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Skin eruptions and

Reaction
นพ.ธีรยุทธ์ สินธวานุรักษ์

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Topic lists
• Urticaria
• Eczema and Dermatitis
• Papulosquamous diseases
• Vesiculobullous diseases
• Erythema multiforme
• Erythema nodosum

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Urticaria

• intensely pruritic, circumscribed, raised,


erythematous plaques, often with central
pallor: variable morphologies

• acute VS chronic

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Morphology
Cholinergic urticaria

Urticaria

Urticaria: dermatographism

Small urticarial papules on red skin (axon reflex


erythema) occurring on the neck within 30 minutes of
vigorous exercise.
Reproduced with permission from: Fitzpatrick, TB, Johnson, RA,
Wolff, K, et al. (Eds). Color Atlas and Synopsis of Clinical
Dermatology, 3rd ed, McGraw-Hill, New York, 1997. Copyright ©
1997 McGraw Hill.

These lesions of dermatographism developed 5 minutes


after stroking the skin with a wooden stick.
Reproduced with permission from: Fitzpatrick, TB, Johnson, RA,
Wolff, K, et al. (Eds). Color Atlas and Synopsis of Clinical
Urticaria is characterized by circumscribed, raised, Dermatology, 3rd ed, McGraw-Hill, New York, 1997. Copyright ©
erythematous, and extremely pruritic lesions. They 1997 McGraw Hill.
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Narcotics/opiates

Muscle relaxants (eg, succinylcholine)

Identifiable causes of urticaria


Causes Radiocontrast agents

Vancomycin

Infections Physical stimuli


Viral Dermatographism

Parasitic Delayed pressure

Bacterial Cold

IgE-mediated allergic cases Cholinergic

Medications Vibratory

Insects Aquagenic

Stinging (yellowjackets, bees, wasps, hornets, fire ants) Solar


Biting (Triatoma [kissing bugs])
Exertion/exercise
Foods
Miscellaneous mechanisms
Blood products (urticarial transfusion reaction)
Nonsteroidal antiinflammatory drugs
Latex (contact or inhaled)
Serum sickness
Contact allergens (animal saliva, raw foods)
Transfusion reactions (distinct from IgE-mediated reactions)
Aeroallergens (rare)
Hormone-associated (progesterone)
Food additives
Stinging nettle
Direct mast cell activation
Narcotics/opiates

Muscle relaxants (eg, succinylcholine)

Radiocontrast agents

Vancomycin

Physical stimuli
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Investigations

• Laboratory studies are normal in most


patients, although a complete blood count
with differential, a CRP or ESR, a TSH level,
and both antithyroglobulin and
antimicrosomal antibodies are suggested.
Biopsy of a fresh lesion is indicated in some
circumstances

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Other urticaria
Urticarial vasculitis

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Treatment (acute)

• mild symptoms of new onset urticaria:


nonsedating H1 antihistamine

• moderate to severe symptoms: add H 2


antihistamine

• severe, persist or angioedema: brief course of


steroid

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Treatment (chronic)
• step1: second generation H1 antihistamine
• step2: Increase dose
• step3: add first generation H1 antihistamine
• step4: Leukotriene modifier
• step5: antiinflammatory agents
• step6: immunosuppressants and
immunomodulatory Rx

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Eczema, Dermatitis

• Seborrheic dermatitis
• Contact dermatitis
• Dyshidrotic eczema
• Nummular eczema
• Atopic dermatitis

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Seborrheic dermatitis
Seborrheic dermatitis Seborrheic dermatitis

Typical involvement of the cheeks and nasolabial folds is This patient has involvement of the retroauricular area.
Reproduced with permission from: Goodheart, HP. Goodheart's
present. photoguide of common skin disorders, 2nd ed., Lippincott Williams
Reproduced with permission from: Goodheart, HP. Goodheart's & Wilkins, Philadelphia 2003. Copyright © 2003 Lippincott Williams
photoguide of common skin disorders, 2nd ed., Lippincott Williams & Wilkins.
& Wilkins, Philadelphia 2003. Copyright © 2003 Lippincott Williams
& Wilkins.

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Seborrheic dermatitis

• role of Malassezia
• association: HIV, Neurologic disorder
• predisposing factors
• Leiner’s disease
• treatment

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Contact dermatitis
Contact dermatitis due to neomycin

allergic contact dermatitis


Contact dermatitis due to nickel

This boy developed an eczematous eruption at the site


This contact dermatitis is secondary to neomycin in ear
where the nickel snap on his blue jeans contacted his
drops. skin.
Reproduced with permission from: Goodheart, HP. Goodheart's
Reproduced with permission from: Goodheart, HP. Goodheart's
photoguide
photoguide of common skin disorders, 2nd ed., Lippincott Williams of common skin disorders, 2nd ed, Lippincott Williams
& Wilkins, Philadelphia 2003. Copyright © 2003 Lippincott Williams
& Wilkins, Philadelphia 2003. Copyright © 2003 Lippincott Williams
& Wilkins.
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2010
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Contact dermatitis
Irritant contact dermatitis

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Dyshidrotic eczema

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Nummular eczema

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Atopic dermatitis

• Incident: 5-20% of children worlwide


• onset before 5 yrs in most of the cases
• 3 age group stage presentation (<2,
2-12, >12)

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AD: Pathogenesis

• Epidermal barrier permeability:


ceramide reduction due to upregulation of
sphyngomyelin deacylase, Filaggrin gene mutation,
Spink 5 def.(a serine protease that inhibit
sc.chymotryptic enz.) Epicutaneous sensitization

• Immune sensitivity
• Genetic
• Staphylococcous aureus

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papules (picture 5). In adults, the flexural areas (neck, antecubital fossae, and popliteal fossae) are most
commonly involved (picture 6); other common sites include the face, wrists, and forearms.

In severe cases, any area of the body can be involved, although it is uncommon to see lesions in the

AD: Diagnosis
axillary, gluteal, or groin area; lesions in these locations should prompt consideration of other diagnoses
such as psoriasis. The presence of pustules within areas of dermatitis suggests secondary infection with
Staphylococcus aureus.

DIAGNOSIS — Atopic dermatitis is diagnosed by observing its representative clinical features. The United
Kingdom working group on AD published criteria for diagnosing atopic dermatitis that include the following
[31]:

• Evidence of itchy skin, including the report by a parent of a child rubbing or scratching.

In addition to itchy skin, three or more of the following are needed to make the diagnosis:

• History of skin creases being involved. These include: antecubital fossae, popliteal fossae, neck, areas
around eyes, fronts of ankles.

• The presence of generally dry skin within the past year.

• Symptoms beginning in a child before the age of two years. This criterion is not used to make the
diagnosis in a child who is under four years old.

• Visible evidence of dermatitis involving flexural surfaces. For children under four years old, this
criterion is met by dermatitis affecting the cheeks or forehead and outer aspects of the extremities.

The UK working group's analysis excluded allergy criteria as originally proposed by Hanifin and Rajka. The
UK working group data have been validated by investigators from the Netherlands [33].

Laboratory testing, including IgE levels, are not used routinely in the evaluation of patients with suspected
atopic dermatitis, and are not currently recommended.

When the diagnosis is uncertain, we suggest that patients be referred to a specialist (eg, dermatologist,
allergist).

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Atopic dermatitis
Atopic dermatitis: infantile Atopic dermatitis: infantile

Confluent erythema, mircovesiculation, scaling, and Confluent erythema, mircovesiculation, papules, crust,
crusting on the face, with similar involvement (to a lesser and scale of a young Asian infant; the shoulders are
degree) on the trunk and arms. The facial involvement is relatively spared, being protected from scratching by
more severe due to easier access to scratching; the baby clothing.
Reproduced with permission from: Fitzpatrick, TB, Johnson, RA,
is squeezing the breast skin to relieve the intense
Wolff, K, et al (Eds). Color Atlas and Synopsis of Clinical
pruritus.
Dermatology, 3rd ed, McGraw-Hill, New York, 1997. Copyright ©
Reproduced with permission from: Fitzpatrick, TB, Johnson, RA,
McGraw-Hill.
วันจันทร์ท่ี 21 มิWolff,
ถน
ุ ายน K, et al (Eds). Color Atlas and Synopsis of Clinical
2010
Atopic dermatitis
Atopic dermatitis
Flexural atopic dermatitis

Severe atopic dermatitis in a 12-year-old girl showing in the


typical location of the popliteal fossae. Note the oozing of serous
fluid from the most involved areas, plus the papular component
and erythema.
Courtesy of Scott Walsh, MD, FRPCP.

Typical appearance of atopic dermatitis in flexura


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of the legs.
AD: Principles of Rx

• Avoid trigger factors:heat, perspiration, low


humidity

• Rx skin infection: Staph. aureus, Herpes


• Control itching: sedating antihistamine
• Rx stress and anxiety

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Psoriasis

• incidence: 1-3%
• onset: bimodal 20-30 and 50-60
• risk factors: genetic, obesity, smoking,
alcohol consumption

• trigger factors: physical trauma,


infection, medication (beta-blockers,
lithium, ACEI, NSAIDs), stress

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Psoriasis

• comorbidities: metabolic dis.(DM, HT),


cardiovascular dis.(MI, artherosclerosis),
increase risk of lymphoma (CTCL, Hodgkin’s
lymphoma)

• clinical presentation: plaque, guttate,


pustular, inversus, erythromderma, nail

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Psoriasis treatments
Localized disease

• Topical steroids
• Tar preparation (crude coal tar, LCD)
• Anthralin
• Calciprotriol

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Psoriasis treatments
• Oral treatment
• Methotrexate
• Retinoids
• Cyclosporin
• Phototherapy
• Biological treatment

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Pityriasis rosea
• acute, seft-limited eruption
• viral etiology?: HHV type6, 7
• Prodrome in few cases, Herald patch
• atypical presentation
• last 4-6 wks. (2-3 mo.)
• recurrent < 10%

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Pityriasis rosea

Pityriasis rosea anterior trunk

Note the herald patch (arrow) and crops of oval lesions


that tend to be oriented along the lines of cleavage of the
skin.
Courtesy of John T Crissey, MD.

The herald patch is visible below the nipple


Courtesy of John T Crissey, MD.
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Lichen planus
• middle aged adult
• last 1-2 yrs., (longer for oral lesions)
• skin, nails, mucous membrane
• pruritic polygonal flat-toped papules,
Wickham’s striae, Koebner’s
phenomenon
• variants: vesiculobullous,
hypertrophic, lichen planopilaris

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Lichen planus

• Drug induced: beta blockers,


methyldopa, penicillamine, quinidine,
NSAIDs, ACEi, sulfonylurea,
carbamazepine, gold, lithium, quinine
• HCV association?
• oral lesion: malignant transformation?

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Lichen planus

• Treatments: topical/ systemic


steroids, retinoids, topical calcineurin
inhibitors, immunosuppressive,
immunomodulators

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Koebner reaction in lichen planus

Patients with lichen planus can exhibit the Koebner


Lichen planus
reaction, in which lesions develop in areas of trauma. In
this patient, the Koebner reaction resulted from
scratching.
Reproduced with permission from: Goodheart, HP. Goodheart's
Photoguide of Common Skin Disorders, 2nd ed, Lippincott Williams
& Wilkins, Philadelphia 2003. Copyright © 2003 Lippincott Williams
& Wilkins.

Lichen planus. Flat-topped, violaceous, polygonal papules


on the flexor wrists are present. There are active and
resolving lesions. Note the postinflammatory
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Hypertrophic lichen planus. Darkly pigmented
hypertrophic lesions are present on the pretibial shaft.
Reproduced with permission from: Goodheart, HP. Goodheart's
Photoguide of Common Skin Disorders, 2nd ed, Lippincott Williams
& Wilkins, Philadelphia 2003. Copyright © 2003 Lippincott Williams
& Wilkins.

Lichen planus

Lichen planus of the nail may present with nail plate


thinning, longitudinal ridging (trachyonychia), fissuring,
and rarely, pterygium. Nail plate thinning and
longitudinal ridging are visible on this patient's nails.

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Oral lichen planus

Penile lichen planus


Lichen planus. Oral lesions with a white, lacy pattern and
an erythematous erosion are present on the buccal
mucosa.
Reproduced with permission from: Goodheart, HP. Goodheart's
Photoguide of Common Skin Disorders, 2nd ed, Lippincott Williams
& Wilkins, Philadelphia 2003. Copyright © 2003 Lippincott Williams
& Wilkins.

Lichen planus. Wickham's striae are visible.


Reproduced with permission from: Goodheart, HP. Goodheart's
Photoguide of Common Skin Disorders, 2nd ed, Lippincott Williams
& Wilkins, Philadelphia 2003. Copyright © 2003 Lippincott Williams
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Pemphigus

• Pemphigus vulgaris
• Pemphigus foliaceus
• Paraneoplastic pemphigus

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Pemphigus vulgaris

• rare: 0.7:100,000, median age: 71


• IgG against Dsg.1 and Dsg.3
• clinical: flaccid bullae over scalp, face,
trunk, oral mucosa
• Dx: histology, immunofluorescent,
ELISA

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Pemphigus vulgaris

Histologic specimen of a bullous lesion in a patient with


pemphigus vulgaris demonstrates the characteristic loss
of cohesion between epidermal cells (acantholysis) with
an intact basement membrane.
Courtesy of Beth G Goldstein, MD and Adam O Goldstein, MD.

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Pemphigus foliaceus

• more superficial (erosion), no mucosal


involvement
• anti-Dsg1 (like exfolatoxin A in 4S)
• special form: fogo selvagem, drug
induced (penicillamine, piroxicam,
captopril, imiquimod)

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Pemphigus foliaceous is characterized by erythema,
scaling, and crusting that first appears on the face and
scalp, and later involves the chest and back.
Reproduced with permission from: Bystryn, J, Ruldolph, J.
Pemphigus. Lancet 2005; 266:61. Copyright © 2005 Nicholas
Soter, MD. Reproduced in Lancet with permission from: the New
York University Department of Dermatology.

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Paraneoplastic
pemphigus
• lymphoreticular tumors eg.
lymphoma, CLL.
• anti Dsg1, anti Dsg3, anti Plakin
• not related to tumor activity
• more sever oral lesions with atypical
mucosal lesions

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Paraneoplastic pemphigus 2

An erosive mucositis was followed by a diffuse symmetric


lichenoid papular eruption. Mucous membrane and
cutaneous lesions cleared when his Castleman tumor was
removed.
Copyright © Chris Ha, MD, Dermatlas; http://www.dermatlas.org.
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Pemphigus Rx
• Systemic glucocorticoids
• Steroid sparings: azathioprine,cyclophosphamide,
dapsone

• anti TNF: sulfazalazine, pentoxyfylline, infliximab,


etanercep

• plasmapheresis
• IVIG
• others:mtx, dapsone, Csp, gold,hydroxychloroquine
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Bullous pemphigoid

• more common (4.3:100,000), 60 yrs


or older
• autoantibody to plakin protein: BP230
(BPAG1) and BP180 (BPAG2)
• BP180 relate to disease activity

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Bullous pemphigoid

• variant: pemphigoid gestationis (late


pregnancy, no fetal risk, affect
subsequent pregnancy)

• variant: cigatricial pemphigoid (oral,


conjunctival, larynx, esophagus, rectal
mucosa; integrin ab., epiligrin ab.)
• drug induced: penicillamine, furocimide

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Bullous pemphigoid

• flexural, groin, axillar, urticarial


lesion, oral lesion in 1/3, pruritus
• diagnosis: clinicals, biopsy,
immunofluorescence, salt-split skin,
ELISA

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Bullous pemphigoid

• treatment: topical, systemic steroid


• steroid sparing: azathioprine, mtx.,
cyclophosphamide, dapsone,
tetracyclin
• prognosis: 50% remission in 2-6 yrs.

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Bullous pemphigoid path

Bullous pemphigoid direct immunofluorescence

Bullous pemphigoid. A subepidermal blister has an


edematous papillary dermis as its base. The roof of the
blister consists of the intact entire epidermis, including
the stratum basalis. Inflammatory cells, fibrin, and tissue
fluid fill the blister.
Reproduced with permission from: Rubin, E, Farber, JL. Pathology,
3rd ed, Lippincott Williams & Wilkins, Philadelphia 1999. Copyright
©1999 Lippincott Williams & Wilkins.

Bullous pemphigoid. Direct immunofluorescence


microscopy reveals linear deposits of C3 and IgG along
the basement membrane zone.
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Bullous pemphigoid

This 82-year-old female with bullous pemphigoid


exhibited pruritic, tense bullae with underlying erythema
on the arms, trunk, and legs.
Copyright © Katsuya Hisamichi, MD, Dermatlas;
http://www.dermatlas.org.
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Cicatricial pemphigoid

The hallmark of ocular cicatricial pemphigoid (OCP) Cicatricial


is pemphigoid
inferior forniceal foreshortening.
Reproduced with permission from: Tasman, W, Jaeger, E. The Wills
Eye Hospital Atlas of Clinical Ophthalmology, 2ed, Lippincott
Williams & Wilkins 2001. Copyright ©2001 Lippincott Williams &
Wilkins.

Severe symblepharon formation can create adhesions


between the eyelid and cornea.
Reproduced with permission from: Tasman, W, Jaeger, E. The Wills
Eye Hospital Atlas of Clinical Ophthalmology, 2ed, Lippincott
Williams & Wilkins 2001. Copyright ©2001 Lippincott Williams &
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Erythema multiforme

• age: adolescent, young adult


• male:female = 3:2
• recurrent rate 30%
• association: HSV1, M.pneumoniae
• clinical: EM minor, EM major, Herpes
associated EM, Mucosal EM

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Immunofluorescence findings are negative or non-specific. In advanced lesions sub-epidermal blister formation may
occur, but necrosis rarely involves the entire epidermis (see eFig. 38-7.1). In late lesions, melanophages may be
prominent.

Figure 38-7

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like erythematous papule or plaque that persists for 1 week or longer (Fig. 38-2). It measures from a few millimeters to
approximately 3 cm and may expand slightly over 24 to 48 hours. Although the periphery remains erythematous and
edematous, the center becomes violaceous and dark; inflammatory activity may regress or relapse in the center, which
gives rise to concentric rings of color (see Fig. 38-2). Often, the center turns purpuric and/or necrotic or transforms into
Erythema
a tense vesicle or bulla. The result is the classic target or multiforme major. Involvement of the lips with a target pattern.
iris lesion.

Figure 38-2 Figure 38-4

Typical target lesions on the palm.


Multiple concentric vesicular rings (herpes iris of Bateman). This pattern may be more frequent i
According to the proposed classification, typical target lesions consist of at least three concentric components: (1) a
dusky central disk, or blister; (2) more peripherally, an infiltrated pale ring; and (3) an erythematous halo. Not all

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lesions of EM are typical; some display two rings only ("raised atypical targets"). However, all are papul
with macules, which are the typical lesions in SJS-TEN. In some patients with EM, most lesions are livid
overlying a just slightly darker central portion, encircled by an erythematous margin (Fig. 38-3). Larger
have a central bulla and a marginal ring of vesicles (herpes iris of Bateman) (Fig. 38-4).

Figure 38-3

Erythema multiforme major. Involvement of the lips with a target pattern.

Figure 38-4

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the throat, larynx, and even the trachea and bronchi.

Figure 38-5

Erythema multiforme major (EMM). Mouth lesions of EMM usually manifest as erosions.

Eye involvement begins with pain and bilateral conjunctivitis in which vesicles and erosions can occur (Fig. 38-6).

Figure 38-6

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Erythema nodosum

• 1-5/100,000, more in women 15-40 yr


• delayed hypersensitivity reaction to
antigen associated with infection,
drug, and other diseases
• tender subcut.nodules on shins,
thighs, trunk, upper extremities

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Septal panniculitis

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Courtesy of Richard S Panush, MD.$$
/%,)$(%/&$1(#$("(0+..),*#2(1#0,*#3&,#/$(/$(,-)(')405(6-)(
$/1&')0(2"$("'0/("77)"*(,/(3)(7#4.)$,)15(
Courtesy of Lee T Nesbitt, Jr. The Skin and Infection: A Color Atlas
and Text, Sanders, CV, Nesbitt, LT Jr (Eds), Williams & Wilkins,
Baltimore. 1995.((
วันจันทร์ท่ี 21 มิถน
ุ ายน 2010
EN: association

• streptococcal infection, leprosy,


medication (omeprazole, HBV
vaccine, OCP, isotretinoin, leukotriene
receptor antagonist: montelukast),
idiopathic
• investigation: CBC, LFT, chest x-ray,
ASO, tuberculin skin test

วันจันทร์ท่ี 21 มิถน
ุ ายน 2010
EN: association
Conditions that may present with erythema nodosum and hilar adenopathy

"#$%&'(&)')!*+',#-.$#,!#/0,.!'/1&,1.2./-!'/!2&)-!%#).)3!41.'-')!5$#%-'%#,,6!('#7/&)-'%8

94+.$%4,&)')!*&%%4$)!'/!5$'2#$6!'/:.%-'&/8

;&%%'('&'(&26%&)')!*5$&2'/./-!%#4).!'/!./(.2'%!#$.#)8

<')-&5,#)2&)')!*)477.)-.(!+6!.5'(.2'&,&7'%!:#%-&$)=!+4-!#,)&!->.!%&/%4$$./-!5$.)./%.!&:!.$6->.2#!24,-':&$2.8

?,#)-&26%&)')!*#%%&25#/'.(!+6!$.)5'$#-&$6!)625-&2)!#/(!->.!5$.)./%.!&:!,4/7!5#$./%>62#,!$#('&,&7'%!:'/('/7)8

@.$)'/'&)')!*5$&+#+,6!$#$.!&4-)'(.!&:!A&$->.$/!B4$&5.8

;>,#26('#!5/.42&/'#.!*4)4#,,6!#%%&25#/'.(!+6!$.)5'$#-&$6!)625-&2)8
!

วันจันทร์ท่ี 21 มิถน
ุ ายน 2010
EN: association

Conditions that may cause erythema nodosum in association with gastrointestinal


symptomatology

"#$%&''&()*+!,)-.%!/01.&1.!2.*+(3.'&!#)/)14'!414&%%+!)554*1!0#!(3.!1.((0#6!)$!6&1(*)0#(.1(0#&%!/01.&1.!&5(070(+8

9.35.(:1!/01.&1.!2)54%&*;)*);6.#0(&%!4%5.*18

<.*10#0&!.#(.*)5)%0(05&!25&#!'0'05!0#$%&''&()*+!,)-.%!/01.&1.!)*!)554*!-0(3)4(!6&1(*)0#(.1(0#&%!5)'=%&0#(1>!
=*),&,%+!*&*.!)4(10/.!)$!?)*(3.*#!@4*)=.8

A&%')#.%%&B!5&'=+%),&5(.*B!1306.%%&!2/0&**3.&!&%-&+1!=*.1.#(8

C&#5*.&(0(01!21D0#!%.10)#1!414&%%+!.&10%+!/01(0#64013./!$*)'!(+=05&%!.*+(3.'&!#)/)14'B!&#/!7.*+!*&*.%+!)554*1!0#!
&/7&#5.!)$!.1(&,%013./!/0&6#)101!)$!=&#5*.&(0(018
!

วันจันทร์ท่ี 21 มิถน
ุ ายน 2010
EN: treatment

• symptomatic treatment
• NSAIDs
• KI
• glucocorticoids

วันจันทร์ท่ี 21 มิถน
ุ ายน 2010

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