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Medical
Dermatology
• Pruritus & Urticaria
• Drug Eruptions
• Other Common Rashes
• Recognize & Refer
Nishit Patel, M.D.
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CONFLICTS OF INTEREST
• No Relevant Conflicts
Special Thanks to Leigh Ann Scalf, MD
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OBJECTIVES
• Learn to diagnose and manage pruritus without a primary
eruption
• Diagnosis and treatment of urticaria
• Identify features of common drug eruptions
• Identify drug rashes that constitute dermatologic emergencies
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OVERVIEW
Pruritus = “Itching”
Urticaria = “Hives”
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PRURITUS WITHOUTPRIMARY LESIONS
In other words…”just itching and scratching.”
So, now what??
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COMMON PRESENTATION
Butterfly area over scapulae often spared because the
patient cannot reach the area to scratch.
Beware: some patients are very flexible and CAN reach
this area!!
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“BY THE BOOK”
The million dollar work-up can be
found in any text book
But….
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PRACTICAL PRURITUS WORK UP
CBC (anemia)
LFT (Hepatic dysfunction)
BUN/Cr (Renal dysfunction)
TSH (Hypothyroidism)
ANA (Lupus)
CXR (Cancer)
All “age appropriate” cancer screenings
Get a complete “ROS”
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URTICARIA
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GROUPING OF URTICARIA
• Acute Urticaria (<6 wks)
• Cause
• 50% idiopathic/unknown
• 40% Upper respiratory tract
infections
• 9% drug reaction
• 1% food related
• Prognosis – Excellent, usually resolves
within days to weeks
• Chronic Urticaria (>6 wks)
• Cause
• 60% - idiopathic/unknown,
autoimmune, infection related
• 35% physical urticaria
• 5% urticarial vasculitis
• Prognosis – 50% of patients with
chronic urticaria will resolve in 1 year.
Can be very difficult to manage.
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URTICARIA / ANGIOEDEMA
Pruritic wheals
Individual
lesions
disappear
within 24 hours.
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DERMATOGRAPHISM
https://upload.wikimedia.org/wikipedia/commons/thumb/4/42/Dermatographic_urticaria.jpg/1200px-
Dermatographic_urticaria.jpg
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May be associated with:
Angioedema
Anaphylaxis with
bronchospasm,
laryngospasm, or
hypotension
URTICARIA / ANGIOEDEMA
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If the patient gives a history of anaphylaxis (throat swelling, difficulty breathing):
Give Rx for Epi-Pen (Twin Ject) and “Emergency Plan”
Refer to Allergist
URTICARIA / ANGIOEDEMA
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URTICARIA / ANGIOEDEMA
Immunologic
Most commonly associated with penicillin and beta-
lactam antibiotics
Nonimmunologic
Aspirin and NSAIDS are the most common causes.
Also caused by radiocontrast. (*Pre-testing does NOT
exclude the possibility of an anaphylactoid reaction to radiocontrast.)
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ACE inhibitors can cause angioedema
African Americans at nearly 5
times greater risk than caucasians
Lisinopril and enalapril > captopril
Blockade of kininase II by ACE
inhibitors may increase the tissue
kinin levels, thus enhancing
urticarial reactions and
angioedema.
URTICARIA / ANGIOEDEMA
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OTHER “URTICARIAS”
• Physical Urticaria
• Urticarial Vasculitis
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“EMPHASIS ON TREATMENT…”URTICARIA
• Anti-Histamines (non/low-sedating), over-the-counter
• Loratidine (Claritin), Cetirizine (Zyrtec), Fexofenadine (Allegra), Levocetirizine
(Xyzal)
• Anti-Histamines (non/low-sedating), prescription only
• Desloratidine (Clarinex) 5mg daily (AM or PM)
• Anti-Histamines (sedating, use at night only)
• Diaphenhydramine (Benadryl) 25mg (at bedtime)
• *Hydroxyzine (Atarax) 10mg/25mg/50mg (at bedtime)
• *Doxepin 10mg/25mg (at bedtime)
• Additional Tx Considerations:
• *Anti-Histamines (H2- Blockers), Prednison, *Montelukast (Singulair),
Omalizumab (Xolair)
* off label usage
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EMPHASIZE TRIGGER AVOIDANCE
• Avoid NSAIDs (non-steroidal anti-inflammatory
medicationsAspirin, Ibuprofen (Motrin), Aleve (naproxen),
Meloxicam, Celebrex, etc.
• Avoid triggers of mast-cell degranulation (histamine release)
• Medications = Opioids (narcotic pain medications), contrast dyes
(radiology imaging), anticholinergic medications, polymyxin B sulfate (
in topical antibiotics)
• Heat/friction
• Alcohol
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OTHER WORKUP TO CONSIDER
• CBC
• CMP
• ESR
• ANA
• TSH
• IgE
• C3, C4
• C1-Inh
(qualitative/quantitative)
• C1q
• Anti-C1q
• CH50
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PEARLS
1) Pruritus without primary lesions should be worked up to rule out any underlying etiology.
2) Urticaria: Individual lesions disappear within 24 hours.
3) Immunologic urticaria: Most commonly associated with penicillin and beta-lactam antibiotics
4) Non-immunologic urticaria: Aspirin and NSAIDS are the most common causes.
5) Antihistamines are the mainstay of treatment for urticaria.
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Drug Eruptions
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DRUG ERUPTIONS, OVERVIEW
Extremely diverse
Almost any drug may be capable of
producing a reaction.
A certain drug may also cause several
different reaction patterns in different
patients.
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IN GENERAL…DRUG ERUPTIONS
Most occur within days to weeks after beginning
the offending agent
Occasionally a reaction begins after long-term use
of a particular drug
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**MORBILLIFORM (AKA: EXANTHEM-LIKE, MACULAR AND PAPULAR, SCARLETINIFORM) ERUPTIONS ARE THE MOST FREQUENT OF
ALL CUTANEOUS REACTIONS TO DRUGS
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EXANTHEMS
“MORBILLIFORM” OR
“SCARLETINIFORM” REACTIONS
Pruritus common
Usually occur with in first 2 weeks of
treatment
Usually start proximally (groin/axillae),
then generalize within 1-2 days
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PATHOGENESIS
NON-IMMUNOLOGIC
IMMUNOLOGIC
*Drug reactions :
-not simply drug allergy
-may result from variations in drug metabolism, immune status, coexistent diseases, and other co-administered medications.
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EXANTHEM-LIKE ERUPTIONS
Most common culprits:
Penicillins
Cephalosporins
Sulfonamides
Carbamazepine
Hydantoins
Allopurinol
Gold
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“EMPHASIS ON TREATMENT…”
“Simple exanthems”(skin only!)
Supportive care
stop offending med, topical steroids, antihistamines
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FIXED DRUG ERUPTION
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FIXED DRUG ERUPTION
Adverse reaction to an ingested drug
Usually solitary
Plaque, bulla, or erosion
Upon rechallenge, FDE occurs at identical site within hours of ingestion
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FIXED DRUG ERUPTION
Usually asymptomatic
May be pruritic or burning
Painful if eroded
Post-inflammatory pigmentary alteration (PIPA) remains between flares – usually hyperpigmentation.
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MOST COMMONLY IMPLICATED DRUGS:
Phenolphthalein
Antimicrobials Tetracyclines
Sulfonamides
Psychoactive agents
Anti-inflammatory agents
OCPs
Quinine
Pseudoephedrine (Sudafed)
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FIXED DRUG ERUPTION
Treatment:
identify and stop offending drug
Non-eroded: potent topical steroid
Eroded: bacitracin or silvadene
PIPA (dermal melanin) does NOT
respond to hydroquinone therapy
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GOOD RASH GONE BAD!
Occasionally, exanthem-like eruptions are
associated with:
Interstitial nephritis
Hepatitis
Lymphadenopathy
So, don’t forget to do a
thorough history and physical!
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1) Drug reactions are DIVERSE.
2) Certain drugs are more likely to produce certain reactions.
3) The most common drug reaction is a moribilliformeruption.
4) Simple “skin-only” exanthems require supportive care…stop offending medication, topical steroids, antihistamines.
5) There can be systemic involvement. *Do a thorough history and physical!!
6) Fixed drug eruptions recur in the same location upon re-exposure to the offending agent
“GOOD RASH” PEARLS
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OTHER COMMON RASHES
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Image from: https://www.merckmanuals.com/-/media/manual/professional/images/4812-pityriasis-rosea-herald-patch-public-
health-image-library-high.jpg?la=en&thn=0
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• A self-limited papulosquamous eruption that is
occasionally pruritic
• Seen mainly in adolescents and young adults, favoring the
trunk and proximal extremities
• Individual lesions are usually oval in shape and their long axis
is oriented along the lines of cleavage
• Less common variants include inverse, vesicular, purpuric and
pustular
PITYRIASIS ROSEA
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Pathogenesis
? Viral etiology
Focus on human herpesvirus-7 (HHV-7) and, less so, on HHV-6
Some studies have shown no difference in prevalence of DNA from HHV-6 or HHV-7 in pts
w PR
Support for viral etiology: prodromal symptoms experienced by some, clustering of cases,
and almost complete absence of recurrent episodes, suggesting immunologic defense against
infectious agent
Epidemiology
Female > male
Affects otherwise healthy adolescents and young adults
Typical eruption lasts 6-8 weeks, then resolves spontaneously
May occasionally last > 5 months
? Slight seasonal variation
PITYRIASIS ROSEA
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“Herald Patch” Large skin- to pink- to salmon-colored patch or plaque with slightly raised
advancing margin Center – fine scaling (like other lesions) Margin - larger, more obvious trailing collarette of scale with the free edge pointing
inwards
Often on trunk, precedes other lesions by hours to days Seen in ~50% of cases
~5% of pts experience a mild prodrome
PITYRIASIS ROSEA - CLINICAL
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Other lesions
Similar to herald patch but smaller
Rapidly appear, usually on trunk and proximal extremities
Long axis following Langer's lines of cleavage “Christmas tree” pattern on back
More papular and hyperpigmentedin pts w/ skin of color
May be pustular initially
Face, palms and soles usually spared
PITYRIASIS ROSEA - CLINICAL
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Pruritus in ~25% of pts
Atypical forms of pityriasis rosea
Inverse - axillae and inguinal areas;
sometimes the face
More common in younger children and in
those with darkly pigmented skin
Other: urticarial, erythema multiforme-
like, vesicular, pustular and purpuric
variants
PITYRIASIS ROSEA - CLINICAL
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Treatment
Patient education and reassurance
Pruritis
Counterirritant antipruritic lotions
Low- to medium-strength topical corticosteroids
Severe cases
UVB – reduces severity of PR but not duration or pruritus
Antihistamines
Short course oral steroids
PITYRIASIS ROSEA - CLINICAL
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ERYTHEMA ANNULARECENTRIFUGUM (EAC)
• Erythema Annulare Centrifugum (EAC)
• Applies to a broad spectrum of clinical findings, “default” diagnosis
• Peak age: 40s
• No known gender difference
• Can last days-decades
• Possibly represents a reaction pattern or hypersensitivity to one of
many Ag’s
• Dermatophytes, candida, other fungi, viruses (pox, EBV, VZV,
HIV), drugs, food, pregnancy, AI endocrinopathies,
hypereosinophilic syndrome, neoplasms
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CLINICAL
• Initial lesions: firm, pink papules that expand centrifugally & develop central clearing
• Can grow to >6cm over 1-2 wks
• Superficial gyrate erythema:
• Minimally elevated
• Central trailing scale (sometimes vesicles @ outer edge)
• +/- pruritus
• Deep gyrate erythema:
• Advancing edge elevated & usually no associated scale
• Majority are non-pruritic
• No scarring, but can get PIH
• Lesions last weeks-months
• No systemic sx’s
• Rare on palms, soles, scalp, mucous membranes
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EAC
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DIFFERENTIAL AND TREATMENT
• DDx: tinea corporis, annular psoriasis, annular urticaria,
allergic urticarial eruption, cutaneous lymphoid hyperplasia,
lymphoma cutis, linear IgA bullous dz, Sjogren’s, LE
• TREATMENT:
• Resolves if underlying d/o is responsible & treated
• Topical steroid to advancing edge
• Tacrolimus, calcipotriol, oral metronidazole, etanercept
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STASIS DERMATITIS
• Disease of adults
• Eruption of lower extremities
• Can see concomitant edema, brownish hyperpigmentation
• Most common site is medial malleolus
• Pathogenesis:
• Venous htn →distension of capillaries → incr permeability → fluid, proteins, RBCs in tissue → protein (fibrin) around blood vessels inhibit O2 diffusion; activation of PMNs & Mφ; release of inflamm mediators; plt accum (focal thrombosis) → fibrosis & tissue remodeling
• Treatment: leg elevation, support stockings, topical steroids, Aluminum acetate compresses
• Higher risk of ACD sensitization with topical antibiotic application
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STASIS DERMATITIS
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• Complicating pathogenic factors: contact (58%-86%) and irritant dermatitis
• Lipodermatosclerosis- progressive induration occurs over years-inverted wine bottle appearance
• Tx: compression stockings/ bandages; exercise calf muscles; venous surgery; wound dressings, topical steroids and emollients
STASIS DERMATITIS
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• Erythematous to skin-colored, sometimes purple–brown or yellowish, waxy indurated nodules or plaques with classic peaud’orange
• Painful, pruritic
• Location: anterolateral aspect of the lower legs or feet
• Non-pitting
• Hypertrichosis and hyperhidrosis
LOCALIZED (PRETIBIAL) MYXEDEMA: CLINICAL
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LOCALIZED (PRETIBIAL) MYXEDEMA
• Induration of the shins due to mucin deposition
• Mucin production stimulated by a serum factor unrelated to
thyroid-stimulating Ig’s
• Associated w/ hyperthyroidism
• Especially Graves disease (1-5% of pts w/ Grave’s)
• W/ exopthalmous (25%)
• May also appear in hypothyroid state following treatment of
Graves
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DDx LSC, hypertrophic LP, lymphedema, obesity-associated
lymphedematous mucinosis, and elephantiasis
Tx Corticosteroids (topically or intralesionally)
Especially if symptomatic
Other: plasmapheresis, gradient pneumatic compression, IVIg, and octreotide
Treating the hyperthyroidism does NOT improve the cutaneous lesions
May clear spontaneously (after an average of 3.5 years)
LOCALIZED (PRETIBIAL) MYXEDEMA
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RECOGNIZE & REFER
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Images from:
• https://www.mayoclinic.org/-/media/kcms/gbs/patient-consumer/images/2013/08/26/10/41/ds00722_im02463_r7_bullouspemphigoidthu_jpg.jpg
• https://jamanetwork.com/data/Journals/DERM/11776/dob40010f1.png
• https://www.dermnetnz.org/topics/bullous-pemphigoid/
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BULLOUS PEMPHIGOID
• Most common subepidermal blistering
disease
• Affects elderly, rarely children
• 90 yo’s have 300X risk of developing
compared to 60 yo’s
• Men>women
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Images from: Dermatology by Jean L., M.D. Bolognia, Joseph Jorizzo, Ronald Rapini C.V. Mosby (June 1, 2003)
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BULLOUS PEMPHIGOID: CLINICAL FEATURES
• Early non-bullous phase
• Nonspecific, pruritus, eczematous, excoriated eruptions, urticarial lesions
• Weeks to months
• May be the only signs of the disease
• Bullous phase
• Erythematous urticarial lesions + tense vesicles/bullae on
normal/erythematous skin
• Symmetrical, predominately on flexural areas and lower trunk
• May form vegetating plaques in intertriginous areas
• Blisters resolve with PIPA, and milia rarely
• Oral involvement in 10-30%
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Images from:
• https://www.facingacne.com/wp-content/uploads/2012/01/Pemphigus-vulgaris.jpg
• https://i.pinimg.com/originals/3f/54/b4/3f54b4e8e3e78d5c4e03b7e3d7fbaeac.jpg
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PEMPHIGUS FOLIACEUS
Images from: https://www.dermquest.com/imagelibrary/large/10559-IMG_9023.JPG
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PEMPHIGUS VULGARIS & FOLIACEUS
• Pemphigus = autoimmune disease of IgG antibodies against keratinocyte
cell surface
• Results in loss of cell-cell adhesion of keratinocytes acantholysis
intraepidermal blisters
• P. vulgaris and P. foliaceus
• Mean age: 50-60 y/o
• Men = women
• 0.76 to 5 per 1,000,000 new cases per year
• Higher in Jewish and Hispanic descendants of the conversos (SW USA)
• 16 to 32 per 1,000,000
• P. vulgaris is more common than P. foliaceus
• Except in Brazil, Finland, and Tunisia
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REFERENCES
Habif: Clinical Dermatology, 4th ed. 2004 Mosby, Inc.
www.dartmouth.edu
Dermatology by Jean L., M.D. Bolognia, Joseph Jorizzo, Ronald Rapini C.V. Mosby (June 1, 2003)
Contact & Occupational Dermatology by James G. Marks, et al (January 15, 2002)
www.aad.org
Fitzpatrick's Color Atlas & Synopsis of Clinical Dermatology by Klauss Wolff, Richard. A. Johnson, Richard Suurmond
Fitzpatrick's Dermatology in General Medicine by Irwin M., Md. Freedberg (Editor), Arthur Z. Eisen (Editor), Klaus Wolff (Editor), K. Frank Austen (Editor), Lowell A. Goldsmith (Editor), Stephen I. Katz (Editor), Thomas B. Fitzpatrick (Editor)