Dermatological Emergencies

Objectives:
- Not given

Main Objective of this lecture is to differentiate betweet SJS – TEN – EM.

Team leader: Ghada Alhadlaq

Members: Bayan Al-Mugheerah – Ghada AlSkait
Revised by: Shrooq Alsomali
Template by group B
Before you start.. CHECK THE EDITING FILE
Sources: doctor’s slides and notes + 436 group B team
[ Color index: Slides| Slides| Important|doctor notes|Extra]
 Clinical Real ER case

Describe the lesions: Approach :

. On face: ill defined - Hx: 3 day onset – Painful – First time – No recent trauma –
erythematous plaque Recent URTI which she took abx for. (onset, progression, drug
with crustation. hx, pain, previous episodes, infections)
On lips: Hemorrhagic - O/E: We should examine her nails, mucous membranes(eye
crustation with ulcers and genitalia) and scalp.
and erosions - LAB: Usually we diagnose clinically but we can order skin
biopsy.
- DDx - Mx
This table is important

Target like
Describe the lesion:
Numerous irregular
erythematous
grouped papules.

• Time interval is very important in differentiating

different drug reactions.
• Exthanthematous = maculopapular.
• Urticaria occurs very fast because its type 1
Describe the lesion: hypersensitivity. Caused by many reasons(drugs)
Numerous erythematous papules, bullae and, • Anaphylaxis is a systemic manifestation more than skin
blistering. and is treated by medicine not derma.
It’s basically a drug induced burn. • Focus on SJS and TEN as they carry high mortality rate
(can reach up to 50%) “Allopurinol+NSAIDs”.

Alarming Morphological patterns :

- Urticaria/ Angioedema .
- Purpura/ Ecchymoses.
- Bullae/ Sloughing.
- Necrosis/Gangrene.
- Exfoliative Erythroderma syndrome.
- Generalized/ widespread rashes in the acutely ill febrile patient.
Dermatologic Emergencies:
- Urticaria/angioedema/anaphylaxis. Swelling of lips, eyes, airway and hypotension.
- Purpura.
- Bullous disease.
- Steven’s Johnson syndrome(SJS)/Toxic epidermal necrolysis(TEN).
- Erythroderma.
 Steven’s Johnson syndrome (SJS) / Toxic epidermal necrolysis (TEN)

- Rare, acute, life-threatening mucocutaneous (skin + mucous-membrane) disease.

- Nearly always drug-related. (patients have problems in drug metabolism)
- Keratinocyte death separation of skin at the dermal-epidermal junction.
- Characteristic symptoms: High fever, skin pain, anxiety and asthenia. Shivering
- It is crucial to diagnose it early so the causal drug can be discontinued. (with every day the risk of death increase)

Review:
It has now become clear that Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are variants within
a continuous spectrum (Same cause – Clinical presentation – Management. They only differ in severity) of adverse
drug reactions.

History:
- EM (erythema multiform) was first described by the Austrian dermatologist Ferdinand von Hebra in 1860.
- In 1922, two US physicians, Stevens and Johnson, described an acute mucocutaneous syndrome in two young boys.
- Characterized by severe purulent conjunctivitis, severe stomatitis with extensive mucosal necrosis, and “EM-like”
cutaneous lesions. It became known as Stevens–Johnson syndrome (SJS) and was recognized as a severe
mucocutaneous disease with a prolonged course and occasional fatalities.
- SJS was later designated as EM major by Bernard Thomas in 1950. However, recent clinical investigations have made
it clear that the term “EM major” should not be used to describe SJS as they are distinct disorders.
- In 1956, Alan Lyell described four pts with an eruption 'resembling scalding of the skin objectively and subjectively',
which he called toxic epidermal necrolysis or TEN. 'Toxic' referred to toxemia – circulation of a toxin – which was
thought to be responsible for the constitutional symptoms and epidermal necrosis.
- Lyell coined the term 'necrolysis' by combining the key CF 'epidermolysis' with the characteristic histopathological
feature 'necrosis'.
- He also described an attack on the mucous membranes as part of the syndrome, with very little inflammation in the
dermis, a feature that was later referred to as 'dermal silence.
- Erythema multiforme, SJS, and TEN were, at the time, considered to be part of a continuous spectrum of cutaneous
reactions.
- It was clear, that HSV was the major cause of EM, and that this virus was not related to TEN.
Recently, Assier et al. clarified this issue by providing clinical evidence that EM and SJS are clinically distinct disorders
with different causes and prognosis.
- Increasingly, SJS, and TEN are considered to be two ends of a spectrum of severe epidermolytic adverse cutaneous
drug reactions, differing only by the extent of skin detachment.

EM was the first to be found, but later American physicians Steven and Johnson found a rash that is more severe
and involves both skin and mucus membranes (conjunctivitis, stomatitis, necrosis). They named at as (EM like) at
first then they changed it named it by their names (Steven-Johnson’s) and the considered it severe mucocutaneous.
What is the difference between SJS and EM? EM is viral (herpes simplex) and SJS is drug induced

• SJS can progress to TEN if left untreated.

• Mainway to differentiate between the two is BSA. Less
than 10% = SJS, >30% = TEN. 10-30% = SJS-TEN overlap. *An extra picture to help you revise
You must include the initial BSA to check progression. Body Surface Area
• Calculating BSA is through areas of epidermal
detachment NOT redness.
 Epidemiology

- Mortality rates range from 25 to 50% (average: 30-35%)

for patients with TEN. 5% for patients with SJS.
- On average, death occurs in every third patient with TEN,
and it is mainly due to infections (S. aureus and
Pseudomonas aeruginosa)
- Drug use is reported in over 95% of patients with TEN.
- Other rare causes include infections and immunization.
- More than 100 drugs have been identified to date as being
associated with SJS/TEN.
- Most common: (know names of drugs NOT only the class)
● Allopurinol “Gout patient”
● Antibiotics (Sulfonamides)
• Its more common here. ● NSAIDs; Diclofenac – Ibuprofen.
• Genetics play a role. ● Anticonvulsants.

‫من باب العلم‬

‫من باب العلم‬

Pathogenesis of SJS/TEN:

- An idiosyncratic, delayed hypersensitivity reaction.

- TEN is associated with an impaired capacity to detoxify reactive intermediate drug metabolites.
- Slow acetylators.
- Immunocompromised pts.
- HIV, With AIDS, the risk of developing TEN is 1000-fold higher than in the general population.
- It is thought to be initiated by an immune response to an antigenic complex formed by the reaction of such
metabolites with certain host tissues.
- There is evidence that systemic lupus is a risk factor
- Genetic susceptibility (increased incidence of HLA-B12 in affected individuals)

Sulfa drops

Keratocytes

I.V immunoglobulin
inhibits FAS-FAS ligament
 • Understanding pathogenesis is essential to understand the management. He took the medication
whether IV – oral or drops the body will react to it as if its an antigen (theory B) and it will go to the
keratocyte which can be an antigen presenting cell and recruits’ T cells and the T cells will act as if it’s a
virus and starts making CD8 T cells and these cells will start producing cytotoxic compounds such as
perforin and granzyme B and will cause necrolysis and apoptosis of skin cells and this is one of the
theories and this is one of the treatment sites. Another theory (theory A) is that there are receptors on
the skin cells called Fas and will become fas and fas ligand and sends signals to the cell to die (Site of
action of immunoglobulins). The last theory (theory C) is through natural killer cells and they will
secrete granulysin which is cytotoxic.

Clinical Features of SJS

- There must be evidence of mucosal involvement.

-Fever, stinging eyes.
- Cough productive of thick, purulent sputum. The cough here is not due to the URTI its due to involvement of the
respiratory mucosa.
- Headache. Malaise, Arthralgia.
- Burning rash begins symmetrically on the face & upper part of the trunk.
- Erythema and erosions of the buccal, ocular and genital mucosa are present in more than 90% of patients. Can even
present without skin involvement!
- The epithelium of the respiratory tract is involved in 25% of patients with TEN, and gastrointestinal lesions (e.g.
esophagitis, diarrhea) can also occur.
The cutaneous lesions are characterized as follows:
- The rash can begin as macules that develop into papules, vesicles, bullae, urticarial plaques, or confluent erythema
- The typical lesion has the appearance of a target – like; this is considered pathognomonic
- In contrast to the typical lesions of erythema multiforme (3 zones), these lesions have only 2 zones of color
- The lesions have a tendency to coalesce.
- Lesions may become bullous and later rupture, leaving denuded skin; the skin becomes susceptible to secondary
infection (Impetigo, yellow golden crust).
- Urticarial lesions typically are not pruritic
- Infection may be responsible for the scarring or if the ulcer is deep (Consult ophtha if injury reached the eye, can
cause blindness) associated with morbidity.
- Although lesions may occur anywhere, the palms, soles, dorsum of the hands, and extensor surfaces are most
commonly affected.
- Nikolsky sign (positive in some area): Applying pressure to normal skin will induce detachment
Signs of mucosal involvement can include the following:
• Erythema
• Edema
• Sloughing
• Blistering
• Ulceration
• Necrosis

• You should examine genitalia. • Skin here is thin so you’ll see erosions not ulcers
(white circle).
• Slit lap examination needed.
• Know how to differentiate between ulcers
• Not to confuse with allergic conjunctivitis this
(bleeding = mid of dermis) and
is serious and you must stop the medication erosions.(superficial)
 Clinical Features of TEN

- Fever, stinging eyes, and pain upon swallowing, any of which can precede cutaneous manifestations by 1 to 3 days.
- Skin lesions tend to appear first on the trunk, spreading to the neck, face, and proximal upper extremities.
- The scalp, distal portions of the arms as well the legs are relatively spared, but the palms and soles can be an early
site of involvement. Less mucous membrane involvement when compared to SJS.
- First, erythematous, dusky-red, or purpuric macules of irregular size and shape, and have a tendency to coalesce.
- At this stage, and in the presence of mucosal involvement and tenderness, the risk of rapid progression to SJS or TEN
should be strongly suspected.
- In the absence of spontaneous epidermal detachment, a Nikolsky sign should be sought by exerting tangential
mechanical pressure with a finger on several erythematous zones. This sign is considered positive if dermo-epidermal
cleavage is induced. Avoid dressing!!
- A target-like appearance.
- This process can be very rapid (hours), or several days.
- The necrotic epidermis then detaches from the underlying dermis, and fluid fills the space between the dermis and
the epidermis, giving rise to blisters
- The blisters break easily (flaccid) and can be extended sideways by slight pressure of the thumb as more necrotic
epidermis is displaced laterally (Asboe-Hansen sign: Pressing on a bulla will cause it to rupture).
- Tense blisters are usually seen only on the palmar & plantar surfaces when the epidermis is thicker more resistant
to mild trauma. How to differentiate from other blistering diseases? In TEN tense blisters involve the palms and soles
only unlike other diseases involving the whole body.

• TEN: Patient is ill probably in ICU if more than 10% of BSA involved its either TEN overlap or TEN.
• Skin looking like Cigarette paper (Positive Nikolosky)
• Dusky-Red – Non blanchable.
• Picture (A) Steven overlap based on BSA. Picture (B) TEN. (important to revise how to calculate BSA).
• The back alone is almost 15% so if you see back involvement defiantly it’s more than 10%
Histology:

• Biopsy is helpful specially to convince other medical teams.

• Biopsy showing inflammation, death and shrinkage of keratocytes.

Pathology of TEN:
A subepidermal blister with overlying confluent
Detachment
necrosis of the entire epidermis ad a sparse
perivascular infiltrate composed primarily of (CD8)
lymphocytes.
Why do we biopsy if it obvious? Sometimes it is not
obvious, we want to see clinically insignificant
detachment
DDx of TEN: (Biopsy can be helpful in differentiating)
- Stevens-Johnson Syndrome
- Staphylococcal Scalded Skin Syndrome (Peds)
- Toxic Shock Syndrome (Adult women)

SJS TEN

Staphylococcal scalded skin syndrome

- usually occur in newborns and young children.

- it is induced by a staphylococcal exotoxin (epidermolysis) that targets desmoglein 1.
- The areas of erythema are tender and widespread, but spare the mucous membranes (very important!!), palms,
and soles.
- The Nikolsky sign may be positive as in TEN (Doctor said it will be (-) in ssss), but it results in a superficial subcorneal
cleavage, not a dermo-epidermal separation. Fragile bullous lesions then develop, and they are rapidly followed by
exfoliation of sheets of epidermis.
- Histologically shows a subcorneal split with normal underlying epidermis.

• Superficial peeling. • Secondary infection NOT

mucosal involvement.

In SSSS: The peeling will occur in areas that are NOT

erythematous
In TEN: The peeling will occur in the dusky
erythematous area.
TEN SSSS
• At the junction. • Superficial dermis only.
• Treatment: STOP • Treatment: ADD
THE MEDICATION. MEDICATION.
 Toxic shock syndrome (TSS) (not common in our society)

- Is an inflammatory response syndrome characterized by fever, rash, hypotension and multiorgan involvement.
- TSS has been typically associated with tampon use in healthy menstruating women. (it’s a risk not a cause)
- The disease is now known to also exist in men, neonates, and non-menstruating women.
- It has been linked to many bacterial infections, including pneumonia, osteomyelitis, sinusitis, and skin and
gynecologic infections.

Staphylococcal TSS (15 - 35 years) higher in women mortality rate is less than 3%
Streptococcal TSS (20 -50 years) both sex mortality rate is 30 - 70%.

- Prodromal period of 2-3 days:

- Fever, nausea and/or vomiting
- Profuse watery diarrhea with abdominal pain.
- Pharyngitis and/or headache, confusion.
- Hypotension
-Negative Nikolsky – No mucous membrane involvement.
- Skin findings:
● Diffuse rash, occasionally patchy and erythematous, with desquamation (this is what makes it a differential
diagnosis) occurring approximately 1-2 weeks later
● Rash initially appearing on trunk, spreading to arms and legs, and involving palms and soles
● Signs of multiorgan involvement

Why does the skin start

peeling and becomes
erythematous? Because the
body can’t detoxify the toxins
anymore

Prognosis of TEN: Management:

Death occurs in 1/3 of pts with TEN (mainly due to

infections). (but we don’t give prophylactic!! We only give if
there’re signs of infection ‫ اول ظهور لبوادر انفكشن‬and we give it
ASAP )
General measures: - (First two most important steps)
Renal function
Metabolic acidosis - Early diagnosis.
- Immediate discontinuation of the causative drug(s)
- Management on a specialist ICU or burn unit.
- Multidisciplinary teamwork. (call Derma – ID – Ophtha –
Pedia – OBGYN – GI – Pulmo)
- Supportive care. (very important)
• A calculation of mortality. - Specific therapy.

Supportive care. Specific therapy

- Pt should be manipulated as little as possible as every - To date, no specific therapy has shown efficacy in
movement is a potential cause of epidermal prospective, controlled clinical trials.
detachment Avoid dressing. - Cyclosporine
- all patient manipulations should be performed - Cyclophosphamide
sterilely. - Systemic steroids (their use has been much debated &
- venous catheters should be placed, if possible, in a remains controversial) more mortality.
region of non-involved skin - Intravenous Immunoglobulins (IVIG): (most survived)
- Non-detached areas are kept dry and not Contain antibodies against Fas that are able to block the
manipulated. binding of FasL to Fas.
- Detached areas, should be covered with Vaseline® - Used in high doses (0.75 g/ kg/day for 4 consecutive days)
gauze until re-epithelialization has occurred. Normally to treat patients with TEN.
skin will heal within 30 days. Keep it dry as possible to
promote healing. Infection or diabetes delay wound
healing.
- Careful monitoring of fluid & electrolyte status with
therapy for any imbalance. Treat as if you would a burn
patient. Risk of renal failure, no urine output, heart
failure, same complications as burn patients.
- Nutritional support.
- Warming of environment to reduce the increase in
metabolic rate.
- Appropriate analgesia. (codeine not NAIDS)
- Prevention, early detection & treatment of infection.
- There is NO evidence that prophylactic antibiotic
provide benefit & most authors reserve antibiotics
therapy for treatment of proven infection (care must be • TEN, there is scarring but at least the patient lived.
taken in screening for sepsis & surveillance of
lines/catheters to allow prompt intervention).
- For the eyes regular examination by an
ophthalmologist is recommended.
- Eyelids should gently cleansed daily with isotonic
sterile sodium chloride solution, and an ophthalmic
antibiotic ointment applied to the eyelids.

• They differ in prognosis.

• SJS hemorrhagic crust.

Erythema multiforme (EM)

- An acute, self-limited, and sometimes recurring skin condition that is considered to be a type IV hypersensitivity
reaction associated with certain infections (HSV), medications, and other various triggers.
- A mild, nonspecific URTI.
- Abrupt onset of a skin rash usually occurs within 3 days, starting on the extremities symmetrically, with centripetal
spreading.
Skin examination:
- The initial lesion is a dull-red, purpuric macule or urticarial plaque that expands slightly to a maximum of 2 cm over
24-48 H
- In the center, a small papule, vesicle, or bulla develops, flattens, and then may clear.
- An intermediate ring develops and becomes raised, pale, and edematous. The periphery gradually changes to
become cyanotic or violaceous and forms typical concentric, “target” lesion.
- Some lesions consist of only 2 concentric rings. Target like
- Some lesions appear at areas of previous trauma (Koebner phenomenon). Explains why it appears more on
extremities.
- Postinflammatory hyperpigmentation or hypopigmentation. But no scarring.
- Nikolsky sign is negative
- The lesions are symmetrical (usual distribution in immune mediated diseases, usually small BSA but sometime might
be generalized), predominantly on the acral extensor surfaces of the extremities, and they spread centripetally to
involve the abdomen and back.
- Lesions may also coalesce and become generalized.
- The palms, neck, and face are frequently involved.
- Mucosal lesions usually heal without sequelae.
- The mucosal involvement SJS is more severe and more extensive than that of EM.
-Usually preceded by herpes infection, ask about herpes “ do you have bullae on the sides of your lips?”
-Its basically an immune reaction to the virus.

• First picture: Bullous target/EM; Dark red borders – edematous ring – center can be red  vesicle or bullae.
• Second picture: White arrow: Target-lesions. Black arrow: Target-like/Targetoid lesions.
• Third picture: lips involvement but not severe.
• Palms are a very common site of involvement and should be one of the first areas you examine.

Investigations: Usually clinical but done for research Treatment:

purposes or if you cannot r/o blistering diseases. - The cause of EM should be identified.
- No specific laboratory tests are indicated to make the - If a drug is suspected, it must be withdrawn as soon as
diagnosis of EM, which should be clinically. possible.
- Specific HSV antigens have been detected within - Infections should be appropriately treated. By ID
keratinocytes by IF study. - Local supportive care for eye involvement is important
- The HSV DNA has been identified primarily within the - Symptomatic Rx, including oral antihistamines, analgesics,
keratinocytes by PCR amplification. local skin care, and soothing mouthwashes (e.g., oral
- Direct IF staining and examination may also identify an rinsing with warm saline or a solution of diphenhydramine;
alternative diagnosis (eg, pemphigoid, immunoglobulin antihistamine, xylocaine; analgesic).
A [IgA] linear dermatosis. - Topical steroids. Because it is type 4 hypersensitivity
- Histopathologic examination of Skin biopsy may be inflammation, not an infection
used to confirm the Dx of EM and to rule out the DDxA ( - Suppression of HSV can prevent HSV-associated EM, but
e.g. blistering disorders) antiviral Rx started after the eruption EM has no effect on
- CXR to to r/o Pneumonia. the course of the erythema multiforme. It isn’t an
infection, is it an immunoreaction to the virus
Course & complications:
- Most patients with (EM) have an uncomplicated
course, healing of the mucosal areas is usually complete.
- Scars and strictures of the esophageal, urethral,
vaginal, and anal mucosa rarely occur. In mucosa, not
skin.
- Severe eye complications (20%), such as purulent
conjunctivitis, anterior uveitis, scarring of the
conjunctiva, symblepharon, may result in permanent
blindness.

• Most common from viral HSV but not the only one
• Bacterial Mycoplasma Pneumoniae clues from
history: Elderly immunocompromised just came
back from hajj with a cough that is not responding
to antibiotics. We ask for CXR and HSV antibodies.

DX? Target-like lesions if blanchable most likely urticaria.

Erythroderma

- Erythro=red. Derma=skin. Causes of Erythroderma:

- its not a diagnosis but rather a clinical - Pre-existing dermatosis (psoriasis, eczema) 50%
presentation. - Drugs 15%
-Generalized redness and scaling of >90% of the - Lymphoma, leukemia 10%
skin surface. - Undetermined 25% Idiopathic
- Considered a serious, at times life-threatening
condition. Clinical features of erythroderma:
- It does not represent a disease but rather a - Erythema precedes exfoliation by 2-6 days.
clinical presentation of a variety of diseases. - Pruritis in 90% of patients. Remember that in TEN and SJS one
- M > F (avg age is ~50 yrs) of the main symptoms was pain NOT pruritis.
- Palmoplantar keratoderma. Thick palms and soles.
- Nail changes in 40%.
- Diffuse non-scarring alopecia.

Systemic manifestations:
- Generalized peripheral lymphadenopathy (50%).
- Pedal or pretibial edema in ~50% of patients.
- Tachycardia, risk of high output cardiac failure (esp. in the
elderly)
- Thermoregulatory disturbances (hyper-hypothermia).
Manifestations based on causative disease: Treatment:
1) Psoriasis: - First thing you need to ask is it psoriasis or lymphoma?
- Nail changes (Oil-drop, onycholysis, nail pits) - Psoriasis? Treat accordingly.
- Lymphoma? Chemo.
2) Atopic dermatitis:
- Otherwise give steroids.
- Pruritus is intense
- Hospitalization may be required.
- Lichenification
- Regardless of cause: Nutritional assessment, correction of fluid
3) Drug reactions: and electrolyte imbalance, prevention of hypothermia and tx of
- Morbilliform or scarlatiniform exanthem secondary infections.
4) Idiopathic erythroderma: - Idiopathic: Topical and systemic corticosteroids. Anti-
- Elderly men histamines.
- Lymphadenopathy and extensive palmoplantar - Treat the cause of erythroderma.
keratoderma. - If caused by psoriasis don’t give steroids as it might cause a
- Peripheral edema flare up.

5) CTCL: Cutaneous T-cell Lymphoma

- Sezary syndrome: Erythroderma, Malignant
(atypical) T lymphocytes and generalized
lymphadenopathy.
- Painful fissured keratoderma, diffuse alopecia,
leonine facies. Lion face.

• Describe the lesion: Scaling over diffuse erythema with

Extra picture sparing on some areas.
• Diagnosis: PRP
6) PRP: pityriasis rubra pilaris (papulosquamous)
• Examine lymph nodes for lymphadenopathy.
- Salmon to orange color, scaly black areas,
• Examine lower limbs for edema.
keratoderma on palms and soles.
• Examine heart for tachycardia and signs of heart failure.
- Follicular keratotic papules on the knees,
elbows and dorsal fingers. • Check temperature for hyper/hypothermia (remember
- Islands of sparing. that skin is important for thermoregulation).

• Sometimes during Psoriatic nail changes:

examination, you -Pitting.
might find clues to -Onycholysis.
the cause; an old -Oil spots.
eczematous lesion
or a psoriatic plaque
on the elbow
Questions:
1) A 4 years old child presented with macular scarlatiniform rash and sandpaper
rash. Nikolsky sign is positive. What is the diagnosis?
A. Kawasaki syndrome
B. Staphylococcal Scalded Skin Syndrome
C. Scarlet fever
D. Drug eruption
Answer: B

2) A 20 year old lady who is epileptic present with 2 days history of fever, sore
throat, malaise & painful cutaneous eruptions with dusky red color, 40% of
epidermal detachment & hemorrhagic crusts of the lips- One month back, the
epileptic medication was changed from valproate to carbamazepine- What is your
diagnosis?
A. TEN secondary to carbamazepine
B. SJS secondary to carbamazepine
C. SJS secondary to valproate
D. TEN secondary to valproate
Answer: A >30%

3) A patient known to have grand mal seizures, just started on carbamazepine. He

came to A/E with 1 week history of fever, malaise, target lesions and erythema and
areas of skin necrosis, with painful crusted lesions on lips. Body surface
involvement is 20%. What is the most likely diagnosis?
A. Steven johnson syndrome.
B. Toxic Epidermal Necrolysis.
C. Erythema Multiforme.
D. Erythrodermic psoriasis
Answer: B (Depends on surface area, this is most likely SJS TEN overlap)

4) 38 years old man referred to the on call dermatologist with a 2-day history of
sore throat, malaise and rash. Three weeks previously his antiepileptic medication
had been changed to carbamazepine, on examination less than 10% of the skin
surface is involved with erythematous, a typical target lesion on trunk, limbs and
face, cheilitis, oral ulcers, conjunctivitis and erosions of the urethra. What is the
most likely diagnosis?
A. Pemphigus vulgaris.
B. Toxic epidermal necrolysis
C. Stevens-Johnson syndrome
D. Erythema multiforme minor
Answer: C

5) Ten year old known to have epilepsy want to start carbamazepine, which HLA
typing
recommend be done before starting the treatment:
A. HLA-B1502
B. HLA-B1301
C. HLA-DCW4
D. HLA-B27
Answer:A