaction and a steam like cloud coming off the skin, but with no heat. If left too long, there can be significant desquamation. Arginine can also be
combined with the Enerpeel carrier and so this neutraliser will ‘hunt down’ the acid, whereas a bicarbonate of soda style neutraliser will only act
superficially.

Jessners Peel (Enerpeel JR)
Jessners based peels contain salicylic acid and so can also assist in the management of post acne oiliness but the two other ingredients of lactic acid and
resorcinol can impact upon hyper pigmentation by interfering with the melanin production. This peel is applied for five minutes and then a remover wipe,
not a neutralizer is used to remove the salicylic acid powder from the surface, while leaving the lactic acid and resorcinol to continue to target the
pigmentation. There are creams such as Tebiskin Lightening Cream which also contain versions of resorcinol and other ingredients to continuously work
to suppress pigment production and these creams have shown comparable efficacy to 4% hydroquinone.
Glossary
• Melanin – skin pigment produced by melanocytes in the epidermis involving the enzyme tyrosinase. Melanin production is increased by ultraviolet light
exposure and by inflammation in the skin.
• Hydroquinone – is a powerful reducing agent used medically to whiten the skin

Treatment of Macrocomedones
Macrocomedones are deep seated comedones that have become so big that they have obliterated the skin ‘pore’. They do
not respond to topical retinoids as even if the retinoid loosens the blockage, it cannot get out of the follicle. They are a
potential contraindication to systemic retinoids as they may develop into deep cystic, inflammatory lesions.
Macrocomedones are treated by light cautery to the skin above the lesions using a hyfrecator at level 2-3. This leaves a
pinpoint scab that falls off after a few days, carrying the macrocomedone with it.
Treatment of Cystic Lesions
Cysts in acne can last for several weeks and are painful and disfiguring. An intra-lesions steroid injection will help to resolve this more quickly. Use a fixedneedle,
diabetic syringe and Depomedrone – 40mg/ml. It is important not to inject too much into the cyst as this could lead to skin atrophy and a
depressed area of skin/ scar. Inject until there is slight blanching of the lesion. If the cyst is very large, try to evacuate some of the pus using a syringe and
needle before injecting the steroid into it.

Light and Laser Treatment
Sunlight
Most patient say that their acne is better after a hot sunny holiday. Occasionally, patient holidaying in a hot humid environment may get an exacerbation
of their acne (see high humidity in Module 1).
Ultraviolet (UV) light will provide a sun tan, which will have a cosmetic effect on the skin. In vitro, UV will inhibit the growth of P acnes and will suppress the
immune function on the skin, so it should have an effect on acne. However, studies in the 1970’s showed that UV light had no effect on tar induced
comedones and a clinical study showed little effect of UV light on inflammatory acne. Historically, UV light was used in acne but poor results resulted in
loss of interest and it is no longer used.
Blue Light
Blue light at 440 nm has been used to treat acne with some success. P acne contains protophorphyrins (see Proliferation of P acnes in Module 1) which
can be excited by light at 440 nm resulting in release of free radicles which will kill the bacteria. Initial studies by Meffert H et al in Berlin in the late 80’s
using a blue light-type high pressure lamp
Small studies showed improvement in acne and reduction of acne lesions following treatment with blue light but as this works as an anti-bacterial agent,
it needs to be used on a daily basis.
Red and Blue Light
In 2000, we published the results of a trial using strip lights producing light at 440 nm (blue light) and 66 nm (red light). The hypothesis was that the blue
light would kill bacteria and the red light would suppress inflammation and aid healing. The results showed that the treatment was effective with 65%
patients achieving a marked improvement of their inflammatory acne.
The main problem was compliance. Patient had to sit with goggles on in front the unit for 5 minutes every day – which a number of our younger patients
found very difficult. A commercial unit was produced but may no longer be available.

Red and Blue LEDs
Omnilux have developed red and blue LED systems for the treatment of acne which require twice weekly treatment in a clinic.
Small studies have shown good efficacy
Photodynamic therapy
This involves the application of topical 5-aminolaevulinic acid as a photosensitizer. This is cconcentrated in sebaceous glands.
The skin is then Illuminated with coherent or laser light with the reduction of reactive oxygen species which destroy P acnes and alter sebaceous gland
function. This is a painful procedure and results in a severe inflammatory reaction in the skin which can last for up to 2 weeks.
Severe inflammatory reaction following
PDT for acne

Lasers
1450 nm Laser with Cooling Spray
Study published in 2002 showed the effect of 1450nm (mid infra-red) laser/ cooling spray in treating truncal acne. Initial animal studies suggested that
the laser would cause short term disruption and rupture of sebaceous glands. Patients were given 4 treatments over 3 weeks, follow up for 24 weeks.
Results showed a statistically significant reduction in number of inflammatory lesions compared to control.
NLite (Regenlite) Laser – 585nm Pulsed Dye
Laser This is a pulse Dye Laser with unique features. It is excellent in its vascular mode to destroy blood vessels but has additional important
medical properties which provide treatment for a range of inflammatory dermatoses – Bio stimulation.
Its unique features are due to the immediate energy rise with the start of the pulse, which is very different to most pulse dye lasers.
Unique pulse of the NLite/Regenlite laser compared to conventional pulse dye
lasers

The NLite also differs from most pulsed dye lasers in being 585nm as opposed to the normal 595 nm. This leads to 300% more absorption by its target,
oxyhaemaglobin
Graph showing absorption of different light wavelengths by oxyhaemaglobin
A clinical study by out group in 2002 and published in the Lancet showed the effectiveness of a single treatment of the face with the NLite laser with follow
up for 3 months during which time no other treatment was allowed. Results showed a fall of 2 grades using the Leeds grading system by the end of the
study.
We have continued to use the NLite laser as monotherapy or in combination with conventional therapy for the last 15 years with good effect.

Scientific studies have shown that the NLite laser has no effects on bacterial numbers in the skin and no effect on sebum production. A single treatment,
however, increases local production of transforming growth factor (TGF)by 1500%.
TGF has three main biological effects:
• Down regulates inflammatory cytokine in the skin
• Up-regulates collagen production by fibroblasts
• Induces regulatory T cells
Increase in TGF at 3 and 24 hours after a single
treatment with NLite laser
It thus reduces inflammation, can increase collagen production, which would help scarring and could eventually induce regulatory T cell which could lead
to tolerisation of the antigens that are causing the acne and result in resolution of the acne.

Module - 6
Advice for the Acne Sufferer

Advice for the Acne Sufferer
A large number of factors will exacerbate acne and patients should be warned about these and given advice
on what they can and cannot use.
Moisturisers
The acne friendly moisturisers that we recommend are Aknicare Cream, Cetaphil lotion and Efficlar lotion.
These are acne friendly and will not induce comedogenesis. All have different characteristics and patients
need to find which one they like to use.
It is important to tell patients that it is not necessarily the oil content that is bad for the skin as even oil free
moisturisers can induce comedogenesis and worsen acne. Tell patients always to look for the sign ‘noncomedogenic’
on any product that they buy.
Sunblocks
Sunblocks are possibly one of the most common causes in terms of exacerbation of acne. A number of my patients have bought sunblocks at the beach
while on holiday to return home with a significant exacerbation of acne. Warn patients to look for non-comedogenic on their sunblock and to avoid those
that do not exhibit this sign. The sunblocks that I recommend is Sunsense SPF 50+ and the Aknicare SPF 30.

Cosmetics
The price and oil free are not good indicators that a makeup is safe to use for the acne sufferer. Even eye
shadow can be comedogenic and many hair products – waxes, gels and pomades can induce blackheads
affecting the forehead – so called pomade acne (Figure 1) Warn patients to look for the label – noncomedogenic
and to avoid all make up that does not show this label.
Washes
Figure 1. Pomade acne in a young man using waxes
on his hair
Patients will often ask advice about an appropriate wash to use. A pH balanced cleanser is all that is required and indeed ordinary soap and water would
be OK. Avoid harsh washes as they can dry the skin and make it too sensitive for the use of topical treatments.
Scrubs
Scrubs do have a place in the management of acne. My favourite for the last 3 decades was Brasivol 1but GSK have
recently discontinued this. Hopefully a smaller company will be able to take it on.
The only equivalent that I have been able to find in Boot's No7 aluminium oxide scrub – Total Renewal. This should
be used after normal cleansing while the skin is still wet. Rub the scrub into areas for 30 seconds and then wash off.
It is marketed as a home micro-dermabrasion and removes the top dead skin cell layers of the skin allowing
comedones to unseat.
Contraceptives in women.
Most hormone based contraceptives employ as part of the preparation, progesterone (See section on oral contraceptives in Module 1). The mini pill, and
all depot contraceptives are progesterone only and the Mirena coil incorporates a slow release progesterone. The majority of progesterones, however, are
second generation progesterones and have androgenic effects which may worsen acne. Third generation progesterones, desogestrel, norgestimate, or
gestodene have no androgenic effects and are thus acne friendly. Studies have shown a higher risk of thromboembolic phenomenon in the third
generation progesterones compared to second generation progesterones at 1.7 to 2.5 times risk but a lower risk of myocardial infarction and possibly of
stroke. Obviously, women need to be counselled about oral contraception.
Avoid Dinette and Yasmin unless there is a clinical need for them as they are often associated with an exacerbation of acne when the pill is stopped.

Module - 7
Acne Scarring

Acne Scarring
Acne scarring can occur with even mild acne. The severity of the scarring appears to correlate more to the individual response to the inflammatory
response in acne than to the severity of the acne.
Scarring in acne is permanent unless it is treated and causes considerable psychological distress to the sufferer. Some feel that the scarring is worse than
the acne.
I will frequently see patients who complain about bad scarring in acne but on examination, they have no
scarring, only post inflammatory hyperpigmentation or post inflammatory hyperemia. These are both selflimiting
conditions, with post inflammatory hyperpigmentation seen mainly in patients with darker skin and
post inflammatory hyperemia seen in patients with very pale skin. There is no way to predict how long these
skin changes will last for but always reassure patients that they are self-limiting.
In patients who want treatment for post-inflammatory hyperpigmentation, they need to be told that there are no very effective treatments available.
Creams containing hydroquinone do not work. Intralesional injections with tranexamic acid (100mg/ml) may be effective but must be repeated every 6-8
weeks.
Post-inflammatory hyperemia can be treated with ablative pulsed dye laser. It will often require several treatments to clear the erythema and each
treatment will result in bruising which can last for up to 2 weeks.

Types of scarring
Scarring in acne can be hypertrophic/ keloidal or atrophic.
Keloid scars
In surgical practice, keloid scars are most commonly seen in patients of Afro-Caribbean decent. In acne, however, the unique inflammatory response leads
to keloid formation in all ethnic groups involving the face, back, chest and upper arms.
Keloids are the result of overactive healing response leading to a raised lumpy scar that
goes beyond the boundary of the initial tissue injury. A 1mm inflammatory pustule can
result in a 5cm keloid. Keloids may be itchy or painful, red or pigmented but cause
major cosmetic problems. They are very visible and if large and on the trunk, will limit
the clothes that the patients can wear as anything tight will show the lumps in the skin.
Treatment of keloids involves the intralesional injection of a depot steroid. I generally use
depomedrome, 40mg/ml. Use a fixed-needle diabetic syringe as you often need to use a lot of
pressure to inject into the keloids and a detachable needle will often pop off. Make sure you are
within the body of the keloid – if you inject under the keloids all you get is atrophy of the lower
dermis and fat and the keloid sinks into a pit but is still present, painful and ugly. Inject until you see
blanching of the keloids. Repeat injections every 6-8 week. There is no way to predict how quickly
keloids will respond. Some respond quickly, others seem to do nothing for months and then
suddenly involute. Ablative pulsed dye laser treatment may accelerate response to intra-lesional
steroids. Very large keloids can be excised but only if followed by local radiotherapy. Excision alone
will lead to recurrence of an even bigger keloids.

Atrophic scars
A large number of treatments have been used to treat atrophic scarring with varying degrees of success. All treatments work in the same principle of
causing an injury to the dermis which leads to a healing response with the induction of new collagen which fills the defect.
Older treatments with dermabrasion and CO 2 laser resurfacing and now rarely used as the success rate was poor and there was considerable down time.
Modern techniques include the Derma roller, automated needling devices and Fraxel laser.
Before deciding on treatment it is important to properly document the type of scar that is present. There are 3 types of atrophic scars that we see in the
acne sufferer:
1. Rolling scars – these look like someone has pressed on the skin and left a dent
2. Box scars – these have sharp edges like a box and can be very small, looking like large skin pores or large looking like craters
3. Ice pick scars – these are deep and fibrotic so feel very hard, and as the name suggests, looks like someone has punctured the skin with a sharp
pick.
Ice pick scars are thankfully rare as the only effective way of getting rid of them is to remove them with a skin punch and repair with a suture. This will leave
a small linear scar.
Rolling and box scars can be free and will flatten completely if the skin is lightly stretched or tethered by scar tissue to deeper areas of the dermis and will
not flatten when the skin is stretched. In such tethered scars additional treatment with subcision may be needed to give good results.
Rolling Scars
Box scars
Ice pick scars

Needling Devices (dermal rollers and automated needling devices)
The Medical Dermal roller and the newer automated needling devices work on the principle of needling. The needles are fine acupuncture
needles which are too thin to leave a permanent mark on the skin but when pushed into the skin will induce a healing response with the
induction of new collagen which will fill the scar and stretch the skin.
Dermarollers
Dermal rollers were developed in Germany and were introduced to the UK by myself in 2009 – prior to that, patients
travelled to Germany to have treatment. The whole affected area is treated i.e. the whole face or back or chest, not just
the scars. The skin is first treated with EMLA cream for 1 hour under occlusion then cleaned and swabbed with alcohol.
The skin treated is with 4 repetitions in 3 different directions – horizontal, vertical and diagonal to optimize the number
of individual piercings that occur. Medical Dermal Roller will produce 250 channels/cm2. The Medical Dermal Roller
comes in a range of fixed needle lengths from 0.5 to 2mm. For acne scarring you need to use 1.5mm needle length.
Treatment will lead to pinpoint bleeding and may be painful. After treatment, clean the skin with sterile normal saline, apply clean gauze and a cold pack
for 10 minutes. After this, any serous exudate will have dried up and the patients can be allowed home. Light moisturizer can be use that night and the
patients can go back to a normal regime the next day. The skin will remain red for up to 4 days.

Automated Needling Device
The automated needling devices are next generation needling systems and have major advantages over the manual rollers. It is an electric pen with 9
acupuncture needles. The needles can be adjusted to varying lengths on a continuous dial from 0.1mm through over 2mm. The speed can also be
adjusted to a maximum speed that will produce 70,000 holes/minute. As the needles go straight in and out, rather than the cycling motion with rollers,
then the automated needling devices are much less painful and redness dissipates much faster.

Fraxel Laser
The Fraxel laser is effectively a CO 2 laser where the laser beam has been fractionated into multiple beamlets. The energy can be adjusted to allow different
depths of the skin to be treated. The basic principle is the same as the Automated needling devices but uses laser rather than needles to injure the skin
and induce a healing response with new collagen induction. The treatment is painful and downtime can be up to 1 week
Trichloracetic Acid (TCA) Chemical Reconstruction of Scarred Skin (CROSS).
This technique was developed in Korea and is particularly useful for small box scars. Up to 100% TCA is used
and carefully applied to the base of the scar using a sharpened orange stick. As soon as frosting occurs, wash off
with normal saline. The TCA causes a very local injury which induces new collagen production and allows the
scar to fill and obliterate the sharp edges. After treatment, frosting lasts for about 30 minutes and is followed by
the development of a soft scab which falls off after a few days. Treatment should be repeated every 6-12 weeks.
Combining this with needling facilitates good results
Frosting following TCA-CROSS
Subcision
Subcision is a very powerful technique that is needed when scars are tethered to deeper structures or in deeper rolling scars where the injury from the
subcision gives good filling of the scar.
Subcision can be performed as an isolated procedure or following automated needling devices treatment.
The scar is marked with a surgical marker and the area infiltrated with lignocaine – if the scars are not
marked before infiltration the local anesthetic will fill the area and it may not be possible to see where the
scar is. Subcision is performed with a 19 gauge NorKor needle which has a cutting blade on the end. This is
inserted into the mid-dermis and pushed back and forth across the scarred area. The needle is then swept
crosswise in a fanning technique with the cutting blade at the advancing edge. Heavy pressure is the applied
to the area to prevent hematoma formation. If hematomas form, they can give a palpable or even visible
lump in the skin that can persist for several weeks.
NorKor Needle

Module - 8
Rosacea

Rosacea
Rosacea is a relatively common disease but is surrounded by misconceptions and controversy:
1. Rosacea is a disease of the elderly, occurring around menopause – WRONG – there are two age peaks for rosacea, one in the late teens and
twenties and a second in the 40s and 50s. It can, however, occur at any age.
2. If you have a red face you have rosacea – WRONG – there are a number of skin conditions that will lead to a red face – seborrheic dermatitis, acne,
atopic eczema, and lupus erythematosus. The hallmark of rosacea is facial flushing, which unlike physiological flushing lasts for longer than 10
minutes and can last for hours or day. It may be asymptomatic or cause severe burning sensation or pain.
3. Rosacea is only seen in Celts and people with pale complexions – WRONG – although commonest in Type I skin it can occur in any ethnic group.
The hallmark of rosacea is facial flushing. This affects the concave areas of the face including the cheeks, forehead, chin and nose. Extra-facial involvement
is unusual but may affect the ears and neck. Some patients only have the flushing or Erythematotelangiectatic rosacea but others will progress to develop
acneiform inflammatory lesions – the Papulopustular rosacea. In some patients, excessive growth of glands and fibrous tissue will lead to swelling of
various parts of the face – Phytomatous rosacea, and up to 50% of patients will develop eye involvement – Ocular rosacea.
Glossary
• Type I skin – this is the Fitzpatrick classification relating to response to sunlight. Type I skin is Celtic skin, people with pale skin, blue eyes and fre3ckles with blond or red
hair. Their skin does not tolerate sun exposure and burns and rarely tans

Types of Rosacea
National Rosacea Society Expert Committee on the Classification and Staging of Rosacea 2004 has reclassified rosacea
into 4 types. In some ways, this is a rather artificial grouping as phytomatous change and ocular involvement are really
sequelae of rosacea rather than being individual entities:
Type I
Erythematotelangiectatic rosacea. In my practice this is the most common form. In some patients it may
progress to Type II, Papulopustular rosacea but it may only manifests as vascular response. Flushing
may be spontaneous or may be precipitated by a trigger factor. The flushing, unlike physiological
flushing, lasts more than 10 minutes and can last hours or days. It may be asymptomatic or cause a
burning sensation or even pain, which may be severe. Trigger factors are very individual to the patient.
Never impose an exclusion diet without first ascertaining what triggers flushing in that patient. In a large
survey conducted in USA the commonest trigger factor was sun exposure, but I have patients who
improve with a sunny holiday. I have patients who can eat a Vindaloo curry but spring onions will cause
a flush and I have patients who can drink beer or white wine but not red wine or spirits. Get your patient
to keep a diary and if they identify something that triggers a flush, try to avoid it.
Type 1 Rosacea in a 22 year old woman
Type II
Papulopustular rosacea. This occurs following a period of flushing or concurrent with flushing. The spots
look like acne which is why rosacea was previously, erroneously called acne rosacea, but in pure rosacea
there are no comedones and the spots may be follicular or interfollicular. Spots may be of any severity and
may become nodulocystic.
Type 2 Rosacea in a 35 year old man

Type III
Phytomatous rosacea. This generally occurs in long standing rosacea and is more common in men but can
occur in women. The increased blood flow through the skin leads to hypertrophic growth of sebaceous glands
and fibrous tissue leading to lumpy swelling of the skin. The commonest is rhinophyma, affecting the nose,
which becomes lumpy and bulbous, often mistaken for the alcoholic nose. It may also occur on the cheeks,
chin and forehead. The swelling is firm and persistent.
Type 3 Rosacea
Rhynophyma in a 60 year old man
Type IV
Ocular rosacea. This can occur with even very mild rosacea and affects up to 50% of rosacea sufferers. Initially the
eyes become dry and gritty, followed by chemosis and red eyes. In severe cases this may lead to keratitis and is a
recognized cause of blindness.
Type 4 Rosacea
Moderate ocular involvement with
chemosis

Pathogenesis of Rosacea
The pathogenesis of rosacea is unclear but a number of hypotheses have been proposed.
1. Rosacea is associated with Helicobacter pylori infections and may be associated with gastrointestinal symptoms. It has been shown that type II
rosacea will improve when patients are treated for H pylori eradication, but this is most likely to be due to the anti-inflammatory effects of the
antibiotics used in this condition and the rosacea relapses once the antibiotics are stopped
2. Rosacea is caused by the demodex mite, Demodex folliculorum. Demodex are a commensal in the skin. In some situations, the density of demodex
increases, mainly due to the use of cream cleansers of the skin and avoidance of soap and water which would normally reduce the level of
demodex. Studies have shown that systemic ivermectin, which clears the skin of demodex mites led to no improvement in rosacea.
3. Rosacea is caused by an abnormality of one of the skin’s antimicrobial peptides. The skin produces a series of naturally occurring antibiotics, the
antimicrobial peptides. These are the cathelicidins and the human defensins. Only one cathelicidin is found in human skin LL37. Studies have
shown in patients with rosacea that cathelicidin processing is disturbed resulting in peptide fragments causing inflammation, erythema and
telangiectasias. More work need to be performed on this.
4. Rosacea is caused by an abnormal vascular response in the skin and can be associates with migraine. This is the most plausible proposal. Blood
vessels in the skin form two plexuses parallel to the surface of the skin – the superficial and deep plexuses. Their primary function is to feed and
oxygenate the skin but the maximal blood flow through the skin is very much higher that the metabolic needs of the skin. The second important
function of the skin vasculature is to cool the body. This is orchestrated via the sympathetic nervous system via receptors in the brain, heart, large
vessels and stomach, which stimulate receptors on the blood vessels – receptors cause vasoconstriction and receptors cause vasodilation. In
rosacea, this system is abnormal leading to flushing. With time, the skin blood vessels become leaky with serous fluid escaping into the dermis,
causing swelling and acting as a focus for inflammation and spot formation.
The fourth proposal is the most likely and gives some direction as to the management of rosacea. The primary abnormality is the vascular instability, with
flushing being the first and cardinal sign of rosacea. This needs to be addressed if rosacea is to be treated properly.
Patient with rosacea have very sensitive skin and patients will often not tolerate a vast array of topical agents including moisturizers and cosmetics. It is
important for patients to try different products to find what their skin will tolerate.
Glossary
• Peptide – a molecule composed of 2 or more amino acids – may result from the breakdown of protein

Module - 9
Treatment of Rosacea

Treatment of Rosacea
Most clinical trials in rosacea have concentrated on the inflammatory lesions of rosacea, mainly ignoring the flushing and
facial redness. The only exceptions are Synchrorose (Rosacure) and topical bromonidine (marketed as Mirvaso gel).
Treatment of type I rosacea
The only medications licensed for the treatment of type I rosacea are Synchrorose (Rosacure) and topical bromonidine. A number of drugs are effective in
controlling flushing but these are used off license.
adrenergic agonists
Systemic adrenergic agonists are very useful in controlling flushing and preventing fixed facial redness. Stimulation of the
causes vasoconstriction.
receptor on blood vessels
Clonidine
Start at 50mcg BD and slowly increase to 75mcg TDS. It is impossible to predict what dose an individual will need to control flushing so start at a low dose
and slowly increase this. The maximal dose that I will use is 75mcg TDS after which I will add in a adrenergic blocker or other drugs – listed below.
At higher doses, clonidine is used to treat hypertension. It works in rosacea by causing vasoconstriction. I have a high success rate with clonidine with
about 60% of patients responding to it as monotherapy or in combination with other drugs.
It can cause tiredness in some patients and may cause problems in patients with concurrent Raynaud’s phenomenon.
Moxonidine
Start at 200mcg OD and slowly increase to 200mcg TDS. This is a good alternative to clonidine and can be tried if the clonidine is not working or causes
unacceptable side effects.

adrenergic blockers (antagonists)
The receptors on the blood vessel cause vasodilation and this can be inhibited by blockers. adrenergic blockers can be used in type I rosacea either
as monotherapy or in combination with an adrenergic agonists. A number of these drugs have been used in rosacea with varying success. These include
propranolol – dose of up to 80mg TDS, atenolol – dose up to 100mg OD and carvedilol – dose up to 25mg BD.
I do not find them as successful as monotherapy compared to adrenergic agonists and they cannot be used in patients who give a history of asthma or
bronchospasm. If used with an adrenergic agonists, the drugs should be withdrawn slowly – never stop suddenly as this could precipitate a hypertensive
episode.
Mirtazapine
This is a centrally acting α 2 adrenergic auto- and heteroreceptors (enhancing norepinephrine release), and selectively antagonizes the 5-HT 2 serotonin
receptors in the central and peripheral nervous system used as an anti-depressant. When used at low dosage, i.e. 15mg/day, it can synergize with the
adrenergic agonists to improve control of flushing. Some patients develop severe with this drug and cannot tolerate it and it may cause weight gain by
increasing appetite.
Topical Bromonidine (Mirvaso gel)
Bromonidine is an adrenergic agonists. It is used for the treatment of glaucoma and for some years, rosacea sufferers have obtained supplies of the eye
preparation, mixed it with hand cream and applied it to the face with varying success. A major problem in these patients was severe rebound that
occurred when the vasoconstrictive effect of the rug wore off.
A commercial product, Mirvaso gel, has been formulated and has undergone extensive tests in USA. The
preparation works very quickly with reduction of facial redness in the first 30 minutes and this effect lasted up to 12
hours.
Since its launch in UK it has given variable results. Some patients find that it does what it says it should do and are
happy to use it. Others find that it does not last as long as 12 hours, and others have problem with rebound flushing
as the drug wears off.
Glossary
• Glaucoma – a condition in which the pressure within the eye increases which can affect vision

Laser and Intense Pulsed Light (IPL)
The only way to remove fixed redness is to ablate the underlying blood vessels using the pulsed dye laser or intense pulsed light (IPL). To be effective, both
will induce bruising of varying intensity. My personal feeling is that laser and IPL will remove ectatic vessels but will not treat Type I rosacea and with
continual flushing, ectatic vessels will reform. There have, however, been reports of pulsed dye laser and IPL use in the treatment of Type I rosacea and
this is an option many patients explore.
I use the RegenLite in the ablative phjase to treat telangiectasias, using a fluence of 6.5j/cm2
In USA a preferred laser is the V-beam Perfecta Laser by Candela, which is a pulsed-dye laser that very good at removing linear spider veins as well as
diffuse redness and also reduces enlarged pores and sagging skin.
The Excel-V Laser by Cutera, is a dual wavelength laser offering versatility to the operator to effectively treat spider veins on the face without damaging the
surrounding skin.
Glossary
• Ectatic – permanently dilated blood vessels or thread veins
V beam Perfecta Laser

Synchrorose
This product contains four synergistic ingredients and is a medically licensed product only available to clinics. A novel ingredient known at a Tryp-2 receptor
antagonist called 4-t-butylcyclohexanol which is the first agent to stop nerve stimulated peptide production irritating the skin by triggering stinging and burning
by activating receptors on skin cells.
4-t-butylcycloheaxanol
Various physiological triggers like food, liquids, temperature change can stimulate nerves which in turn activate receptors on keratinocytes (epidermal skin cells)
which release peptides (protein fragments) which cause a stinging and burning sensation. Rosacea sufferers receptors are much more reactive to these stimuli.
4-t-butylcyclohexanol inhibits the effect of these nerve stimulated peptides thereby calming and soothing rosacea symptoms before they show. Regular use of
these agents can have a profound effect on rosacea symptoms and also other nerve stimulated redness.
Dimethly Sulfone
Also known as methyl sulfonyl methane (MSM) is the second ingredient and works synergistically with the butylcyclohexabol in that it suppresses the activity of
key skin inflammatory agents including the key cytokine interleukin 1 alpha which triggers erythema and swelling. MSM also reduces the activity of vaso
endothelial growth factor and tumour necrosis factor1 alpha. Rosacea sufferers may be hyper-reactive to these skin chemicals which may exacerbate
telangiectasia and phymatous development. In combination these agents have a synergistic effect on rosacea symptoms and development as each is beneficial
to the other.
Polyglutamic Acid
The third ingredient is Polyglutamic Acid which is a long chain of repeating units of glutamic acid, and creates a
physical smooth, elastic, self moisturising and soft film for improved sensory perception and protection of the outer
layer of the skin, a reinforcement of the skin’s support structure, stimulates the production of skin lipids improving skin
sensitivity (less sensitive), stimulates the renewal of the epidermis (also improves sensitivity), raises the tolerance
threshold to rosacea triggers especially external ones (raises TTT (Trigger Tolerance Thresholds)).
Silymarin
A bioflavanoid complex from milk thistle known as Silymarin in the fourth ingredient in Synchrorose and this works in
synergy with MSM to suppress erythema. The retail version of Synchrorose does not contain silymarin, but is the
updated formula and should not be confused with the old MSM/silymarin only formula.

Treatment of Type II Rosacea
Topical antibiotics
Metronidazole - Topical metronidazole
Available as 0.75% and 1% gels and creams. Some gels contain cellulose and this leaves a surface film which some
patients find unacceptable
Topical metronidazole is marketed for the treatment of rosacea and is successful in treating the inflammatory
spots in rosacea but will have no effect on flushing or facial redness.
Topical erythromycin and clindamycin
Topical erythromycin and clindamycin are effective in treating inflammatory rosacea but the alcoholic solutions and gels may be too irritant to be
tolerated by the rosacea sufferer. Dalacin T lotion (1% clindamycin) may be better tolerated.
Topical pimicrolimus
Topical azaleic acid
The 15% azaleic acid cream (marketed as Finacea ) is effective in treating inflammatory lesions of rosacea and
may have a very mild effect on facial redness. The 20% azaleic acid preparation (marketed as Skinoren) is
generally too irritant for the rosacea sufferer.
Topical pimicrolimus (marketed as Elidel cream) is a non-steroidal anti-inflammatory agent. One study has shown that it
is effective in treating inflammatory lesions of rosacea and gave similar results to topical metronidazole. Neither gave
response to flushing or telangiectasia.
Topical Ivermectin
Topical ivermectin (marketed as Soolantra) has potent anti-inflammatory effects and is very effective in Type 2
rosacea, suppressing the inflammatory lesions but with little effect on the redness. I find that it is more effective than
topical metronidazole.

Systemic antibiotics
Tetracyclines
The tetracyclines are generally reported to be the most effective treatment for rosacea. It should be noted, that tetracyclines, as with all systemic
antibiotics, have their main effect in inflammatory lesions of rosacea and have little or no effect on flushing and redness. As bacteria are not implicated in
the pathogenesis of rosacea, the main effect of the tetracyclines is their potent anti-inflammatory effect. Oxytetracycline at 250-500mg BD would be a
suitable dose.
Doxycycline, at 100mg OD is a popular choice in rosacea as it is frequently used in ocular rosacea. Always warn
patients to take this drug with food, as the capsule of the antibiotic can adhere to the oesophagus causing a
chemical burn. It can also cause significant photosensitivity.
A low dose, slow release doxycycline (40mg/day marketed as Efracea) has been developed for the treatment of
inflammatory rosacea. The blood levels with this preparation never reach antibiotic levels, so should have no effect
on the gastrointestinal tract and should not induce vagina candidiasis.
Trimethoprim
Trimethoprim is a good second line antibiotic for the treatment of inflammatory rosacea. It can be prescribed at 200-300mg BD. It is generally well
tolerated but there is a low incidence of allergic reaction to the drug, with the development of a widespread itchy rash after 10 days of taking the drug. If
this happens, the drug should be stopped and the rash will settle after a few days. If itching is severe it can be treated with a mild topical steroid or
calamine lotion.
Oral metronidazole
Oral metronidazole – dose 200mg TDS, is very effective in severe inflammatory rosacea not responding to other antibiotics. Patients should be advised to
avoid alcohol while taking this antibiotic as it can have an Antabuse effect.
Glossary
• Antabuse – a drug used to treat alcoholism – it leads to alcohol being converted into formaldehyde which causes severe vomiting

Oral Isotretinoin
Oral isotretinoin is used to treat Type 2 rosacea which has failed to respond to conventional antibiotics. It does seem to work but rapid relapses when the drug is
withdrawn is the norm. Indeed, in my experience oral isotretinoin seems to precipitate rosacea in susceptible patients who are being treated for acne and I have a
number of patients whose rosacea started when they took oral isotretinoin.
Laser treatment
As in acne, the bio-stimulatory effect of the NLite (Regenlite) laser, used at low fluencies – 2.5-3.5J/cm 2 can be very effective in inflammatory rosacea. Treatments need
to be repeated every 3 months.
Treatment of type III rosacea
Phytomatous change in the skin will not respond to medical treatment. Oral isotretinoin (1mg/kg/day) will reduce the swelling but it relapses when the drug is
withdrawn.
It is important to treat the active rosacea so that the disease does not progress, but the only effective treatments are surgical, debulking changes on the cheeks,
forehead and chin. The nose can be carved back to its original shape and size.
Treatment of Type IV rosacea
There seems to be poor correlation between severity of rosacea or response to treatment of Type I and Type II rosacea and the severity of ocular rosacea. Always ask
patients with rosacea if they have any ocular problems. Some patients will respond to oral doxycycline but I generally refer patients to the ophthalmologist for
treatments which will often involve eye toilet and use of artificial tears.