Episode Transcript
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(00:08):
Hello and welcome to this Rash Decisionspodcast, where we look at skin-related
issues, conditions and treatmentsin an interesting and informed way.
I'm Dr Roger Henderson, GP,with a long-standing interest
in this area of health.
And I'm Dr George Moncrieff.
I was also a GP, though I've now retiredfrom my practice and I was the Chair
(00:30):
of the Dermatology Council for England.
Now today, George and I are going tobe talking about acne, and as we all
know, this is a huge area with ourskin-related conditions workload.
So we're going to be lookingat what we should know about
it before we look to treat it.
And the treatment of acne itselfwill be the subject of our next
(00:50):
podcast in about two weeks time.
So make sure you check that one out.
I can give you a quick heads up alreadyand tell you it's an absolute cracker.
But first of all, George, I thinkit's a really good idea to talk about
the aetiology of acne because thisinforms our treatment choices and also,
(01:15):
it's really far from simple isn't it?
It's fascinating to be honest.
Acne is caused by acombination of genetic makeup.
So, for example, if your father is moreimportant than your mother, as far as
severity of acne is concerned, the malegenes are more likely to trigger acne.
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And then an interplay between that andyour hormones, often unbalanced hormones,
early in teenage years and that's whywe see acne, particularly in teenagers.
But what's going on in acne?
Well, these hormones drive, in somebodygenetically prone, increased sebum
production by the sebaceous glands.
And that sebum is not onlyincreased in volume, it's thicker.
(02:00):
They also increase the numberof cells around the infundibular
opening of the pilosebaceous unit.
As you know, every hair folliclehas its own individual grease
gland, the pilosebaceous unit,and that becomes blocked.
And what's going on, isa degree of seborrhoea.
Now, anything in the body thatblocks, whether it's your middle ear
(02:21):
cavity, your sinuses, your appendix,your fallopian tubes, or your
pilosebaceous unit, once it's blocked,you get bacteria growing behind it.
And the bacteria that grows inthis situation is the cutibacterium
acnes, though we used to call itproprionibacterium acnes, it's sort
of an obligate anaerobe, and that thencauses the inflammatory lesions we see.
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So it's seborrhoea, increased cellsfalling into that grease, blocking
the hair follicle opening, thepore, and causing an open comedone.
Then colonisation causing the inflammatorylesions, which will go on to pustules
or closed comedones and then the moreinflammatory lesions that we see.
What about the factors affecting acne?
(03:06):
We start to strain to areasof myth and disinformation.
I have to say, especially with socialmedia on the rise and rise, it's amazing
what patients will sit in front of youand tell you what they think, about what
works for their acne and what they'vetried and what they shouldn't try.
And even in our lifetimes asmedical students and doctors,
(03:29):
George, that has flip-flopped.
I'm thinking of things like...
like diet here.
Well, yes diet's very interesting.
Like me, I'm sure you were taughtthat you should dispel any myths that
diet has a part to play in acne, andyou should go out of your way to tell
patients it doesn't play a part...
and would you believe it that wasbased on some terrible studies?
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Fulton had four patients who, aftera week, reported no difference.
And Anderson, I think, had about 70students, who he either gave a candy
bar to or something else, and after fourweeks there was no significant difference.
Now, studies like that would neverget close to getting published
in a peer-reviewed journal.
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These were really shockingly bad studies.
But, for some reason, the professionleapt onto that evidence, if you
can call it evidence, and deniedpatients who said to them that they
thought their diet was aggravating it.
We all see patients who say,I had some chocolates and the
next day my acne was worse.
There have been some more scientificpapers done this century, both looking
(04:34):
at the Aché hunter-gatherers in,in Paraguay and the Kitavan tribe
in Papua New Guinea, where there's,for example, 2000 individuals.
They eat a diet of fish and fruit,and they have no acne at all.
If they're given a westernised diet, theyget acne, which then gets better when
they go back to their normal healthy diet.
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So, certainly junk foods and things,anything that causes a glycaemic load.
So, particularly cocoa and sugars,which are rapidly absorbed.
Interestingly, ice creamcan increase acne fourfold.
And whey powder, a lot of skimmedmilk, because it's so thin,
is fortified with whey powder.
(05:14):
And individuals who sometimes go togyms and want to build up their bodies,
they're drinking four pints of milka day, but they don't want to put on
too much weight, other than muscleweight, they'll drink skimmed milk.
That's a huge amount of whey powder.
And these, sugars essentially, increaseinsulin growth factor one, which then
stimulates the production of androgens.
(05:35):
So.
Yep, I think it does matter.
NICE, in their guidance for acne lastyear, acknowledged that diet had a part to
play in many patients with acne, but theywent on to say that we would not suggest
doctors spend time discussing it withpatients because it's too complicated.
I ask you, it's not complicated tosay to a patient, "Do you find eating
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chocolates or eating a lot of icecream makes things worse, or are
you drinking a lot of skimmed milk?"
It doesn't take me very long.
They went on to say, furthermore, we'reanxious that discussing diet in a young
person might trigger an eating disorder.
Come on.
It's a bit like saying I didn'twant to ask this patient about
suicidal ideation because they weredepressed, you know, that that's
(06:20):
going to cause them to commit suicide.
I find it astonishing that that wasthe view that they took, but they did
acknowledge that diet plays a part.
I mean, talking about hormones, certainlyandrogenic hormones will make acne worse,
so in particular, anabolic steroids.
If somebody is taking anabolicsteroids, from the gym or wherever,
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and they've got acne, which is usuallythe case, there's no point coming to
see me because nothing I can do isgoing to make a lot of difference.
They need to be off the steroids andnot plan to get back on them again
for our treatments to have any impact.
The first-generation combinedpills could make acne worse.
All combined pills have ethinylestradiol,from 20, 30 or some of them 35 micrograms.
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But what distinguishes one fromanother is whether it's the androgenic
progesterone, like levonorgestrelor norethisterone, in Rigevidon® or
Binovum®, for example, TriNovum®.
Or a progesterone like gestodene anddesogestrel, which are usually marginally
antiandrogenic and usually slightly help.
(07:27):
Or a combined pill, such asone that contains drospirenone
or cyproterone acetate.
Oestrogen makes acne better.
So what you want in acne is anoestrogen dominant pill and a
non androgenic progesterone.
So the most oestrogen dominantpills have 35 micrograms.
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And, you want them to have somethinglike drospirenone, which is a
spironolactone-like progesterone.
In America, spironolactoneis licensed for acne.
It's not in this country,but I have used it for acne.
And you need to use quite high dosesto be effective, like 100, 200, or even
more milligrams a day, and it's thereforelimited by gynaecomastia or mastodynia.
(08:15):
But drospirenone is a spironolactoneprogesterone in things like
Yacella and Lucette® and Yasmin®.
Or you can go for a trueanti-testosterone, cyproterone acetate.
But, so we'll be talking abouttreatment next time in more detail.*;
So I think this is a perfect timefor us to take the opportunity just
to say a few words about our kindsponsor, AproDerm®, and their range
(08:38):
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In many ways as a GP, it hasoften been tricky to find an
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We know it's not as simple as onecondition, one type of emollient.
It's often a case of a patient trying anemollient and then going back and forth
with several prescriptions and visits tous, and other practices or other doctors.
(09:00):
Which is not ideal for them or for us.
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(09:21):
So the point here is that with just oneprescription, we can give our patients
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Now, obviously this gives patientschoice, it aids compliance, vitally
important, whilst at the same timesaving time, money, and most importantly
fewer visits for the patient.
(09:42):
Now as a GP that ticks every box andit sounds like a perfect answer for me.
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(10:04):
I have to say that Inow love them even more.
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Stress definitely plays a part.
I'm sure like me, you've seen patientsbefore doing a webinar or presentation or
(10:29):
an exam or an interview, you get spots.
And we all know thatstress does play a part.
Cosmetics can certainly clog up poresif people are using thick cosmetics
and we'll probably come on to that.
And UV light, we know that a littlebit of sensible, non-burning sunlight
definitely seems to help acne.
When I, see a very muscular well-builtyoung man in my surgery with
(10:56):
acne, it's a default question...
Exactly.
...to ask them, you know, doyou take anabolic steroids?
I almost go straight to the chase and sayhow often do you take anabolic steroids,
but one or two don't, but the rise ofbody dysmorphia in young men, driven
by social media, is certainly somethingthat I never saw at the start of my
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medical career and now see quite a bit.
And I think it's probably under, notover, reported, and as you say, one of
the problems with any young man, takinganabolic steroids is, whatever we throw
at them, it's not going to work becausethose steroids are going to overpower any
possible treatment that we could throwat them and you sometimes have to have
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the, the stern words, you know, do youwant to keep taking steroids or do you
want your acne, but you can't have both.
And usually they'll say, well, I like myacne better because my girlfriend doesn't
like the look of it, but then often, whenthey lose their muscle mass and you tend
to find they sometimes go back on it...
Exactly, yeah.
...But it's always worth askingthat question with someone with acne
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who is well-built, very muscular,always think anabolic steroids.
Now many patients of mine dobelieve that acne, is acne, is acne.
But one of the things I have learnt,over too many years of treating them,
is that there's a massive range ofpresentations, including the 'no need
to treat, so mild', to the Roaccutane®specialist referral level with
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horrendous scarring, which I thinkwe've failed, if we get to the scarring
point, and also clinical findings.
So there's this massive sortof A to Z range, isn't there?
Greasy skin, distribution,pigmentation, scarring, morphology.
We've got to treat each patientas they sit in front of us
rather than just lumping everyonewith acne into the same boat.
(12:51):
Yeah.
So most patients with acnehave a degree of seborrhoea.
So their skin looks quiteshiny and it looks oily.
And of course that's quite good for dryskin conditions like eczema and so on.
But you'll notice that the patient hasa rather oily, greasier complexion.
Acne, 99% of patients withacne, it'll affect their face.
(13:12):
I say almost 100%.
And about 80%, it affects thefront of the chest and around about
80/90% affects the back, rightdown sometimes to the buttocks, it
can go right the way down there.
And I think of acne as beinginflammatory or non-inflammatory.
So, when non-inflammatory, we'retalking about open comedones, these
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blocked pores, just basically dead cellsfilled with melanin that have fallen
into the sebum and blocked that pore.
And you sometimes see thatin young teenagers or even
younger children aged 11 or 12.
And if you do see significant opencomedone disease at that age, it is a
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marker for more severe disease to come.
And then you get the more inflammatoryend of the spectrum with papules
and pustules and then it can go onto nodules and cysts and of course
that is likely to heal with scarring.
Sometimes you see very mild acne, veryfew, just one or two inflammatory lesions,
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but each one of them has been attackedand the patient has excavated and torn
it out to try and get, rid of the spot.
They've picked it and pulled away atit, and that will cause scarring and
the condition we call acne excoriée.
And then, typically in darkerskin, the darker skin types, the
inflammation can cause quite markedpost-inflammatory hyperpigmentation.
(14:34):
Now I can't remember the last time Iinvestigated someone with acne unless
I was thinking this acne is actuallysecondary to polycystic ovarian syndrome.
I know adrenal hyperplasia could do it.
I don't think I've ever seen a case.
(14:55):
But, pretty much, I'm fairly safein saying that most of us don't
go out of our way to investigateacne straight off the bat, do we?
No, I don't think so.
Those are the two main situations.
I obviously had a young man andI was suspicious that he was
still taking anabolic steroids.
I would not embark on treatment until I'ddone the tests to check that he wasn't.
(15:19):
So I do a quick testthere for testosterone.
But no, I think polycystic ovariansyndrome is so common, affecting perhaps
even one in four women of childbearingyears, that even in my non-overweight
women, if they got persistent acne, oreven acne, I would just be thinking,
are we dealing here with PCOS?
And then address that.
Yep, Yeah.
There are two types ofadrenal hyperplasia.
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There's the classic, which is exceedinglyrare, one in 30 to 50,000 people,
but there's the non-classical adrenalhyperplasia, which possibly affects up
to half a percent of the population.
And they, unlike the classical, don'tpresent with adrenal failure, but instead
they present with hyperandrogenism.
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Massive hirsuties, male patternbaldness, and severe acne.
So I specifically think about thatin my individuals whose acne is
particularly recalcitrant or has comeback after a course of isotretinoin.
And it's very easy to testfor, you just do a 9am
17-hydroxyprogesterone blood test.
It's very cheap.
(16:24):
And of course, if that's abnormal,it's quite possible that they won't
be able to mount a good adrenalresponse to a severe stress situation.
So, where they'd have a major operationor a heart attack at a later stage in
their life, if they know they've gotadrenal hyperplasia, the non-classical
pattern, maybe the treatment they receivewill be, they'll be onto the case faster.
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Then if that weren't the case, they couldhave an Addisonian type crisis, I suspect.
So, you're doing them a doublefavour and managing their acne
in that situation, if they've gotnon-classical adrenal hyperplasia.
It's very simple.
You just give them the steroid replacementthat they need, and their acne melts away.
So it is, it is rare, yes, butthe way it manifests is with
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extreme hirsuties in somebody withresistant and recalcitrant acne.
That's a really helpful aide-mémoire,that one, because I think that's
one we often forget with allthe common things being common.
But that's a really useful one toclose this, little chat off, I think.
Actually, you know, you've onlyrecently chaired a whole day's
conference on rare conditions.
And, I think the message fromcame out that there are so many
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rare conditions, that we commonlyencounter something less common.
That's right.
One of the statistics thatabsolutely rocked me back is that
one in 17 people in the UK havea condition classified as rare.
Not one in 1,700, not one in17,000, one in 17 and that
really puts it in perspective.
So...
Certainly does.
...thinking about adrenal hyperplasiain our acne patients is a good rule.
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It's so important for us inprimary care to remain alert to
that possibility at all times.
Absolutely.
So, George and I do hope you foundthis chat about this most common
of skin problems interesting.
And you found the overviewhelpful and you've remembered some
things you may have forgotten.
And hopefully it's allowed you to havea little more confidence next time you
are in your surgery and speaking tosomeone sitting in front of you with acne.
(18:15):
So, Roger and I hope you'll join usnext time when we'll be discussing the
crucial area of how best to treat acne,including when to refer to secondary care.
We'd also like to thank our sponsorAproDerm® for all their help in putting
these Rash Decisions podcasts together.
We couldn't have done it without them.
So, until the next time,it's goodbye from George.
Goodbye.
(18:36):
And as always, it's goodbye from me.
Goodbye.