NON-SCALY PLAQUESGroup 2Sy A, Sy J, Sydiongco, Tacata, Tady, Tamondong, Tan E, Tan G, Tan M, Tan S

FIXED DRUG ERUPTION

SY, Aaron Keefe S.

FIXED DRUG ERUPTION

recur at the same site with each exposure to medications

Six or fewer lesions occur, frequently one

May be present anywhere on the body, but half occur on the oral and genital mucosa

Clinical Features Begins as a red patch Evolves to an iris or target

lesion identical to erythema multiforme that may eventually blister and erode

Lesions of genital and oral mucosa presents as erosions

Most lesions are 1 to several cm in diameter.

New lesions may be added with continiued /repeated ingestion of the medication.

Pathophysiology Exact mechanism is

unknown Recent research suggests a

cell-mediated process that initiates both the active and quiescent lesions.

Lesion contain intraepidermal CD8+ T-cells with the phenotypic markers of effector memory T-cells.

Skin-resident T-cells rapidly produce IFN-γ on exposure to medication.

Histologic Features• An interface dermatitis

occuring with intraepidermal and subepidermal vesicle formation, necrosis of keratinocytes and a mixed superficial and deep infiltrate of neutrophils, eosinophils, and mononuclear cells.

• Stratum corneum is normal in acute stage.

• Papillary dermal fibrosis and deep perivascular pigment incontinence are commonly present from prior episodes.

Etiologic Agents

Medications usually taken intermittently.

NSAIDS, esp. Pyrazole derivatives, Paracetamol, Naproxen, Oxicams, & Mefenamic Acid – predilection for the lips

Sulfonamides, Trimethoprim or the combination – resp. for majority of genital fixed drug eruptions

Possible Etiologic Agents

Include: Barbiturates Tetracyclines Phenolphthalein

(in laxative) Acetaminophen Ceterizine Celecoxib

Dextromethophan Hydroxyzine Lamotrigine Phenylpropanolam

ine Erythromycin Chinese &

Japanese herbs

Patch Testing needed to determine

which drug may be involved

Patch tests with various concentrations of the offending medication can reproduce the lesion on an affected but not unaffected skin.

Most useful in pyrazolone derivative-related reactions.

Nonpigmenting Fixed Drug Eruption

large, tender, often symmetrical eythematous plaques

Resolve completely within weeks.

Pseudoephedrine hydrochloride – most common cause

Baboon Syndrome – buttocks, groin, axilla

Treatment Main goal - identify the causative agent and avoid

it. Lesions of fixed drug eruption resolve

spontaneously with avoidance of the inciting drug.

ERYSIPELASSy, Jamelle D.

ERYSIPELASSt. Anthony’s fire / ignis

sacer

an acute beta-hemolytic group A streptococcal infection of the skin involving the superficial dermal lymphatics

group B – perineal erysipelas

ERYSIPELAS

local redness, heat, swelling, & a highly characteristic raised, indurated border

PMN leukocytosis skin lesions: transient

hyperemia vesicles or bullae

legs and face are the most frequent sites affected

ERYSIPELAS

• septicemia, deep cellulitis, or necrotizing fasciitis

complications:

• operative wounds, fissures, abrasions or scratches, unclean tying of the umbilical cord, venous insufficiency, obesity, lymphedema, and chronic leg ulcers

predisposing causes:

• contact dermatitis from plants, drugs, or dyes, and with angioneurotic edema

may be confused with:

TREATMENT

Pharmacologic

• Vigorous antibiotic therapy for at least 10 days

• systemic penicillin

• erythromycin

Non-pharmacologic

• Ice bags and cold compresses

CELLULITISSydiongco, Paula

Diffuse suppurative inflammation of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin

Malaise, chills, fever, and toxicity may occur

Lymphangitis, regional lymphadenopathy, or both may be present

In severe cases, patients may develop hypotension and area infiltrated and pits on pressure

No racial and sex predilection

No age predilection; individuals older than 45 years

• Facial cellulitis is more common in children younger than 3 years.

• Perianal cellulitis is predominantly a disease of children.

Site of infection may occur anywhere on the body, but the leg is the most common site of the infection, followed by the arm, and then the head and neck areas. • following surgery or trauma

wounds, cellulitis can develop in the abdomen or chest areas.

• morbid obesity, it can also develop in the abdominal area

Incubation• 24 hours or can take days to

develop.Duration• less than a week to

disappear with antibiotic therapy.

• months to resolve completely in more serious cases and can result in severe debility or even death if untreated.

• Not properly treated, it may appear to improve but can resurface months or even years later.

break in the skin such as a fissure, cut, laceration, insect bite, or puncture wound

Risk factors: tinea pedis; elderly and those with immunodeficiency; diabetic people; Immunosuppressive drugs; Chickenpox and shingles; chronic venous insufficiency and varicose veins; pregnancy and obesity

Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis

The vast majority of cases are caused by Streptococcus pyogenes or Staphylococcus aureus

Cellulitis• S pyogenes

• Immunocompetent adults• Perianal cellulitis (children)

• perianal erythema and pruritus, purulent secretions, painful defecation, and bleeding in the stools

• S aureus• Children

• Pasteurella multocida• dog or cat bite or scratch

• Pseudomonas aeruginosa• after a puncture wound

• Non–group A streptococci (ie, groups B, C, and G)• lymphatic obstruction or venectomy for coronary artery

bypass graft• Aeromonas hydrophilia, Vibrio vulnificus

• after exposure to freshwater or seawater

Haemophilus influenzae cellulitis• Haemophilus influenzae type B• Children < 6 y.o.• Rare in countries where vaccination is available• Bacteremia may lead to meningitis, orbital cellulitis,

osteomyelitis, or pyarthrosis• Culture, needle aspirate• Cefotaxime and ceftriaxone; Rifampin

Pneumococcal facial cellulitis• S pneumoniae• Young children• Extremity involvement: DM, subs. abuse• Head, neck & upper torso involvement: SLE, nephrotic

syndrome, hematologic dso.• Fever, leukocytosis, and septicemia• Penicillin, vancomycin

Helicobacter cellulitis• Helicobacter cinaedi

• Fever, bacteremia, cellulitis and arthritis• HIV- infected patients; malignancy,

diabetes; and acoholism• distinctive red-brown or copper color w/

minimal warmth• Ciprofloxacin

Tuberculous cellulitis• Mycobacterium

• TB px taking chronic corticosteroids• Past history of pulm. TB• Four drug treatment

Diagnosis

Cellulitis is most often a clinical diagnosis

Blood cultures usually are positive only if the patient develops generalized sepsis

Resemble Cellulitis: • deep vein thrombosis: compression leg ultrasound• Lyme disease has been misdiagnosed as staph- or strep-

induced cellulitis (bullseye rash does not always appear): to rule out Lyme disease is with a blood test, which is recommended during warm months in areas where the disease is endemic.[2]

Complications

Gangrene Metastatic abscess

Grave sepsis

Children and

compromised adults

Treatment & PreventionRest affected limb & cleaning the wound site and treatment with oral antibiotics

Early lesions:

• Intralesional inj of triamcinolone acetonide 1:10

Mild cellulitis:

• Flucloxacillin monotherapy (to cover staphylococcal infection)

Moderate cases or where streptococcal infection is suspected:

• combined with oral phenoxymethylpenicillin or intravenous benzylpenicillin, or ampicillin/amoxicillin ; cefazolin or vancomycin

Severe cases:• require admission and intravenous (IV) therapy.

Wound:• cleaned and dressed appropriately done daily or when they become wet or dirtyMedical advice should be

sought:• wound deep or dirty and retained foreign bodies

URTICARIATACATA, PatriciaTADY, Clarissa Marie

URTICARIA (HIVES)

characterized by wheals surrounded by a red halo or flare

severe itching, stinging or pricking

annular or polycyclic pattern clearing of central region and coalescence of lesions

URTICARIA (HIVES)

Subcutaneous swellings (angioedema) may accompany the wheals target the

gastrointestinal and respiratory tracts resulting in abdominal pain, coryza, asthma and respiratory problems.

ACUTE VS. CHRONIC URTICARIA

•days to weeks •Produce evanescent wheals that

rarely last >12h•Resolution within 6 weeks of onset

ACUTE

•Daily episodes of urticaria and/or angioedema lasting >6w

•Physical urticaria commonCHRONIC

COMMON TRIGGERS

Opiates Polymyxin B Tubocurarine Aspirin and other

NSAIDS Tartrazine Benzoate

ETIOLOGIC FACTORS

•Most frequent cause of acute urticaria

•MOST COMMON: Penicillin and related antibiotics

•Allergic rhinitis or asthma, nasal polyps and food induced anaphylaxis

A.DRUGS

•frequent cause of acute urticaria whereas in chronic urticaria food is a less frequent factor

•MOST COMMON: Chocolate, shellfish, nuts, peanuts, eggs and milk

•Serum radiallergosorbent tests(RASTs) can be used to detect specific IgE and elimination of diets can be of benefit.

B. FOOD

ETIOLOGIC FACTORS•Natural food additives: yeasts,

salicylates, citric acid, egg and fish albumin

•Synthetic additives: azo dyes, sulfites, penicillin, benzoic acid derivatives

•With the exception of sulfite and penicillin, most food additives can be avoided by eating only meat produce and dairy products

•Packaged food are largely prohibited.

C. Food

Additives

ETIOLOGIC FACTORS

•Streptococcal infections •Chronic viral infection (Hep B & C)•Helminths (ascaris,

ankylostoma,filaria)D. Infection

s•Severe emotional stress no matter

what the primary cause•Initiating stimulus in CHOLINERGIC

URTICARIAE. Emotional Stress

•Associated with carcinomas and Hodgkin’s diseaseF.

Neoplasms

ETIOLOGIC FACTORS

•Grass pollens, house dust mites, feathers, formaldehyde, etc.G.

Inhalants

•Induced by ingestion of alcoholH.

Alcohol

•Rarely causes urticaria

I. Mentho

l

PATHOGENESIS

Capillary permeability

Release of histamine from the MAST CELLS (PRIMARY EFFECTOR in urticarial reactions)

Serotonin, leukotrienes, prostaglandins, proteases and kinins – other substances that may cause vasodilation and capillary permeability

DIAGNOSIS• Clinical grounds• Fixed lesions >24h: Urticarial vasculitis,

granuloma annulare, sarcoidosis, cutaneous T – cell lymphoma

• Skin biopsy: if wheals last >24hCLINICAL EVALUATION• Detailed history and physical examination• Radiologic sinus evaluation • Blood count to detect eosinophilia • Review of medications in chronic urticaria • Skin biopsy

ANAPHYLAXIS

An acute and often life

threatening immunologic

reaction

Scalp pruritus, diffuse

erythema, urticaria and angioedema

Most common causes of serious anaphylactic reactions:• Penicillins,

radiographic contrast agents

• Hymenoptera stings, shellfish and other food allergens

Treatment Acute Urticaria

Antihistamines Non-sedating Histamines pose a lower risk

of psychomotor problem in adults. Avoid the trigger if the cause can be

identified Systemic corticosteroids For severe reactions, respiratory and

cardiovascular support is essential. Intubation and tracheotomy may be

required.

Chronic Urticaria Mainstay treatment: Antihistamines

Should be taken on a daily basis and not prescribed to be taken as needed

Second generation antihistamine produce less sedation in most patients

Second line treatment Phototherapy Calcium channel antagonist Antimalarial medications Methotrexate

Corticosteroids produce long term side effects Local treatment

Tepid or cold tub baths Topical camphor and menthol

OTHER URTICARIAL VARIANTS

Angioedema

▫Acute, evanescent, circumscribed edema

▫Area of predeliction: Eyelids, lips, lobes of ears, external

genitalia, or mucous membranes of the mouth, tongue, or larynx

▫ Swelling occurs in the lower layers of the skin or in the subcutaneous tissues

▫ Frequently begins during night and is found on awakening

▫ Two subtypes: Deep form Angioedema associated w/ C1 esterase inhibitor

deficiency

Hereditary Angioedema (HAE)▫ Quincke edema▫ 2nd – 4th decade, Autosomal dominant inheritance▫ Swelling: Asymmetrical without urticaria or itching In subcutaneous tissues and abdominal organs mimicking surgical emergencies, and the upper airway (larynx) – life-threatening▫ Little response to antihistamines, epinephrine, or steroids▫ High mortality rate – death often caused by laryngeal edema▫ 3 phenotypic forms: Type I Type II Type III ▫ Trigger factors: minor trauma, surgery, sudden changes in temperature, or sudden emotional stress

http://www.cfp.ca/content/vol54/issue3/images/large/365fig1.jpeg

Acquired C1 Esterase Inhibitor Deficiency

Usually occurs after 4th decade of life No family history Not associated w/ pruritis or urticaria Two subtypes: A. Acquired angioedema-I

▫ Rare disorder associated with lymphoproliferative diseases

▫ Treatment: Replacement of C1-EI with concentrates or FFP; antifibrinolytic agents; synthetic Danazol

B. Acquired angioedema-II▫ Extremely rare disease▫ Treatment: Immunosuppresive therapy; Synthetic

corticosteroids (temporarily effective); Plasmapheresis

Episodic Angioedema with Eosinophilia

Uncommon disorder w/ no underlying disease

Isolated facial edema May occur with fever, weight gain,

eosinoophilia and elevated eosinophil major basic protein

Treatment: administration of systemic steroidal medications, antihistamines, and IVG

Schnitzler Syndrome

▫Rare disorder▫Combination of chronic, non-pruritic

urticaria, fever of unknown origin, disabling bone pain, hyperostosis, increased erythrocyte sedimentation rate, and monoclonal IgM gammopathy

▫Age of onset: 29-77 years old; affects both sex

▫Effective therapy has not been determined

▫Bone pain and urticarial lesion respond to systemic corticosteroids

Physical Urticarias Occur most frequently in ages 17-40 years

old Most common form

dermatographism > cholinergic > cold urticaria

Chronic idiopathic urticaria: Dermatographism, delayed pressure, cholinergic,

and cold urticaria Other forms:

Adrenergic Urticaria Vibratory Angioedema

Heat Urticaria Aquagenic Urticaria Solar Urticaria Pressure Urticaria

( Delayed Pressure)

Dermatographism▫Sharply localized edema or wheal

with a surrounding erythematous flare occurring within seconds to minutes after the skin has been stroked

▫Affects 2-5% of the population▫Arise spontaneously after drug-induced

urticaria and persist for months▫H2 antihistamine may be of benefit

Cholinergic Urticaria▫ Produced by the action of AcH on the mast cell▫ Characterized by minute, highly pruritic,

punctuate wheals or papules 1-3 mm in diameter and surrounded by areas of erythema

▫ Area of predilection: trunk and face ▫ Persists for 30-90 min and followed by a refractory

period with no lesions of up to 24 hours▫ Palms and soles are spared▫ Trigger factors: exercise, emotional stress,

increased environmental temperature, or intradermal injection of nicotine picrate or methacholine

▫ Treatment: adequate dosage of antihistamines; Danazol in refractory cases

Cold Urticaria Exposure to cold may develop edema and wheals

on the exposed areas; usually on the face and hands

Urticaria does not develop during chilling but on rewarming

Types: Primary – no underlying systemic disease - Tx: Doxepin, Cyproheptadine;

Acrivastine and Cetirizine Secondary - Associated with underlying

systemic disease such as

cryoglobulinemia Familial Cold Urticaria- produces a

Burning sensation with cyanotic centers

and surrounding white halos

lasting for 24 – 48 hrs - Leukocytosis - Tx: Stanozolol

therapy

ERYTHEMA MULTIFORMETamondong, RoxanneTan, Ernie Joe

Erythema Multiforme

Erythema multiforme minor Herpes simplex-associated erythema

multiforme (HAEM) Strongly associated with preceding

herpetic infection

Clinical features

Self-limited Recurrent disease Young adults 1-4 weeks Sharply marginated, erythematous

macules

Raised, edematous papules

24-48 hrs

Classic target or iris lesion

A ring of erythema that forms around the periphery, and centrally the lesions are flatter, more purpuric, and dusky

3 zones: Central dusky purpura Elevated, edematous pale ring Surrounding macular erythema

Typical target lesions best seen in palms and soles

Lesions appear symmetrically and acrally

Initial involvement most frequently of the dorsal hands

Dorsal feet, extensor limbs, elbows, knees, palms and soles

10% of cases, more widespread lesions occur on the trunk

Mucosal involvement in 25% of cases and is limited to the oral mucosa

Atypical HAEM

Outbreaks of unilateral or segmental papules and plaques that may be few in number or solitary

Lesions may be up to 20cm in diameter

Plaques- erythematous and evolve to have a dusky center, which desquamates

Subcutaneous nodules may be present

Histology: features of EM and HSV can be seen

Acyclovir – prevents the lesions Prednisone – increase the frequency

of attacks

Etiologic factors Preceding orolabial HSV infection Appear 1-3 weeks (average of 10 days)

after the herpes outbreak Not all episodes of EM may follow every

episode of herpes

Pathogenesis

due to an allergic reaction(medication) or infection(HSV or Mycoplasma)

involves damage to the blood vessels of the skin followed by damage to skin tissues.

Activated T lymphocytes are present in lesions of Erythema Multiforme. Epidermis – Cytotoxic or Suppressor cellsDermis – Helper T-cells

EM minor is linked to HLA type HLA-DQ3

Histopathology

Histologic Features are NOT predictive of etiology due to similar feature from

EM to TEN(Toxic epidermal necrolysis) Extent of epidermal involvement depends

on the duration of the lesion and where in the lesion the biopsy is taken

Biopsy- “basket-weave stratum corneum” - suggest acute process where in

there was not enough time to produce abnormal keratin

Histopathology

Vacuolar interface dermatitis is present with vacuoles and foci of individual cells necrosis out of proportion to the no. of lymphocytes

Dermal infiltrate is largely mononuclear and tends to be primarily around the upper dermal vessels and along the dermo-epidermal junction.

Eosinophils may be present but rarely prominent and not predictive of etiology

Histopathology of EM must be differentiated from the following:

Fixed Drug Eruption

Graft vs Host disease

Pityriasis lichenoides

Lupus erythematosu

s-deeper infiltrate-w/ eosinophil and neutrophils- papillary dermal fibrosis- melanophages around post-capillary venules

-More compact stratum corneum -Epithelial disorder resembling Bowens Disease

-w/ lymphocyte in every vacuole- w/ erythrocyte extravasasion - neutrophil margination within dermal vessels

-Compact hyperkertosis- a deeper periadnexal infiltrate- dermal mucin and basement membrane thickening

Differential Diagnosis when Bullae are prominent:

Pemphigus Bullous pemphigoid

Paraneoplastic pemphigus

- Prominent mucous membrane involvment

- Lesions are small - erythema prominent at periphery of the bulla

-May produce atypical target lesions- mucosal involvement - vacuolar interface dermatitis - appear very similar to EM major

Treatment

Most cases are self limited and symptomatic treatment may be all that required-Anti-histamine, Moist compress, Topical anesthetics and Acetaminophen

Prevention:Sunscreen lotion and sunscreen-containing lip balm – prevent UVB induced outbeaks of HSV

Therapy:Oral Anti-viral (acyclovir, valacyclovir or famciclovir)Dapsone – antibacterial that inhibits synthesis of dihydrofolic acid - alternative drug when anti-virals are not effectiveSystemic Steroids – control inflammationIntravenous Immunoglobulin – to stop disease process

EXFOLIATIVE DERMATITIS

Genevieve Lynn C. Tan

Exfoliative Dermatitis

Dermatitis exfoliativa Pityriasis rubra (Hebra) Erythroderma (Wilson – Brocq)

Exfoliative Dermatitis

Extensive erythema and scaling

Entire body surface is dull scarlet

Small, laminated scales

No vesicles and pustules

Extensive telogen effluvium

Etiology

Result of generalization of preexisting chronic dermatosis (61%)

Medications allopurinol, sulfas, gold, phenytoin, phenobarbital,

isoniazid, carbamazepine, cisplatin, dapsone, mefloquine, tobramycine, minocycline, nifedipine and iodine

Inadequate intake of branched chain amino acids in infants with MSUD

Idiopathic

Etiology

Sezary syndrome Generalized

exfoliative dermatitis with intense puritus

Leonine facies Alopecia Palmoplantar

hyperkeratosis Onychodystrophy

Criteria for diagnosis of Sezary syndrome: Absolute Sezary cell count of at least

1000/mm3 CD4/CD8 ratio >10 Increase Lymphocyte count with evidence

of T cell clone Chromosomally abnormal T cell clone

Etiology

Hodgkin’s Disease Generalized exfoliative dermatitis Fever Lymphadenopathy Hepatosplenomegaly ESR

Histopathology

Nonspecific Hyperkeratosis Mild acanthosis Focal parakeratosis

Treatment

Drug-induced – stop drug Application of mild corticosteroid

after soaking and occlusion under sauna suit

Acitretin, cyclosporin, methotrexate for psoriatic erythroderma

Isotretinoin, acetretin, methotrexate for PRP

Azathioprine and methotrexate for idiopathic erythroderma unresponsive to therapy

HANSEN’S DISEASE

Tan, Marie DoloresTan, Samantha

Hansen’s Disease Also known as LEPROSY

Chronic, systemic, infectious disease caused by Mycobacterium leprae

Granulomatous or neutrophelic lesions in different parts of the body like: Skin Mucous Membrane Nerves Anterior Segment of the Eye Bones Viscera

Hansen’s Disease

Mycobacterium leprae

Weakly acid fast Grows 32-35°C Cultivated in mouse pads and

armadillos Favors intracellular location Only bacterium to invade

peripheral nerves Phenolic Glycolipid (PGL-1) – unique

to leprosy bacillus

Epidemiology

10-15 million worldwide

Asia (Indian Subcontinent), Sub-Saharan Africa, South and Central America, Pacific Islands, and the Philippines

Most cases in tropical and developing world

More common in people who are of low economic status, w/ inadequate housing, unsuitable sanitation, poor nutrition, and lack of education

Epidemiology

Men > Female Occurs in all ages Peak presentations in children aged

10-20 years old and in adults 30-60 years old

Mode of transmission: controversial (respiratory route: infectious droplets from nasal secretions)

Genetic susceptibility

PATHOGENESIS

Patient’s immune reaction to the leprosy bacillus: critical element in determining the outcome of infection.

TUBERCULOID LEPROMATOUS

Granulomas Well-formed, contain helper T-cells

Poorly-formed, predominant suppressor T-cells

Cytokine profile IFN-γ, IL-2 IL-4, -5, and -10 prominent

Cell-mediated immunity

Good Downregulated

DIAGNOSIS Identification of M. leprae in the affected tissue

Skin biopsies Skin or nerve lesions Stain: visualize the bacillus with Fite-Faraco stain

Slit smears Lesions and cooler areas of the skin Stain: acid-fast stain Multibacillary: organisms found on the skin smears Paucibacillary: negative skin smears (and 5 or fewer

lesions) Serologic tests

Detects antibodies against M. leprae-unique antigens (PGL-1)

PCR detects small numbers of organisms in infected tissue

Diagnostic procedures

Histamine Test

Metacholine Sweat Test

Skin Sensory Test

Lepromin Test (Mitsuda Reaction)

Hansen’s Disease

Presents with a broad spectrum of clinical diseases

Exposure

No clinical disease

(Spontaneous cure)

Develops clinical disease

Paucibacillary

Multibacillary

Early indeterminate leprosy

Insidous onset Slight prodromal symptoms “Numbness” – first clinical manifestation First lesion is a solitary, ill-defined

hypopigmented macule (sometimes erythematous) Succeeding lesions common: Cheeks, upper arms,

thigh, and buttocks Peripheral Nerves not enlarged No plaques No nodules No or very few bacilli on biopsy

SPECTRUM OF HOST-PARASITE RESISTANCE in leprosy

High resistance Unstable resistance No resistance

Tuberculoid (TT)

BorderlineTuberculoid (BT)

Borderline (BB)

Borderline Lepromatous (BL)

Lepromatous (LL)

Lesions 1-3 Few Few or manyasymmetrical

Many Numerous and asymmetrical

Smear for bacilli

0 1+ 2+ 3+ 4+

Lepromin test

3+ 2+ + + 0

Histology Epithelioid cells decreasing → Increasing histiocytes, foam cells, granuloma, xanthoma-like

Nerve destruction, sarcoid-like granuloma

Tuberculoid leprosy Solitary, large, few (<3), asymmetrically

distributed lesions Sharply defined and elevated border that

slopes down to flattened atrophic centers– “Saucer Right Side Up” appearance

Palpable indurations Dry hairless hypo/hyperpigmented lesions Lesions are anesthetic/hyposthenic and

anhidrotic Enlarged peripheral nerves (great auricular

nerve and ulnar nerve) Muscular weakness and atrophy Common sites of lesion: Face, Limbs or Trunk

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Borderline tuberculoid leprosy

Lesions are similar to tuberculoid lesions, but smaller and more numerous (>10-20)

Satellite lesions around large macules or plaques

Less hair loss Nerves slightly enlarged Common sites of lesion:

face and limbs

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Borderline leprosy Small, numerous (but

countable), cutaneous lesions Generalized, but

asymmetrical lesions Erythematous, irregularly

shaped, ill defined borders Erythematous plaques with

islands of normal skin – “Swiss Cheese Appearance”

Nerves are slightly enlarged, thicker, and tender

Anesthesia is only moderatewww.aifo.it/.../online/courses/lepdd

Borderline Lepromatous Leprosy

Numerous (too many to count), symmetrical lesions: macules, papules, plaques, and nodules

Ill-defined outer border and sharply marginated inner border - “Inverted saucer shaped” or “Punched Out”

Reverse configuration of tuberculoid type

Nerve lesions appear later, enlarged, tender, or both

Anesthesia is often absent

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Lepromatous Leprosy Numerous, symmetrical

macules, papules, plaques, and nodules

Lepromas (nodules) on the earlobes, nose, lips, eyebrows

Little or no loss of sensation over the lesions

No nerve thickening No changes in sweating “Leonine Fascies” Madarosis – lateral thinning of

eyebrows Nasal ulceration

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TreatmentWHO Western Pacific recommendation

Reactional states

Characteristic and clinically important aspect of Hansen’s disease

Experienced by 50% of patients after institution of multidrug therapy

Triggers: intercurrent infections, vaccination, pregnancy, vitamin A, iodides, bromide

Severe, abrupt 2 Forms

TYPE 1 TYPE 2Caused/Mediated By:

Cell-mediated Immune complexes

Occur In: Borderline Leprosy(BT, BB, BL)

Lepromatous patients(BL, LL)

Management of reactions Even though reactions may appear after drug

treatment is instituted, it is not advisable to discontinue or reduce anti-leprosy medication.

MILD REACTIONS No neurologic complications or severe systemic

symptoms Supportive treatment, bed rest, aspirin or NSAIDs

TYPE 1 REACTIONS Prednisone Clofazimine

TYPE 2 REACTIONS (ENL) Thalidomide: drug of choice; potent teratogen Systemic corticosteroids

prevention

BCG vaccination alone provides about 34% prevention against infection

BCG + heat-killed M. leprae increases protection to 64%

Treat active multibacillary patients and examine exposed persons on an annual basis to detect early evidence of infection

Chemoprophylaxis in hyperendemic regions Once yearly multidrug therapy with single dose

rifampin+minocycline+clofazamine