CUTANEOUS MANIFESTATIONS OF HUMAN IMMUNODEFICIENCY VIRUS INFECTION - PowerPoint Presentation

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CUTANEOUS MANIFESTATIONS OF HUMAN IMMUNODEFICIENCY VIRUS INFECTION

BYDR. JAHNABIMODERATORDR. BHASKAR GUPTA, PROF and HODDEPT OF DERMATOLOGY

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IntroductionHIV is a

lymphotropic human retrovirus.Acquired - sexually, - from blood or blood products, or - vertically from an infected mother during pregnancy, birth or breastfeeding. The virus infects immunocompetent cells including CD4+ T cells and macrophages.

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History

In 1981, Pneumocystis jiroveci (formerly carinii) pneumonia, Kaposi sarcoma, and chronic ulcerative herpes simplex virus (HSV) infections in homosexual men in association with reduced cell-mediated immunity were reported . Soon thereafter, the underlying condition was termed

acquired immune deficiency syndrome (AIDS

).

In 1983, The causative T-

lymphotropic

retrovirus was identified and named the

human immunodeficiency virus (HIV).

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Epidemiology

Globally in 2016, nearly 37 million people were estimated to be living with HIV.Affect specific population- sex workers, injectable drug abusers and men who have sex with men( MSM).

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Pathophysiology

VirologyTwo main types : HIV‐1 and HIV‐2.HIV-1 most common cause globally,HIV-2 infection -West Africa.

HIV-2 is associated with

- slower progression of

immunosuppression

,

- decreased infectivity, and

- resistance to non-nucleoside reverse transcriptase inhibitors.

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HIV-1 divided into

- groups, subtypes (or clades), sub‐subtypes and circulating recombinant forms (CRFs) . Groups

:

M (major) - pandemic

N (new) – West Central Africa.

O (outlier) - endemic in Cameroon and

neighbouring

countriesnine subtypes of HIV‐1 identified: A–D, F–H, J and K. subtype or

clade

F -- two sub‐subtypes or

subclades

F1 and F2.

CRF01- AE

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HIV is a single‐stranded RNA virus.

three major structural genes: gag (coding for nuclear proteins), pol (coding for reverse transcriptase) and env (coding for the envelope).Transcription regulatory genes including

rev, tat and

nef

,

small accessory genes important for infection

vif

, vpu, vpr.

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During HIV-1 infection, the viral envelope proteins

gp120 and gp41 initially interact with the CD4 molecule followed by a second interaction with a chemokine

receptor, usually

CCR5 on

monocytes

/macrophages or CXCR4 on T-cells

.

Following binding, changes in conformation induce fusion of the viral envelope with the plasma membrane, and the virus particle is thereby internalized.

RNA genome is transcribed by a reverse transcriptase enzyme that produces a DNA copy of the HIV RNA

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viral DNA copy is spliced into the host DNA through the action of an

integrase enzyme Transcription of viral DNA into RNA yields genomic material for new viral particles or it can be translated into viral proteins. Cleavage of the latter into structural components of the virus is accomplished by proteases.

Intact viruses are then produced and host cells are destroyed.

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Infection by the transmitted/founder virus is followed by a rapid increase in HIV replication. After ~6 months, the viral load falls to a set point that is determined by the host’s innate natural killer (NK) cell response plus an adaptive immune response by CD8+ cells and neutralizing antibodies.

initial antibody response develops within 1–3 months after transmission and is strain-specific. CD8+ cytotoxic T cells

directed

against HIV begin to function within 10 days of exposure.

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Initial infection results in a reduction in circulating CD4+ T cells, which is followed by a recovery to nearly normal levels and a subsequent slow fall of about 50 to 100 cells/mm3 per year.

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Natural history

HIV disease is a continuum that progresses from primary infection to death via a sequence of opportunistic infections and neoplasms that mark the gradual deterioration of the immune systemFor untreated infections, the median time for progression to AIDS is ~10 years. AIDS is defined by a CD4+ cell count of <200/mm3 or <14% CD4+ T cells and/or the presence of an AIDS-defining condition.10–15% of untreated patients referred to as “long-term non-

progressors

”, have their HIV infections for ≥10 years with no symptoms and CD4+ T-cell counts of >500 cells/mm3.

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AIDS defining illness

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Dermatological manifestations in HIV infection

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WHO CLINICAL STAGING OF HIV/AIDS IN THE SETTING OF CONFIRMED HIV INFECTION

Clinical stage 1 – asymptomatic; immunologic correlate*: >500 CD4+ cells/mm3 • Asymptomatic • Persistent generalized

lymphadenopathy

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Clinical stage 2 – mild; immunologic correlate

*: 350–499 CD4+ cells/mm3All agesHerpes zoster

• Fungal nail infection

•

Pruritic

papular

eruptions• Angular cheilitis

• Recurrent oral ulcerations

• Recurrent/chronic upper respiratory tract infections(sinusitis,

otitis

media/

otorrhea

, tonsillitis,

pharyngitis

Adults

Seborrheic

dermatitis

• Moderate unexplained weight loss (<10%

of body weight

Children

Extensive warts

• Extensive molluscum contagiosum

• Unexplained persistent parotid

enlargement

• Unexplained persistent

hepatosplenomegaly

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Clinical stage 3 – advanced; immunologic correlate*:

200–349 CD4+ cells/mm3 All agesPersistent oral candidiasis

Oral hairy

leukoplakia

Acute necrotizing ulcerative

stomatitis

, gingivitis, or

periodontitis Unexplained chronic diarrhea (>1 month in adults, >2 weeks in children)

Unexplained persistent fever (≥37.6°C intermittent or constant, for >1 month)

Pulmonary tuberculosis (current)

Unexplained anemia (<8 g/

dL

),

neutropenia

(<0.5 × 109/L) or chronic thrombocytopenia (<50 × 109/L)

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AdultsUnexplained severe weight loss (>10% of body weight) Severe bacterial infections such as pneumonia, empyema, pyomyositis

, bone or joint infection, meningitis,

bacteremia

Children

Unexplained moderate malnutrition or wasting not adequately responding to standard therapy

Recurrent severe bacterial pneumonia

Symptomatic lymphoid interstitial

pneumonitis

Lymph node tuberculosis

Chronic HIV-associated lung disease including

bronchiectasis

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Clinical stage 4 – severe/AIDS-defining conditions; immunologic correlate*:

<200 CD4+ cells/mm3 All ages

Chronic herpes simplex infection (

orolabial

, genital, or

anorectal

of >1 month’s duration or visceral at any site)

Kaposi sarcomaExtrapulmonary

cryptococcosis

including meningitis

Disseminated endemic mycosis (

coccidioidomycosis

or

histoplasmosis

)

Disseminated non-

tuberculous

mycobacterial

infection

.

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Unexplained severe wasting, stunting or severe malnutrition not responding to standard therapy (HIV wasting syndrome)

Cytomegalovirus infection (retinitis or infection of other organs; onset at age >1 month)HIV encephalopathyProgressive multifocal leukoencephalopathyExtrapulmonary

tuberculosis

Candidiasis

of the esophagus, trachea, bronchi, or lungs

Pneumocystis

pneumonia

Central nervous system toxoplasmosis (onset at age >1 month)Chronic cryptosporidiosis (with diarrhea)Chronic

isosporiasis

Symptomatic HIV-associated nephropathy or symptomatic HIV-associated

cardiomyopathy

Cerebral or B-cell non-Hodgkin lymphoma, or other HIV-associated solid tumor

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Adults

Atypical disseminated leishmaniasisRecurrent severe bacterial pneumoniaRecurrent non-typhoidal

Salmonella

bacteremia

Invasive cervical carcinoma

Children

Recurrent severe bacterial infections such

as

empyema

,

pyomyositis

, bone or joint

infection, or meningitis (but excluding

pneumonia

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Acute HIV syndrome

About 3–6 weeks following primary infection, the majority (80%) of individuals infected with HIV develop an acute influenza or mononucleosis-like syndrome.C/Ffever, lethargy, rash Rash - in 40–80% of patients; distinct, well-demarcated, nonpruritic macules

and papules typically

generalised

favoring the upper chest and back (particularly the

clavicular

region), forehead, and scalp.. lasts 4–5 days .

myalgias/ arthralgias, cervical and

axillary

lymphadenopathy

,

pharyngitis

, night sweats, and nausea/vomiting/ diarrhea.

Less commonly reported findings include

leukopenia

, thrombocytopenia, weight loss, aseptic meningitis, anorexia, abnormal liver function tests, and oral and genital ulcers.

last for 2–3 weeks and resolve gradually as levels of plasma

viremia

decrease.

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HIV-RELATED INFECTIOUS SKIN CONDITIONS

Viral infectionsHerpes simplex virus (HSV)Varicella - zoster virus(VZV)Molluscum contagiosum virus

Human

papilloma

virus (HPV)

Epstein–Barr virus (EBV)

Cytomegalovirus (CMV)

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Herpes simplex virus (HSV)

Relatively immunocompetent individuals usually have typical, self-limited HSV disease.As immunity wanes, recurrences increases and lesions take longer to heal, potentially evolving into chronic, extensive, deep, and painful ulcers perioral region,

anogenital

region, and digits.

Atypical morphologies, such as

folliculitis

,

hyperkeratotic, verrucous papules and nodules



observed in advanced HIV disease.

Higher doses and longer courses of antiviral medications are typically required.

Resistance to acyclovir.

Alternative --

foscarnet

,

cidofovir

, and

imiquimod

.

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Chronic ulcerative herpes

simplex virus infection in an HIV-infected patient.

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Varicella - zoster virus(VZV)

Varicella tends to have new lesion formation over a longer period of timea higher lesion count7–15-fold higher incidence of herpes zoster compared to the general population.chronic non-healing ulcers, hyperkeratotic

verrucous

plaques, and

multidermatomal

disseminated skin lesions.

complications - bacterial superinfection, systemic involvement, and multiple recurrences.HIV-infected patients without VZV immunity should receive

varicella

–zoster immune globulin within 10 days of exposure to VZV.

Antiviral treatment - continued until clinical resolution occurs.

Patients treated with ART may experience paradoxical worsening of herpes zoster when their CD4+ T-cell counts rise.(IRIS)

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Molluscum contagiosum virus

Commonly occursMore persistent with reduced CD4+ T-cell counts (<100/mm3)Larger >1cm ,coalescent, verrucous, and widespread lesionsPredonimantly facial

Do not manifest

pathognomonic

classic morphology and are not typically domed in shape and lack the characteristic central

umbilication

.

Atypical lesion- resemble folliculitis, abscesses, warts, and cutaneous horns.Progressive and recurrent.

Resolve spontaneously after initiation of ART but can also present as a manifestation of IRIS.

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Human papilloma virus (HPV)

prevalence is higher HIV-infected individuals have reduced HPV clearance, more treatment-resistant mucocutaneous lesions, and accelerated development of HPV-associated carcinoma

Increase risk of

-

epidermodysplasia

verruciformis

 SCC -

cervical intraepithelial

neoplasia

.

- Anal HPV is present in >90% of HIV-infected MSM

- High-grade anal intraepithelial

neoplasia

(AIN) and anal cancer

- penile cancer

On ART- Enlargement or inflammation of pre-existing warts and an eruption of new warts can occur in the setting of IRIS.

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Human

papillomavirus

-induced invasive

squamous cell carcinoma in a 32-year-old man with human immunodeficiency virus infection

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Epstein–Barr virus (EBV)

Oral hairy leukoplakia (OHL) results from EBVinfection of the oral mucosa and typically presents as hyperkeratotic, corrugated white plaques with hair-like projections on the lateral aspect of the tongue.more prevalent in men and those with CD4+ T-cell counts below 200/mm3

represents a predictor of rapid disease progression if ART is not initiated.

topical or oral

antiherpetic

antiviral medications and topical

podophyllin

, tretinoin, or gentian violet may be of benefit.but recurrence is common

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Oral hairy

leukoplakia

. White plaques with

vertical corrugations on the

inferolateral

aspect of the tongue

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Cytomegalovirus (CMV)

Reactivation of CMV - CD4+ T-cell counts that are <100/mm3, significant cause of morbidity and mortality in patients with AIDSCutaneous presentations are uncommon include ulcers favoring the anogenital area, verrucous

or

hyperpigmented

plaques,

prurigo

nodularis-like lesions, purpuric papules, vesicles, and morbilliform eruptions. Ulcerative lesions are often co-infected with HSV or VZV.

Treatment and prophylaxis –

cART

Intravenous

foscarnet

,

ganciclovir

and

cidofovir

are specific treatments

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Cytomegalovirus infection: nodular

prurigo

‐like eruption on the back

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Bacterial infections

recurrent and potentially severe cutaneous bacterial infectionslocalized or widespreadStaphylococcus aureusBacillary angiomatosisMycobacteria

Syphilis

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Staphylococcus aureus

Most common bacterial pathogen in HIV infected individualsCutaneous presentations include impetigo, folliculitis, furunculosis, wound infections, cellulitis

, and rarely botryomycosis.

higher prevalence and incidence of

methicillin

-resistant

S.

aureus (MRSA) colonization of the skin.The lower extremities, buttocks, and scrotum are commonly affected.

risk factors

-

a low CD4+ T-cell count,

- recent treatment with antibiotics

- hospitalization, and

- illicit drug use.

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Bacillary angiomatosis

rare condition - vascular proliferation Gram-negative bacilli Bartonella henselae and B. quintana

.

severely

immunocompromised

, usually with CD4+ T-cell counts <100/mm3

favors the skin and subcutaneous

typically present with a single to numerous, firm, red or violaceous papules and nodules; these lesions may be painful, ulcerate, or bleed profusely after trauma.

Large subcutaneous nodules – ulcerate

Treatment consists of

doxycycline

or

macrolides

.

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Mycobacteria

reactivation of, Mycobacterium tuberculosis seems to occur early in HIV Infection and cutaneous tuberculosis is common.clinical presentation lupus vulgaris , scrofuloderma

, scattered

violaceous

papules , acute

miliary

tuberculosis of the skin,

keratotic papules, nodules and palmoplantar keratoderma

,

pilonidal

sinus, and

tuberculides

.

Tuberculous

lymphadenitis has been said to be a characteristic manifestation in HIV.

Non-healing ulcer and

verrucous

lesions over

perianal

area.

Atypical

mycobacterial

infection-

Mycobacterium

avium

-

intracellulare

,( CD4- <50/

microlt

)

which presents with

violaceous

papules, nodules, and ulcers.

M. Avium, M. kansasii , M. haemophilum

,

M.

fortuitum

, M.

lentiflavum

and M.

marinum

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Histopathological

features such as caseating granuloma may be absent due to diminished cell‐mediated immunity.Prophylaxis and treatment-cART and specific conventional antituberculous

drugs are used.

Atypical

mycobacterial

infection is treated with a

macrolide

and ethambutol.

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Syphilis

HIV-infected patients --present with multiple primary chancres, concomitant lesions of primary and secondary syphilis, palmoplantar keratoderma, annular plaques, and lues maligna

.

Prodromal

symptom precedes the appearance of papules, pustules, and necrotic nodules with ulceration and crusting

lesions are symmetrically distributed,

palms and sometimes oral mucosa

Greater severity of neurosyphilis

The recommended stage-specific treatment regimens are the same as those for HIV-negative persons, but with longer monitoring.

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Secondary syphilis presenting as

lues

maligna

.

This HIV-positive man had a fever, headache,

arthralgias

, and

myalgias

together with this widespread eruption of pustules and crusted

papulonodules

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Fungal infections

CandidiasisDermatophytosesHistoplasmosisCryptococcosisOther fungal infections Cutaneous sporotrichosis

,

paracoccidioidomycosis

,

blastomycosis

,

nocardiasis , rhinosporidiosis , primary cutaneous aspergillosis,

mucormycosis

.

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Candidiasis

Most common fungal infection in those with HIV infection(90% of advanced disease)Oropharyngeal candidiasis is often the first clinical manifestation of HIV infectionOropharyngeal

candidiasis

typically presents in four different clinical patterns:

(1)

pseudomembranous

(thrush), (2)

hyperplastic,(3) erythematous (atrophic), and (4) angular cheilitis

Candida

albicans

is the most frequent species isolated. Treatment is

with single‐dose oral

fluconazole

or localized oral

miconazole

. Resistance can occur.

Chronic

paronychia

, and

onychodystrophy

, refractory vaginal, esophageal, and disseminated

candidiasis

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Dermatophytoses

More widespread, atypical in appearance, and refractory to treatmentAtypical presentation – pseudoimbricata, facial papule mimicking eosinophilic folliculitis,extensive and deep , invasive

dermatophytosis,including

Majocchi’s

granuloma

.In severely immunosuppressed patients with AIDS, the lesions may have little inflammation and often lack the elevated border and central clearing typical of

tinea

(

anergic

form)

Proximal

subungual

onychomycosis

ART has markedly diminished the incidence of these infections.

Tt



topical

and/or systemic antifungal therapy with

imidazoles

or

triazoles

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Invasive Fungal Infections

Cryptococcus neoformansmost common life-threatening fungal infection associated with advanced HIV disease Disseminated infection with a CD4+ T cell count <50/μL. head and neck

In HIV/AIDS,

cryptococcal

skin involvement should be suspected when

papulonodular

necrotizing skin lesions with central

umbilication, like molluscum contagiosum , are encountered in the context of neurological or pulmonary disease.subcutaneous nodules,

cellulitis

, palpable purpura,

violaceous

plaques

mimicking

Kaposi sarcoma, and

pyoderma

gangrenosum

–like lesions

Violaceous nodules and ulcerations may also be seen on the palate and tongue.

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Cutaneous diagnosis is by skin biopsy with special stains for the

cryptococcal capsule (e.g. mucicarmine) and culture, or Tzanck preparation.Intravenous liposomal amphotericin and oral fluconazole

are the mainstays of treatment.

Primary and secondary prophylaxis is with oral

fluconazole

.

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Histoplasmosis

Histoplasma capsulatumDisseminated - CD4+ T cell count <50/μL and presents with fevers, weight loss, pulmonary symptoms,

lymphadenopathy

,

hepatosplenomegaly

, and rash.

multiple morphologies, including erythematous papules, necrotic

umbilicated papules and nodules mimicking molluscum, folliculitis,

acneiform

eruptions

, rosacea-

like

eruptions

,

psoriasiform

eruptions

,

ulcers, vegetative plaques, and

pyoderma

gangrenosum

- like lesions.

face, extremities and trunk.

Histoplasma

capsulatum

can be demonstrated by

Gomori

methenamine

silver stain of a skin biopsy section

Treatment is by

cART

and

itraconazole

and/or

amphotericin

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Penicilliosis

CD4+ T cell count <50/μLSkin lesions in 70% of patients, andtypically consist of umbilicated papules favoring the face, pinnae, upper trunk, and arms.

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Parasitic infestation

ScabiesLeishmaniasisStrongyloidiasisAcanthamebiasisDemodicosis

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Scabies

mite Sarcoptes scabiei var. hominis,In advanced HIV disease, who are not able to control mite replication, are at risk for developing crusted scabies.

Crusted scabies commonly presents with extensive thick

hyperkeratotic

plaques with dirty gray brown scale.

atypical locations such as the scalp, beard area, palms, and soles.

not

pruritic, or minimally pruritic

a gram of crust may harbor thousands of mites

–extremely contagious.

Ivermectin

(200

μg

/kg weekly) 3–7 doses, depending on the severity of the infection.

topical

scabicide

(every 2–3 days × 1–2 weeks) and

keratolytic

cream to improve penetration of the agent.

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INFLAMMATORY DERMATOSES

Seborrheic dermatitisPsoriasisAtopic eczemaErythrodermaEosinophilic folliculitisPruritic

papular

eruption

Granuloma

annulareDrug reaction

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Seborrheic dermatitis

Affects 20–85% of HIV-infected individualsall stages of HIV diseaseAn acute onset or sudden flare of extensive or severe seborrheic dermatitis raise the possibility of HIV infection.

Typical features + a

papular

component, exuberant facial plaques, and widespread involvement with evolution to

erythroderma

may occur with waning immunity.

Refractory to standard therapy.

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Psoriasis

HIV-associated psoriasis is characterized by greater disease severity, frequent exacerbations, atypical presentations, resistance to treatment, and a higher prevalence of psoriatic arthritishallmark of HIV-associated psoriasis is multiple morphologic subtypes in the same patient.guttate, inverse and erythrodermic

psoriasis are the most common.

HIV-associated psoriasis that is not responding to topical medications, therapeutic options include phototherapy (e.g. narrowband UVB), systemic

retinoids

, and ART

Immunosuppressive agents should be reserved for patients with refractory disease, and ART plus concomitant prophylaxis for opportunistic infections is recommended.

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Eosinophilic folliculitis

intensely pruritic, erythematous, follicular-based papules that are often excoriatedScalp, face, neck, and upper trunkadvanced HIV disease and CD4+ T-cell counts <250–300/mm3.

pathomechanism

-An exaggerated reaction to

Malassezia

,

Demodex

, or other organisms normally present within the follicular infundibula.

Differ by intractable itch, lack of

circinate

lesions or

palmoplantar

involvement, and failure to respond to

indomethacin

.

Tt

– topical corticosteroids,

tacrolimus

and

permethrin

; oral antibiotics,

itraconazole

,

dapsone

and

retinoids

; and UVB phototherapy.

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Pruritic papular eruption

severe pruritic and skin-colored to erythematous, non-follicular papulesdistributed symmetricallyextremities and trunk

eruption is typically associated with multiple excoriations, marked

postinflammatory

hyperpigmentation, and scarring.

marker of severe

immunosuppression

as more than 80% of HIV-infected individuals with PPE have been reported to have CD4+ T cell counts <100/μL.

Etiopathogenesis

- unclear,

But PPE may represent a hypersensitivity reaction to arthropod bites.

extremely difficult to treat effectively.

Topical corticosteroids, antihistamines, oral antibiotics

UVB phototherapy and ART may be of benefit.

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Atopic eczema

In adults reports of patients whose atopic eczema recurred or worsened during the course of HIV infection. Others believe atopic eczema is not affected by HIV.

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ErythrodermaErythroderma in HIV disease may be related to drug hypersensitivity,atopic dermatitis,

psoriasis,

seborrheic

dermatitis,

photosensitivity dermatitis,

coexisting human T-cell

lymphotrophic virus-1 infection, pityriasis rubra pilaris

,

cutaneous T cell lymphoma.

In a young black patient,

erythroderma

may be a marker for HIV infection.

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Drug reaction

Cutaneous side effects of non‐ARV drugs in patients with HIV/AIDSMorbilliform toxic erythemaErythema

multiforme

, SJS, TEN, DRESS

Erythroderma

Anaphylaxis,

urticaria

, angio-oedemaXerosis

,

cheilitis

Lichenoid

reactions

Psoriasis

Photodermatoses

Purpura

Oro‐genital ulceration

Vasculitis

Fixed drug eruptions:

•

Pentamidine

: also causes ulcers at the site of injection

•

Foscarnet

: penile ulceration

Palmar

/plantar

keratoderma

:

glucan

Flagellate

erythema

:

bleomycin

Eosinophilic

folliculitis

:

foscarnet

Acrocyanosis

: butyl nitrite

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Drugs implicated in EM, SJS, TEN, and dress syndrome in patients with HIV/AIDS

Abacavir• Allopurinol• Amprenavir (APV)a

•

Carbamazepine

•

Clarithromycin

• Co‐

trimoxazole (sulfamethoxazole

trimethoprim

)

•

Efaviren

•

Etravirie

•

Flucoazole

•

Griseofulvin

•

Indinavir

(IDV, IND)

•

Isoniazid

•

Lamivudine

(3TC)

•

Nevirapine

•

Nitrofurantoin

(in pregnancy)

•

Phenytoin

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Probenecid

•

Pyrimethamine

•

Raltegravir

(RAL)

•

Saquinavir

(SQV, SAQ)

•

Stavudine

(d4T)

• Streptomycin

• Sulfadiazine

•

Sulfadoxine

• Thalidomide

•

Thioacetazone

(

thiacetazone

)

•

Vancomycin

•

Zidovudine

(AZT, ZDV)

• Traditional Chinese medicines

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Photosensitivity Reactions

Porphyria cutanea tarda (PCT)Chronic actinic dermatitis lichenoid photoeruption,

photosensitive

granuloma

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Metabolic Changes

HIV/ART-associated lipodystrophyMalnutrition71

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Cutaneous neoplasm

Kaposi sarcomaSCCBCCMelanomaLymphoma72

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Kaposi sarcoma

KS typically presents as red–purplish patches, papules, plaques, and nodules. The lesions can ulcerate face, upper body, oral cavity, and genitaliaLymph node involvement can result in lymphedemaART is often an effective treatment for KS and represents a reasonable initial

monotherapy

for limited disease.

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Squamous and Basal Cell Carcinomasand Melanoma

2- to 3-fold increased risk of basal cell carcinoma (BCC) and SCC. Onset- younger age ,Multifocal and located on the trunk or extremities.SCCs tend to favor the head and neck, have a high risk of recurrence and metastasis.Superficial BCCs of the trunk- m/c. BCC do not behave more aggressively.

HPV infection with high-risk genital ,

anogenital

, oral, digital, and AEDV-associated cutaneous SCCs.

risk factors for non-melanoma skin cancer - sun exposure, blond hair, blue eyes, and a family history of skin cancer.

Melanomas in HIV-infected patients are often multiple, frequently metastasize, and are associated with a poor prognosis.

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