infecticus skin desease dr.arif.ppt

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INFECTIOUS SKIN DISEASES

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Primary factors regulating infection of human skin

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Primary factors regulating infection of human skin

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BACTERIAL SKIN INFECTION(PYODERMAS)

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Bacterial infection of the skin can be thought of

in four major categories:

• primary skin infection• secondary infection of a primary skin

disease (e.g. infected atopic dermatitis)• skin lesions as manifestations of primary

infection in some other organ system, usually the blood

• reactive skin conditions resulting from bacterial

infection (e.g., erythema nodusum due to streptococcal pharyngitis)

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Cutaneous and subcutaneous infection due to staphylococci and streptococci

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ImpetigoTwo clinical patterns: • non-bullous : caused by S. aureus and Group A streptococcus• bullous : caused by S. aureus

• Lesions commonly arise on the skin of the face (esp.around the nares) or extremities after trauma

• Pruritus or soreness of the area is a common complaint

Non bullous-impetigoHistory• In a typical sequence, S. aureus spreads from nose to normal skin (app. 11 days later) and then develop into skin lesions (after another 11 days)

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…Non bullous-impetigo

Cutaneous Lesions

• Initial: transient vesicle or pustule• quickly evolves into a honey-colored crusted plaque (can enlarge to >2cm in diameter)• surrounding erythema may be present• constitutional symptoms are absent• regional lymphadenopathy may be present in up to 90% of pts w/prolonged, untreated infection

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Non bullous-impetigo

Erythema and crusting on the nose and moustache area (A), which can spread to involve the entire centrofacial region (B)

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Bullous-impetigo

Cutaneous Lesions• Occurs more commonly in the newborn and in older infants• Characterized by the rapid progression of vesicles to flaccid bullae• Bullae usually arise on areas of grossly normal skin• The Nikolsky sign (sheet-like removal of epidermis by shearing pressure) is not present• Bullae initially contain clear yelow fluid becomes dark yellow and turbid, and their margins are sharply demarcated without an erythematous halo• The bullae are superficial, and within a day or two, they rupture and collapse, forming thin, light-brown to golden- yellow crusts

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Bullous-impetigo

(A). Multiple vesicles with clear and turbid contents that (B) coalesce to form flaccid bullae

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Staphylococcal ecthyma

• cutaneous pyoderma characerized by thickly crusted erosions or ulcerations• is usually a consequence of neglected impetigo• untreated staphylococcal/ streptococcal impetigo can extend more deeply, penetrating epidermis, producing a shallow crusted ulcer

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Staphylococcal ecthyma

Multiple thickly crusted ulcers on the leg

• The ulcer has a “punched out” appearance when the dirty grayish-yellow crust and purulent material are debrided

• The margin of the ulcer is indurated, raides, and violaceous, and the granulating base extends deeply into the dermis

• The lesions are slow to heal, requiring several weeks of antibiotic tx for resolution

• Management: same as for staphylococcal impetigo

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Folliculitis• pyoderma that begins within the hair follicle• is classified according to the depth of invasion (superficial and deep), and microbial etiology

Superficial Folliculitis• a small, fragile, dome-shaped pustule occurs at the infundibulum (ostium or opening) of a hair follicle, • often on the scalp of children and • in the beard area, axillae, extremities, and buttocks of adults

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Superficial Folliculitis. Multiple pustules confined to the beard area

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Deep Folliculitis

• Sycosis barbae is a deep folliculitis with perifollicular inflammation occurring in the bearded areas of the face and upper lip• if untreated, the lesions may become more deeply seated and chronic • lokal tx w/ warm saline compresses and local antibiotics (mupirocin or topical clindamycin) may be sufficient to control infection• More extensive cases require systemic antibiotic tx

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Sycosis barbae Deep staphylococcal folliculitis of the mustache region

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Furuncles and Carbuncles

Furuncle/ boil • is a deep-seated inflammatory nodule that develops around hair follicle, • usually from a preceding, more superficial folliculitis • often evolving into an abscess

Carbuncle• more extensive, deeper, communicating, infiltrated lesion that develops when suppuration occurs in thick inelastic skin when multiple, closely set furuncles coalesce

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Furuncles and Carbuncles

Furuncle of the upper lip. The lesion is nodular, and the central necrotic plug is covered by purulent crust. Several small pustules are seen lateral to the center of the lesion

Multiple furuncles. Multiple abscesses on the buttocks. The lesions healed w/

scarring after a prolonged course of dicloxacillin

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Furuncles and Carbuncles

Carbuncle. This lesion represents multiple confluent furuncles draining pus from multiple openings

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Simple furunculosisLocal application of moist heat

Carbuncle/ furuncle w/ surrounding cellulitis/ w/associated feverShould be treated w/ a systemic antibiotic (as for impetigo)

Severe infection/infection in dangerous areaMaximal antibiotic dosage should be employed by the parental route

Treatment

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Erysipelas• is a distinct type of superficial cutaneous cellulitis w/ marked dermal lymphatic vessel involvement • is caused by group A -hemolytic streptococcus (very uncommonly group C or G streptococcus), rarely caused by S. aureus.

painful, warm erythema of the lower extremity with well-defined borders

painful, edematous erythema with sharp margination on both cheeks and the nose.

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Cellulitis

• extends deeper into the dermis and subcutaneous tissue• the most common etiologic agents: S. aureus and • occasionally other bacteria are identified (group B streptococci in the newborn, pneumococci, Gram- negative bacilli, and in immunocompromised individuals, a variety of microorg., including yeasts and molds)

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Cellulitis• can be differentiated from erysipelas by the lack of distinct margins between affected and normal skin, a deeper, firmer form of tender induration, fluctuance, and occasionally the presence of crepitus on palpation

Cellulitis after puncture trauma. The forearm is swollen, erythematous,& tender. There is abscess formation,

blistering, and crusting

Cellulitis. The lower extremity is swollen, erythematous,& tender. There is blistering, and crusting

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Mild cases of early erysipelasOutpatienti.m. procaine penicillin (600.000 unit twice daily) orOral penicillin V, 500mg every 6h orDicloxacillin 500 mg 4x/dOral cephalosporinsMacrolides and clindamycin (in penicillin-allergic patients)

More extensive streptococcal infectionsHospitaizedi.v. aqueous penicillin G (1 to 2 million units every 4-6h)

Local measuresBed rest and elevation of the involved area to reduce local edema

Treatment

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• Caused by Corynebacterium minutissimum• Occur in flexural areas, esp. in the groin and in between toes; macules/patch with fine scales and sharply defined borders• Wood’s lamp: lesions are coral red because bacteria produce fluorescent porphyrins• Treatment: erythromycin (topical or oral)

Erythrasma

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FUNGAL INFECTION

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• Group of organisms that include yeast and molds which are usually not pathogenic

• Grow best in unsanitary conditions with warmth, moisture and darkness

• Infections generally occur in keratinized tissue found in hair, nails and stratum corneum

• Dermatophytes (Ringworm fungi)• Cause of most skin, nail and hair fungal

infections

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• is a dermatophytosis of the scalp and associated hair

• it may be caused by any pathogenic dermatophyte from the genera Trichophyton and Microsporum exepting T. concentricum

Tinea capitis

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36“Black dot” tinea capitis caused by Trichophyton tonsurans

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Tinea capitis caused by Microsporum audouinii

Tinea capitis “gray patch” type. A large, round hyperkeratotic plaque of alopecia due to breaking off of hair shafts close to the surface.

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Kerion: red, oozing, hairless plaque

Permanent scarring alopecia post kerion

Kerion: heavily crusted, hairless plaque

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• Refers to all dermatophytoses of glabrous skin except the palms, soles, and groin

• The classic presentation is an annular lesion w/ scale across the entire erythematous border.

• The border is often vesicular and advances centrifugally.

• The center of the lesion is usually scaly but may exhibit clearing

• Lesions may be serpiginous and annular “ring-worm”-like)

Tinea corporis

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Tinea corporis: large gyrate plaque with advancing border, typical “ringworm-like” configuration

Tinea imbricata: concentric ring of scale caused by T. concentricum

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Annular tinea corporis on the thigh. Note

multiple, confluent annular lesions w/ a

scaly and partially vesicular border. This

type of lesion is usually seen w/ zoophilic

dermatophytic infection

Polycyclic pattern of tinea corporis resembling psoriasis

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• Usually appears as multiple erythematous papulovesicles w/ a well-marginated, raised border

• Pruritus is common, as is pain w/ maceration or secondary infection

Tinea Cruris

Tinea cruris. Scaling erythematous plaque w/

sharp margins in the inguinal and pubic region

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• Tinea pedis may present as any of the four forms, or a combination thereof

•Chronic intertriginous type (Interdigital type)

•Chronic hyperkeratotic type•Vesiculo-bullous type•Acute ulcerative type

Tinea Pedis and Tinea Manus

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Tinea pedis, interdigital. The area

is macerated and has opaque white scales and some

erosions

Tinea pedis. Superficial white scales in a moccasin-type

distribution.Note archiform pattern of the scales, which is

characteristic

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“Two feet-one hand” presentation

of Trichophyton rubrumTinea pedis, bullous type. Ruptured

vesicles, bullae, erythema, and erosion on the plantar aspect of

the great toe

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• Any infection of the nail caused by dermatophyte fungi, nondermatophyte fungi, or yeast

• 4 clinical types:•Distal subungual onychomycosis•Proximal subungual onychomycosis•White superficial onychomycosis•Candidal onychomycosis

Onychomycosis

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A. Distal subungual onychomycosis occuring simultaneously with superficial white onychomycosis

B. white superficial onychomycosis

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Candidiasis• Diverse group of infections caused by Candida albicans or by other members of the genus Candida• These organisms typically infect the skin, nails, mucous membranes, and gastrointestinat tract, but they also may cause systemic disease

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Pseudomembranous candidiasis or thrush. Note the characteristic white patches on the palate

Candida perleche w/ erythema and fissuring at the corners of the

mouth

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Note the superficial erosion and moist area

with ulceration which are surrounded by erythematous papules. These satellite

lesions are typically associated w/ chronic

which are found outside the larger affected areas

Hyperplastic candidiasis of the tongue

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Red, partially eroded plaques on the vulva surrounded by a delicate collar in an infant. Outside the main lesions are few pustular satellite lesions

Candida in potassium hydroxide preparation showing pseudohyphae and yeast forms

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Oral candidiasis• Uncomplicated: Nystatin suspension (400.000-600.000 unit 4x/d) or• In recurrent cases, oral azoles are proven to be more effective

Candidal intertrigo• Topical antifungals including nystatin and topical imidazole cream• Miconazole powder can be use to dry moist intertriginous areas

Candidal paronychia• Chronic paronychia due to Candida is resistant to therapy• Topical imidazole in solution form is the ideal tx• Oral ketokonazole may be used

Treatment

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• Caused by Pityrosporum orbiculare, previously called Malassezia furfur• Sharply defined, yellowish-brown macules w/ tiny scales• KOH prep: spaghetti and meatball-like hyphae and spores

Pityriasis versicolor

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Tinea versicolor infant Tinea versicolor, upper chest in teenager

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• TERIMA KASIH

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• AUTOIMMUNE SKIN DISEASES

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1. What is autoimmune disease?

2. Describe skin diseases caused by autoimmune mechanism?

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AUTOIMMUNE SKIN DISEASES

• BULLOUS DISEASES GROUP • RHEUMATIC DISEASES GROUP• OTHER

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Bullous Disease Group• Pemphigus vulgaris• Pemphigus foliaceus• Bullous pemhigoid• Herpes gestationes• Epidermolysis bullosa• Dermatitis herpetiformis• Chronic Bullous Dermatosis of Childhood

(CBDC)

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PEMPHIGUS• A group of disorders with loss of intra-epidermal

adhesion• Cause: autoantibodies directed against proteins of

desmosomal complex that hold keratinocytes together.

• Classification:• Pemphigus vulgaris • Pemphigus foliaceus• Pemphigus erythematosus• Pemphigus vegetans

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Pemphigus vulgaris• severe and potentially fatal autoimmune

blistering disorder affecting the skin and mucous membranes caused by autoantibodies against desmogleins.

• Incidence : 0.1-0.5/100,000 population/yr• Pathogenesis:

• Genetic predisposition: HLA-DRQ402, -DQ0505• Autoantibodies against desmoglein 3 (Dsg3), and

desmoglein 1(Dsg1)• The bound antibodies activate proteases that damage

the desmosome acantholysis• Serum Ab titer correlates with severity of disease and

course

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Skin biology

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Damages of desmoglein in Pemphigus

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Protein DiseaseDesmoglein 1 Pemphigus foliaseus, striate palmoplantar

keratoderma, S4, bullous impetigoDesmoglein 3 Pemphigus vulgarisDesmoglein 4 Autosomal recessive hypotrichosisPlakoglobin Palmoplantar keratoderma with wooly hair and

arrythmogenic right ventricular cardiomyopathy (Naxos disease)

Plakophilin 1 Ectodermal dysplasia/skin fragility syndrome (skin erosions, dystrophic nails, sparse hair, and painful palmoplantar keratoderma)

Plakophilin 2 arrythmogenic right ventricular cardiomyopathy Desmoplakin Lethal acantholytic epidermolysis bullosa, striate

palmoplantar keratoderma type I, Palmoplantar keratoderma with left ventricular cardiomyopathy and wooly hair, autosomal dominant arrythmogenic right ventricular cardiomyopathy

Diseases caused by desmosomal disturbances

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Clinical pictures

• Predilection : scalp, face, intertriginous areas, mechancal stressed areas, nail fold, oral mucosa

• The blisters are not stable, as he epidermis falls apart --> erosion & crusts

• 3 stages:• Oral involvement -- 70 % • Localized areas (e.g. scalp)• Generalized disease

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Diagnosis• Clinical pictures• Nikolsky sign :

• Gentle rubbing results in development of new blisters

• Asboe-Hansen sign :• Pressure at edge of blister makes it spread

• Histology• Immunofluorescence

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Differential diagnosis• Skin lesions:

• Erytema multiforme/ Stevens Johnson Syndrome

• Bullous impetigo• Hailey-Hailey disease

• Oral lesions:• Erosive candidiasis• Chronic recurrent aphthae• Herpetic gingivo-stomatitis

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Pemphigus foliaceusPemphigus foliaceus• Represent 10 – 20 % all pemphigus• Clinical pictures :

• Recurrent crops of vesicles/blisters easily rupture, leaving crusted erosion

• Predilection: head, neck, upper trunk, and rarely mucous membrane• Mostly affect adult usually midlife

• Nikolsky sign positive• Histopathology :

• Superficial blisters with split in the granular layer or directly beneath the stratum corneum

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Differential Diagnosis

• Seborrhoic dermatitis• Photodermatoses• Lupus erythematosus• Erythroderma• Drug eruption

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Management• Systemic :

• Corticosteroids (1-2 mg/kg/day)• Cyclophosphamide (7.5-10 mg/kg/day)• Cycloporine (5.0-7.5 mg/kg/day• Azathioprine (2.5 mgkg/day)

• Topical:• Antiseptic and anticandidal• Oral anesthetic gel

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Bullous Pemphigoid• Subepidermal blistering disease caused by

autoantibodies against components of the hemidesmosomes in the basement membrane zone (BMZ) (i.e. BPAG1/BP230 and BPAG2/BP180)

• Incidence:• Most frequent autoimmune bullous disease,

affects more elder people (50-60 yrs)• Men more common affected

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HD

MBLL

LD

AF

MB

ZONA MEMBRAN BASAL/DERMAL-EPIDERMAL JUNCTION

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• Clinical pictures:• Initialized by pruritus, urticarial lesions then

followed by development of blisters• The blisters are stable and tense as the roof

are entire epidermis, contain fluid serum• Oralmucosa involvement <20%• Nikolsky sign negative

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• Histology:• Subepidermal blisters containing eosinophils• Lamina lucida remains on the roof,and lamina

densa on the floor• Immunofluorescence:

• Band of IgG and C3 along BMZ

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Management

• Systemic:• Prednisolone 1 mg/kg daily --> tappered to

maintenance dose 8 mg/day• Sparing agents :

• Azathioprine, mycophenolate mofetil• Methotrexate 15-20 mg/ week

• Topical;• High potent corticosteroids• Antiseptics (Povidone iodine)

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• TERIMA KASIH

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RHEUMATIC DISEASES GROUP

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Systemic Lupus Erythematosus

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What is SLE?

• Prototypic autoimmune disease- loss of immune distinction between self and foreign

• Combination of a genetically susceptible individual exposed to an environmental trigger

• Tissue damage occurs by the deposition of autoantibodies in target tissues triggering inflammation.

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Demographics of SLE• 10/1 prevalence in females versus males

• 3-4/1 prevalence in African Americans and Hispanics compared to Caucasians

• Occurs in up to 1% of young black women and is one of the leading causes of natural death in this group

• Incidence has more than doubled in the last 20 years

• Morbidity and mortality is markedly higher in African Americans and Hispanics compared to Caucasians

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SLE: 1982 Classification Criteria*Malar Rash Renal Disorder

Discoid Rash Neurologic DisorderPhotosensitivity Hematologic DisorderOral Ulcers Immunologic DisorderArthritis Antinuclear AntibodySerositis

**Must have Four Criteria Simultaneously or Serially.Must have Four Criteria Simultaneously or Serially. ACR

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Systemic Lupus Erythematosus:1982 Classification Criteria

DefinitionsMalar Rash Fixed Erthema, Flat, or Raised,

sparing the Nasolabial folds

Discoid Rash Raised patches, Adherent keratotic scaling, Follicular plugging; older

lesions may cause scarring

Photosensitivity Skin rash from sunlight

ACR

96Malar rash with discoid features

97Malar rash- note nasolabial sparing

98Malar rash again with nasolabial sparing

99Lupus rash in sun exposed areas (photosensitivity)

100Lupus alopecia

101Vasculitic rash of the hand in lupus

102 Subacute cutaneous lupus associated with anti-Ro antibodies

103Rash in neonatal lupus- will fade as mom’s antibodies are cleared

104Vesicular rash from lupus- lupus can do anything in the skin

105 Lupus band test- IgG deposition at the dermal/epidermal interface

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Systemic Lupus Erythematosus:1982 Classification Criteria

Definitions(continued)Oral or

Nasopharyngeal Usually PainlessUlcers

Arthritis Nonerosive, Inflammatory in two or more peripheral joints

Serositis Pleuritis or Pericarditis

ACR

107Oral ulcers in a patient with lupus- note hard palate location

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Jaccoud’s arthropathy in lupus- joint deformities are reducible-no erosions

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Libman Sachs endocarditis in lupus- sterile deposits usually mitral valve

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Systemic Lupus Erythematosus:1982 Classification Criteria

Definitions(continued)

Renal Disorder Persistent Proteinuria or Cellular Casts

Neurologic Disorder Seizures or Psychosis

Hematologic Disorder Hemolytic Anemia, Leukopenia (<4,000/mm3), Lymphopenia(<1,500/mm3), or Thrombocytopenia (<10,000/mm3)

ACR

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Systemic Lupus Erythematosus:Renal Histology

Normal Light Microscopy, but Immunoglobin or Complement Protein Deposits Present

Mesangial Lupus Nephritis

Mild Focal Glomerulonephritis

Diffuse Proliferative Glomerulonephritis

Membranous Glomerulonephritis

Interstitial and Tubular Nephritis ACR

112WHO Class IV diffuse proliferative glomerulonephritis in SLE

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Renal Disease in Lupus• Renal disease is the leading determinant of

morbidity and mortality in SLE

• Vast majority of renal disease is WHO Class III or IV proliferative nephritis

• African Americans with lupus nephritis have a 5-10 fold increased risk of renal failure compared to age/sex matched Caucasians despite similar treatment

114Glomerular staining with anti-IgG indicating immune complexes

115Left- normal glomerular loops Immune complex deposits

116Podocyte foot process fusion More immune complexes

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SLE: Nervous System DisordersSeizures Ataxia

Headache Rigidity, Tremor

Stroke Syndromes Chorea

Transverse Myelitis Aseptic Meningitis

Coma Psychiatric Disorders

Dementia

ACR

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119 Choroid bodies in a patient with SLE

120Retinal vasculitis with hemorrhage- associated with CNS lupus

121Infarcted brain tissue Bland CNS vasculopathy of SLE

122MRI showing gray matter lesions the L posterior brain

123 Large infarct in a patient with CNS lupus

124LE cells are dropped and anti-phospholipid antibodies added

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Laboratory Evaluation of SLE• Screening test is the ANA (antinuclear antibody) which is

positive in >95% of patients with SLE

• Four patterns- speckled, homogeneous, rim and nucleolar (seen in scleroderma)

• The speckled pattern is associated with antibodies to Sm, RNP, Ro and La

• The rim pattern is associated with antibodies to double stranded DNA

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Laboratory (continued)• Antibodies to Sm are felt to be specific for

SLE- if you have them you have lupus

• Anti-RNP antibodies are seen in lupus and mixed connective tissue disease

• Anti-Ro and La antibodies are seen in SLE and in Sjogrens syndrome

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Laboratory Monitoring of Disease Activity

• The serum tests useful for following lupus disease activity are anti-dsDNA antibodies and complement levels (C3C4 or CH50).

• In some patients anti-dsDNA antibody levels parallel disease activity

• With active disease complement proteins are consumed thus serum C3, C4 and CH50 decrease

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Laboratory Monitoring (Continued)

• CBCs are useful to monitor for development of Coombs positive hemolytic anemia as well as immune neutropenia and immune mediated thrombocytopenia

• Urine analysis will demonstrate increased proteinuria and an active sediment (RBCs, WBCs and casts) with active lupus nephritis

• All of these measures should improve with therapy

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Current Treatment Options in SLE

• Mild to moderate disease (rash, arthritis)- plaquenil, NSAIDs, MTX, ?DHEA

• Severe disease (renal, CNS)- cyclophosphamide, Cell Cept, IVIg, ?plasmapheresis

• Refractory severe disease- bone marrow ablation +/- stem cell transplant, rituximab

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NSAIDs

• Useful for arthritis and pleuritis/pericarditis of lupus

• Careful monitoring of effects on renal function

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Hydroxychloroquine (Plaquenil)• An antimalarial

• Useful for treating arthritis and skin rash

• Improves the chronic fatigue of some patients

• Yearly opthamologic exams to monitor for development of macular changes

• ?? May prevent development of more severe disease- almost all lupus patients are on it

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Methotrexate

• A chemotherapeutic agent but used at very low doses to treat almost every rheumatic disease

• In lupus is good for skin disease, arthritis, and pleuritis

• Liver toxicity and bone marrow suppression so must monitor blood tests

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Treatment of Mild to Moderate Symptoms of SLE

(Dehydroepiandrosterone, DHEA)

• Overall a modest effect on lupus symptoms. It has no effect on serious disease like CNS or renal

• Side effects include acneiform dermatitis in 40% and hirsutism of varying degrees on all patients. No notable LFT abnormalities

• Potentially useful as a adjunct for steroid sparing

• No data on its effectiveness in men

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Treatment of Mild to Moderate Symptoms of SLE (thalidomide)

• SLE patients with refractory skin disease were treated with 25-50mg/day.

• After 5 days, 7/16 had marked improvement and an additional 6/16 had some improvement. Maximum response was seen at 16 weeks.

• In a second study of 18 patients, all responded

• No effect on other signs and symptoms of disease

• 6/8 responders relapsed when taken off medication

• Significant problem with peripheral neuropathy that in 25% does not resolve with discontinuing therapy

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Treatment of Severe Life Threatening or Organ Threatening Disease

• Cytoxan is the gold standard- a potent and toxic alkylating chemotherapeutic agent given as a once a month IV pulse

• Puts most patients into remission but lots of side effects- infection, malignancy, cytopenias etc

• Particularly troublesome in young women is the induction of premature ovarian failure

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Treatment of SLE- IV Ig

• Utility in the acute treatment of ITP is well proven

• Utility in other manifestations of lupus are less well known

• European group treated patients with IV Ig once a month

following IV CTX and maintained remission

• Lowers anti-DNA levels and raises complement levels

• Consideration for refractory patients or those in whom

immunosuppression is a concern or in the pregnant patient

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Lupus Nephritis Treatment Summary

• Cytoxan remains the gold standard for initial therapy.

• New immunomodulators may offer similar efficacy with less toxicity.

• Most patients will require long term treatment with immunosuppression; less toxic therapies than CTX may be as efficacious.

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Atherosclerosis and Lupus• Patients with SLE have a significant increased risk of

developing early atherosclerosis

• Hypertension and hypercholesterolemia are common in lupus but are not predictive of ASCVD

• Mortality from SLE has increased 60% over the last 10 years in black females with SLE

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Atherosclerosis and Lupus

• Important to control hypertension, follow and treat hyperlipidemia and stop smoking

• In a recent study only 10-30% of SLE patients had their cholesterol checked and less than 50% with known increased lipids were treated

• Use of statins may be beneficial in both treating SLE and controlling hyperlipidemia

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• TERIMA KASIH