INFECTIOUS SKIN DISEASES

Primary factors regulating infection of human skin

Primary factors regulating infection of human skin

BACTERIAL SKIN INFECTION

(PYODERMAS)

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

Cutaneous and subcutaneous infection due to

staphylococci and streptococci

Impetigo
Two clinical patterns:
non-bullous : caused by S. aureus and Group A
streptococcus
bullous :
caused by S. aureus

Non bullous-impetigo
History

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)
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
8

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

Non bullous-impetigo

Erythema and crusting on the nose and moustache area (A),

which can spread to involve the entire centrofacial region (B)
10

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 goldenyellow crusts
11

Bullous-impetigo

(A). Multiple vesicles with clear and turbid contents that (B)
coalesce to form flaccid bullae
12

13

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

14

Staphylococcal ecthyma
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

Multiple thickly crusted ulcers on the leg

15

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
16

Superficial Folliculitis.
Multiple pustules confined to the beard area
17

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

18

Sycosis barbae
Deep staphylococcal folliculitis of the mustache region
19

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

20

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

21

Furuncles and Carbuncles

Carbuncle. This lesion represents multiple confluent

furuncles draining pus from multiple openings

22

Treatment
Simple furunculosis
Local application of moist heat
Carbuncle/ furuncle w/ surrounding cellulitis/
w/associated fever
Should be treated w/ a systemic antibiotic (as for
impetigo)
Severe infection/infection in dangerous area
Maximal antibiotic dosage should be employed by the
parental route

23

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

24
margination on both cheeks and the nose.

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, Gramnegative bacilli, and in immunocompromised individuals,
a variety of microorg., including yeasts and molds)

25

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. The lower extremity is swollen,

erythematous,& tender. There is blistering,
and crusting

Cellulitis after puncture trauma. The

forearm is swollen, erythematous,& tender.
There is abscess formation, blistering, and 26
crusting

Treatment
Mild cases of early erysipelas
Outpatient
i.m. procaine penicillin (600.000 unit twice daily) or
Oral penicillin V, 500mg every 6h or
Dicloxacillin 500 mg 4x/d
Oral cephalosporins
Macrolides and clindamycin (in penicillin-allergic patients)
More extensive streptococcal infections
Hospitaized
i.v. aqueous penicillin G (1 to 2 million units every 4-6h)
Local measures
Bed rest and elevation of the involved area to reduce local
edema

27

Erythrasma
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
Woods lamp: lesions are coral red because bacteria
produce fluorescent porphyrins
Treatment: erythromycin (topical or oral)

28

29

FUNGAL INFECTION

30

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
31

32

33

Tinea capitis
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

34

35

Black dot tinea capitis caused by Trichophyton tonsurans

36

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.
37

Kerion: heavily crusted, hairless plaque

Kerion: red, oozing, hairless

plaque
Permanent scarring alopecia post kerion

38

39

Tinea corporis

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-wormlike)
40

Tinea corporis: large gyrate plaque with

advancing border, typical ringworm-like
configuration

Tinea imbricata: concentric ring of

scale caused by T. concentricum

41

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

42

Tinea Cruris

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. Scaling erythematous

plaque w/ sharp margins in the
inguinal and pubic region
43

Tinea Pedis and Tinea Manus

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

44

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
45

Two feet-one hand presentation

of Trichophyton rubrum

Tinea pedis, bullous type. Ruptured

vesicles, bullae, erythema, and
erosion on the plantar aspect of the
great toe
46

Onychomycosis

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

47

A. Distal subungual onychomycosis occuring

simultaneously with superficial white
onychomycosis

B. white superficial onychomycosis

48

49

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

50

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

Candida perleche w/ erythema and

fissuring at the corners of the mouth

51

Hyperplastic candidiasis of the tongue

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
52

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
53

Treatment
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
54

Pityriasis versicolor
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

55

Tinea versicolor infant

Tinea versicolor, upper chest in teenager

56

TERIMA KASIH

57

AUTOIMMUNE SKIN DISEASES

58

1.

What is autoimmune disease?

2.

Describe skin diseases caused by

autoimmune mechanism?

59

AUTOIMMUNE SKIN DISEASES

BULLOUS DISEASES GROUP

RHEUMATIC DISEASES GROUP
OTHER

60

Bullous Disease Group

Pemphigus vulgaris
Pemphigus foliaceus
Bullous pemhigoid
Herpes gestationes
Epidermolysis bullosa
Dermatitis herpetiformis
Chronic Bullous Dermatosis of Childhood
(CBDC)
61

62

63
11

64

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

65

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
66

Skin biology

Damages of desmoglein in Pemphigus

67
1

Diseases caused by desmosomal disturbances

Protein

Disease

Desmoglein 1

Pemphigus foliaseus, striate palmoplantar

keratoderma, S4, bullous impetigo

Desmoglein 3

Pemphigus vulgaris

Desmoglein 4

Autosomal recessive hypotrichosis

Plakoglobin

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
68
1
ventricular cardiomyopathy

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
69

70

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
71

72

73

Differential diagnosis

Skin lesions:
Erytema multiforme/ Stevens Johnson
Syndrome
Bullous impetigo
Hailey-Hailey disease

Oral lesions:
Erosive candidiasis
Chronic recurrent aphthae
Herpetic gingivo-stomatitis
74

Pemphigus 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

75

76

77

Differential Diagnosis

Seborrhoic dermatitis
Photodermatoses
Lupus erythematosus
Erythroderma
Drug eruption

78

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
79

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
80

ZONA MEMBRAN BASAL/DERMAL-EPIDERMAL JUNCTION

HD
LL
MB
MB

LD

AF
81

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

82

83

84

85

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

86

87

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)
88

TERIMA KASIH

89

RHEUMATIC DISEASES GROUP

90

Systemic Lupus Erythematosus

91

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.
92

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

93

SLE: 1982 Classification

Criteria* Renal Disorder
Malar Rash
Discoid Rash
Photosensitivity
Oral Ulcers
Arthritis
Serositis

Neurologic Disorder
Hematologic Disorder
Immunologic Disorder
Antinuclear Antibody

*Must have Four Criteria Simultaneously or Serially. ACR94

Systemic Lupus Erythematosus:

1982 Classification Criteria
Definitions
Malar Rash Fixed Erthema, Flat, or Raised,
the Nasolabial folds

sparing

Discoid Rash
Raised patches, Adherent keratotic
scaling, Follicular plugging; older
lesions may cause scarring
Photosensitivity

Skin rash from sunlight

ACR

95

Malarrashwithdiscoidfeatures

96

Malarrashnotenasolabialsparing

97

Malarrashagainwithnasolabialsparing

98

Lupusrashinsunexposedareas(photosensitivity)

99

Lupusalopecia

100

Vasculiticrashofthehandinlupus

101

SubacutecutaneouslupusassociatedwithantiRoantibodies

102

Rashinneonatallupuswillfadeasmomsantibodiesarecleared

103

Vesicularrashfromlupuslupuscandoanythingintheskin

104

LupusbandtestIgGdepositionatthedermal/epidermalinterface

105

Systemic Lupus Erythematosus:

1982 Classification Criteria
Definitions
Oral or
Nasopharyngeal
Ulcers

(continued)
Usually Painless

Arthritis
Nonerosive,
Inflammatory in
two or more peripheral joints
Serositis

Pleuritis or Pericarditis
ACR106

Oralulcersinapatientwithlupusnotehardpalatelocation

107

Jaccoudsarthropathyinlupusjointdeformities
arereduciblenoerosions

108

LibmanSachsendocarditisinlupussteriledeposits
usuallymitralvalve

109

Systemic Lupus Erythematosus:

1982 Classification Criteria
Definitions
(continued)
Renal Disorder Persistent Proteinuria or
Casts

Cellular

Neurologic Disorder Seizures or Psychosis

Hematologic DisorderHemolytic Anemia,
Leukopenia (<4,000/mm3),
Lymphopenia(<1,500/mm3), or
Thrombocytopenia (<10,000/mm3)
110
ACR

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

111

WHOClassIVdiffuseproliferativeglomerulonephritisinSLE

112

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
113

GlomerularstainingwithantiIgGindicatingimmunecomplexes

114

LeftnormalglomerularloopsImmunecomplexdeposits

115

PodocytefootprocessfusionMoreimmunecomplexes

116

SLE: Nervous System Disorders

Seizures

Ataxia

Headache

Rigidity, Tremor

Stroke Syndromes

Chorea

Transverse Myelitis

Aseptic Meningitis

Coma

Psychiatric Disorders

Dementia
ACR

117

118

ChoroidbodiesinapatientwithSLE

119

120
RetinalvasculitiswithhemorrhageassociatedwithCNSlupus

InfarctedbraintissueBlandCNSvasculopathyofSLE

121

MRIshowinggraymatterlesionstheLposteriorbrain

122

LargeinfarctinapatientwithCNSlupus

123

LEcellsaredroppedandantiphospholipidantibodiesadded

124

125

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
126

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
127

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
128

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

129

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
130

NSAIDs

Useful for arthritis and pleuritis/pericarditis of

lupus

Careful monitoring of effects on renal function

131

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
132

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
133

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

134

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

135

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
136

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
137

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.

138

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
139

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
140

TERIMA KASIH

141