primary care dermatology society winter 2010 - pcds · nodular prurigo nodular prurigo is a common...
TRANSCRIPT
Good news! Our efforts to prevent the imposition of Generic Substitution have been
successful, at least for now, since the Department of Health has decided to drop the
idea. In conjunction with the All Party Parliamentary Group on Skin and a group of
concerned patient groups as well as a few non dermatological pharma companies the
PCDS raised awareness of the risk of what would have amounted to a limited list.
Those of us old enough to remember the previous attempt at the imposition of a
black list of dermatological products in the 1990s will be less excited about the
winning of this round. I sadly predict that we will face increasing efforts to limit the
choice our patients will have in the future as the effects of the white paper and the
credit crunch begin to bite. We have a duty to maintain the best possible range of
treatments for our patients since the requirements of different types of skin are so
varied and make a huge difference to patients’ wellbeing.
More good news lies in the new development we have planned for next year. We
have planned an extra eight one day “Essential Dermatology” meetings to add to the
two already planned. These are a development of our previous Basic Dermatology
meetings and are designed to be aimed at your dermatology naive colleagues and
VTS registrars. We plan to take the roadshow around the country and have prepared
the series of presentations which will be presented by some of the committee and
local members who have volunteered to help. It is especially important for education
Primary Care Dermatology Society Winter 2010
Bulletinpcds.org.uk
2nd Floor, Titan Court, 3 Bishop Square, Hatfield AL10 9NA T: 01707 226024 F: 01707 226001 E: [email protected] W: pcds.org.uk
Chairman’s Report
The PCDS Trustee Committee
Mr Peter Lapsley Dr Tom PoynerDr Stephen Hayes Dr Jane Rakowski Dr Julia Schofield
Forthcoming MeetingsMembers of the corporate membership scheme
2011
Basic Dermoscopy MeetingManchester Conference CentreThursday 24th February
PCDS Ireland Annual MeetingGalwayFriday 4th & Saturday 5th March
Spring MeetingSheffieldFriday 18th March
Essential DermatologyManchester Conference CentreFriday 1st April
Improvers Skin Surgery CourseLitchdon Medical Centre, BarnstapleFriday 8th & Saturday 9th April
European MeetingGrand Hyatt, BerlinFriday 13th to Sunday 15th May
Summer MeetingFriday 10th & Saturday 11th JuneThe Grand Hotel, Brighton
Autumn MeetingThursday 22nd SeptemberLady Margaret Hall, Oxford
Skin Surgery CourseSaturday 15th & Sunday 16th OctoberDurham
Advanced Dermoscopy CourseThursday 27th OctoberBMA House, London
Scottish MeetingSaturday 12th & Sunday 13th NovemberWesterwood HotelCumbernauld
Dermol knocks out Staph...
…and soothesitchy eczema
The Dermol family of antimicrobialemollients – for patients of all ages who suffer from dry and itchy skin conditions such as atopiceczema/dermatitis.
• Specially formulated to be effective and acceptable on sensitive eczema skin
• Significant antimicrobial activity against MRSA and FRSA (fusidic acid-resistantStaphylococcus aureus)1
• Over 10 million packs used by satisfied patients2
Dermol® 200 Shower Emollient andDermol® 500 Lotion Benzalkonium chloride0.1%, chlorhexidine dihydrochloride 0.1%,liquid paraffin 2.5%, isopropyl myristate2.5%. Dermol® Cream Benzalkoniumchloride 0.1%, chlorhexidine dihydrochloride0.1%, liquid paraffin 10%, isopropylmyristate 10%.Uses: Antimicrobial emollients for the management of dry andpruritic skin conditions, especially eczema and dermatitis, and foruse as soap substitutes. Directions: Adults, children and theelderly: Apply direct to the skin or use as soap substitutes.
Dermol® 600 Bath Emollient Benzalkoniumchloride 0.5%, liquid paraffin 25%, isopropylmyristate 25%.Uses: Antimicrobial bath emollient for the management of dry,scaly and/or pruritic skin conditions, especially eczema anddermatitis. Directions: Adults, children and the elderly: Add to a bath of warm water. Soak and pat dry.
Contra-indications, warnings, side-effects etc: Please refer toSPC for full details before prescribing. Do not use if sensitive toany of the ingredients. In the unlikely event of a reaction stoptreatment. Keep away from the eyes. Take care not to slip in thebath or shower. Package quantities, NHS prices and MAnumbers: Dermol 200 Shower Emollient: 200ml shower pack£3.55, PL00173/0156. Dermol 500 Lotion: 500ml pump dispenser£6.03, PL00173/0051. Dermol Cream: 100g tube £2.86, 500gpump dispenser £6.63, PL00173/0171. Dermol 600 Bath
Emollient: 600ml bottle £7.55, PL00173/0155. Legal category: PMA holder: Dermal Laboratories, Tatmore Place, Gosmore,Hitchin, Herts, SG4 7QR. Date of preparation: January 2010.
References:1. Gallagher J. Rosher P. Temple S. Dixon A. Routine infection
control using a proprietary range of combined antisepticemollients and soap substitutes – their effectiveness againstMRSA and FRSA. Presented as a poster at the 18th Congress ofthe EADV in October 2009, Berlin.
2. Dermol Range – Total Unit Sales since launch. DermalLaboratories Ltd. Data on file.
Adverse events should be reported. Reportingforms and information can be found atwww.yellowcard.gov.uk. Adverse events shouldalso be reported to Dermal.
www.dermal.co.uk
2
at GP level to be provided by those experienced in delivering the care being taught.
The aim is to inspire and enthuse as well as provide the essential elements of
day-to-day dermatology. Following the Health Care Needs Assessment by Dr Julia
Schofield, we know that dermatology contributes to 24% of consultations. In addition
delegates will be provided with a memory stick which will include the presentations
and extended details of all the subjects covered. Guidelines, further reading
suggestions and references will also be provided to make the stick almost a
complete, up-to-date, dermatology manual.
Please encourage your colleagues and registrars to attend when we are in your area
since I am very conscious of the risk of deskilling generic GPs as the attention has
been towards GPSI development. Details of venues and dates as well as booking
details can be found on the website or by calling the PCDS office.
The usual range of meetings have also been arranged for next year maintaining our
high standard and variety. These do not just happen and there is a great deal of
thought and research which goes into the planning. The venues have to be assessed
and our increased attendance numbers and range of sponsors cause a happy difficulty
in finding venues with sufficient facilities and size at a price we, and you, can afford.
The administration team (Siobhan and Carol) spend a lot of time and effort visiting and
planning hotel arrangements and we are so grateful to them for all their hidden work
which only comes to notice when, rarely, hotels let us down in some way.
Dr Elizabeth Ogden is our main educational advisor and her knowledge of speakers is
a huge asset to the rest of us who help with the different meetings. She is always
keen to hear of good speakers and interesting subjects for future meetings so please
drop us an email if you hear one. We are especially interested in presenters new to
the Society.
Happy new year to all our members and good luck for 2011.
Stephen Kownacki
Executive Chair
Editorial Winter 2010
Scottish Meeting The Scottish meeting was an overwhelming success again
this year. The venue was the Radisson Blu Hotel,
Edinburgh. I’m sure that those of you who were brave
enough to venture North of the Border would all agree.
The hotel was ideally situated on the Royal Mile with close
access to local attractions and shops . There was also the
Salisbury Craggs at the bottom of the mile for those who
fancied a breath of very fresh air. The speakers were of a high
standard and the talks were varied and interesting. Stephen
Hayes will be summarising the salient points from Jonathan
Bowing’s Dermoscopy workshop later, for those who did not
attend. I particularly enjoyed a lively debate between Julian
Peace and George Moncrieff on behalf of Primary Care and
Chris Bower and Peter Lapsley representing Secondary Care on
whether BCC’s could be safely managed in the community. All
parties represented themselves very well. The winners were
primary care; not surprising in view of the audience. However,
it was a close call. I’d like to thank all the speakers on behalf of
the Committee and Carol, Siobhan and Iain for organising an
excellent event. A very energetic Ceildih followed the dinner on
Saturday evening. There was some over exuberant flinging
around of partners. I hope everyone enjoyed it despite several
people having bruised limbs the next day!
6 7
Melanoma Taskforce and SkinCancer Visions 2015 Report
On November 1st, the Melanoma
Taskforce published their
recommendations for Prevention,
Diagnosis and Treatment of the disease.
The Taskforce included patient group and
charity representatives (including Cancer
Research UK, The Teenage Cancer Trust,
SKCIN, Factor 50 and the Skin Care
Campaign), MPs, GPs, Skin Cancer
Nurses, Dermatologists, Oncologists and
Surgeons, as well as representatives from
the National Cancer Action Team and the
National Cancer Intelligence Network.
Key recommendations included:n Public awareness campaigns on the
dangers of overexposure to the sun
and the importance of early detection
of skin cancer should be more
targeted on the most susceptible
groups
n Better training for GPs and information
for pharmacists, hairdressers,
physiotherapists, swimming
instructors and others who come into
contact with peoples’ skin, on how to
spot the signs of skin cancer
n Further regulations on sun bed use to
ensure all salons are supervised and
all adult users of sun beds are provided
with health information warnings about
the dangers of sun bed exposure
n Prioritise the development of a Quality
Standard for melanoma; standards that
will mandate innovation in skin cancer
service design, incentivise the best
use of clinical expertise and drive
improvements in patient outcomes
throughout the patient pathway
The Taskforce has made submissions to
the Department of Health consultations
on the Cancer Reform Strategy and the
NHS White Paper.
This is obviously a step in the right
direction but it may be some time for the
message to filter through to address the
learning needs of health care
professionals and give dermatology the
place it deserves as an important part of
the core curriculum .
New Anti-wrinkle Treatment –whatever next?
After a series of tests, French scientists
at the Centre d’Etudes et de Recherches
Cosmetologique (CERCO) have proved
that a Dutch anti-wrinkle bra, La
Decollette does really work. Their test
results show that cleavage wrinkles
disappear after 24 hours and skin is
smooth again after about two weeks. It
is worn at night and prevents the
formation of permanent vertical wrinkles
developing. Three dimensional
techniques employing lasers and
cameras were used to measure the
wrinkles. I’m not sure of the number of
patients included in the study. Perhaps
they should branch out to balaclavas
next it may save patients having to pay
for expensive injections!
Nightmare last night – I woke up with
palpitations and in a cold sweat thinking
that Christmas was around the corner.
Clearly that would be awful; I’m too
busy to prepare for such festivities…
reality dawns only 28 days and
counting-less by the time you read this.
Season Greetings.
Helen Frow
8 9
Nodular Prurigo
Nodular prurigo is a common skin disease in which
multiple, intensely pruritic, excoriated nodules are found
on any area of the body. Patients with nodular prurigo
complain bitterly about the itch as well as the eroded,
oozing lumpy appearance of their skin and, of course, the
associated loss of confidence and self esteem concomitant
with such disease. Chronic rubbing of the skin causes
lichenification (thickening) of the skin, and excoriation from
scratching results in eroded plaques or nodules. Pigmentary
changes often result from such repetitive trauma to the skin.
Nodular prurigo affects all ages, races and both genders, but is
probably more common in middle aged and elderly individuals.
Patients with nodular prurigo freely admit that they scratch at
their skin and that the intractable itch drives their symptoms.
Although there is usually not much in the way of obsessive or
compulsive symptoms, there is often a habit associated with
scratching and patients will note that the condition deteriorates
at times of stress. This can prove a useful way of treating the
patient with ‘habit reversal’ techniques (below).
The causes of nodular prurigo include those of any unremitting
itch:
• Chronic liver disease
• Chronic renal disease
• Infections
• HIV
• Hepatitis B and C
• Syphilis
• Malignancy
• Lymphomas
• Haematological Malignancy
• Others
• Anxiety or other psychiatric condition
• Medication
• ACE inhibitors
• Anti-psychotics
• Others
• Idiopathic
• Metabolic disease such as hyper- and hypothyroidism and
diabetes mellitus
• Long standing skin disease such as eczema
Most patients present initially to their general practitioners, and
most are treated effectively in primary care.
Treatment of Patients with Nodular Prurigo inPrimary Care1 Establish the diagnosis by history and examination
2 Exclude (as best as possible) differential diagnoses such as
a. Immuno-bullous disease for example pemphigoid in a
nodular prurigo pattern
b. Lichen planus
c. Cutaneous neoplasia (especially cutaneous lymphoma)
d. Other dermatoses such as eczema, psoriasis and contact
dermatitis
3. Look for an underlying cause (above). This will include
routine blood tests (FBC, renal, liver and thyroid function,
glucose). It may include HIV and hepatitis serology and,
sometimes, a skin biopsy. If a skin biopsy is taken,
immunofluorescence is important to exclude immuno-
bullous disease (though this is more likely to be performed
by GPwSIs or in secondary care)
4. Patch tests can be useful to exclude a contact dermatitis
component (via the local secondary care unit)
5. Referring the patient to advocacy groups such as
www.nodular-prurigo.org.uk
6. Enter into a dialogue about treatment options
It is very important to remember that treatment for nodular
prurigo is often applied in a step-up and step-down manner
similar to the treatment of asthma and atopic eczema. This
means that patients will start off on easily administered
treatment such as emollients and topical steroids and then, if
not responding, ‘step-up’ to ADDITIONALLY using treatments
such as antihistamines and UVB. Once control of the nodular
prurigo is effected, patients can ‘step-down’ to treatments with
less risk of side effects and toxicity.
EmollientsEmollients are the first line treatment for nodular prurigo, and
will be necessary once the condition has been successfully
treated to avoid a recurrence. Emollients are used either directly
onto the skin or as bath emollients, and are important because
they help repair the skin’s barrier function and because they act
as anti-pruritics. Some emollients (for example Balneum Plus
cream and bath emollient) contain specific agents (such as
lauromacrogols) which can help reduce itch. Patients like to
choose their own emollient and, where possible, it is best to
give patients a trial of a variety so that they can pick the
emollient which suits them best.
Topical Steroids Topical steroids act as anti-inflammatories and as such will have
an indirect anti-pruritic activity. Stronger topical steroids are
usually required to treat nodular prurigo as the skin is thickened
(so absorption reduced) and the inflammation is relatively deep
and active. Most Dermatologists tend to use ointments rather
than creams as the creams often contain preservatives to
which the patient can be allergic. Clobetasol (despite being
super potent) is best used initially for most patients with
nodular prurigo. The strength of the steroid can then be titrated
down after a few weeks. A great treatment option is also
Healan Tape (steroid, fluandrenalone, impregnated sticking
tape) which can be applied overnight to each of the individual
nodules and then removed the following day.
Topical Calcineurin InhibitorsThese agents can be very useful in nodular prurigo of the face,
but are probably too expensive and too problematic (burning
and itching side effects) to be used extensively.
BandagingWraps and impregnated bandages are great treatments for
nodular prurigo as they provide an extra layer between the
patient’s skin and his or her nails. The impregnations in some
bandages (such as ichthopaste and viscopaste) can have
additional anti-pruritic and anti-inflammatory properties.
Nursing colleagues will initially need to demonstrate the
application of these bandages, but, once patients have learned
how to apply them, they are relatively easy to use. Using
steroids beneath the bandages augments the action of the
steroids, so topical steroids need to be reduced in potency
when using bandages. Nevertheless it is essential that topical
steroids are used at the same time as the bandages.
AntihistaminesSedating anti-histamines are usually best in nodular prurigo as
the patient often has disturbed sleep patterns and because the
pruritus is often worse in bed. Hydroxyzine 25 to 50mg at
night is the most common dose to use, but lower doses
(10mg) are possible in patients who find the sedation too
much with higher doses. Non-sedating antihistamines during
the day (or night) can be useful for those who cannot tolerate
sedating medication (for example patients who are driving for
an occupation).
Treatment for Nodular Prurigo in SecondaryCareIf a referral to secondary care is necessary because,
• The diagnosis is in doubt
• The patient has not responded to initial treatment
• The nodular prurigo is severe
• The patient is thought to have an underlying cause such as
bullous pemphigoid and a skin biopsy is necessary
• The patient needs patch testing
• The patient is demanding a referral to secondary care, after
any relevant biopsies or patch tests are performed, the patient
can be treated in ADDITION to topical treatments with;
UVB and PUVAUltra-violet light treatment using narrow band UVB (which only
uses the relatively less harmful UVB light) and PUVA
(ultra-violet A light plus psoralen medication) may be beneficial
for severe pruritus. UVB and PUVA work by reducing pruritus,
and by reducing the cutaneous inflammation. But the adverse
effects of prolonged UV exposure need to be explained before
such treatment is commenced and a formal consent is
important. Most recalcitrant nodular prurigo patients will
respond to UVB or PUVA and can then be switched back to
topical treatments once their skin is clear.
Post inflammatory hyperpigmentation Excoriated nodules Excoriations and hypopigmented scarring
10 11
place and frequency of most scratching, and then over the
following weeks attempts to reduce that scratching habit.
Usually the patient has a counter and can count the number of
times he or she scratches at the skin. Initially, the patient will
record a high frequency of scratching ‘episodes’, which will
gradually tail off as habit reversal starts to work. But person-
centred cognitive behavioural therapy (CBT) can also be
invaluable in the management of nodular prurigo, both to address
any self-esteem issues and to manage anxiety and depression.
CBT can also act as a mirror to reflect life-events and issues back
to the patient, so that the patient can address these. In
addressing life-issues the patient may well be addressing the
cause of the nodular prurigo itself.
ConclusionsNodular prurigo is a common condition which can be difficult to
treat. Using a step-up and step-down model of care and engaging
the patient in the management of their condition is key to
successful treatment.
Dr Anthony Bewley FRCP
Consultant Dermatologist, Whipps Cross University Hospital
& Barts and the London NHS Trust
Dr Bowling told us that despite the
doubters, dermoscopy is becoming
steadily more accepted as a tool
which provides additional diagnostic
evidence, reducing needless benign
excisions while reducing missed
melanomas. In Oxford, the ratio of
benign to malignant moles excised has
now been reduced by dermoscopy to an
astonishingly low 2:1, even better than
the 5:1 which has been reported by
Argenziano. Without dermoscopy this
ratio can be as high as 18:1 or higher, an
argument which apart from the issue of
needless scars should interest
Commissioners. Cutting out benign
lesions pointlessly is neither good
medicine nor good economics.
This was the 4th time I have heard Dr
Bowling present, but the slides were
new and the presentation adapted to the
changing dermoscopic scene. He
mentioned his personal series of 1,000
melanomas including many unusual
presentations, but, recognising we GPs
will not see many melanomas, he
concentrated mainly on using
dermoscopy to make the referral
decision. The goal is positive
identification of benign lesions, referring
whenever dermoscopy could not enable
safe reassurance. Secondary care does
not necessarily want fewer referrals, just
better grading. He mentioned the terrors
of the web which sometimes had
patients planning their funerals in the 10
days waiting for the skin cancer clinic
appointment – at which he would take 3
seconds to diagnose a seborrhoiec wart
or haemangioma.
Beware nonspecific lesionsA very slow growing 5cm irregularly
shaped and pigmented lesion on a man's
back yielded no useful dermoscopic
criteria – but it was impossible to
confidently assign the lesion to a benign
diagnostic category, which equals a
referal. It was dermatofibrosarcoma
protuberans (DFSP), a rare sarcoma
which grows so slowly it may be ignored,
but can still kill. Again, if it looks wrong
and can't be proved benign, refer. Rare
things are rare, but do occur, and as with
Merkel cell cancer, (a dangerous cancer
mainly of older men’s’ head and neck
which is on the increase and like DFSP
lacks dermoscopic features) are often
missed. We were reminded that the
ABCD rule doesn’t work for nodular
lesions, and is anyway a crude tool
compared to systematic examination of
lesion architecture by dermoscopy, our
window into the histopathologist’s world.
BCC pigment and pseudolacunaeLacunae are a stereotypical dermoscopic
feature of haemangiomas, often allowing
extremely confident diagnosis and
avoiding referral. They can be red, blue,
purple or black (when thrombosed), and
may be mixed within a lesion, BUT the
colour within each individual lacuna
should be homogenous. ‘Lacunae’ which
are grey, brown or of mixed/granular
colours occur in basal cell cancers as we
were shown, catching some of us out.
We spent half an hour looking at
pigmentation in BCCs. Dr Bowling said
once you got used to seeing BCC
pigment through the dermoscope; you
get your eye in and see it more often on
naked eye appearance – something I
have noticed. Fully pigmented BCCs are
uncommon, but probably 40% of BCCs
have some pigment, a dermoscopic
feature often allowing a firm diagnosis.
The pigment in BCCs is not melanocytes,
but melanin in abnormal basal cells. Leaf
like structures, ovoid globules and
cartwheel structures are among the
irregular blue, brown and grey pigmented
structures seen in BCCs, all part of the
chaos that occurs in a growing tumour.
Dr Bowling stressed that the morphology
of a malignant tumour changes
dynamically over time. Even the most
experienced dermoscopist cannot always
tell a pigmented BCC from a melanoma.
Reduced referrals
We saw 30 plain views and then
dermoscopic views of the same tumours
and marked to refer or reassure. On a
show of hands, there was a significant
Improvers’ Dermoscopy Workshop
I know we have written often about dermoscopy: this report concentrates on someadvanced teaching points presented by the UK’s top Dermoscopist with whom thePCDS has been working for several years
2.5 hours with Jonathan Bowling, Edinburgh
1. Nodular Prurigo UK. http:// www.nodular-prurigo.org.uk /
2. Hyde JN, Montgomery FH. A practical treatise on disease of the skin for the use of students and practitioners. 1909; 174-175
3. Finlay AY, Khan GK. Dermatology Life Quality Index (DLQI): A simple practical measure for routine clinical use. Clinical and ExperimentalDermatology 1994; 19: 210-216.
As a retired nurse I have a continuing
interest in health matters. Being
someone who has had a lifetime of
deriving satisfaction from caring for
others both professionally and in a
voluntary capacity, when I was
diagnosed with nodular prurigo (NP) and
found no support organisation for this
condition, I decided to start a website dedicated to this –
Nodular Prurigo UK1.
NP (Pruritus Nodularis, Hyde’s Disease) is a chronic skin
condition first described by Hyde & Montgomery2. It has no
known cause or specific treatment. I was diagnosed 3½ years
ago, but had suffered for about 1½ years before this. Having
had other skin conditions most of my life (urticaria, eczema) it
had been assumed both by my GP and me that this was just
an extension of these. It was not until another partner in the
practice specialising in skin disorders ordered a skin biopsy
that a precise diagnosis was reached. Treatment then has
been various and ultimately unsuccessful, now reaching into
immunosuppressant drugs.
With all my own experience I recognised that a website giving
clear information and acting as a contact point for people
affected by NP through a support forum, would be a useful
addition to the online support dermatological networks. Having
started in March 2010 it is still early days, but if the demand is
sufficient there is always the possibility of Nodular Prurigo UK
becoming a charity or not-for-profit organisation. This project is
currently self-funded, donations, however, will always be
welcome!
Please visit the website and get in touch with any comments,
items for publication or suggestions to improve the site. You
might also encourage anyone affected by NP to visit the site
and help me build statistics on their experiences by completing
the two online questionnaires – the Dermatology Life Quality
Index (DLQI)3 and a Treatment Survey.
Rebecca Ditman SRNNodular Prurigo UK
Nodular Prurigo UK – A New Support Service
Psychotropic Medication• Tricyclics can be wonderfully useful in treating nodular
prurigo. Starting at low doses (such as amitriptylline10mg at
night) and increasing to higher doses is usually key. Remember
to warn patients of the side effects and check that they have no
cardiac history. Also remember to be up front with patients that
this medication is used as an anti-depressant in some (most
patients with nodular prurigo are not depressed and the clinician
can be clear that the medication is not being used for that
purpose and not at an anti-depressant dose). Some tricyclics
have additional anti-histamine properties (for example doxepin)
which can be useful
• SSRIs can also be helpful especially if the patient has an
affective disorder such as anxiety and/or depression
• Rarely agents such as opiate receptor antagonists, pregabalin
and gabapentin have been reported to benefit patients with
nodular prurigo, but this would be under Specialist supervision
PsychotherapyHabit reversal therapy for the itch-scratch cycle associated with
nodular prurigo may be helpful. This is a behavioural therapy
technique whereby the patient initially acknowledges the time,
12 13
This 69 year old man presented with a widespread, intensely itchy, rash,
that had been steadily worsening over the past year. Have a look at the
illustrations and ask yourself
What would you include in your differential diagnosis?
• What tests would you perform?
• Would a skin biopsy help?
• What are the treatment options?
The keys to the clinical diagnosis here are
1) The distribution of the very itchy rash
2) The presence of vesicles on close examination (Fig 1)
Dermatitis herpetiformis (DH) presents with intensely pruritic or stinging
polymorphous lesions, symmetrically located on extensor surfaces, especially
elbows (Fig 2), knees, scapulae, shoulders (Figs 3), sacrum, buttocks (Fig 4),
hairline and scalp (Fig 5). Close examination may show the characteristic vesicles
(Fig 1). Hence the name herpetiformis = looks like herpes. Usually itch is of such
intensity that vigorous itching and scratching removes the vesicles, leaving
widespread erosions, crusted papules, and areas of post-inflammatory
hyperpigmentation.
A not unusual presentation, especially early on, is with erythema, urticarial
plaques and papules. Rarely DH is asymptomatic. Often the patient describes
itching, burning, and stinging 8 to 12 hours before lesions develop.
DH can start at any age with a peak age of onset between 20 and 40 years. It
persists indefinitely.
It is one of the group of autoimmune blistering diseases and is associated with
many other autoimmune disorders, such as pernicious anemia, Sjögren
syndrome, Lupus erythematosus, and diabetes mellitus. The
finding, on a skin biopsy, of granular deposition of
immunoglobulin A (IgA) detected with direct
immunofluorescence (DIF) confirms diagnosis.
Nearly all DH patients have clinical or more usually subclinical
small bowel villous atrophy (gluten-sensitive enteropathy).
Indeed DH represents the cutaneous manifestation of
gluten-sensitive enteropathy, an immunologic reaction to
ingested gliadin, Circulating IgA antibodies against
endomysium and tissue transglutatminase (tTG) may be
detected on serology.
Patients are at increased risk of developing non-Hodgkins
lymphoma. However the risk is low. One follow up study
showed a risk of 1% of 1104 patients, with onset from 2 to 31
years after diagnosis of DH.
Treatment
Gluten free diet is the treatment of choice. Six to twenty-four
months of strict diet reduces or may eliminate the need for
medication. It treats the enteropathy (which is usually present)
and is protective against small bowel lymphoma.
Dapsone Starting at a dose of 25 mg to 50 mg daily gives rapid symptom
relief, often within hours of the first dose, with no new lesions
erupting after 2 to 3 days. The average daily dose is usually 50
to 75mg. The dose should be titrated down once satisfactory
response is achieved. Maintenance dose may be as low as 25
mg per week.
Dapsone causes haemolysis, methaemoglobinaemia, jaundice
and neuropathy. The haematological side effects tend not to be
a problem with a daily dose of 100 mg or less. Table 1 outlines
a schedule for monitoring dapsone.
Irish people have a very high incidence of Coeliac disease and
DH. Those of you who practice in areas of the UK with historic
high immigration from Ireland should consider the diagnosis of
DH when faced with a widespread, blistering, itchy rash in one
of your patients.Johnny Loughnane
What’s Your Diagnosis?
reduction in intention to refer with
dermoscopy, with initially suspicious
looking lesions resolving into
haemangiomas, seborrhoiec warts
and benign naevi. He made the point
that we tended to teach little
dermoscopy of benign intradermal
naevi which often look like small
papular non pigmented BCCs. The
blood vessels were the main clue,
the short curvilinear vessels (I have
heard them called comma vessels
elsewhere) in the shape of letters C,
J, E and S distributed evenly though
the lesion, not so long or well
focused as the typical arborising
telangiectatic vessels of BCCs. Very
helpful.
Horror slide
The horror slide of the presentation
was a warty pigmented scalp lesion
on a white man from a hot country.
Dermoscopy showed numerous
milia like cysts and comedo like
openings, so I thought it was a
seborrhoiec wart. However, Dr
Bowling, and the histopathologist,
thought it was a melanoma. The
clues, apart from the high risk history
including recent change, were the ill
defined edge and irregular dark
pigment, but the dermoscopic
resemblance of this warty melanoma
to a benign seborrhoiec wart scared
me witless and I consider myself an
experienced dermoscopist.
Admittedly he said it was easier in
the flesh than from the image (a
problem for teledermoscopy). A
good reminder that there is no
'always' or 'never' in medicine and
that we should beware
overconfidence. Community based
dermoscopy is already (albeit
patchily) achieving its potential to
reduce referrals by screening out
benign lesions, but let’s be careful
out there.
Stephen Hayes
Fig 1 Fig 2 Fig 3 Fig 4 Fig 5
Before initiation of therapy
1. Complete history/examination
2. Severe cardiac/lung disease – dose adjusted as it causessome degree of hemolysis
3. C/I – G6PD,severe hepatic abnormality, pregnancy and breastfeeding
4. FBC – plus differential, reticulocyte count, Urea, creatinine, LFT,G6PD
Follow-up visits
5. Periodic neurologic evaluation
6. FBC/differential and reticulocyte count every 2 weeks first 3 to6 months, then every 2 months
7. Liver and renal function tests and urinalysis monthly first 3 to6 months, then every 2 months
Table 1. Monitoring Patients on Dapsone
14 15
The revised BAD UK Guidelines forthe Management of Cutaneous Melanoma 2010
Tony, a 52 year old patient was seen in out-patient clinic this
week and informed of his diagnosis – a nodular melanoma of
Breslow thickness 4.3 mm. His outlook is not good. Tony had
been referred 14 weeks ago as a routine referral with a
relatively non-specific lump on his skin. Could the revised
Guidelines have helped improve Tony’s chance of survival?
Before I attempt to answer this question I would like to
highlight four areas within the revised Guidelines that are of
value to GPs and other primary care health professionals:
• Who is at risk of melanoma?
• Sun protection and vitamin D3
• When should family members be referred?
• Hormones and melanoma
Who is at risk of melanoma?
Slightly increased risk (1-3 times that of the general population)
• Risk factors – skin that burns easily, red or blond hair, a high
density of freckles, any family history of melanoma
• Management – give advice on sun-protection and
self-examination
Moderately increased risk (8-10 times that of the general
population)
• Risk factors – large numbers of moles, some of which may
be atypical in appearance, a personal history of melanoma,
organ transplant recipients
• Management - patients with large numbers of moles of
which some are atypical should be referred to a
Dermatologist for assessment and photography, otherwise:
• Counsel about the risk
• Give advice on sun protection
• Monthly self-examination
High-risk (more than 10 times that of the general population)
• Risk factors – patients with giant congenital melanocytic
naevi, those with a strong family history (see later)
• Management - long-term Dermatology follow-up needed
Sun protection and vitamin D3
Adequate sun exposure to allow vitamin D synthesis or
sufficient dietary intake of vitamin D3 is essential to human
health. It is now recognised that a balanced approach needs to
be given to our population:
• All individuals and especially children should not get sunburnt
• Sunbeds should be avoided - a recent meta-analysis has
shown that the use of sunbeds, particularly under the age of
35 increases the risk
• Those at risk should limit their recreational sunlight and at the
same time consider supplementing their intake of vitamin D3
in the absence of any contraindications. Foods containing
vitamin D3 include cod liver oil, fortified milk, salmon,
mackerel, sardines, egg yolk and beef liver
• It is inappropriate to greatly reduce sun exposure in those at
low-risk
When should family members be referred?
• 3 or more cases of melanoma or pancreatic cancer
• 2 cases of melanoma in a family PLUS any of the following:
• the presence of multiple primary melanomas in one of the
affected individuals
• the presence of multiple atypical moles
Family members should be referred routinely to a clinic
managing inherited predisposition to cancer (involving
Dermatologists and/or Clinical Geneticists)
Melanoma – pregnancy and hormonalmedications
• Pregnancy - there is no evidence that melanoma at or around
the time of pregnancy affects the outcome for mother or
baby, but the social and family effects of developing
recurrent melanoma during pregnancy or after birth are great
and so appropriate counseling is needed
• The COCP – there is no evidence that this plays any role in
the natural history of melanoma
• HRT – there is no evidence that this plays any role in the
natural history of melanoma, neither does it worsen the
prognosis in stage I or II melanoma
Follow up of patients with melanoma
• Patients with in situ melanomas do not require follow up
• Patients with invasive melanomas have differing risk of
relapse according to their stage group
• Patients with stage IA melanoma should be seen two to four
times over up to 12 months, then discharged
• Patients with stage IB–IIIA melanoma should be seen
3-monthly for 3 years, then 6-monthly to 5 years
• Patients with stage IIIB and IIIC and resected stage IV
melanoma should be seen 3-monthly for 3 years, then
6-monthly to 5 years, then annually to 10 years
• Patients with unresectable stage IV melanoma are seen
according to need
But what about Tony?
Effective management of melanoma is based around early
diagnosis and surgical excision, and with this in mind I don’t
believe that the revised Guidelines are going to help the likes
of Tony. Why is this?
• There are massive pressures on GPs to refer almost
everything that could vaguely be a melanoma
• Our secondary care 2-week clinics are now awash with
seborrhoeic keratoses and other benign lesions, which are
pushing up waiting lists for routine referrals
• As with Tony, significant numbers of melanoma may not
be obvious – up to 50% of melanomas arrive on routine
referrals and these patients may now be waiting longer to
be seen
• The new Guidelines do little to address the educational
needs of the community and simply state ‘Melanoma
remains relatively uncommon and therefore the opportunity
to develop diagnostic skills is limited in primary care‘
• The Guidelines do little to assist GPs to help sort out which
lesions should be referred – essentially unless the lesion is a
normal looking mole arising in puberty the Guidelines
recommend the patient should be referred
So how could Tony have fared better?
If we could take out of our secondary care clinics many of the
skin lesions that are obviously benign, then the patients
referred routinely such as Tony would be been seen quicker
and their prognosis improved.
We cannot keep on dismissing the potential to improve the
dermatology know how of GPs, and a move towards better
training and education for GPs is paramount to improved
survival rates for melanoma. Most working in primary care are
not going to become experts in the diagnoses of skin lesions
but there is certainly a great opportunity to help GPs recognise
what is very likely to be normal such as itchy moles that look
normal and which are not changing, or moles that become
raised and ‘wobbly’ while maintaining their symmetry.
And what about the role of Dermoscopy in primary care? GPs
across the county are showing a substantial interest in this
diagnostic aid, and while I cannot recommend GPs using a
dermatoscope to make a diagnosis of melanoma, with
appropriate training it surely has a place to help confirm benign
lesions such as seborrhoeic keratoses, angioma and
dermatofibroma?
Close working relationships between primary and secondary
care are also important and this is why I was concerned to read
that the authors of the revised Guidelines are all based in
secondary care. The only mention of primary care was the
RCGP, I am not aware of any contact with the PCDS, which
after all has over 1000 members with a keen interest in
dermatology.
So how do I qualify to pass comment on the strengths and
weaknesses of the BAD Guidelines? I work with patients in
general practice, as a GPwSI in dermatology and skin surgery
and also in an under-resourced dermatology out-patient
department. I also have a very personal experience – it was
over 10 years ago that I sat in my GP office and saw the report
of a 4mm pigmented lesion that had been removed from my
left shoulder, unfortunately it was not a short one, however I
was one of the lucky ones as it was only a melanoma-in-situ.
For more information on melanoma please refer to the relevant
chapter in the A-Z of clinical guidance on the PCDS website.
Dr Tim Cunliffe
16 17
Dr Snippit’s Clippings
News from IrelandIn 2011 the Annual Meeting of the PCDSI will take place in
Galway for the first time ever. The Radisson Hotel, in the
center of town, is our venue. Two very full days of
dermatology education have been arranged for Friday 4th and
Saturday 5th of March.
Connemara, an area of beautiful mountains and rugged coastline is
situated West of the City. The centre of Galway is within walking
distance of our conference venue. You might therefore consider a
short spring break, combining two days of intensive dermatology
education with a relaxing few days on Ireland’s West Coast.
The programme includes sessions on atopic eczema, psoriasis,
skin problems in different patient groups, dermoscopy, skin
infection, difficult cases, paediatric dermatology etc. Our speakers
are from Ireland, England, Wales and Scotland. There will be some
parallel sessions, where we aim to cater for delegates varying
knowledge and expertise in dermatology.
Please check out our website, www.pcdsi2011.com, for a detailed
programme, registration form and accommodation details.
I accepted an invitation to join the Expert Skin Cancer Group
advising the National Cancer Control Programme. The Chair is Dr
Patrick Ormond from St James Hospital, Dublin. The Group have
been meeting regularly, drawing up Guidelines on Referral of
Patients with Suspected Skin Cancer. A one page Guideline Sheet
and a Standard Referral Form are at present being piloted in the
Cork area. Initially they will be restricted to suspected cases of
Melanoma. After assessment of the pilot, there will be a final
refinement of the Guideline and Referral Form, after which they
will be introduced throughout the Country. It is planned that extra
Consultant Dermatologist appointments will be made to cater for
expected increased workload in secondary care. In the present
financial state of the country we can only assume that this will not
constitute a flood of appointments.
Johnny Loughnane
Tubercles from tattoos
The BMJ of 30th October1 carries an interesting story about an
outbreak of Mycobacterium chelonae (no, I’d never heard of it
either) in France. A large outbreak over 8 months was due to
contaminated tattoo ink. 48 patients presented with skin
lesions, mainly pustules, occurring several days to a month
after visiting 2 particular tattooists in Le Havre. The germ was
cultured from ink bottles, which had been refilled from a large
bottle and rinsed with tap water. The report is accompanied
with an image of a wolf tattoo sporting a crop of pustules and
papules. They all got better with antibiotics, but are stuck with
the tattoos. Silly habit.
Vitiligo and other Auto Immune Diseases
The same BMJ had a
patient authored item about
Vitiligo. Darryl Monte,
assisted by Vitiligo Society
lead Jennifer Viles and
Dermatologist David
Gawkrodger, told us about
his journey. Steroid cream was tried, then ‘holistic’
homeopathy, and then (after a possibly stress induced relapse)
PUVA, which achieved rapid repigmentation on the face.
However, his legs got worse. A change to narrowband UVB
partially improved the face, but not hands and feet. He had 250
UV treatments in all. He has also tried tacrolimus, again on
anecdotal evidence, and feels that the affected areas of skin
are thinner, especially the hands.
Mr Monte felt his main problem from vitiligo was other
peoples’ attitude towards his appearance, describing the
psychological effect as ‘quite painful’. He subsequently
developed diabetes and then rheumatoid disease – which was
dramatically improved by etanercept. Dr Gawkrodger notes
that etanercept didn’t help the vitiligo, and that ‘there is still no
really effective treatment’ and calls for more research.
Dr Snippit’s sympathy for the patient’s suffering almost, but
not quite, prevents him from wondering about the risk/benefit
ratio of unproven treatments, including steroid and
phototherapy, for unreliable relief of benign disorders. And if
research does give us a monoclonal antibody or similar for
vitiligo, what will it cost compared to, say, a Specialist
Dermatology Nurse’s annual pay? If NICE goes, we GPs will
be responsible for decisions about such things.......
Missed Melanoma...again
If in some areas of medicine we lack good evidence, in other
areas we don’t always make best use of the evidence we
have. Father-of-four Jon Edmonds, 42, alleges a Bristol Plastic
Surgeon refused to remove a bleeding mole from his shoulder
because it was a 'cosmetic' procedure. Now he has
metastatic melanoma and is suing the NHS for £300,000. He
told reporters 'The failure to carry out that minor and
inexpensive procedure is now likely to cost the NHS a very
large sum of money.2’
Mr Edmonds's GP correctly referred him to a Pigmented
Lesion Clinic in October 2005 after noticing a mole on his left
shoulder but he was told it was a bite or sting. His friends
subsequently encouraged him to get it reviewed in February
2008 when it changed, but he evidently felt reassured by the
original advice. When his GP re-referred him in June 2009
after colour change, it was metastatic.
His lawyer said: ‘Jon should have had this mole cut out in
2005. The fact that he wasn't even followed up compounded
the error. He is now left with a far less favourable prognosis
than he should have been, and in the circumstances we are
pursuing the claim as quickly as we can, and expect to
recover very substantial damages for Jon.'
Two words: sad, instructive. But Dr Snippit hopes that Daily
Mail readers will not conclude that the NHS should always
remove moles, even if they are ‘only cosmetic’. That is not the
lesson this tragedy teaches.
Incidentally, it is whispered in high places that the continuing
uncertainty over vitamin D and the benefits of UV is being
gently stirred and spiced up by the tanning lobby. Surely not?
Next thing you know we’ll hear of a Secretary of State for
Health working for a tobacco company. No, there’s no way
that could ever happen.
Oral Isotretinoin and Attempted Suicide
We all know of the teratogenic effects of
Roaccutane (now available as generic
isotretinoin), although when Dr Snippit once
warned a female patient it was as bad as
Thalidomide, she asked ‘What’s Thalidomide?’.
But anxiety about mood change and suicide still
prevents some patients with severe scarring
acne from receiving therapy. The BMJ of 20th
November3, 4 carried a report and editorial based
on 21 years of health records to try to ‘untangle
whether the drug itself or severe acne’ causes
increased suicide risk. The answer apparently is,
it’s a bit of both, but the absolute risk is tiny
anyhow. Suicide attempts in the treatment group
were already rising before treatment began. The
authors concluded ‘The data support our
hypothesis that severe acne, regardless of
exposure to isotretinoin, carries an increased risk of
attempted suicide.... A physician would thus need
to start treatments in more than 2000 new patients
during one year to see one additional suicide
attempt (note, ‘attempt’, not completed suicide)
due to treatment. Nevertheless, the most important
proactive measure to be taken would be to closely
monitor all patients’ psychiatric status, not only
during treatment but also for at least a year after
treatment with isotretinoin.’
In other words, as far as we can tell, acne is
associated with increased levels of depression and
self harm, and oral isotretinoin apparently causes a
tiny increase in self harm events, with a number
needed to harm (NNH) of over 2,000. Helpful to
have a nice round-and reassuring-figure like this to
hand when counseling severe acne patients about
risk and benefits. But do read the whole study and
editorial. Nice bit of work.
Season’s Greetings from Dr Snippit
1. BMJ 30th October 2010 volume 341 page 938
2. http://www.dailymail.co.uk/health/article-1329078/Father-4-cancer-sues-NHS-doctor-dismisses-mole-insect-bite.html#ixzz15GwtDQvi
3. http://www.bmj.com/content/341/bmj.c5866.full?sid=cec75596-1d87-4f29-8fd3-c4a352a8d925
4. http://www.bmj.com/content/341/bmj.c5812.full
September – November 2010
So, the baking days of summer have
been replaced with the mists and
mellow fruitfulness of autumn –
without the inconvenience of all that
baking, of course...As the nights grow
longer, what could be better than
curling up with a few juicy journals?
An unexpected side effect of the
demonization (rightly so, IMHO) of
sunbeds is that the permatanned are
constantly looking for new ways to keep
up that all year round glow of...’health’.
Synthetic analogues of melanocyte
stimulating hormone – so called
melanogenic peptides – have recently
become available1. However, despite
these products still being under test by
the regulatory authorities, for it seems
likely they may have therapeutic
applications, they are already widely
available on the t’interweb, in tanning
salons and in some gyms. They are
self-administered by sub-cutaneous
injection. This is obviously not an ideal
situation. Not only are these products of
unregulated purity and potency, they also
have sometimes unexpected effects on
pre-existing melanocytic naevi, or even
cause new naevi to erupt. In addition, the
risks of blood borne virus transmission
from shared or dirty needles doesn’t go
away if the drugs are ‘tanning products’.
Another of the series of evidence based updates comes next, this time on atopic
eczema2. It would appear that research into eczema is alive and well – 260
randomised controlled trials have been conducted in the past 10 years. Evidence
was presented of the risks of oral corticosteroids in severe flares of eczema, the
efficacy of pro-biotics in the prevention of eczema (only if given to mothers in the
last trimester of pregnancy!), the confusion surrounding allergy testing (no
concensus has been reached) and the benefits of structured educational
programmes for both sufferers and carers. This is a ‘hot topic’ at the moment and
our German friends seem to be leading the way with this particular intervention.
The PCDS has a meeting, next May, in Berlin, and one of our speakers will be
detailing the German experience.
It has long been my belief that dermatology has taken over the mantle of the last
true general hospital speciality. If any further evidence is required, consider the
example of psoriasis3. We are increasingly being asked to look upon psoriasis as a
multi-system disease that just happens to have a primary cutaneous manifestation.
From America comes evidence that psoriasis carries with it an increased risk of
cardiovascular death – this is not unsurprising, chronic inflammation has been long
known to cause this. What is surprising is that psoriasis also carries an increased
risk of mortality from kidney disease, infection and dementia. Whether this is a
consequence of the disease or the treatments for the disease remains unclear.
Lichen sclerosus is a relatively common, autoimmune, inflammatory dermatosis. It
has a predilection for the genital skin of both sexes, but also can affect the
extra-genital skin. Rather oddly, it has a bi-modal distribution in both sexes too,
affecting pre-pubertal and post menopausal girls and women, but also young boys
and adult men. A biopsy is often necessary to make the formal diagnosis,
particularly on extra-genital skin where it can be hard to distinguish it from
morphoea. A timely set of guidelines4 (there seem to be some of these every
quarter...) have been produced to guide treatment and longer term care. Topical
steroids remain the mainstay of therapy, although other treatments are gaining
credence – particularly tacrolimus. The fear, as always, is that lichen sclerosus can
progress to squamous cell carcinoma – the risk, however, appears small – less than
Journal Watch
5%. Secondary care follow up is recommended for patients who have continuing
symptoms despite adequate treatment, previous SCCs, those who have treatment
unresponsive disease and those patients who present with atypical forms of the
disease. Follow up is deemed unnecessary for patients who use less than 60g of a
superpotent topical steroid in a 12 month period for symptom control.
Onto another troubling disease, but this time with a more public expression...
rosacea. Whilst some diseases – take another bow, psoriasis – have had their
impact analysed and quantified, others have had less time spent on them5. The
DLQI is the most widely used tool to define impact on quality of life, rosacea can
be shown to have a moderate impact on quality of life. The DLQI can also be used
to look at the impact of interventions, we can thus say that, because of their
relative efficacy compared to other therapeutic agents, topical metronidazole, oral
tetracyclines and oral isotretinoin have a positive life quality effect. Nice to know,
isn’t it?
Personally speaking, I always find it helpful to have another bit of evidence to beat
smokers over the head with so I am eternally grateful to Meding et al6.
What-do-you-know, smoking increases the severity of hand eczema and it has a
dose response relationship! So, if you have hand eczema, and you smoke – the
more you smoke, the worse the eczema is likely to be. The authors mention
possible confounding factors, I will choose to ignore these for the time being.
There has recently been an unaccustomed outbreak of common sense with the
shelving of the plans for generic substitution in pharmacies. One of the greatest
concerns revolved around the substitution of emollients. Aqueous cream is,
currently, the cheapest emollient cream but its use as a leave on emollient has
long been questioned. This study7 shows why. The application of aqueous cream
to normal skin resulted in a reduction in thickness of the stratum corneum, and
increased transepidermal water loss – implying a marked reduction in the barrier
function of healthy skin. This obviously calls in to question the propriety of using it
as a leave on emollient on already compromised skin.
Just when you thought it was safe to venture outside again – after all, we have all
taken on-board the SunSmart advice, haven’t we? – we now have to fear the
effects of sub-erythemal UV exposure8. Thankfully, this is a review article and
doesn’t suggest living in a cave, but the evidence is accumulating that even
avoiding sunburn doesn’t necessarily prevent photo-damage to skin. Helpfully, we
are advised that, taking a lunchtime meal, outside, in Paris, in June will result in a
skin exposure of 50% of the minimal erythema dose to exposed skin. I feel more
research in to this is essential and I propose to put myself forward as a suitable
test subject.
In the UK, however, we appear to have taken on-board the sun-protection issue to
such an extent that we are in danger of heading the other way – into sub-optimal
levels of exposure. Admittedly, using an experimental population from Manchester
may skew the results somewhat, but in this study9, only by the end of summer
can optimal levels of Vitamin D be detected in the blood – even then, many
subjects never reached this level. It is just this level that is necessary to maintain
us through the long winter months. Currently, the majority of the population, it
would seem, becomes vitamin D deficient during the dark half of the year. We
have already discussed in a previous issue that supplementation of the diet is the
most viable option to correct this – this paper provides more evidence for this.
So now we’re all feeling relaxed, it’s time
to talk about stress10. Stress affects many
diseases, and its effects on psoriasis are
well documented. Evidence is here
presented to suggest that this is, indeed,
more than skin deep. Stress, particularly
moments of high stress affect circulating
cortisol levels and it is this that influences
disease outcomes in patients with
psoriasis. It is also suggested that chronic
stress creates a ‘psycho-physiological
state’ of persistently lowered cortisol
levels and it is this that leads to the
deleterious effects of new stressors on
the skin.
Experimental data is often subject to
confounding factors that can muddy the
conclusions somewhat. In particular, the
effects of treatment on chronic diseases
can be particularly confusing. For example,
the incidence of cancer in patients with
atopic dermatitis exceeds that of the
general population11. Specific subtypes of
cancer, such as lymphoma, are also
over-represented within this population.
These are not just cutaneous cancers –
more evidence of the systemic nature of
many of ‘our’ diseases. So, does the
chronic stimulation of the immune system
lead to these neoplasms developing, or is
it the effects of immunosuppressive
treatments? Further research is needed…
For our final paper, we return to ultraviolet
radiation. We’ve had damage and
deficiency, so it only seems fair to show a
beneficial side to this part of the
electromagnetic spectrum. UVB, and in
particular, narrow band UV has become a
standard therapy in the treatment of
psoriasis. There is, however, significant
individual variation in both the number of
treatments necessary to achieve
remission and also in the duration of that
remission12. There are clinical predictors of
early success – milder disease, female
gender, lower body weight and a higher
prior exposure to therapeutic UVB. Only
one factor seemed to predict length of
remission – the more treatments needed
18 19
In patients with severe chronic hand eczema:With Toctino 30mg used for 12–24 weeks:
Clear/almost clear hands in nearly half of patients1
Improvement in 4 out of 5 patients2
Effective treatment of both hyperkeratotic and inflammatory symptoms1
Two thirds of patients remain in remission 6 months after achieving clear/almost clear hands3
Simple once daily oral dose and minimal monitoring4
PRESCRIBING INFORMATION: TOCTINO® (ALITRETINOIN) 10mg OR 30mg CAPSULES. Before prescribing Toctino please refer to the full Summary of Product Characteristics. Name of the medicinal product: Toctino (alitretinoin) 10mg or 30mg Capsules. Non proprietary name: Alitretinoin. Presentation: Soft capsules containing 10mg or 30mg of alitretinoin. Indication: Severe chronic hand eczema in adults that is unresponsive to treatment with potent topical corticosteroids. Predominantly hyperkeratotic features are more likely to respond to treatment than pompholyx. Dosage and administration: Toctino should only be prescribed by dermatologists or physicians with experience in the use of systemic retinoid therapy. The recommended dose range is 10-30mg once daily, to be taken orally with a meal. The recommended starting dose is 30mg once daily. A dose reduction to 10mg once daily may be considered in patients with unacceptable adverse reactions to the higher dose. “High risk” patients with diabetes, obesity, cardiovascular risk factors or lipid metabolism disorders should be initiated on 10mg once daily and titrated up to 30mg once daily if necessary. A treatment course can be given for 12 to 24 weeks depending on response. In the event of relapse, patients may benefit from further treatment courses. Prescriptions for women of childbearing potential should be limited to 30 days and dispensed within 7 days of the prescription in accordance with the Pregnancy Prevention Programme.Contraindications:
If pregnancy occurs, Toctino should be stopped immediately and the patient referred to a physician specialising or experienced in teratology for advice. Toctino
is contraindicated during breastfeeding. Toctino is contraindicated in patients with hepatic insufficiency, severe renal insufficiency, uncontrolled hypercholesterolaemia, hypertriglyceridaemia, hypothyroidism, hypervitaminosis A, hypersensitivity to alitretinoin, other retinoids or excipients, allergy to peanut or soya, hereditary fructose intolerance and concomitant tetracycline treatment. Precautions and warnings: Not recommended in patients under 18 years of age. Male fertility may be compromised. Patients should be reminded not to share medication or donate blood during therapy or for 1 month following therapy with Toctino. Psychiatric disorders have been seen with other retinoids, therefore particular care should be taken in patients with a history of depression. Patients should be observed for signs of depression and referred for appropriate treatment if necessary. Effects of UV light may be enhanced and patients should avoid excessive exposure to sunlight, unsupervised use of sun lamps and should use appropriate sun protection of at least SPF 15. Patients experiencing visual difficulties should be referred to an ophthalmologist and treatment discontinuation may be required. Decreased night vision has been reported and patients should be warned asymptoms of benign intracranial hypertension including headache, nausea and vomiting, visual disturbances and papilloedema should discontinue treatment immediately. Serum cholesterol and triglycerides should be monitored. Treatment should be discontinued if hypertriglyceridaemia cannot be controlled at an acceptable level or if symptoms of pancreatitis occur. In “high risk” patients with diabetes, obesity, cardiovascular risk factors or lipid metabolism disorders, more frequent serum lipid checks may be necessary. Dose reduction or discontinuation should be considered in the event of persistent clinically relevant elevation of liver transaminases. If severe diarrhoea is observed, diagnosis of inflammatory bowel disease should be considered and treatment discontinued immediately. Severe allergic reactions necessitate interruption of therapy and careful monitoring. Please refer to the Toctino Summary of Product Characteristics for further details. Interactions: Concomitant use of St John’s Wort may cause failure of combined hormonal contraceptives. Concomitant use of vitamin A or other retinoids may cause hypervitaminosis A. Concomitant use of tetracyclines may increase the risk of
benign intracranial hypertension. Common adverse effects: Very common (≥10%): headache, hypertriglyceridaemia, hypercholesterolaemia, decreased HDL. Common (≥1%; <10%): anaemia, increased iron binding capacity, decreased monocytes, increased thrombocytes, decreased TSH, decreased free T4, conjunctivitis, dry eyes, eye irritation, flushing, increased liver transaminases, dry skin and lips, cheilitis, eczema, dermatitis, erythema, alopecia, arthralgia, myalgia, increased blood creatine phosphokinase. Serious adverse effects: Uncommon (≥ 0.1%; <1%): blurred vision, cataract, epistaxis, ankylosing spondylitis. Rare (≥0.01; <0.1%): benign intracranial hypertension, vasculitis. Overdose: reversible adverse effects consistent with retinoid toxicity, including severe headache, diarrhoea, facial flushing and hypertriglyceridaemia. Please refer to the Toctino Summary of Product Characteristics for full details of adverse effects with Toctino. Storage instructions: Store in original packaging and protect from light. Marketing authorisation number and NHS List Price: PL32205/0001/0001 Toctino 10mg 30 capsule pack £411.43; PL32205/0001/0002 Toctino 30mg 30 capsule pack £411.43 Legal Category: POM. Name and address of authorisation holder: Basilea Medical Ltd., 14/16 Frederick Sanger Road, The Surrey Research Park, Guildford, Surrey, GU2 7YD. Toctino® is a registered trademark of Basilea Pharmaceuticals International AG. Date of preparation of prescribing information: August 2008. ALI080051 recertified Oct 2010.
Adverse events should be reported. Reporting forms and information can be found at www.yellowcard.gov.uk. Adverse events should also be reported to Basilea Pharmaceuticals on 01483 790023.
Pregnancy is an absolute contraindication to treatment with Toctino. Use during pregnancy or in women of childbearing potential is contraindicated unless all conditions of Pregnancy Prevention Programme are met. If pregnancy does occur in spite of the pregnancy prevention precautions during treatment with Toctino or in the month following discontinuation of therapy, there is a high risk of very severe and serious malformation of the foetus. Please refer to the Toctino Summary of Product Characteristics for further details.
References: 1. Ruzicka T et al. Efficacy and safety of oral alitretinoin (9-cis retinoic acid) in patients with severe chronic hand eczema refractory to topical corticosteroids: results of a randomised, double blind, placebo-controlled, multicentre trial. Br J Dermatol 2008; 158(4): 808-817. 2. Data on file ALI100031, July 2010. 3. Ruzicka T et al. Re-treatment study of alitretinoin (9-cis-retinoic acid) in severe chronic hand eczema refractory to topical treatment. Poster 280 presented at EADV 2007. 4. Toctino SPC accessed on the EMC www.medicines.org.uk/emc/.
ALI100115 Oct 2010
20
I am writing this during the falling of the first snows of Autumn! So
much for global warming. It is also in the midst of the debacle of the
football referees withdrawing their services. I can’t remember the
last time we had such a plethora of good strikers in Scottish football.
It was good to see so many of you at the Radisson Blu in Edinburgh.
I hope you all enjoyed it and that all the bruises on arms etc have
disappeared. The report of the meeting and another on the
dermoscopy workshop are elsewhere in the bulletin so I shall not expand further except
to say that I hope as many of you if not more can come next year to the Westerwood
Hotel in 2011.
I mentioned in the last bulletin that I would like to set up a database of dermatology
educational meetings etc in Scotland so that doctors can tap into it to see if there is
anything local to them for CPD points etc. I have had no response yet – so please let me
know of anything, dermatology wise, happening in your area so that we can spread the
word. It’s good to talk! My niece is in South America at present and has been told that
the latest chat up line in Chilean clubs is “your place or mine?” – that’s a new one…
In my part of the world, we are trying to set up some interactive educational evenings in
the CHP to look at patient pathways in dermatology and orthopaedics, so if anyone in
NW Glasgow CHP area wishes to know if and when they are happening, please send me
an email at [email protected].
Also in the CHP area we are possibly piloting an integrated care program for psoriasis
patients including the annual review mentioned in the new SIGN guidelines – watch this
space. I have also had talks with Martin Whitehead, the Oncology Policy Manager of
Bristol Myers Squibb about setting up a Melanoma Taskforce in Scotland along similar
arrangements as to the one already set up in England. If anyone has a burning desire to
be involved once again email me and I will pass your details on to them.
I attended the PSALV (Psoriatic Arthritis Patient Group) dinner in Holyrood on 17th
November which included presentations on the new SIGN guidelines. The GP annual
review for psoriasis patients was once again mentioned and being the only person there
admitting to be a GP I was asked to comment. I pointed out that it will only appear on
our radar if it is included in QoF payments. The MSP at our Table had not heard of these
and made a note to find out more. I also heard the 2 sides of the alcohol debate from an
SNP and Labour MSP which proved interesting. The main argument against was that at
45p a unit it was a tax on the poor and if it was 80p there would have been more of a
debate. The pub next to my surgery has changed its name to Moderation ,so when I ask
my patients about their drinking habits they now all tell me they drink in ………………
That’s all for now. Have a Merry Christmas and a Happy New year.
Iain Henderson
News From North ofthe Border
to achieve clearance meant a
shorter duration of remission. Life’s
hard sometimes. There were also
genetic indicators also, but these
will be harder to determine in a
clinical setting – most people, in my
experience, do not know if they are
homozygous for the C-allele of the
Taq1 VDR polymorphism. If only
people knew themselves better.
Julian Peace
References1. Langan, Nie and Rhodes - Melanotropicpeptides: more than just ‘Barbie drugs’ and‘sun-tan jabs’? BJD2010:163;451-455.
2. Flohr and Powell - Eczema: an EvidenceBased Update. Report from the 9thNottingham Evidence Based Update Meeting,13 May 2010, Loughborough, U.K.BJD2010:163;456-457.
3. Abuabara et al – Cause Specific Mortality inpatients with severe psoriasis – a populationbased cohort study in the UK.BJD2010:163;586-592.
4. Neill et al – BAD guidelines for themanagement of lichen sclerosus 2010-10-31BJD2010:163;672-682.
5. Aksoy et al – The impact of rosacea onquality of life: effects of demographic andclinical characteristics and various treatmentmodalities.BJD2010:163;719-725.
6. Meding at al – Tobacco smoking and handeczema: a population based study.BJD2010:163;752-756.
7. Tsang and Guy - Effect of Aqueous CreamBP on human stratum corneum in vivo.BJD2010:163;954-958.
8. Seite et al - Photodamage to human skin bysuberythemal exposure to solar ultravioletradiation can be attenuated by sunscreens: areviewBJD2010:163;903-914.
9. Webb et al - The role of sunlight exposure indetermining the vitamin D status of the U.K.white adult population.BJD2010:163;1050-1055.
10. Evers et al - How stress gets under theskin: cortisol and stress reactivity in psoriasis.BJD2010:163;986-991.
11. Arana et al - Incidence of cancer in thegeneral population and in patients with orwithout atopic dermatitis in the U.K.BJD2010:163;1036-1043.
12. Ryan et al - Clinical and genetic predictorsof response to narrowband ultraviolet B for thetreatment of chronic plaque psoriasis.BJD2010:163;1056-1063.