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Reports written by Dr. Déborah Salik (Dermatologist, Belgium), Dr. Josefina Marco Bonnet (Dermatologist, France), Dr. Laura Bouchard (Dermatologist, Finland) and Dr. Joël Claveau (Dermatologist, Quebec)
Related topics
Speakers: Prof. Carle Paul, Dr. Myrto Trakatelli and Dr. Lise Boussemart
Reports written by Dr. DĂ©borah Salik
To start, the participants introduced themselves and said what they expected to get out of the workshop.
Next, they brainstormed to establish the core values of the workshop: trust, caring, listening, kindness, indulgence, patience, firmness, respect, experience, impartiality, confidentiality, sharing emotions, honesty, self-criticism, tolerance, reflection, spontaneity, efficiency, non-judgement.
“Leadership is the art of persuading people to work toward a common goal” - D. Goleman
The concept of social intelligence was first brought to light by E. Thorndike.
In 1980: H. Gardner introduced the concept of multiple intelligences.
In 1990: P. Salovey and J. D. Mayer coined the term “emotional intelligence”.
In 2000: R. Boyatzis and D. Goleman developed a model of emotional intelligence, broken down into domains and competencies, and evaluated and validated the tool.
The vast majority of the skills developed in higher education are cognitive skills. They provide a core set of technical skills leading to a diploma. Future differentiation will be based on emotional skills, i.e.
The dimensions of emotional balance according to R. Davidson are as follows:
There are 12 competencies of emotional intelligence:
The key domains in social and emotional intelligence are as follows:
There are various styles of leadership: coercive, authoritative/visionary, democratic/inclusive, and coaching/mentoring.
The main objectives in leadership are trust, authenticity, empathy, and logic. Trust is central to building relationships in leadership.
The concept of leadership is influenced by personal impact. This is the positive or negative individual impact we have as a leader in a relationship.
There is no impact on age, gender, nationality, culture, biography or reputation, but this is part of personal impact.
However, certain aspects can be modulated: physical presence, clothing, appearance, listening skills, competence, language and choice of words, politeness, and courtesy.
There are three levels of listening
Similarly, there are various types of listeners. We can adopt an attentive, intermittent, distracted, weak, elective, opportunistic, confirmation bias, deficit-based, contradictory, or convergent approach.
In listening and understanding, some cues can be important, such as eye contact, facial expressions, nodding, and body language. The listener should avoid interrupting and external distractions (text messages, telephone calls) should be eliminated. No judgement, no interpretation.
It is necessary to create a transition cycle and establish a connection. We attach to a secure base. We establish connections with people, values, and objectives. When change occurs, we are separated from the things and people to which/whom we are connected. We experience emotions in response to change that vary in intensity.
Unresolved grief/losses can prevent us from fully connecting with other people.
A secure base leader may be a person, a connection, or a goal – something that creates a feeling of protection. They are a source of energy that will inspire us and enable us to take risks and achieve fulfilment. We can take the example of a parent and their child.
The components of our secure base are essential for learning and making sense of things; they influence the way we think.
A secure base leader offers help. They are a good listener who deciphers verbal and non-verbal cues and is attentive to needs. Rather than defending a position, they ask questions to learn more. They do not think for others. “They have unconditional positive regard toward the other person” - C. Roger. They see potential, even if the other person does not. They are reliable and available to the other person and will encourage them if they have any problems.
Empathy is the intuitive ability to put ourselves in another person’s shoes and sense what they are feeling. It is a powerful tool for emotional intelligence.
There are three types of empathy:
Empathy helps us understand other people and ourselves. It is essential in human relations and in doctor-patient and leader-team relationships.
It is a skill that can be developed through mirror neurons.
Here are a few techniques for cultivating empathy during a consultation:
There are no right or wrong answers here.
It is important to create space to encourage exploration and ask open-ended and hypothetical questions, to redirect the attention of the person asking the question. This helps clarify the unknown and lowers the stakes when it comes to deciding whether to adopt a particular course of action; it also invites us to consider different possibilities.
There are various types of questions to ask:
Conflict can be defined as a difference between two or more people, causing tension, an emotional response or disagreement when trust is broken or absent.
Conflict is caused by the breakdown of a relationship or the inability to deal with loss or grief.
Who am I when faced with a conflict?
Analyse the conflict, and identify the
What is the other person’s goal? Where is the tension?
What are your areas of common interest?
To negotiate with “difficult” people, we can try using the “noble storytelling” technique, considering the:
There are also eight principles of conflict management:
Speakers : Dr. C. Devin, Prof. Florent Grange, Dr. Aude Nassif, Dr. Laura Fertitta and Dr. Arnaud Porquet
Report written by Dr. DĂ©borah Salik
Mastocytosis is a disorder characterised by mast cell infiltration in organs. The WHO classification distinguishes between cutaneous mastocytosis and systemic mastocytosis (indolent, aggressive, with clonal haematological disease).
The pathophysiology is generally known as being linked to a mutation in the KITD816V gene, but this alone does not explain the different phenotypes of the disease. Other genes and signalling pathways are probably involved
This study focused on a patient with a form of congenital aggressive systemic mastocytosis, which accounts for less than 0.05% of mastocytosis cases and could be genetic in origin. He had a KIT mutation, multi-organ involvement (skin, bone marrow, liver, spleen), and recurrent anaphylaxis
An analysis of his exome found a homozygous, loss-of-function SLC26A2 variant (R279X (c.C835T, pArg279Trp). This variant is responsible for a sulphation defect in solid cancers, which probably plays a role in cancer plasticity. Inhibition of sulphation increases KIT proliferation and phosphorylation.
Sulphate reduces KIT proliferation and phosphorylation.
A second transcriptomic study in 33 patients with sporadic systemic mastocytosis showed a decrease in the PAPSS2 transcript (tumour suppressor gene).
These two genes regulate cell proliferation and tyrosine phosphorylation and could be new therapeutic targets in mastocytosis.
XP is a particularly rare condition in Nepal. All the patients affected exclusively have the XPC pR415X mutation in its homozygous state, suggesting a founder effect of this mutation. This variant is characterised by the occurrence of extremely early carcinomas.
The aim of this study was to assess the preventive habits of XP patients in Nepal:
There is therefore a lack of knowledge as well as inadequate access to healthcare and sun protection. The obstacles are related to poverty, lack of health insurance, early school leaving, social exclusion, isolation, and distance from medical clinics. There is therefore a need to inform and educate the population (parents, families, youth workers) and put in place social and community assistance.
This study helped identify needs in order to improve the provision of care.
The genetics of Verneuil’s disease still remain unclear.
We reported an association between HS and gene variants involved in immune deficiency and/or immune response.
Regarding genetic factors, the following have been found:
A new hypothesis has been put forward: HS may be associated with immune deficiency genes.
Neurofibromatosis type 1 (NF1) is an autosomal dominant genodermatosis linked to mutations in the NF1 gene (tumour suppressor gene).
There is a constant presence of tumours such as neurofibromas (NFs), which are
Patients develop malignant peripheral nerve sheath tumours (MPNSTs), which are the main cause of death. The formation of these MPNSTs appears to be based on the conversion of NFp to dysplastic NFs.
The number of NFsc is independent of mortality, but if the number of NFsc is greater than 10, then there is a risk associated with the presence of NFi.
A risk phenotype can therefore be described in the presence of one NFi or more than 10 NFsc. The aim of this study was to investigate the mortality of NF1 patients as a function of these phenotypes.
Case-control studies in patients with at least two NFsc:
Results:
The presence of NFsc > 2 was associated with a significant increase in mortality (five MPNSTs among the patients who died).
The prevalence of vascular dysplasias (VDs) in NF1 ranges from 0.4 to 6.4%.
The most common are renal artery stenosis and arterial aneurysm, with frequent arterial disease. The complications can include stenosis, aortic narrowing, Moyamoya disease or a life-threatening aneurysm/pseudoaneurysm.
The frequency of these abnormalities is unknown and there are no recommendations for screening.
The study presented was conducted on 123 patients with 210 vascular dysplasias.
Study results:
In conclusion:
VD is common (18.5%) and is often asymptomatic in NF1 patients. In the event of optic pathway glioma, systematic screening for cerebral VDs is necessary. If a VD is present, screening for VDs in other regions should be performed.
Speakers: Dr. M. Saint-Jean, Dr. Lucie Peuvrel and Dr. C. Abadie
Report written by Dr. DĂ©borah Salik
The basic working tool is the patient’s family pedigree, which is created during the consultation. Based on this consultation, we can determine whether there is a suspected genetic predisposition:
The oncogenetic consultation should be carried out with the patient’s agreement and informed consent.
The genetic test involves DNA sequencing from blood and a buccal smear, followed by a laboratory analysis of the DNA sequencing results, after which the patient is called in for a consultation.
The consultation takes place in parallel with a consultation with a psychologist.
If a genetic predisposition is identified:
Classification of variants (ACMG classification):
If a genetic predisposition is identified, there are:
It should be noted that the family has an obligation to inform other family members.
Obstacles in oncogenetic consultations include:
There are:
The genetic panel for melanoma is as follows: CDKN2A - CDK4 - BAP1 - MITF - MC1R - ACD - POT1 - TERT and TERF2IP
(+ initial digital video-dermoscopy at M0, M3, M12 and then half-yearly, and annual whole-body imaging)
Rare variant
Leading tumour spectrum
Monitoring from the age of 18:
Monitoring:
Clinical signs:
Mucocutaneous lesions (>95%)
Thyroid involvement >70%
Digestive involvement
Mammary involvement (>65%)
Urogenital involvement
Neurological involvement (40%)
Incidence: 8-9/100,000
Genes coding for TSC1 and TSC2, autosomal dominant transmission
Reduced life expectancy
Clinical manifestations:
Good genotype/phenotype correlation but possibility of a mosaic form of tuberous sclerosis complex.
Monitoring should include an annual dermatological examination.
As regards drug treatments, prescription of:
1/3,000 births
Complete penetrance at eight years of age; children have almost all (97%) the diagnostic criteria.
Highly variable phenotype.
Mutation in a tumour suppressor gene: NF1 acts in the MAP-kinase pathway, enabling cells to survive and proliferate.
Neurofibromin negatively regulates the RAS pathway by converting active RAS-GTP into inactive RAS-GDP.
Kinetics of the lesions
Before one year: characteristic bone lesions and café au lait spots
Three years: Lisch nodules
Four to six years: optic pathway glioma or lentigines
Investigation of complications during:
The presence of vesicles or bullae is rare in Kawasaki disease and should lead to the consideration of other diagnoses.
This means we should watch out for the polymorphism of mucocutaneous eruptions in Kawasaki disease.
Toxic shock syndrome
Speakers: Dr. Anne Welfringer-Morin, Dr. Laura Polivka and Prof. Christine Bodemer
Report written by Dr. Deborah Salik
Localised cutaneous morphea is not associated with a vascular disorder or the presence of autoantibodies. There may be a triggering factor.
The clinical evaluation can be difficult, as morphea “en coup de sabre” can resemble vitiligo.
There are various types of morphea: linear, limited, generalised, deep, mixed, and eosinophilic fasciitis.
Linear morphea:
Limited morphea:
Generalised morphea:
Pan-sclerotic morphea:
Prescription of general corticosteroid therapy: IV methylprednisolone, 30 mg/kg (max 1,000 mg), three days/month for three to six months, or oral prednisolone, 0.5 to 1 mg/kg for two to four weeks, then tapering off over three to six months.
+ Combined with methotrexate at a dose of 15 mg/m2/week for at least 12 months.
Prescription of topical corticosteroids:
Alternative:
For the 30% of patients who do not respond to methotrexate, there are various alternatives:
Morphea progresses unpredictably; recurrences are not uncommon and can sometimes occur 20 years later. Plaque morphea progresses over three to five years, while linear forms stabilise within two to three years.
Around 20-25% of recurrences occur within 20 months of stopping treatment.
Progression to the systemic form is exceptional, and a work-up should only be carried out if a warning sign appears.
This is rare and accounts for 3% of patients with systemic sclerosis.
The average age is 9.9 years and the female-to-male ratio is 9:1 after eight years.
It is characterised by:
Inflammatory myopathies in children include dermatomyositis (DM) (pure, amyopathic, overlap) and polymyositis.
These often occur at a very early stage, in particular gottron papules and facial erythema (including chin involvement which is characteristic in DM). There is also thickening of the cuticles associated with an abnormal periungual capillary network.
Capillary dilation can be seen on the gums (a sign of enlarged capillaries).
Facial oedema may be indicative of dermatomyositis or else of a viral infection, which could itself be a trigger for DM.
There may also be pigmentation disorders or areas of calcinosis.
Lipodystrophy is more likely to be seen in the course of DM; it is less commonly a telltale sign.
Corticosteroids 1 to 2 mg/kg/day, oral or IV
For the skin:
Prevention of osteoporosis, photoprotection, monitoring of growth retardation, ophthalmological monitoring.
There is no effective treatment for calcinosis.
If the patient does not tolerate methotrexate or if this treatment is not effective after 12 weeks:
Plasma exchange/immunoadsorption for patients with vasculopathy.
Relevance of JAK inhibitors in the management of DM.
This is where the cold triggers spasms in small blood vessels of the extremities.
We should look for signs of secondary Raynaud’s by carrying out a work-up including: CBC - ESR - CRP - ANA - Capillaroscopy.
Possible diagnoses:
Progresses to disease for 23.6% of children with Raynaud’s phenomenon (median time to disease onset of 2.4 years)
Abnormal prolonged vasoconstriction triggered by cold due to hypoxia, generating a local inflammatory reaction in predisposed individuals.
E.g. Aicardi–Goutières syndrome.
The first descriptions of vitiligo date back 3,500 years. This condition was often mistaken for leprosy. Its worldwide prevalence is 0.5 to 1%.
The skin plays an important role in our interactions with the world; this is particularly true for skin colour. Half of patients surveyed say that vitiligo affects their quality of life, and if it occurs on visible areas such as the face or more than 5% of body surface area, they are even more stigmatised.
Patients report rude remarks and being stared at. A negative impact on patients’ sexuality has also been attributed to the condition.
It is estimated that patients with vitiligo are five times more likely to suffer from depression.
These patients present with anxiety and low self-esteem; they often experience depression, stigma and somatisation, all of which have a major impact on their quality of life.
Vitiligo patients also experience workplace discrimination.
Sixty-five percent of patients in Europe have been told their vitiligo could not be treated.
The key points of the international expert group’s recommendations
Objectives
The combination of an immunomodulator and phototherapy is the most effective.
Patients should be assessed every six months (or every three months if they are undergoing phototherapy).
With current treatments, complete repigmentation is achieved:
It is necessary to wait six to 24 months before the response can be assessed.
JAK1/2 inhibitor constituting the first treatment for non-segmental vitiligo in adults and children aged 12 and over; used as monotherapy twice a day.
It is also effective on the body, but less so than on the face.
After one year, patients no longer see their vitiligo and do not experience hyperpigmentation with repigmentation.
This treatment is well tolerated, although a moderate and transient acneiform reaction and mild local pruritus may occur.
Tolerance at two years is excellent.
How to prescribe and manage phototherapy
Recurrence for optimum results: three times a week, although twice a week remains acceptable.
The maximum dose is 1,500 mJ/cm2 for the face and 30,000 mJ/cm2 for the body.
Do not apply any products for four hours before phototherapy (except mineral oils on hyperkeratotic areas of elbows and knees).
hen the child is able to remain in the booth and keep the protective shells on, i.e. around the age of 7-10 years, depending on the child’s level of maturity.
Can be exposed if the eyes are kept closed and the face is covered during the session.
Patients with vitiligo have protective properties against melanoma and are four times less likely to develop it. No increased risk of Bowen’s disease with phototherapy. The risk of melanoma is not increased. The risk of actinic keratosis (AK) may be increased after 200 sessions.
Association between lymphoma and tacrolimus and phototherapy: No increased risk of any cancer.
For active vitiligo:
Active vitiligo should be treated urgently:
These treatments halt progression in 85% of cases.
For example: an adult patient treated with Medrol (methylprednisolone) 16 mg twice weekly (8 mg for older children, 4 mg for younger children, equivalent to 2 mg drops for very young children) but with side effects: weight gain, insomnia, adolescent growth (maximum three months because of impact on growth).
The other possible treatments are as follows:
Upadacitinib, baricitinib, povorcitinib
Speakers: Dr. Emmanuel Mahé and Prof. Anne-Claire Bursztejn
Report written by Dr. DĂ©borah Salik
The clinical features of psoriasis progress differently according to age.
In infants, the appearance of plaques is rare. Napkin and inverse psoriasis are more common.
In older children, scalp involvement, palmoplantar forms and guttate psoriasis predominate. Balanitis or inverse psoriasis, sometimes with fissures, may also be observed.
Children may present with facial psoriasis, around the eyes or mouth or on the cheeks.
Psoriasis of the scalp may be seen in the form of pityriasis amiantace, seborrhoeic dermatitis, or plaque psoriasis.
Palmoplantar forms are often difficult and fissured.
There is also linear psoriasis, which is highly resistant to treatment.
The Psoriasis Area Severity Index (PASI) has never been evaluated in children, even though it is the US Food and Drug Administration’s (FDA) benchmark score for studies.
In terms of quality of life, the Dermatology Life Quality Index (DLQI) is the main score used in studies. It is essential to listen to children and how they feel from day to day, and put them in situations (for example, holding a pen with psoriasis with fissures, going to the swimming pool, etc.).
American paediatric recommendations for assessing severity:
The prevalence ranges from 1 to 15% and is highly dependent on the type of study, recruitment, and the age of the population.
Is systemic screening necessary? What is the therapeutic impact? What are the benefits of ultrasound imaging of the joints?
The co-morbidities of psoriasis can cause anxiety in parents.
What about the risks of depression, smoking, alcoholism, myocardial infarction, and the progression of the psoriasis itself?
The form of psoriasis is stable (pustular or plaque form) and persists over time.
In terms of severity, there is no difference in adulthood.
There is no evidence that the earlier the disease appears, the more severe it will be.
Age at onset has no impact on the frequency of co-morbidities in adulthood.
Age at onset also has no influence on the occurrence of psoriatic arthritis in adulthood.
Age at onset of psoriasis does not affect the risk of consuming alcohol or tobacco, the level of education, age at marriage, etc.
Present in 1 to 2.5% of the general population and 0.37 to 14% of the paediatric population.
There are many associations, so it is not necessarily psoriasis. There are also familial forms, probably of genetic origin.
When a child is faced with difficulties endangering their health or safety...
Child abuse is not just about physical or sexual violence. It encompasses actions, or a lack thereof, that cause major disruptions to a child’s life or that hinder their physical, mental or sexual development.
No forms of child abuse are harmless.
The figures have been rising since the COVID pandemic, linked to an increase in domestic violence and lifestyle changes (teleworking).
The perpetrators of abuse are mainly adults, but they can also be adolescents or children. They are most often close family members, in 95% of cases.
The protection of children is everyone’s business.
A doctor must act as a child’s advocate if they consider that the child’s health interests have been misunderstood or are being inadequately protected by those around them.
Many people who have been victims of maltreatment or sexual abuse do not show any specific signs. More often than not, the accumulation of mild signs will provide grounds for suspicion.
Identify warning signs, assess the overall situation, and write to the relevant authorities
Speakers: Dr. Patricia Senet, Prof. Émilie Sbidian and Prof. Laurence Le Cleach
Report written by Dr. Joséfina Marco-Bonnet
5FU or laser therapy before PDT is superior to PDT alone.
The guidelines are very heterogeneous.
For BCC, monitoring every six to 12 months for five years.
For high-risk SCC, monitoring every three months for two years, then every six to 12 months for three to five years.
HCV is four times more common in lichen planus (LP) patients and LP is three times more common in HCV-positive patients. However, the results vary depending on the:
There is no significant difference in acute side effects or anticholinergic effects between the H1 antihistamines tested.
Bilastine 20 mg has the fewest neurological effects. Ebastine 10 mg, levocetirizine 5 mg, mizolastine 10 mg and rupatadine 20 mg also have few neurological effects. Those with the most adverse events, particularly neurological adverse events, are mizolastine 10 mg and cetirizine 10 mg.
Clobetasol 40g/day is superior to prednisone (0.5 to 1 mg/kg/day) in terms of healing after 21 days and mortality after one year.
Clobetasol 10-30 g/day is as effective as clobetasol 40 g/day.
Doxycycline 200 mg/day is not as good as prednisolone 0.5 mg/kg/day for healing after 21 days but this is not true for mortality after one year.
No studies have been conducted for AD.
For psoriasis, depression is associated with female gender and psoriatic arthritis but not with age, severity, or systemic treatment. Anxiety is associated with female gender, severity, and psoriatic arthritis, but not with age or systemic treatment. Based on a single study for each of the following factors, there is no association with place of residence, occupation, genital or facial involvement, psoriasis phenotype, or co-morbidities (bipolar disorder, cardiovascular disease, diabetes, schizophrenia). The results are contradictory for level of education, age at onset, ethnicity, and history of depression.
AD patients fear the long-term side effects of topical corticosteroids (TCs) in terms of skin atrophy (moderate level of certainty).
They are concerned that TCs will become ineffective if used over a long period of time (low level of certainty).
They prefer:
These are aimed at reducing the risk of serious side effects (cardiovascular disorders, blood clots, serious infections, cancer) associated with JAK inhibitors when used to treat chronic inflammatory diseases.
JAK inhibitors should only be used in the absence of appropriate therapeutic alternatives in patients:
Moreover, they should be used with caution in patients with risk factors for blood clots in the lungs or deep veins.
The dose should be reduced for certain groups of patients at risk of venous thromboembolism, cancer, or major cardiovascular events.
The JAK inhibitors covered by these recommendations are baricitinib, tofacitinib, upadacitinib, filgotinib, and abrocitinib.
Not all drugs have been compared with each other. Adalimumab is superior to apremilast and etanercept. Guselkumab is superior to ixekizumab. The three drugs that work best are guselkumab, adalimumab, and bimzelx.
In palmoplantar pustulosis, studies show no difference between the various drugs.
Speakers: Dr Bruno Matard (Croissy-sur-Seine), Dr Philippe Assouly (Malakoff) et Dr Pascal Reygagne (Paris)
Report written by Dr. Joséfina Marco-Bonnet
It is important to consider:
It is diagnosed by cytodiagnosis and CBC. It is treated with Class II topical corticosteroids.
It can be caused by pyogenic bacteria, C. acnes, yeasts of the Malassezia genus, or gram-negative and other bacteria. It can also be idiopathic.
The usual bacteriological samples should therefore be taken, and an anaerobic culture for C. acnes as well as mycological samples should be requested. Treatment is usually empirical.
It is important to explain to the patient that there is follicular dysbiosis and that the goal of zero pustules is impossible, but that we are aiming for an acceptable situation where the length of exposure to systemic treatments is minimised.
Treatment includes:
A mycological sample should always be taken to rule out a kerion.
Prescribe a course of oral antibiotics for forms with secondary infection, before and/or during treatment with isotretinoin.
The benchmark treatment is isotretinoin 0.5 to 1 mg/kg for several months.
Fluctuating cysts should also be drained with a needle and injected with triamcinolone acetonide (10 to 20 mg/ml).
If this fails, excision surgery is required. This is a treatment of last resort for patients who have been warned of the risk of scarring and keloids.
Early treatment is necessary to avoid scars, which are difficult to manage.
It can affect the entire scalp. In the early stage, histology shows neutrophils, while in the late stage, there are lymphocytes, plasma cells, and a few perifollicular granulomas. No evident lichen-type lymphocytic infiltrate is found.
Clinically, it resembles lichen planopilaris, but with outbreaks of pustules and scabs as it progresses. Adult ringworm should always be ruled out.
There are some other tricky forms:
An ovarian tumour should be considered in the presence of male-pattern AGA (receding hairline) of recent onset.
The new treatment in 2023 is oral minoxidil (Lonoten®) 0.5 to 1 mg in women and 2.5 to 5 mg in men.
Patients should be informed of the risks of hypertrichosis (15%), dizziness (2%), headaches (0.5%), oedema (1%), and tachycardia (1%).
This is an off-label treatment whose efficacy should be assessed after around six months.
It can even be used if there is an allergy to minoxidil lotion. It should be used with caution in brown-haired female patients from the Mediterranean region and in patients who are taking more than three blood pressure medicines.
This is alopecia associated with an increase in the skin’s thickness to 9 to 15 mm (it is usually 4.5 to 6 mm). This occurs because the hypodermis is thickened (x2). This produces an elastic, spongy “cotton wool-like” consistency.
It affects women (9/10) with black skin. There is no treatment.
An underlying cause should always be sought so it can be treated (trauma, inflammatory disease, etc.).
Of sudden onset (postoperative > 4 hrs, coma, lack of nursing care, forceps, hairdressing equipment, EEG electrodes) with pain and oedematous pink patches.
Dermoscopy shows initial inflammation, black dots, broken hairs, dystrophic hairs, and vellus hairs.
The risk factors are intubation > 24 hrs, operation time > 10 hrs + Trendelenburg positioning, hypoxia, hypotension, hypothermia, diabetes, and war.
Hair loss occurs within three to 30 days. It spontaneously resolves within a few months.
Twenty percent of cases progress to scarring alopecia.
Clinically, this is characterised by well-defined patches, diffuse erythema, diffuse scales, no significant central atrophy, central recurrences, dilated ostia, dyschromia, and telangiectasias. It is important to look for involvement of the face and ears, which is common.
Dermoscopy shows:
Treatment is as follows:
Complications such as ulceration and SCC can occur.
Based on the experience of the Sabouraud team, in cases of LPP refractory to conventional treatments, ciclosporin may be an option at a dose of 4 to 5 mg/kg/day for four months. The success rate is 77%, but this is only a suspensive treatment, with a 12-month relapse rate of 80%.
LPP treatments in 2023
Dermoscopy is reliable for diagnosing ringworm.
For trichophytic ringworm, comma and corkscrew hairs are visible.
For microsporic ringworm, Morse code-like and zigzag hairs are observed
Speaker: Prof. Thierry Passeron
Report written by Dr. Josefina Marco Bonnet
The VIOLIN study showed that vitiligo is a condition that affects quality of life and is associated with co-morbidities such as depression in addition to autoimmune diseases such as autoimmune thyroiditis (x2), alopecia (x2), psoriasis, and atopic dermatitis (AD).
No treatment had been prescribed for 83.8% of patients.
The objectives of treating vitiligo are to:
The patient should always be asked for their treatment objectives, and medical decision-making should be shared.
When faced with vitiligo, it is important to recognise the active forms, as these require urgent treatment!
The treatment that blocks flare-ups in over 90% of cases is UVB therapy (two or three times a week) combined with mini-pulses of cortisone (twice a week for three to six months).
For example: methylprednisolone (Medrol®) 16 mg twice weekly in adults, 8 mg in older children, 4 mg in younger children, 2 mg drops in very young children.
During puberty, treat for a maximum of three months.
Combination treatments are the gold standard for the repigmentation of vitiligo.
For the face and sensitive areas: tacrolimus 0.1% twice a day (off-label use).
For the rest of the body: strong topical corticosteroids (TCs) once a day, five days a week.
These treatments should be combined with either:
Prevention is important as 40 to 50% of vitiligo lesions recur during the first year after repigmentation.
If the depigmentation is limited: tacrolimus 0.1% twice a week, with no need for sun exposure. It reduces the risk of recurrence to 9.7%. TCs are probably just as effective, but the effect has not been demonstrated.
If the depigmentation is diffuse, UVB therapy two to four times a month as maintenance treatment (expert opinion).
Ruxolitinib cream is recommended for non-segmental vitiligo with facial involvement in adults and adolescents over the age of 12. Long-term treatment is required.
Four percent of patients achieve F-VASI90 at Week 104.
It does not work as well on the body and hands. Forty percent of patients are satisfied.
Treatment must be continued, otherwise 60% of patients relapse. However, a response is obtained again when treatment is resumed.
For patients showing the least response, if treatment is continued, they continue to improve.
Tolerance is good. “Acne” and mild pruritus are the main adverse events.
Oral JAK inhibitors should be used for diffuse vitiligo. They represent real therapeutic progress. It takes several months to achieve satisfactory repigmentation. The studies carried out have focused on these medicines used as monotherapy. There is:
Only a combined approach can achieve fully satisfactory results.
There are other avenues to explore:
Speaker: Dr. S. Georgin-Lavialle
Report written by Dr. Josefina Marco Bonnet
The findings in favour of an AID include:
There are three main pathways:
Inflammasome diseases include hereditary periodic fever syndromes, cryopyrin-associated autoinflammatory syndromes (CAPS), TRAPS, and MKD.
In Familial Mediterranean fever (FMF), the pathognomonic sign is pseudo-erysipelas of the ankle; it is complicated by amyloidosis. It can be associated with psoriasis and Verneuil’s disease.
In CAPS, the dermatological sign is cold-induced urticaria. It is important to investigate a family history of deafness, aphthosis, clubbing of the fingernails and toenails, and a permanent increase in CRP in adults (between 20 and 50 years of age).
In TRAPS, which is a rare disease, there is a rash during bouts of fever, periorbital oedema, and CRP of 400 during flare-ups, which returns to normal between flare-ups.
What do we need to know about haploinsufficiency of A20 (HA20), a disease of the NF-NK pathway?
It is a cosmopolitan autosomal dominant disease that begins in childhood (before the age of 10 in 94% of cases, often in the first year of life). It should be considered in the presence of oral or bipolar (Behçet-like) aphthosis, abdominal pain, bloody diarrhoea, an inflammatory context (permanently elevated CRP), onset in childhood, or a family context.
An AID of the NF-NK pathway should be considered when there is:
In the presence of stroke, an AID should be considered in the event of livedo, recurrent ulcers, necrosis, or inflammation (increased CRP). This starts before the age of 10. Protein electrophoresis should be ordered. It is secondary to ADA2 deficiency (DADA2).
Diseases of the interferon pathway correspond to the JAK pathway. There are loss-of-function as well as gain-of-function mutations associated with inflammation that can go as far as autoimmunity. These are STAT diseases.
Dermatologically, STAT3 (gain-of-function) mutations result in alopecia, eczema, and psoriasis.
Dermatologically, STAT6 (gain-of-function) mutations produce severe and resistant atopy, food allergies, asthma, chronic diarrhoea, serosal calcifications, hyper IgE syndrome, and hypereosinophilia.
Early onset, inflammation (of mucous membranes+++), severe and recurrent infections, cytopenia and sometimes eczema and cutaneous vasculitis should suggest actinopathy.
Monogenic AIDs that begin in adulthood include VEXAS, CAPS, and systemic inflammatory trunk recurrent acute macular eruption (SITRAME).
SITRAME is probably an interferonopathy that causes an erythematous-macular rash on the trunk with fever. Blood IgE and IL-18 levels should be measured.
In conclusion, there are many new monogenic AIDs, so they should be kept in mind. It is important to measure CRP, perform a CBC and protein electrophoresis test, draw up a family tree, and discuss a genetic analysis using next-generation sequencing.
Speakers: Dr. F. Ballanger, Dr. O. Cogrel and Dr V. Bernard
Report written by Dr. Joséfina Marco-Bonnet
This is usually moderate but chronic acne that recurs and responds slowly to treatment. It is a peripheral hormonal condition with a major impact on quality of life. AFA patients have reactive skin and a tendency to pick at their acne, which can leave scars.
This is a therapeutic challenge.
One treatment option is spironolactone (off-label use) at a dose of 50 to 200 mg per day. Peak efficacy is reached within three to five months. No work-up is required.
No association has been found between spironolactone use and cancer (breast, ovarian, bladder cancer). There is no increased risk of thromboembolism with spironolactone.
Certain drugs interact with spironolactone:
Several questions still remain:
Recommendation:
In cases of moderate hirsutism and/or acne in non-menopausal women, treat with:
Combined contraceptives:
In the absence of CIs, a combined contraceptive containing levonorgestrel or norgestimate (the only one with the same relative risk of thrombosis as combined contraceptives containing levonorgestrel) should be prescribed as first-line treatment.
In practice, there are no proven benefits of one combined contraceptive over another for acne or hirsutism.
Vascular risk factors should systematically be investigated before prescribing any medication.
Endometriosis is currently treated with dienogest administered continuously at a dose of 2 mg/day, but this does not have MA for contraception.
Contraindications:
In conclusion, in cases of moderate to severe AFA:
For moderate to severe acne + hyperandrogenism:
For very severe acne with major repercussions:
Future topical treatment: Clascoterone
This is the first topical anti-androgen medication; it was approved by the FDA in August 2020. This 1% cream should be applied twice a day for 12 weeks. It is indicated for moderate to severe facial acne in patients over the age of 12 (both boys and girls).
It is not available in France.
To diagnose PCOS, two of the three Rotterdam criteria must be met and other causes of hyperandrogenism (non-classic 21-hydroxylase deficiency, Cushing syndrome, adrenal or ovarian androgen-secreting tumours) and menstrual cycle disorders (hyperprolactinaemia, functional hypothalamic amenorrhoea, other gonadotropin deficiency) must be ruled out.
Rotterdam criteria:
The hormone test to be carried out after three months off hormonal contraception, between D2 and D15 of a spontaneous cycle or one triggered by duphaston, in the morning, includes:
Pelvic ultrasound should not be performed before eight years post-menarche. It is not essential if two other Rotterdam criteria are present. PCOS is diagnosed if there are more than 20 x 2-9 mm follicles per ovary or if ovarian volume is greater than 10 cm3.
Pelvic ultrasound can be replaced with an AMH test for the diagnosis of multifollicular ovaries. This test is difficult to interpret and should only be performed at the request of an endocrinologist or gynaecologist.
Described in 1972 by Kligman and Mills, this is acne worsened by unsuitable cosmetics (products that are too greasy or too oily, make-up powders, harsh cleansers, hair products that affect the temples and forehead, topical corticosteroids); it mainly affects patients with pigmented skin. It is moderate, polymorphic acne. When acne occurs due to friction, it is known as acne mechanica.
The treatment of acne on pigmented skin is different. The need to use photoprotection and manage hyperpigmentation should be emphasised.
For very mild acne: topical retinoids +/- benzoyl peroxide (BPO); if erythema: topical corticosteroids for two to three days.
For mild acne: topical retinoids +/- BPO; if this fails: cyclins.
For moderate acne: cyclins or isotretinoin 0.2 mg/kg/day or spironolactone.
For severe acne: cyclins for one month, then isotretinoin 0.2 mg/kg/day.
For very severe acne: isotretinoin + general corticosteroid therapy.
This is acquired pigmentation resulting from inflammation that can take the form of scarring. It can affect all skin types. The risk factors are phototype III/IV, a high degree of inflammation, delayed treatment, and a tendency to pick at and rub the skin.
Treatment varies depending on acne activity. For active acne and AMH:
If there is no active acne:
- First-line treatment: azelaic acid, hydroquinone, topical retinoid alone.
- Second-line treatment: kojic acid, arbutin, vitamin C.
The whole face should be treated over a long period of time, suitable cosmetics should be used, SPF50 photoprotection should be applied, scrubs and rubbing should be avoided, and the role of make-up should be optimised.
There is a probable clinical spectrum between acne conglobata and Verneuil’s disease.
Isotretinoin should be used with caution as there is a risk of aggravation, especially if the patient is male and has a BMI>25.
Facial abscesses can be treated with long-acting corticosteroid injections (10 mg/ml), sometimes combined with oral corticosteroid therapy.
If the acne is resistant to isotretinoin, it can be treated as hidradenitis suppurativa with biotherapy.
Scar management is difficult, which is why early treatment is essential.
Post-acne keloid scars can be treated with:
Atrophic scars on the trunk are impossible to treat.
Atrophic scars on the face are difficult to manage because they are deep and irregular and have a sclerotic base. The degree of sclerosis should be assessed by a stretch test and based on the appearance of the scar base. The more severe the sclerosis, the more difficult it is to correct.
Treatment:
Ice pick scars should be treated by punch excision, TCA Cross, radiofrequency therapy, or laser resurfacing.
Shallow U-shaped scars should be treated by punch excision, dermabrasion, microneedling, radiofrequency therapy, or laser resurfacing. Deep U-shaped scars should be treated by subcision, TCA Cross, punch excision/elevation, or laser resurfacing.
Slightly sloping U-shaped scars should be treated by subcision, fillers, dermabrasion, microneedling, radiofrequency therapy, or laser resurfacing.
Inflammatory scars should be treated early with vascular laser, IPL, or LED light therapy.
Lasers can even be used under isotretinoin.
Speakers: Prof. Antoine Mahé, Prof. Antoine Petit and Dr Emilie Baubian
Report written by Dr. Joséfina Marco-Bonnet
According to the data in the literature, they are not exceptional.
They are common among African Americans and in Asia (Thailand, Singapore, India) but are much rarer in Sub-Saharan Africa.
Clinical forms vary depending on the phototype and geographical location:
Management includes photoprotection and tolerance induction in CAD.
It is more frequent on black skin (prevalence of 65% vs 25% on white skin). It is a frequent reason for consulting because it has a major impact on quality of life. Treatment is difficult, with a risk of worsening the PIH.
SPF30+ photoprotection with an anti-visible light filter and good UVA protection is necessary.
Start with a hydroquinone-corticosteroid-retinoid combination for three months.
Local treatments should be tested behind the ear. These are the same treatments used for melasma.
Preparation is necessary: sunscreen for two months before the peel and for three months afterwards; start tretinoin six weeks and stop two to three weeks before the peel.
If tretinoin is poorly tolerated, depigmenting dermocosmetic cream for six weeks before the peel, continuing afterwards.
There are also alternative treatments: PRP, bakuchiol, or oral or local tranexamic acid.
It is more common on black skin. There are more severe lesions and sequelae (alopecia, pigmentation disorders) that affect quality of life. The risk of scarring is also increased, as is the prevalence of severe depression (x2), anxiety disorders, panic disorders, suicidal risk, alcohol addiction, and agoraphobia.
In terms of treatment, photoprotection against UV rays should be put in place, and an inducing drug should be sought out and discontinued.
First-line treatment: apply topical corticosteroids and if there is resistance, use local tacrolimus 0.1% (off-label use).
If there is resistance to local treatment, prescribe hydroxychloroquine (6.5 mg/kg/day), which leads to clinical improvement in 80% of cases.
In the event of failure, it is important to ensure that the drug is being taken correctly by measuring hydroxychloroquine levels in the blood, and check that there are no inducing factors such as sun exposure or smoking.
After failure of or resistance to synthetic antimalarial drugs, try thalidomide or methotrexate (off-label use). As third-line treatment, combine belimumab (MA) with standard therapy
Speakers: Prof. Marie-Thérèse Leccia, Prof. Brigitte Dréno, Dr. Jean-Paul Claudel and Dr. Fabienne Ballanger-Desolneux
Report written by Dr. Laura Bouchard
Professor Leccia spoke about the role of hormone treatments in the management of acne.
Second-generation combined oral contraceptives (COCs, ethinylestradiol + progestin) containing norgestrel or levonorgestrel (“androgenic” progestin) are preferred to third- and fourth-generation pills containing desogestrel, gestodene or norgestimate (“non-androgenic” progestin) because of a lower thrombotic risk.
Following a campaign undertaken in 2012-2014 by the French National Agency for Medicines and Health Products Safety (ANSM) on the thromboembolic risk associated with third- and fourth-generation pills, a health survey conducted in France in 2016 revealed a decline in the use of the pill as a method of contraception, particularly among young women aged 20-29.
In the contraception study published by the ANSM in conjunction with the Epi-Phare Scientific Interest Group (GIS Epi-Phare) covering a 10-year period from 2012-2022, oral contraception containing oestrogen and progestin had sharply decreased (-36%), while the use of progestin-only pills had increased by 50%.
Sales of levonorgestrel intrauterine devices (IUDs), used mainly by women over the age of 35, had remained stable, and copper IUDs accounted for more than half of all IUD sales in France.
The ANSM conducted an information campaign for professionals to ensure that first- and second-generation pills are systematically favoured, and that the use of third- and fourth-generation pills is the exception rather than the rule.
Second-generation pills are preferred for patients with an oestrogenic profile (heavy, painful periods, mastopathy), and third- or fourth-generation pills for patients with an androgenic profile (acne, hirsutism).
A study by Barbieri et al. (Obstet Gynecol 2020):
Indications for cyproterone acetate + ethinylestradiol (Diane 35®) (third generation)
Cyproterone acetate (Androcur® and generics)
Spironolactone and acne:
Review by Layton et al. (Am J Clin Dermatol 2017): efficacy of spironolactone in acne
Study: Santer et al. (BMJ 2023):
Speaker: Dr. Jacques Savary
Report written by Dr. Laura Bouchard
There are some cases of melanoma associated with pregnancy: they are diagnosed during pregnancy or in the year following childbirth.
Is the risk of melanoma increased by pregnancy? The results are very contradictory.
Melanoma is the most common form of cancer in pregnant women (31%).
1% of melanoma cases are diagnosed in women during pregnancy.
1/3 of women with melanoma are of childbearing age.
Speakers: Dr. Gerard Toubel, Dr. Jean-Michel Mazer and Dr. François Will
Report written by Dr. Laura Bouchard
For more than 10 years, Rox Anderson’s research group in Boston has been trying to find a wavelength that would selectively treat the sebaceous glands. The success of laser hair removal has shown that selective photothermolysis of the stem cells around hairs is effective.
The group used a free electron laser (choice of wavelength and power) to develop a laser that would selectively target sebum. They found three wavelengths that were selectively absorbed, but only the ~1700 nm wavelength penetrated deeply enough.
Tests on scalp biopsies showed that laser-induced heating of the sebaceous glands caused atrophy of the gland without any necrosis around it (Sakamoto et al, Lasers Surg Med 2012).
In 2011, Jeffrey Orringer’s research group in Ann Arbor published a study with a 1708 nm laser that destroyed lipid-rich targets such as sebaceous glands down to a depth of 1.65 mm in the skin. Ex vivo tests on human skin nevertheless caused epidermal and dermal burns when no cooling method was used, but contact cooling effectively protected the skin’s surface (Alexander et al, Lasers Surg Med 2011).
At the 2019 Annual Conference of the American Society for Laser Medicine and Surgery (ASLMS), the first oral presentation addressed the results of treatments with the 1726 nm laser on patients (Tanghetti et al, oral presentation ASLMS 2019).
The authors achieved selective photothermolysis of sebaceous glands on the face and back. They subsequently developed an integrated cooling system and in March 2022, Cutera launched the first commercial laser using the AviClear© 1726 nm wavelength.
In November of the same year, Accure launched a laser using the same wavelength but a slightly different technology: Accure Laser System©. The Accure laser is precisely driven by skin temperature and relies on air cooling, whereas AviClear operates at a certain fluence and uses contact cooling. Accure is sold to dermatologists and plastic surgeons, while AviClear also targets the medical spa market and other non-medical users.
The AviClear clinical trial included 104 patients with moderate to severe acne (https://www.accessdata.fda.gov/cdrh_docs/pdf21/K213461.pdf).
Open-label study with 17 patients aged 18 to 36 treated with AviClear (Goldberg et al, J Cosmet Dermatol 2023)
Another open-label study, conducted by David Goldberg using the same laser, showed statistically significant reductions in inflammatory lesions of 52% and 56% after four and 12 weeks. However, 24 months post-treatment, there was a 97% reduction. There was also a high level of satisfaction among the treated subjects (70%).
The AviClear protocol consists of three treatments one month apart and Accure consists of four treatments.
These lasers are not yet available in Europe and the price is not known, as the machine is rented in the United States.
The price of three treatments with AviClear is around $3,000 in the United States.
These lasers are an alternative to isotretinoin for patients who are unable or unwilling to take medication. As with isotretinoin, there is an initial flare-up of acne and it takes some time to see a result.
Speakers: Dr. Marie-Sylvie Doutre and Prof. Bernard Cribier
Report written by Dr. Laura Bouchard
The differential diagnosis should be made with lupus erythematosus and Pseudopelade of Brocq.
To differentiate between lichen and lupus, we need:
Treating lichen planopilaris is difficult.
It is a scarring alopecia so do not wait to start therapy.
Prescribe:
A specific form of lichen planopilaris that is particularly prevalent in postmenopausal women, and sometimes younger men and women. We are seeing increasing numbers of familial cases. Potential role of environmental factors and solar filters?
It is mainly seen on the forehead, but it can also affect the retroauricular area and the neck. The eyebrows are often affected too, sometimes initially. It can also impact the eyelashes, axillary hair, pubic hair and hair on the limbs.
In 20–25% of cases, there are small facial papules that are the same colour as the patient’s skin or slightly pinkish, on the forehead, temporal area and sometimes on the cheeks.
The histology is similar to that of sebaceous hyperplasia, BUT only sebaceous glands remain once the vellus follicles have disappeared.
Dr M.S. Doutre (Bordeaux, France) and Prof. B. Cribier (Strasbourg)
Carried out based on:
Local treatments:
Study on the safety and efficacy of high doses of clobetasol propionate 0.05% to treat lichen planus (Melin et al., J Dermatol 2023). The study was carried out on 57 patients with an average affected surface area of 27% (10–40) and pruritus (55/57 patients). Prescription of:
JAK inhibitors (Motarnad-Sanaye et al., J Dermatol Treat 2022, Abduelmula et al., J Cutan Med Surg 2023):
Presents as grey-blue or brown-black macular lesions, without a prior erythematous phase. They are usually seen on the face and neck, and are often slightly itchy. They evolve over months or years.
Most often seen in females, with a dark phototype.
This pathology has bothersome negative aesthetic impacts.
Seen in axillary, inguinal and inframammary folds. Lichen planus pigmentosus is difficult to treat.
Local treatments:
Systemic treatments:
Laser treatment:
Often 2 or 3 lines of treatment, often for patients who are not satisfied aesthetically.
Seen in phototype IV or V patients with macules or pigmented plaques which are erythematous to begin with (sometimes forgotten) and progress to slate grey, “ashy” lesions. Usually found on the torso and limbs, possibly on the neck and face.
Heterogeneous pigmented lesions in patients with dark phototypes, located in exposed areas. It is considered to be a contact photodermatosis.
New disorder with pigmented lesions on the face and neck
A recently described pathology (Litaiem et al., Clinics in Dermatology 2022).
It affects phototype III–V patients and appears in the form of brown plaques or diffuse reticulate hyperpigmentation. In the cases described, there are no scales, no atrophy, no telangiectasias and no immunological anomalies.
Speaker: Prof. Brigitte Dréno
Report written by Dr. Laura Bouchard
Prof. Brigitte Dréno spoke about the importance of the microbiome for the healing of wounds.
A rupture in the skin barrier destroys the microbiome that exists on the skin and creates an area rich in skin nutrients that favours the growth of opportunistic commensal or pathogenic microbes (Tomic-Canic et al., Am. J. Clinical Dermatol. 2020).
This leads to dysbiosis or a loss of diversity in the microbiome.
The dysbiosis caused by a wound can differ according to its origin: diabetic ulcer, pressure ulcer, burn, etc. This is found when analysing microbiota using bacterial cultures or ribosomal RNA testing (White & Grice, Cold Spring Harbor Perspect. Biol. 2023).
The profile of the skin microbiome differs between the upper layers and deeper layers of the epidermis, and there is a dermal microbiome (Nakatsuji et al., Nat. Commun. 2013).
The new microbiome appears two weeks after the formation of a wound and resembles that of the deeper layers of the epidermis and of the dermis. This suggests that the bacteria in the deeper layers of the skin colonize the healing wound on the surface.
Additionally, the skin microbiome blocks the penetration of pathogenic bacteria.
Pathogenic microbes adhere to corneocytes using their membrane proteins, which bind to specific receptors on the corneocytes (pattern-recognition receptor (PRR) proteins).
The commensal bacteria produce antimicrobial peptides (AMPs), with two types:
The stratum corneum is covered in antimicrobial peptides called “antibiotic-like peptides” and thus forms an antimicrobial barrier.
If the pathogenic microbe crosses the stratum corneum, the epidermis develops a new strategy to block the invasion of the skin (Timar et al., Mol. Immunol. 2006; Chehouad et al., Proc. Natl. Acad. Sci. 2013; Ersanli et al., Biology 2023)
The skin microbiome has three targets for healing wounds (Canchy et al., Eur. J. Acad. Venereol. 2023). Commensal bacteria:
The microbiome:
Each commensal bacterium has a protective function in the barrier.
If its activity becomes excessive, the skin microbiome can have a negative impact:
If a person has chronic inflammation that is not prevented by the skin microbiome, in 60% of wounds, bacteria will develop a biofilm in the bed of the wound and make it harder to heal.
The profile of the commensal bacteria may be to help in antimicrobial defence, improve the skin barrier, boost the immune response, and recruit T-cells. However, in another environment, it can have the opposite effect and favour chronic inflammation.
Stress controls the skin microbiome, inducing chronic inflammation.
Stress mediators (cortisol, catecholamines, acetylcholine, neuropeptides, etc.) influence the wound’s microbiome (Holmes et al., Adv. Wound Care 2015):
Stress can be physiological or psychological and controls the skin microbiome via neurogenic inflammation.
Stress → signals from the brain → production of substance P by nerve endings near the sebaceous glands → activation of substance P receptors on the sebaceous glands → increased production of sebum → induced alterations of the microbiome (notably S. aureus and S. epidermidis).
Substance P (N’Diaye et al., Front. Microbiol. 2016):
The healed wound never returns to a normal microbiome. As such, a therapeutic approach is required.
Therapeutic approaches for restoring balance to the skin microbiome in the healed area of the wound:
Probiotics – new prototypes from lactic acid bacteria.
Speaker: Prof. J.C. BĂ©ani
Report written by Dr. Laura Bouchard
Answers to questions: Doubts, polemics, controversies
The allergic reactions caused by SPPs are above all photoallergies. They are particularly due to oxybenzone or benzophenone-3 (BP-3) and octocrylene (OCT) (allergies which are more common in children). This is because impurities from benzophenone (BP) remain when OCT is synthesised, and OCT produces BP when it breaks down
SPPs containing OCT should therefore be discarded after a certain period of time
Certain solar filters have systemic toxicity as they penetrate the skin. This is the case with oxybenzone, which penetrates the skin to a significant extent and which was found in plasma levels that were much higher than the other filters in all the studies. It is also found in urine, amniotic fluid and breast milk.
We must also be careful with endocrine disruptors:
Certain solar filters are found in the environment:
Conclusion:
Solar filters are just one small source of the filters we are exposed to.
The cosmetics industry should:
No studies recommended avoiding using SPPs.
Speaker: Prof. Thierry Passeron
Report written by Dr. Laura Bouchard
Prof Thierry Passeron gave a presentation on care for vitiligo, along with the results of local treatment with the JAK-1 and -2 inhibitor ruxolitinib, which will soon be available in France.
The goals of therapy are to halt depigmentation, induce repigmentation (between 6 and 24 months), and prevent recurrences.
Care according to the Worldwide expert recommendations for the diagnosis and management of vitiligo: Position statement from the International Vitiligo Task Force Part 1: towards a new management algorithm. Van Geel et al., J. Eur. Acad. Dermatol. Venereol. 2023.
Conclusions
Speakers: Dr. Olivia Boccara, Dr. Stéphanie Mallet, Dr. Thomas Hubiche, Dr. Sophie Leducq, Prof. Sébastien Barbarot, and Dr. Christine Léauté-Labrèze
Report written by Dr. Joël Claveau
This very clinical session was split into five sections: naevi in children, warts and molluscum contagiosum, scalp pathologies in children, atopic dermatitis and infantile haemangiomas. Each speaker reviewed recent publications and some of the treatment algorithms that had the greatest impact on everyday practice.
In the first section which covered naevi in children, a large study in the Journal of the American Academy of Dermatology revealed that melanomas before the age of 12 are extremely rare. There are just 5 to 10 cases of paediatric melanomas in France each year in under 18s. In children under 10, there were no recorded deaths, melanomas are non-spreading and do not resemble naevi. This supports the idea that this population should not be considered “young adults”, as they are two entirely different cases. As such, the diagnostic criteria for adult melanomas do not apply to children. The situation only becomes similar to that of adults in adolescence (superficial spreading melanoma (SSM) with ABCD criteria). To conclude, the speakers mentioned that a melanoma together with (even giant) congenital naevi is exceptional and that a Spitz naevus is often clinically concerning but biologically benign.
In the second section on warts and molluscum contagiosum, we were reminded that there are a number of therapeutic options. This includes, first of all, abstention from therapy since 52% of cases resolve themselves in 15 months, cryotherapy, salicylic acid, localised chemotherapy and immunotherapy. However, high-quality meta-analyses have shown that each of them is only slightly more effective than a placebo. There is a slight increase in efficacy when the methods are combined. It is therefore important to correctly choose the patients who require treatment, i.e. those with bothersome, painful and visible lesions. We should choose the therapeutic option that is the least traumatising. Lastly, in cases of anal or genital condylomas, we should check for sexual abuse, maternal-foetal transmission in the very young and transmission within the family.
When it came to childhood pathologies of the scalp, we were shown a very interesting classification algorithm to help identify pathologies in our surgeries. Firstly, you must distinguish congenital or early-onset alopecia from acquired forms. The first category can be further split into scarring disorders including aplasia cutis congenita, which requires swift treatment, as opposed to non-scarring alopecia such as neonatal occipital alopecia and congenital triangular alopecia. On the other hand, acquired forms include alopecia areata, ringworm and induced pathologies such as trichotillomania and traction alopecia. Next, hair shaft abnormalities are rarer pathologies that require specialist treatment. In terms of pathologies that change the colour of the hair, there is greying or premature loss of hair colour associated with a number of aetiologies to be investigated with blood tests, and Green hair syndrome resulting from deposits of copper sulphate crystals in pool water. Lastly, the category for tumour lesions includes sebaceous naevi and congenital naevi.
Similarly to the previous section, the speakers presented a very clear decision-making algorithm to help clinicians faced with atopic dermatitis. First of all, remember that it is important to consider differential diagnoses such as newborn rash, scabies, psoriasis and mycosis fungoides as well as specific phenotypes in patients with darker skin who present with follicular hyperkeratosis. Secondly, we should assess the severity of the atopic dermatitis using global assessment and quality of life scores such as the Atopic Dermatitis Control Tool (ADCT) and the Investigator Global Assessment (IGA). Alongside this, we must assess the associated comorbidities of asthma and food allergies, which can be reduced with early treatment of atopic dermatitis. All these prior assessments help define a personalised, 3-part treatment covering patient education, local treatment and systemic treatment. Education is based on local treatments, understanding the disease and regular cleansing. Local treatment comprises corticosteroids during the initial treatment phase, and calcineurin inhibitors as maintenance therapy. As for systemic treatment, it is constantly evolving and involves numerous biological agents such as dupilumab, tralokinumab and JAK inhibitors which replace older first-line molecules such as methotrexate and ciclosporine.
The final session covered the treatment of infantile haemangiomas and, unsurprisingly, focused on systemic beta-blockers. The speakers mentioned that propranolol is the only treatment authorised for sale in France (AMM) and that it is essential that this treatment begins as early as possible. The haemangioma regresses entirely or almost entirely in 60% of cases at 3 mg/kg/day when treatment begins within 3 months of birth. It is also effective in 76% of cases of severe forms if treatment continues up to 12 months, though recurrence is possible when treatment stops. Atenolol is also offered as an alternative although the molecule has not been authorised for sale in France (AMM). If this fails or in case of contraindications for propranolol, we can suggest rapamycin. Corticosteroids are now only suggested as a second- or third-line treatment. Surprisingly, timolol, a topical beta-blocker, was not more effective than the placebo and is therefore a secondary option which should not delay initiation of propranolol when necessary.
Speakers: Dr. Emmanuelle Amsler, Dr. Brigitte Milpied, and Prof. Marie-Sylvie Doutre
Report written by Dr. Joël Claveau
This practical session was informative and interactive and mainly consisted of overviews of clinical cases. After the initial presentation of each case, there was an educational questionnaire linked to the diagnosis, the investigations or the therapy. The right answer was then presented during case feedback, together with a description of the pathology and a quick review of the relevant literature.
The first case covered a chronic, recurring eczematous rash on the face and hands. It was a photoallergy induced by contact with chlorpromazine after repeatedly preparing this antipsychotic medication. The key here was sufficient case history, enabling us to identify that this medication had been handled.
The second case was the sudden appearance of a unilateral erythema on an upper limb, affecting the elbow, back of the hand and periungual areas on the fingers. The right answer to the quiz was carrying out a blood test for Lyme borreliosis, which would have strong positive results. The issue was therefore acrodermatitis chronica atrophicans, presenting with purplish acral inflammation followed by an atrophic, fibrosing phase. Treatment with doxycycline was necessary.
The third case looked at a recurring exanthema on the trunk with infection, with no other related symptoms. The correct response was measuring CRP, which is always high in acute cases of this stereotypical rash. The disorder in question is called SITRAME (systemic inflammatory trunk recurrent acute macular eruption), which is a recently described autoinflammatory syndrome that always affects the trunk and sometimes the arms.
The fourth case was that of a middle-aged male presenting with a well-delineated pruriginous papulopustular eruption on his back, which appeared after facial surgery. It was a case of allergic contact eczema caused by betadine, the product used for preoperative disinfection. It was diagnosed with a positive patch test.
The fifth case covered the recurrent appearance of papulovesicular lesions on the upper limbs and hands after taking paracetamol. For this case, the examination to be requested was a skin biopsy, which would reveal pseudo-bullous lesions with neutrophilic infiltration. This result enabled a diagnosis of Sweet syndrome, or neutrophilic dermatosis. We were reminded that this syndrome has numerous histological subtypes. The literature only reported a single case like this patient’s linked to taking paracetamol.
The sixth case was recurrent periorbital swelling followed by significant facial oedema in a young female patient. The correct response was allergic contact eczema caused by epoxy resin. This is a common allergen in professional environments, but apparently it is becoming increasingly common in non-professional cases as it is used for crafting projects. As such, this dermatosis is becoming increasingly prevalent.
The seventh case tackled pruritic nodules on the outer arms which had been progressing for several years. The questionnaire should cover vaccination history and other injections in the location of the lesions. The additional investigation should include a deep biopsy, which would reveal nodular infiltration and lymphocytic hyperplasia. The diagnosis was reactive pseudolymphoma caused by vaccination. Tetracyclines are suitable as first-line treatment, but thalidomide is often more effective.
The eighth case saw a patient being treated with nivolumab for metastatic melanoma, presenting with fixed, recurring pseudo-bullous lesions which appeared after around 3 months. The diagnosis made was fixed pigmented erythema following the periodic injection of the iodinated contrast products used in imaging to monitor melanoma. The diagnosis was confirmed with a patch test on damaged skin. We were reminded that these new contrast agents cause delayed reactions compared with the immediate reactions of older-generation products.
The ninth case was a middle-aged man with a fungated lesion on the head of his penis, which his GP believed was a carcinoma. The key to diagnosis was a complete cutaneous examination which revealed a palmoplantar keratoderma. This led to a blood test for syphilis, which gave a strong positive and revealed a primary syphilis infection.
The tenth case involved a young girl with papules where a mosquito spray had been applied. The patient was referred with a suspected contact allergy. However, additional history revealed that she had been experiencing cold-induced urticaria for several years. The key to diagnosing this case was listing the ingredients in the mosquito spray, since it contained menthol. The product had a cooling effect which was triggering the reaction.
Lastly, the eleventh case looked at a patient who had undergone a thyroidectomy and whose scar became very inflamed a few days after the procedure. The key here was to look at the different products used during the surgery. The culprit was in fact the wound adhesive, containing the allergen 2-octyl cyanoacrylate. During the allergological investigation, the patient had a significant positive reaction to the product in the patch test. The speakers mentioned that this issue is growing rapidly, particularly among paediatric patients, as wound adhesive is increasingly used due to its cosmetic advantages compared to conventional sutures.
Speakers: Dr Candice Lesage (Montpellier, France), Dr Laetitia Visseaux (Reims, France), Prof. Florent Grange (Besançon, France), Prof. Olivier Dereure (Montpellier, France)
Report written by Dr. Joël Claveau
This session was highly relevant given that the indications for new cancer therapies are constantly increasing. The three main classes of systemic agents used in oncology are chemotherapy, targeted therapy and immunotherapy. Regardless of their type of practice, clinicians will encounter various types of dermatoses since these skin toxicities are highly prevalent. From the outset, we were told that the dermatologist’s role is to assess and manage the toxicity, to enable the agent to continue to be used where possible and, finally, to be able to recognise severe presentations. The key to good patient management is assessing the patient quickly and maintaining good relations with oncological, allergological and pharmaceutical colleagues. It is important to inform patients of the expected effects as part of a preventive approach, i.e. the importance of skin care, moisturising and providing information leaflets. When a rash appears, drug investigation is crucial in determining the causal agent.
For the 3 types of treatment, being able to recognise severe reactions is essential. They may occur immediately (IgE-mediated type), such as anaphylaxis, urticaria and angioedema. Cetuximab is the prototype of this reaction, but several other agents, such as taxanes, can cause it. In some cases (e.g. cetuximab), the infusion rate may be slowed for prophylaxis. Shock is treated with adrenaline and injectable corticosteroids. Other delayed severe toxidermias include toxic epidermal necrosis (TEN/Lyell), Stevens-Johnson syndrome, DRESS (drug reaction with eosinophilia and systemic symptoms) and AGEP (acute generalised exanthematous pustulosis). We should look for signs of severity such as facial oedema, mucosal involvement, the presence of vesicles or bullae, Nikolsky’s sign, purpura, skin pain and fever. Biological tests are used to identify haematological, hepatic or renal disorders. Toxicity must be graded in order to adapt treatment and follow-up. Anti-BRAF agents are associated with complete or incomplete DRESS (without eosinophilia). The delay is generally shorter than with other agents, and corticosteroid therapy very often ensures rapid and complete remission. The therapy cannot always be reintroduced. Contrary to typical Lyell’s syndrome, systemic steroids are usually recommended in cases secondary to anti-cancer immunotherapy.
Chemotherapy causes skin toxicities secondary to damage to rapidly renewing cells such as keratinocytes. Firstly, there is hand-foot syndrome, which is more inflammatory. We can try to prevent it with suitable shoes and insoles, avoiding rubbing and consulting a podiatrist if necessary. Emollients and very strong topical corticosteroid therapy under occlusion are recommended as treatment. More rarely, capecitabine-associated adermatoglyphia may also be encountered. In terms of pigmentation disorders, we most often see diffuse or localised hyperpigmentation which may have a coppery-brown pseudo-Addisonian appearance. It can also affect appendages such as the hair (methotrexate), nails (5FU, taxanes) and mucous membranes. Bleomycin flagellate dermatitis may also be encountered. Reticular hyperpigmentation has been described with paclitaxel. Toxic erythema is a bilateral inflammatory condition affecting the acral regions after 2 to 4 weeks of treatment. Late-onset cutaneous porphyria can also occur with tamoxifen and cyclophosphamide.
The class of targeted therapies (anti-EGFR, anti-BRAF, anti-MEK, etc.) present frequent and very specific cutaneous toxicities depending on their target. With anti-EGFR treatments, we very frequently observe acneiform eruptions and paronychia. They are also known to cause hand-foot syndromes, which are initially inflammatory, sometimes bullous and finally hyperkeratotic. They present differently from chemotherapy-related hand-foot syndrome. Encorafenib is most often responsible here, but it can also be observed with various targeted therapies. With melanoma, anti-BRAF agents are often used in combination with anti-MEK agents. Adding in anti-MEK reduces cutaneous effects to around 25%. However, certain pathologies or situations require the use of anti-BRAF monotherapy, resulting in various manifestations of hyperkeratosis ranging from keratosis pilaris to keratoacanthoma and multiple acrochordons. The mechanism is linked to overactivation of the MAP kinase pathway. There may also be various eruptive pigmented lesions. The induction of wild-type BRAF melanomas has even been reported. Cystic acne can also occur. However, certain dermatoses occur even with the addition of anti-MEK, such as photosensitivity associated with Vemurafenib (induced by UVA). Strict, broad-spectrum photoprotection is recommended. Certain reactions are due to the use of anti-MEK monotherapy (affecting up to 60% of patients), such as folliculitis similar to that seen with anti-EGFR treated with cyclins, topical corticosteroids and photoprotection. Finally, in high-grade squamous cell carcinomas treated with Cetuximab or Panitumumab, a very significant inflammatory reaction may be observed at the site of actinic keratoses and may even cause sterile erosive and pustular dermatoses.
The final section dealt with the cutaneous toxicities of immunotherapy. There are three groups of molecules: anti-CTLA4, anti-PD1 and anti-PDL1. These different agents can provoke numerous reactions via an immune mechanism. The toxicity spectra are quite similar regardless of the indication. The main signs are maculopapular, eczematous and lichenoid eruptions, psoriasis and vitiligo. The cutaneous effects of Pembrolizumab and Nivolumab are almost identical. Reaction intensity is usually grade 1–2 and permanent discontinuation of treatment is rare (5%). Rash and pruritus are often the first immunological reactions to occur, before any other non-dermatological reactions. Rash is the most common reaction (20–25%), it occurs early and is often self-limiting. The appropriate use of sufficient quantities of topical steroids, together with good skin hydration, usually prevents the need for systemic steroids. It is generally quite rare for therapy to have to be stopped. There is also the appearance of vitiligo (2–10% of cases), which is usually delayed, after a few months of treatment, and is almost exclusively associated with melanoma immunotherapy. Its occurrence is associated with a better anti-cancer response. However, rashes are more frequent and often more severe with dual immunotherapy (Ipilimumab + Nivolumab). Finally, numerous rarer dermatoses have also been described with immunotherapy: pemphigoid, panniculitis, mucositis, sarcoidosis, cutaneous lupus, Grover’s disease, etc.
