Vates Gamification

YOUR MISSION:

Select a case, interpret the information and answer questions to diagnose and manage the patient's condition. See how you score!

Can you diagnose and treat these cases?

Case	Case description	Completed
Case 1:	A 14-year-old male is presenting with a solitary erythematous plaque on his leg - can you help to diagnose and treat his condition so that he can confidently return to school?
Case 2:	A 47-year-old male is presenting with multiple, well-defined, erythematous papules and plaques on his forearm - can you help to diagnose and treat his condition to relieve his symptoms?

Case 1: Image provided by Dr Yvette Fernández, Mexico (GSK Medical Scientific Advisor, Dermatology).

Case 2: Image and case study provided by Dr Gary Ong (GSK Global Medical Director – Dutasteride AGA, Vates, Zanamivir and Supplements).

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Cases completed	Total score
Case 1 Case 2	0 0

Patient vignette and clinical history

Background: The patient was a 14-year-old male high school student, who was diagnosed with ADHD when he was 18 months old

Clinical presentation: Solitary erythematous plaque on the front of one leg, without pruritus

Duration and temporal pattern of signs/symptoms and signals: 6 months

Comorbidities and associated treatments: ADHD treated with lisdexamfetamine, aripiprazole, and magnesium valproate

Other information: No other relevant medical history, including allergies

Psychosocial impact: Concerns about social stigma upon returning to school with his skin condition

ADHD, attention deficit hyperactivity disorder.
Image and case study provided by Dr Yvette Fernández, Mexico (GSK Medical Scientific Advisor, Dermatology).

Physical examination

General physical examination: Non-contributory

Location of lesion: Anterior aspect of the right leg

Description of skin lesions: Solitary, well-defined, erythematous plaque (measuring 6.0 x 5.5 cm) topped with silver-white scales

Case study provided by Dr Yvette Fernández, Mexico (GSK Medical Scientific Advisor, Dermatology).

Question 1: Diagnostic tests

Which of the below diagnostic tests would be appropriate for this patient? (Please select one option)

Skin biopsy Patch testing Skin scraping KOH test

KOH, potassium hydroxide.

Question 1: Correct diagnostic test

Skin biopsy

Skin biopsies and histological findings can be used for clarification when diagnosing steroid-responsive dermatoses, if necessary¹

Continue through the slides to see the differential diagnoses for this patient, as well as the methods that can be used to differentiate the final diagnosis from other similar dermatoses

1. Gisondi P, et al. J Clin Med 2020;9:3594

Differential diagnosis (1/4)

During diagnosis, the following differentials should be considered, as well as the patient’s history and medications

Condition	Lichen planus	Nummular (discoid) eczema
Cause	A T-cell mediated autoimmune disorder, in which inflammatory cells attack an unknown protein within the skin and mucosal keratinocytes¹	Impairment of the cutaneous lipid barrier, precipitated by various factors such as ageing, infection, and certain drugs and alcohol^4,5
Location	The flexor surfaces of the wrists, forearms, and legs²	The lower extremities are most commonly involved, followed by the upper extremities and trunk⁴
Onset	Primarily middle-aged adults (>40 year olds) with equal sex incidence^1,3	Bimodal distribution, affecting females from 15–25 years of age and males from 50–65 years of age⁴
Signs/symptoms	Ranges from asymptomatic to intense pruritus^1,2	Xerosis and pruritus⁴
Lesion appearance and borders	Lesions are typically purple, pruritic, planar plaques/papules that tend to heal with residual post-inflammatory hyperpigmentation. Lesions may be polygonal and often have a shiny surface covered in fine white lines (Wickham’s striae).² The lesions may appear in a linear configuration, following the lines of trauma (Koebner phenomenon)²	Lesions typically begin as papules or vesicles that coalesce into plaques.³ Established lesions will appear in a symmetrical distribution, and be sharply defined, round or coin-shaped, erythematous and eczematous plaques ranging from 1–10 cm⁴

Both images are reproduced with the permission of Wiley Journals. The first image was first published in Herzum A, et al. Clinical Case Reports 2021;9:e05092. https://doi.org/10.1002/ccr3.5092. The second image was first published in Knöpfel N, et al. Pediatr Dermatol 2018;35:611–615.

1. DermNet NZ. Lichen Planus. Available at: https://dermentnz.org/topics/lichen-planus. (last accessed November 2021); 2. Usatine RP and Tinitigan M. Am Fam Physician 2011;84:53–60; 3. Gorouhi F, et al. Sci World J 2014;742826. doi: 10.1155/2014/742826; 4. Robinson CA, et al. Nummular Dermatitis. In: StatPearls [Internet]. Treasure Island, 2021; 5. Bonamonte D, et al. Dermatitis 2012;23:153–157.

Differential diagnosis (2/4)

Condition	Mycosis fungoides var pagetoid reticular	Lichen simplex chronicus
Cause	A form of cutaneous T-cell lymphoma with an unknown cause, but genetic predisposition, chemical exposure, and chronic antigen stimulation have been theorised to play a role¹	Unknown, but localised areas of the skin itch spontaneously, leading to an itch-scratch cycle that provokes lesions³
Location	Typically the distal extremities, trunk and thighs^1,2	Usually easy-to-reach areas, such as the head, neck, arms, scalp, and genitals³
Onset	Mycosis fungoides usually occurs in late adulthood (median 55–60 years);¹ however, cases of PR have been reported in patients of all ages²	Middle-to-late adulthood, peaking at 30–50 years of age³
Signs/symptoms	Pruritus¹	Pruritus, erythema³
Lesion appearance and borders	Usually presents as a single, erythematous, slowly growing, scaly or verrucous plaque²	Typically presents as a single or multiple discoloured lesions with dry, patchy areas of skin that are scaly and thick. The lichenification of lesions may occur due to chronic scratching³

PR, pagetoid reticulosis.

All images are reproduced with the permission of Wiley Journals. The first image was first published in Torre-Castro J, et al. J Cutan Pathol 2020;47:466–469. The second image was first published in Lotti T, et al. Dermatol Ther 2008;21:42–46.

1. DermNet NZ. Mycosis fungoides. Available at: https://dermnetnz.org/topics/mycosis-fungoides. (last accessed November 2021); 2. Larson K and Wick MR. Dermatophatology (Basel) 2016;3:8–12; 3. Charifa A, et al. In: StatPearls [Internet]. Treasure Island, 2021.

Differential diagnosis (3/4)

Condition	Atopic dermatitis (AD)	Seborrhoeic dermatitis
Cause	Unknown cause, but AD is identified as a disease of the immune system; cytokines are a critical factor, causing barrier defects and inflammation¹	The cause is unclear but the skin reactions are thought to result from an inflammatory response to a common skin organism, Malassezia yeast^6,7
Location	Can be anywhere on the body, but usually the flexor regions²	Usually appears on body areas with a large density of sebaceous glands, such as the scalp, face, chest, back, axilla and groin⁷
Onset	Infants usually present with acute AD between 3 and 6 months of age, whereas older children and adults present with chronic AD^3,4	Most commonly occurs in infants within the first 3 months of life and in adults at 30–60 years of age⁸
Signs/symptoms	Pruritus, xerosis, erythema⁵	Pruritus, erythema^7,9
Lesion appearance and borders	Acute form: Vesicular, weeping, crusting eruptions² Subacute form: Dry, scaly, erythematous papules, and plaques² Chronic form: Lichenification of plaques²	Typically presents as well-delimited, erythematous plaques with greasy-looking, yellowish scales of varying extents. The distribution of lesions is commonly symmetrical. Patches may be flaky, large, oily or include dry scales⁹

The first image is used with permission from DermNet NZ. The second image is used with permission from DanDerm.

1. DermNet NZ. Causes of atopic dermatitis. Available at: https://www.dermnetnz.org/topics/causes-of-atopic-dermatitis. (last accessed November 2021); 2. Berke R, et al. Am Fam Physician 2012;86:35–42; 3. Avena-Woods C. AM J Manag Care 2017;23(8 Suppl):S115–S123; 4. Langan SM, et al. Lancet 2020;396:345–360; 5. Saeki H, et al. J Dermatol 2009;36:563–577; 6. Gaitanis G, et al. Clin Microbiol Rev 2012;25:106–141; 7. Clark GW, et al. Am Fam Physician 2015;91:185–190; 8. Schwartz RA, et al. Am Fam Physician 2006;74: 125–130; 9. Borda LJ and Wikramanayake TC. J Clin Investig Dermatol 2015;3:10.13188/2373-1044.100019.

Differential diagnosis (4/4)

Condition	Generalised plaque psoriasis	Drug-induced psoriasis
Cause	Unknown, but there are various precipitating factors; these include genetics, infection and stress¹	Exposure to certain drugs can elicit the induction or exacerbation of psoriasis^4,5
Location	Usually the scalp, elbows, knees, and sacral area. However, any area of the skin may be involved, including the palms and soles, as well as the genital regions²	Plaques commonly occur on the scalp, elbows, knees, buttocks, and/or genitals⁶
Onset	Can occur at any age, but has two age onset peaks: the first at age 20–30 years and the second at age 50–60 years¹	There is a latency period between starting the medication and the onset of psoriatic lesion(s), the length of which can vary between drugs⁵
Signs/symptoms	Pruritus and erythema³	Erythema^7,6
Lesion appearance and borders	Well-delimited, thick, erythematous plaques, covered by silvery white scales. These lesions can range from small erythematous, scaly papules to large, thick plaques. Multiple symmetrical lesions usually appear bilaterally.^2,3	Similar to generalised plaque psoriasis, but may be missing the well-demarcated borders or lack the coarse scaling⁴ Psoriasiform skin lesions may be present in some cases^4,7

The first image is used with permission from DanDerm. The second image is reproduced with the permission of Wiley Journals. It was first published in Mendieta KI, et al. Pediatr Dermatol 2018;35:e136–e137. doi:10.1111/pde.13418

1. Menter A. Am J Manag Care 2016;22(8 Suppl):s216–224; 2. Menter A, et al. J AM Acad Dermatol 2020;82;1445–1486; 3. Armstrong AW and Read C. JAMA Dermatol 2020;323:1945–1960; 4. Balak D and Hajdarbegovic.E. Psoriasis (Auckl) 2017;7:87–94; 5. Tsankov N, et al. 2000;1:159–165; 6. DermNet Nz. Drug-induced psoriasis. Available at: https://dermnetnz.org/topics/drug-induced-psoriasis. (last accessed November 2021); 7. Sehgal VN, et al. J Dermatol Venereol Leprol 2008;74:94–99.

Question 2: Diagnosis

What would be your chosen diagnosis for this patient based on the options below? (Please select one option)

Lichen planus Atopic dermatitis Nummular eczema Seborrhoeic dermatitis Lichen simplex chronicus Drug-induced psoriasis Generalised plaque
psoriasis Mycosis fungoides var pagetoid reticular

Question 2: Correct diagnosis

Correct answer:

Drug-induced psoriasis

Click the buttons below to find out more:

Diagnostic considerations Disease background Precipitating factors

Diagnostic considerations and final diagnosis

Diagnosis: The following methods can be used to differentiate drug-induced psoriasis from other similar dermatoses:¹

Record a precise medical history to determine the causative drug¹

Distinguishing clinical features and plaque type by morphology²

Skin biopsies and histological findings may be required for further clarification³

Final diagnosis: Drug-induced psoriasis, likely due to aripiprazole⁴

The exact mechanisms of drug-associated psoriasis are not known and most likely vary between different drugs⁴
Case reports have shown a possible association between antipsychotics and the development or worsening of psoriatic rash. Immunomodulatory effects of antipsychotics may be involved in immune-mediated conditions⁴
There may be an association between ADHD and psoriasis⁵
- A population-based cross-sectional study reported a positive association between ADHD and psoriasis, potentially due to pleiotropic genetic effects in shared risk pathways. However, other factors associated with ADHD may also provoke psoriasis

ADHD, attention deficit hyperactivity disorder.

Skin biopsy icon made by Pixel perfect from www.flaticon.com.

Case study provided by Dr Yvette Fernández, Mexico (GSK Medical Scientific Advisor, Dermatology).

1. Dermnet Nz. Drug-induced psoriasis. Available at: https://dermnetnz.org/topics/drug-induced-psoriasis. (last accessed November 2021); 2. Nair PA and Badri T. Psoriasis. In: StatPearls [Internet]. Treasure Island; 2021; 3. Gisondi P, et al. J Clin Med 2020;9:3594; 4. Bujor CE, et al. BMC Psychiatry 2017;17:242; 5. Hegvik T, et al. Eur Child Adolesc Psychiatry 2018;27:663–675.

Disease background: Psoriasis (1/2)

Psoriasis is a chronic, relapsing and remitting, non-infectious inflammatory skin disease^1,2

Plaque psoriasis, also known as psoriasis vulgaris, is the most prevalent form of psoriasis¹ and usually affects the elbows, knees, scalp, and sacral area³
The condition typically presents as well-delimited, thick, erythematous plaques covered by white scales, which if removed may reveal pinpoint bleeding from the dilated capillaries (Auspitz sign)⁴
Psoriasis involves infiltration of the skin by activated T-cells that stimulate proliferation of keratinocytes. This dysregulation in keratinocyte turnover results in the formation of thick plaques⁵

Auspitz sign

The image is reproduced with the permission of Wiley Journals. It was first published in Nasca MR, et al. Br J Dermatol 2019;180:e178.

1. Rendon A and Schäkel K. Int J Mol Sci 2019;20:1475; 2. Samarasekera EJ and Smith CH. Clin Med (Lond) 2014;14:178–182; 3. Menter A, et al. J AM Acad Dermatol 2020;82;1445–1486;

4. Armstrong AW and Read C. JAMA Dermatol 2020;323:1945–1960; 5. Nair PA and Badri T. Psoriasis. In: StatPearls [Internet]. Treasure Island; 2021.

Disease background: Psoriasis (2/2)

Individuals can present with plaque psoriasis of differing severity, which is classified as mild, moderate or severe. Psoriasis severity should be assessed by a minimum of two indices, usually BSA and PGA. However, PASI and DLQI should be considered for patients who undergo phototherapy or systemic therapy¹
Classification of plaque psoriasis severity¹

Severity BSA, % PGA PASI DLQI
Mild <3 1–2 <5 <5
Moderate 3–10 3 5–10 5–10
Severe >10 4 >10 >10
The signs of psoriasis are different for every individual; however, some signs are common in all types of psoriasis, such as erythema, skin thickening and scales.² It’s also important to remember that multiple forms can be present in an individual at any given time³

BSA, body surface area; DLQI, dermatology life quality index; PASI, psoriasis area and severity index; PGA, physician global assessment.

The table is reproduced with the permission of Wiley Journals. It was first published in Imafuku S, et al. J Dermatol 2018;45:805–811.

1. Imafuku S, et al. J Dermatol 2018;45:805–811; 2. Mayo Clinic. Psoriasis. Available at: https://www.mayoclinic.org/diseases-conditions/psoriasis/symptoms-causes/syc-20355840. (last accessed December 2021);

3. American Academy of Dermatology Association. Types of Psoriasis: Can You Have More Than One. Available at: https://www.aad.org/public/diseases/psoriasis/treatment/could-have/types. (last accessed December 2021).

Intrinsic precipitating factors for psoriasis

The cause of psoriasis is unknown; genetic predisposition, altered epidermal kinetics and various intrinsic precipitating factors play a role

Genetics^1–3

It is well established that psoriasis runs in families

Psychological stress⁴

Mental stress is thought to exacerbate psoriasis, although further studies are needed to elucidate the exact association

Comorbidities⁴

Obesity, diabetes mellitus, dyslipidaemia, and hypertension are associated with psoriasis

Psychological stress and comorbidities icons made by Pixel perfect from www.flaticon.com.

1. Hawkes JE, et al. J Allergy Clin Immunol 2017;140:645–653; 2. Tsoi LC, et al. Nat Commun 2017;24;8:e15382; 3. MSD Manual. Psoriasis. 2020. Available at: https://www.msdmanuals.com/en-gb/professional/dermatologic-disorders/psoriasis-and-scaling-diseases/psoriasis. (last accessed November 2021);

4. Kamiya K, et al. Int J Mol Sci 2019;20:4347.

Extrinsic precipitating factors for psoriasis

The cause of psoriasis is unknown; various extrinsic precipitating factors may play a role

Infection¹

The association between psoriasis and streptococcal infection is well recognised

Smoking^1,2

There is an established association between psoriasis and smoking

Air pollutants and sun exposure¹

Certain groups of patients can develop psoriasis after UV exposure

Mechanical stress¹

In patients with psoriasis, skin lesions may appear in uninvolved areas after various injuries, known as Koebner phenomenon

Drugs^1,3,4

The onset and exacerbation of psoriasis is associated with certain drugs, such as beta-blockers, lithium, antimalarials, NSAIDs, and anti-psychotics
(e.g. aripiprazole)

NSAIDs, non-steroidal anti-inflammatory drugs; UV, ultraviolet.

1. Kamiya K, et al. Int J Mol Sci 2019;20:4347; 2. Li W, et al. Am J Epidemiol 2012;175:402–413; 3. Bujor CE, et al. BMC Psychiatry 2017;17:242; 4. Tsankov N, et al. Am J Clin Dermatol 2000;1:159–165.

Question 3: Psoriasis severity

If a patient’s psoriasis covered 4% of their body surface area, what would the severity of their psoriasis be classified as?

Severe Mild Moderate

r

Question 3: Psoriasis severity answer

Moderate

According to the BSA assessment, psoriasis is classified as moderate when 3–10% of the skin is affected¹

Click the button below to find out more:

Disease background

BSA, body surface area.

1. Imafuku S, et al. J Dermatol 2018;45:805–811.

Disease background: Psoriasis

Individuals can present with plaque psoriasis of differing severity, which is classified as mild, moderate or severe. Psoriasis severity should be assessed by a minimum of two indices, usually BSA and PGA. However, PASI and DLQI should be considered for patients who undergo phototherapy or systemic therapy¹
Classification of plaque psoriasis severity¹

Severity BSA, % PGA PASI DLQI
Mild <3 1–2 <5 <5
Moderate 3–10 3 5–10 5–10
Severe >10 4 >10 >10
The signs of psoriasis are different for every individual; however, some signs are common in all types of psoriasis, such as erythema, skin thickening and scales.² It’s also important to remember that multiple forms can be present in an individual at any given time³

BSA, body surface area; DLQI, dermatology life quality index; PASI, psoriasis area and severity index; PGA, physician global assessment.

The table is reproduced with the permission of Wiley Journals. It was first published in Imafuku S, et al. J Dermatol 2018;45:805–811.

1. Imafuku S, et al. J Dermatol 2018;45:805–811; 2. Mayo Clinic. Psoriasis. Available at: https://www.mayoclinic.org/diseases-conditions/psoriasis/symptoms-causes/syc-20355840. (last accessed December 2021); 3. American Academy of Dermatology Association. Types of Psoriasis: Can You Have More Than One. Available at: https://www.aad.org/public/diseases/psoriasis/treatment/could-have/types. (last accessed December 2021).

Therapeutic management for drug-induced psoriasis

The first step in the management of drug-related psoriasis, when possible, is discontinuing and replacing the causative drug. However, if skin lesions show no improvement upon discontinuation, treatment may be needed¹

PSORIASIS SEVERITY

Severe
(>10%)^*

Moderate
(3-10%)^*

Mild
(<3%)^*

Systemic non-biological therapy² Phototherapy and photochemotherapy³ Biological therapy⁴

Potent or very potent TCSs⁵ Phototherapy and photochemotherapy³ Systemic non-biological therapy² Biological therapy⁴

Potent or very potent TCSs⁵ Vitamin D analogues⁵ Phototherapy and photochemotherapy³

Treatment options

First-line therapy:

Potent or very potent TCSs (e.g. clobetasol propionate)⁵
Vitamin D analogues (e.g. calcipotriene and calcitriol)⁵
Phototherapy and photochemotherapy (e.g. UVB, PUVA)³

Second-line therapy:

Systemic non-biological therapy (e.g. methotrexate, cyclosporine, and retinoids)²

Third-line therapy:

Biological therapy (e.g. TNF antagonists and anti-IL antibodies)⁴

Adjuvant therapy:

Moisturisers, emollients, and skin barrier creams⁵

*Body surface area percentage.

Anti-IL, anti-interleukin; PUVA, psoralen-ultraviolet A therapy; TCS, topical corticosteroid; TNF, tumour necrosis factor; UVB, ultraviolet B.

1. Balak D and Hajdarbegovic E. Psoriasis (Auckl) 2017;7:87–94; 2. Menter A, et al. J Am Acad Dermatol 2020;82;1445–1486; 3. Elmets CA, et al. J Am Acad Dermatol 2019;81;775–804; 4. Menter A, et al. J Am Acad Dermatol 2019;80:1029–1072; 5. Elmets CA, et al. J Am Acad Dermatol 2021;84:432–470.

Question 4: Treatment selection

Would the use of moderately potent, potent, or very potent topical corticosteroids be appropriate for this case?

Yes No

Question 4: Correct answer

YES

The use of moderately potent to very potent topical corticosteroids for up to 4 weeks is recommended for the treatment of plaque psoraisis¹

Continue through the slides to see the treatment chosen for this case

1. Elmets CA, et al. J Am Acad Dermatol 2021;84:432–470

Case 1: Treatment objective and selection

Objective: Effective and rapid response to treatment

Treatment chosen: Dermovate (clobetasol propionate) cream twice daily for 3 weeks, plus an emollient

This treatment was chosen due to its safety, effectiveness, and cosmetic acceptability, which would promote therapeutic adherence
Systemic treatment was avoided due to the risk of adverse events, particularly as there was only one lesion to treat
The frequency and duration of treatment was selected as there was a solitary lesion that was scaly and infiltrated

Case study provided by Dr Yvette Fernández, Mexico (GSK Medical Scientific Advisor, Dermatology).

Guideline-based rationale for treatment choice

Guidelines		Treatment decisions
“The first step in the management of drug-related psoriasis is stopping and replacing the offending agent when possible”¹		The patient was considered to be mentally stable by their psychiatrist, so aripiprazole was discontinued, and the patient was monitored carefully
“The use of class 1,* class 2,^† and class 3–5^‡ topical corticosteroids for up to 4 weeks is recommended for the treatment of plaque psoriasis not involving intertriginous areas”²		A very potent topical corticosteroid was prescribed for 3 weeks to treat the solitary erythematous plaque, as there was no involvement of an intertriginous area
“The use of an emollient in conjunction with topical corticosteroids for 4 to 8 weeks^§ can be used to help reduce itching, desquamation, and total body surface area and prevent quick relapse of psoriasis when topical corticosteroids are discontinued”²		An emollient was prescribed adjunct to the topical corticosteroid treatment

*Very potent topical corticosteroids;^3,4 ^†Potent topical corticosteroids;^3,4 ^‡Moderately potent topical corticosteroids.^3,4 ^§ Treatment with Dermovate should not be continued from more than 4 weeks⁵

1. Balak D and Hajdarbegovic E. Psoriasis (Auckl) 2017;7:87–94; 2. Elmets CA, et al. J Am Acad Dermatol 2021;84:432–470; 3. Gabros S, Nessel TA, and Zito PM. Topical Corticosteroids. In: StatPearls [Internet]. Treasure Island, 2021; 4. National Eczema Society. Available at https://eczema.org/wp-content/uploads/Topical-steroids-Sep-19-1.pdf. (last accessed January 2022); 5. Dermovate local prescribing information based on UK V11.

Treatment outcome

Follow-up period: 4 weeks

Response: Yes

Course of action: The lesion had total resolution and the patient did not relapse. It was recommended that the patient continue with a mild cleanser and emollient

Next steps: Psoriasis is associated with various triggering factors that can elicit a reaction; therefore, the patient was advised to avoid triggers such as mechanical stress, air pollution, smoking, alcohol, and certain drugs

Additionally, the patient should be monitored for comorbidities, such as obesity, dyslipidaemia, and hypertension, as psoriasis is associated with triggers that can elicit disease

Before treatment

After treatment

Image and case study provided by Dr Yvette Fernández, Mexico (GSK Medical Scientific Advisor, Dermatology).

Patient vignette and clinical history

Background: 47-year-old male, office worker

Patient history: Onset of itch and burning sensation after application of ‘Sandalwood’ perfume made in India

The perfume was previously used, but the concentration may have been more concentrated at the bottom of the bottle
History of fatty liver and high cholesterol, no prior history of atopic dermatitis
Previous history of a fixed drug eruption, which was resolved

Presenting symptoms: The first instance of dermatitis was at the site of contact with the perfume, on the left antecubital fossa. There was also a contiguous spread beyond the site of contact

Duration and temporal pattern of signs/symptoms and signals: 1 day, acute onset after application of perfume

Medical history: On statins. Non-smoker, and no alcohol intake

Allergies: Iodinated contrast agents

Image and case study provided by Dr Gary Ong (GSK Global Medical Director – Dutasteride AGA, Vates, Zanamivir and Supplements).

Physical examination

General physical examination of skin: Erythema, oedema, and pruritus on the left antecubital fossa

Description of skin lesions: Multiple, well-defined, erythematous papules and plaques with some vesicles

Any other relevant information: Pruritus resulting in scratching

Case study provided by Dr Gary Ong (GSK Global Medical Director – Dutasteride AGA, Vates, Zanamivir and Supplements).

Question 1: Diagnostic tests

Which of the below diagnostic tests would be appropriate for this patient? (Please select one option)

Patch testing Skin scraping KOH test All of the above

KOH, potassium hydroxide.

Question 1: Correct diagnostic test

All of the above

Patch-testing, skin biopsies and skin scraping may be used, if necessary.^1,2 Skin scraping for KOH testing may be used to identify or rule out fungal infections such as tinea corporis³

Continue through the slides to see the differential diagnoses for this patient, as well as the methods that can be used to differentiate the final diagnosis from other similar dermatoses

1. Usatine RP and Riojas M. Am Fam Physician 2010;82:249–255; 2. Kostner L, et al. Immunol Allergy Clin North Am 2017;37:141–152; 3. Ely JW, et al. Am Fam Physician 2014;90:702–710.

Differential diagnosis (1/2)

During diagnosis, the following differentials should be considered, as well as the patient’s history of fragrance use

Condition	Atopic dermatitis (AD)	Tinea corporis
Cause	Unknown cause, but AD is identified as a disease of the immune system; cytokines are a critical factor, causing barrier defects and inflammation¹	A superficial fungal skin infection caused by dermatophytes and their ability to attach to the keratinised tissue of skin^6,7
Location	Can be anywhere on the body, but usually the flexor regions²	Typically the exposed skin of the neck, trunk, and/or extremities⁶
Onset	Infants usually present with acute AD between 3 and 6 months of age, whereas older children and adults present with acute and chronic AD^3,4	Can occur at any age, but is most common in prepubertal children⁷
Signs/symptoms	Pruritus, xerosis, erythema⁵	Pruritus, erythema⁶
Lesion appearance and borders	Acute form: Vesicular, weeping, crusting eruptions² Chronic form: Lichenification of plaques²	The lesions usually present as annular or ovoid with patches and plaques; may be single or multiple, and generally range from 1–5 cm; have sharp active margins with raised, erythematous, scaly edges that may contain vesicles; and spread centrifugally from the core, leaving a central clearing and mild residual scaling, giving rise to the term ‘ringworm^6,7

The first image is used with permission from DermNet NZ. The second image is reproduced with the permission of Wiley Journals. It was first published in Ohno S, et al. J Dermatol 2008;35:590–593.

1. DermNet Nz. Causes of atopic dermatitis. Available at: https://www.dermnetnz.org/topics/causes-of-atopic-dermatitis. (last accessed November 2021); 2. Berke R, et al. Am Fam Physician 2012;86:35–42; 3. Avena-Woods C. AM J Manag Care 2017;23(8 Suppl):S115–S123; 4. Langan SM, et al. Lancet 2020;396:345–360; 5. Saeki H, et al. J Dermatol 2009;36:563–577; 6. Yee G and Al Aboud AM. Tinea Corporis. In: StatPearls [Internet]. Treasure Island, 2021; 7. Ely JW, et al. Am Fam Physician 2014;90:702–710.

Differential diagnosis (2/2)

Condition	Irritant contact dermatitis (ICD)	Allergic contact dermatitis (ACD)
Cause	Skin injury due to direct cytotoxic effects and inflammation following irritant contact (e.g. detergents and abrasives)¹	T-cell mediated, delayed hypersensitivity reaction following contact with usually innocuous allergens⁴
Location	Areas that come in contact with the irritant; typically the hands and mouth¹	Any exposed skin, often the hands and face⁵
Onset	Acute form: Rapid (within minutes of irritant contact)² Cumulative form: Delayed (hours–days)²	Delayed (hours–days)⁴
Signs/symptoms	Burning, pruritus, pain^1,2	Intense pruritus, pain, erythema, swelling, and dry, scaly skin^5,6
Lesion appearance and borders	Acute form: Papules and blisters may be present. This may be followed by weeping, scab formation and scaling³ Cumulative form: The lesions appear more exudative and scaled, with skin thickening and indistinct demarcation around the lesions³	Acute cases may involve a dramatic flare with erythema, vesicles, and bullae; chronic cases may involve lichen with cracks and fissures5 Clinical signs of ICD and ACD often overlap, but ACD tends to manifest as acute to subacute dermatitis, with pruritus as its cardinal symptom⁷ ACD development depends on the concentration of an allergen and duration of exposure: strong allergens may result in sensitisation within a week, whilst weak allergens may take months to years to promote sensitisation⁸

The first image is used with permission from DanDerm. The second image is reproduced with the permission of Wiley Journals. It was first published in Mohamed M, et al. Australas J Dermatol 1999;40:164–166.

1. Usatine RP and Riojas M. Am Fam Physician 2010;82:249–255; 2. Veien NK. Clinical features of contact dermatitis. In: Textbook Quick Guide to Contact Dermatitis. Springer, Berlin, Heidelberg. 2016. pp 9–31; 3. Brasch J, et al. Allergo J Int 2014;23:126–138; 4 DermNet NZ. Allergic contact dermatitis. Available at: https://www.dermnetnz.org/topics/allergic-contact-dermatitis. (last accessed November 2021); 5. Murphy PB, et al. Allergic Contact Dermatitis. In: StatPearls [Internet]. Treasure Island, 2019; 6. Kostner L, et al. Immunol Allergy Clin North Am 2017;37:141–152; 6; 7. Sasseville D. Allergy Asthma Clin Immunol 2008;4:59–65; 8. Brites GS, et al. Pharmacol Res 2020;162:105282. doi:10.1016/j.phrs.2020.105282.

Question 2: Diagnosis

What would be your chosen diagnosis for this patient based on the options below? (Please select one option)

Irritant contact dermatitis Allergic contact dermatitis Atopic dermatitis Tinea corporis

Question 2: Correct diagnosis

Correct answer:

Allergic contact dermatitis

Click the buttons below to find out more:

Diagnostic considerations Disease background Precipitating factors

Diagnostic considerations and final diagnosis

Diagnosis: It can be difficult to differentiate between various dermatoses, but the following steps can be used to aid diagnosis:

Record a precise medical history¹

Thoroughly inspect the clinical appearance of the dermatitis^1,2

Patch-testing, skin biopsies and skin scraping may be used, if necessary^1,2

Final diagnosis: Allergic contact dermatitis (ACD) secondary to perfume³

In response to contact with an allergen identified as the patient’s ‘Sandalwood’ perfume³
A perfume may consist of 10–300 basic components obtained from >500 raw materials⁴
- Determining the specific offending allergen can be very difficult. Most contact dermatitis clinics use a fragrance mix and Balsam of Peru to test for fragrance allergies

Patch-testing icon made by Pixel perfect from www.flaticon.com.

1. Usatine RP and Riojas M. Am Fam Physician 2010;82:249–255; 2. Kostner L, et al. Immunol Allergy Clin North Am 2017;37:141–152; 3. Case study provided by Dr Gary Ong (GSK Global Medical Director – Dutasteride AGA, Vates, Zanamivir and Supplements); 4. Johansen JD and Lepoittevin JP. Fragrances. In: Contact dermatitis. Springer Link; 2010. pp 607–627; 5. Uter W. Fragrances. In: Quick Guide to Contact Dermatitis. Springer, Berlin, Heidelberg. 2016. pp 139–145.

Disease background: Allergic contact dermatitis (ACD)

ACD is a type IV or delayed-type hypersensitivity reaction that occurs when the skin comes into contact with an allergen¹

In ACD, the reaction is usually localised to the area of contact, but may be diffuse or patchy within the exposed area²

A distinction should be made between the sensitisation and elicitation phases of ACD:³

Sensitisation includes the events following the first contact with an allergen, where an individual becomes sensitised without a visible ACD reaction
Following sensitisation, elicitation results in the clinical manifestation of ACD following the next contact with the allergen

Sensitisation occurs over days, weeks or even years^3,4

Elicitation occurs within 48–72 hours after the next exposure to the allergen^1,3

Timer icon made by Pixel perfect from www.flaticon.com

1. DermNet NZ. Allergic contact dermatitis. Available at: https://www.dermnetnz.org/topics/allergic-contact-dermatitis. (last accessed November 2021); 2. So JK, et al. Curr Treat Options Allergy 2015;2:333–348; 3. Rustemeyer T, et al. Mechanisms in Allergic Contact Dermatitis. In: Quick Guide to Contact Dermatitis. Springer, Berlin, Heidelberg. 2001. pp 15–58; 4. Brites GS, et al. Pharmacol Res 2020;162:105282. doi: 10.1016/j.phrs.2020.105282.

Precipitating factors for allergic contact dermatitis^1–3

Genetics¹

Variations in genetics can make certain people more susceptible to ACD

Occupation^1,2

People working in specific occupations are at risk of developing ACD due to exposure to potential sensitisers. For example, exposure to formaldehyde in the beauty, construction and healthcare industries

Sex^1,3

There is a higher prevalence of ACD in women; this has been associated with increased exposure to allergens (e.g. nickel through piercings)

Age^1,4

ACD is more likely to affect young patients, with a prevalence of 15% in 12–16 year olds

Nickel^1,3

Nickel is a common contact allergen globally

AD

Incidence of AD¹

A history of AD can lead to a reduced skin barrier function, which facilitates the penetration of allergens

ACD, allergic contact dermatitis; AD, atopic dermatitis.

1. Peiser M, et al. Cell Mol Life Sci 2012;69:763–781; 2. Qin R and Lampel HP. Curr Treat Options Allerg 2015;2:349–364; 3. Meding B, Contact Dermatitis 2000;43:65–71; 4. Mortz CG, et al. Acta Derm Venereol 2002;82:352–358.

Therapeutic management for allergic contact dermatitis

A key factor in the management of ACD is the avoidance of contact with the respective allergen¹ Therapy for ACD persisting despite removal of the allergen should follow the management of atopic/endogenous dermatitis²

ACD LOCALISATION

Extensive
(>20% of skin)

Localised

Systemic therapy¹ Phototherapy²

Potent or very potent TCSs (a lower potency can be used for areas with thin skin)¹ Cool compress¹ Phototherapy²

Treatment options

First-line therapy:

Potent or very potent TCSs (e.g. clobetasol propionate)¹
Systemic therapy (e.g. triamcinolone, methotrexate, cyclosporine)¹
Cool compress used to soothe symptoms for acute ACD¹

Second-line therapy:

Phototherapy (e.g. short-wave ultraviolet light and PUVA)²

Adjuvant therapy:

Emollients, moisturisers, and barrier creams may be used as a secondary prevention strategy¹
Secondary infection should be treated with appropriate antibiotics

ACD, allergic contact dermatitis; PUVA, psoralen-ultraviolet A therapy; TCS, topical corticosteroid.

1. Usatine RP and Riojas M. Am Fam Physician 2010;82:249–255; 2. Johnston GA, et al. Br J Dermatol 2017;176:317–329 3. Hian YL and Goh CL. The principles and practice of contact and occupational dermatology in the Asia-Pacific region. World Scientific; 2001. pp 71–72.

Question 3: Treatment selection

Would systemic therapy be appropriate for this case?

Yes No

Question 4: Correct answer

NO

Systemic therapy is considered a first-line treatment for patients with extensive (>20% of skin affected) allergic contact dermatitis¹

Continue through the slides to see the treatment chosen for this case

1. Usatine RP and Riojas M. Am Fam Physician 2010;82:249–255

Case 2: Treatment objective and selection

Objective: Effective and rapid response to treatment

Initial treatment chosen: Hydrocortisone cream, twice a day to the affected area, was prescribed for a week

However, the patient returned for a review after 3 days as there was no response to the treatment

Second treatment chosen: Dermovate (clobetasol propionate) cream applied twice daily

Since the patient was not responding to the low potency topical corticosteroid (TCS), the decision was made to use a high potency TCS and then step down to lower potency TCS, if necessary
No antibiotics were required as there was no secondary infection noted

Case study provided by Dr Gary Ong (GSK Global Medical Director – Dutasteride AGA, Vates, Zanamivir and Supplements).

Guideline-based rationale for treatment choice

Guidelines

Treatment decisions

“In patients with contact dermatitis, the priority is to identify and avoid the causative substance”¹

The patient was instructed to avoid their Sandalwood perfume

“Hydrocortisone 1% is available over-the-counter for the treatment of mild-to-moderate eczema* not involving the face or genitals”²

“Localised acute allergic contact dermatitis lesions are successfully treated with mid- or high-potency^† topical steroids”²

As the patient’s allergic contact dermatitis was mild, hydrocortisone(a mild potency topical steroid) was initially chosen

A very potent topical corticosteroid was prescribed when the patient did not respond to the initial treatment

“Emollients, moisturisers, or barrier creams may be instated as secondary prevention strategies to help avoid continued exposure”¹

Once the papules and plaques had resolved, the patient was instructed to moisturise the area

*Therapy for allergic contact dermatitis persisting despite removal of the allergen should follow the management of atopic/endogenous dermatitis;³ ^†Potent to very potent topical corticosteroids.^4,5

1. Usatine RP and Riojas M. Am Fam Physician 2010;82:249–255; 2. NICE Clinical Guidelines, Topical corticosteroids. 2021; 3. Johnston GA, et al. Br J Dermatol 2017;176:317–329; 4. Gabros S, Nessel TA, and Zito PM. Topical Corticosteroids. In: StatPearls [Internet]. Treasure Island, 2021; 5. National Eczema Society. Available at https://eczema.org/wp-content/uploads/Topical-steroids-Sep-19-1.pdf. (last accessed January 2022).

Question 4: Guideline recommendations

Is the following statement true or false? Guidelines recommend that localised acute allergic contact dermatitis lesions can be successfully treated with potent or very potent topical corticosteroids

TRUE FALSE

Question 4: Correct answer

True

Localised acute allergic contact dermatitis lesions can be successfully treated with potent or very potent topical steroids¹

Continue through the slides to see the treatment outcome for this case

1. Usatine RP and Riojas M. Am Fam Physician 2010;82:249–255

Outcome following initial hydrocortisone cream treatment

Follow-up period: 3 days

Response: No – further erythema was observed and the pruritus had not subsided

Course of action: The patient was not responding to hydrocortisone cream; therefore, a change was made to Dermovate (clobetasol propionate) cream, which was applied twice daily

Before hydrocortisone cream treatment

Day 3 after starting hydrocortisone cream treatment

Image and case study provided by Dr Gary Ong (GSK Global Medical Director – Dutasteride AGA, Vates, Zanamivir and Supplements).

Outcome following treatment with Dermovate
(clobetasol propionate) cream

Follow-up period: 3 days after initiation of Dermovate cream

Response: Yes – erythema and pruritus had subsided. Crusted lesions were observed in the left antecubital fossa

Course of action: Treatment with Dermovate cream was discontinued as the patient’s acute lesions had resolved. Moisturiser use was advised

Next steps: Advice was given to the patient to avoid the perfume, which was likely the cause of the allergic contact dermatitis

Before Dermovate cream treatment (after hydrocortisone cream treatment)

Day 6 after starting treatment with Dermovate cream

Image and case study provided by Dr Gary Ong (GSK Global Medical Director – Dutasteride AGA, Vates, Zanamivir and Supplements).

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Severity	BSA, %	PGA	PASI	DLQI
Mild	<3	1–2	<5	<5
Moderate	3–10	3	5–10	5–10
Severe	>10	4	>10	>10