C18 Dermatologic manifestations in HIV disease
Epidemiology of skin diseases in HIV/AIDS
Skin disorders are commonly encountered in HIV-infected patients, and they may be the first manifestation of HIV disease. Up to 90% of HIV-infected persons suffer from skin problem during their course of illness.[1] The frequency and distribution of dermatologic diseases in HIV infection vary widely. This can be partially explained by the difference in study design, stage of HIV disease, pattern of prevailing infections and use of highly active antiretroviral therapy (HAART). In a cross-sectional study of 186 HIV positive patients in Hong Kong, 175 (94%) had suffered from one or more cutaneous disorders. The most common skin disorder identified was fungal infection, followed by eczema and seborrhoeic dermatitis.[Box 18.1]
Box 18.1. Common cutaneous lesions in HIV patients in Hong Kong (n=186)
| Cutaneous lesions | number | (%) |
|---|---|---|
| Dermatophytosis: Tinea pedis, cruris, corporis onychomycosis | 89 | (47.8) |
| Eczema | 49 | (26.3) |
| Lipodystrophy | 22 | (11.8) |
| Nail conditions: melanonychia, nail dystrophy, chronic parochynia, Subungual haemtoma; ingrowing toenail | 20 | (10.8) |
| Folliculitis: bacterial folliculitis, eosinophilic folliculitis, pityrosporum folliculitis | 19 | (10.2) |
| Pruritic papular eruption (PPE) | 14 | (7.5) |
| Cheilitis / dry lips | 11 | (5.9) |
| Viral infection: Common Wart; post-herpetic neuralgia, Molluscum contagiosum | 9 | (4.8) |
| Skin pigmentation: melasma; easy suntan, generalised hyperpigmentation | 9 | (4.8) |
| Drug eruption | 6 | (3.2) |
| Other conditions included exaggerated insect bite reaction, xerosis, keratosis pilaris, Kaposi’s sarcoma, urticaria and vitiligo. An individual may have more than one dermatosis. 175 (94%) had got one or more dermatological conditions. | ||
In general, declining immunity is associated with increased number and severity of skin disorders.[2] Skin lesions are more likely to have unusual appearance and disease course, and could be recalcitrant to standard treatments in advanced HIV infection.
Approach to skin conditions in HIV/AIDS
Framework of HIV dermatoses
A myriad of skin disorders is implicated in managing people with HIV/AIDS. The spectrum of skin disorder depends on:
- immunologic stage, as reflected by CD4 count
- the use of HAART
- pattern of endemic / opportunistic infections
- pattern of other inflammatory dermatosis and neoplasm
(a) immunologic stage, as reflected by CD4 count[Box 18.2]:
In general, the lower the CD4 count, the higher the chance of opportunistic infection. Nonetheless, psoriasis is one inflammatory dermatosis that has paradoxical behaviour with HIV infection. Studies revealed that pre-existing psoriasis may undergo severe exacerbation in HIV infected patients and become more severe with progression to AIDS.[3]
Box 18.2. Relationship between skin manifestation and CD4 count in HIV infection
| Clinical status and ranges of CD4 cell count | Skin Problems |
|---|---|
| Early infection; CD4 >500/μ | Acute retroviral syndrome Kaposi’s sarcoma Wart Vaginal Thrush |
| Mild Immunosuppression; CD4 200-500/μ | Oral Thrush Recurrent Herpes simplex and zoster Recalcitrant seborrhoeic dermatitis Oral Hairy Leukoplakia Recalcitrant Psoriasis Hyperkeratotic Warts |
| Significant Immunosuppression; CD4 100-200/μ | Disseminated herpes infection Eosinophilic Folliculitis Wide spread molluscum Extensive Kaposi’s sarcoma |
| Advanced Immunosuppression; <100/μ | Cutaneous Penicilliosis Non-healing and large herpes Cutaneous Cryptococcus Disseminated CMV infection |
(b) the use of HAART
The advent of antiretroviral therapy has changed the spectrum of skin disorders by improving host immunity, which in turn reduces the occurrence of Kaposi’s sarcoma (KS) and some skin conditions.[1] However, the restoration of immunity especially in those with more advanced HIV disease could lead to changes in the manifestations of many opportunistic infections and diseases. These are referred as “immune reconstitution inflammatory syndrome (IRIS)”.[Chapter C17] The spectrum of dermatological manifestations in IRIS is summarised in Box 18.3.
Box 18.3. Dermatological manifestation of IRIS
| Non-infectious Inflammatory skin diseases | |
| I. Follicular Inflammatory eruptions | |
| Acneiform eruption or rosacea like eruption: | New onset or upsurge of folliculitis including eosinophilic folliculitis |
| II. Neoplastic lesions | |
| Kaposi’s sarcoma (KS) | Paradoxical increase of cutaneous KS, increasing nodularity and vascularity of existing lesions or increasing oedema |
| Non-Hodgkin’s lymphoma (NHL) | Newly developed shortly after HAART |
| Cutaneous Infectious skin diseases | |
| III. Viral Infection | |
| Varicella Zoster vir us (VZV) infection | Increased incidence, usually uncomplicated and responsive to usual treatment |
| Herpes Simplex virus (HSV) | Increased incidence, also extensive and haemorrhagic, may be associated with myelopathy and encephalitis |
| Human papillomavirus (HPV) | Increased new onset of numerous cutaneous warts, may transform to a giant Buschke-Lowenstein tumour or new onset of epidemodysplasia verruciformis-like cutaneous eruption |
| Molluscum contagiosum virus (MCV) | Increased incidence and inflame; may become exuberant Molluscum contagiosum |
| IV. Mycobacteria | |
| MTB | Nodular lesions, skin changes overlying inflamed lymph nodes |
| Leprosy | Reversal reaction |
| Others | |
| V. Autoimmune and other conditions | |
| IRIS has been reported to be associated with other autoimmune disease such as lupus erythematosus, Gravis thyroiditis, alopecia universalis[4] and vitiligo.[5] Severe inflammatory seborrhoeic dermatitis with secondary alopecia was reported in a patient one month after initiation of HAART.[6] | |
| VI. Granulomatous inflammation | |
| Granulomatous reaction to tattoo | Precipitate foreign body reaction in existing tattoo[6] |
People living with HIV/AIDS (PLWHA) are more likely than non-infected persons to have adverse drug reactions. The use of antiretroviral agents, almost without exceptions, carries the potential risk of causing mucocutaneous adverse reactions.[Box 18.4][7] Some of these adverse effects can be class-specific whereas others are specific to the individual drug. It is often difficult to differentiate and identify the culprit of skin rash as combined use of antiretrovirals is the standard involving simultaneous initiation of 3 drugs. It is even more complicated in those taking other drugs for opportunistic infections. Besides, some adverse effects may have strong labelling effect. For instance, a man who has sex with men (MSM) may be driven away from HAART because of lipodystrophy. The adverse mucocutaneous effects of antiretrovirals is summarised in Box 18.4.[8-15]
Box 18.4. Adverse mucocutaneous effects of antiretroviral agents
| Nucleoside/Nucleotide reverse transcriptase inhibitors (NRTI) Cutaneous adverse effects are mostly specific to individual medications i.e. not class specific; mitochondrial toxicities associated with this class may contribute to lipodystrophy which has a stronger relationship with stavudine (d4T) and didanosine (ddI), though these are no longer commonly prescribed. |
|
| Abacavir (ABC) | Rashes described as maculopapular, urticarial, EM, diffuse erythema, Sweet’s syndrome |
| Didanosine (ddI) | Dry mouth, leucocytoclastic vasculitis, Stevens-Johnson syndrome (SJS), papuloerythroderma of Ofuji, alopecia |
| Emtricitabine (FTC) | Dry skin, maculopapular, urticarial and vesicobullous rash, palmoplantar hyperpigmentation |
| Lamivudine (3TC) | Allergic contact dermatitis |
| Stavudine (d4T) | Peripheral oedema Morbilliform to vesicular rash with mucosal involvement; urticarial rash: low incidence and usually self-limited |
| Tenofovir (TDF) | Morbilliform to vesicular rash with mucosal involvement; urticarial rash: low incidence and usually self-limited |
| Zidovudine (ZDV) | Mucocutaneous & nail hyperpigmentation, hypertrichosis, leucocytoclastic vasculitis, paronychia, fever associated with a variety rash described as lichenoid, morbilliform, urticarial, erythema and toxic epidermal necrolysis (TENS) |
| Non-nucleoside reverse transcriptase inhibitors (NNRTI) NNRTI may cause morbilliform rash which may be part of systemic hypersensitivity syndrome. Of all NNRTS, nevirapine has highest incidence of skin rash whereas rilpivirine has the lowest. |
|
| Efavirenz (EFV) | Morbilliform usually self-limited and hence may not be necessary to be ceased solely for skin rash; history of nevirapine rash does not preclude the use of EFV |
| Nevirapine (NVP) | Morbilliform rash, DRESS (also described as drug-induced hypersensitivity syndrome (DIHS) in the HIV literature), Acute generalised exanthematous pustulosis (AGEP), oral ulcer, SJS |
| Rilpivirine (RPV) | Maculopapular to morbilliform rash; less common compared with NNRTIs |
| Protease Inhibitor (PI) PI may contribute to HIV-associated lipodystrophy syndrome in varying degree and may have stronger relationship with central fat accumulation. |
|
| Atazanavir (ATV) | Mild rash usually not requiring treatment cessation; asymptomatic jaundice |
| Darunavir (DRV) | Not specific, may have SJS, EM |
| Fosamprenavir (FPV) | Self maculopapular rash, SJS (containing sulfa moiety and therefore should be used with caution if there is history of sulfonamide reaction |
| Indinavir (IDV) | Retinoid effects like dry skin, paronychia, cheilitis, alopecia; morbilliform rash |
| Lopinavir (LPV) | DIHS |
| Ritonavir (RTV) | Circumoral paraesthesia, disulfiram reaction |
| Saqinavir (SQV) | Self-limited fixed drug eruption |
| Integrase Inhibitor (INSTI) INSTI is the new class of ART which is not commonly associated with mucocutaneous lesions. |
|
| Raltegravir (RAL) | Uncommonly with DRESS |
| Dolutegravir (DTG) | Uncommonly with DIHS |
| Entry and Fusion Inhibitor | |
| Enfuvirtide (INN) | Uncommonly with DRESS |
| Dolutegravir (DTG) | Uncommonly with DIHS |
| Entry and Fusion Inhibitor | |
| Enfuvirtide (INN) | Local injection site reactions |
| Maraviroc (MRV) | Non-specific rash |
| AGEP: Acute generalised exanthematous pustulosis; DIHS: drug-induced hypersensitivity syndrome; DRESS: Drug reaction with eosinophilia systemic syndrome; EM: Erythema Multiforme; SJS: Stevens Johnson Syndrome; TEN: Toxic epidermal necrolysis. | |
(c) pattern of endemic / opportunistic infections
Recognition of the pattern of dermatological manifestations of opportunistic infection in HIV disease may be contributory to disease diagnosis, staging and choice of specific therapeutic agents. Examples include multi-dermatomal herpes zoster infection that is associated with immunodeficiency resulting from HIV/AIDS; recurrence of persistent oral thrush, persistent non healing large aphthous ulcer and extensive hyperkeratotic wart which suggests HIV infection not limited to a particular geographical location; penicilliosis with or without dermatological manifestations which is unique with HIV infection in Hong Kong and Southeast Asia. The pattern of endemic / opportunistic infection is summarised in Box 18.5.
(d) pattern of other inflammatory dermatoses and neoplasms
With advanced disease and low CD4 count, more cutaneous infections may occur whereas the signs and symptoms of inflammatory dermatoses may become less obvious or atypical.[Box 18.2] However, such inflammatory dermatoses can offer clues which alert clinicians of the diagnosis of HIV/AIDS. For example, as mentioned above, sudden onset, or exacerbation of psoriasis or recalcitrant seborrhoeic dermatitis may herald the diagnosis of HIV. Other examples are eosinophilic folliculitis and type VI pityriasis rubra pilaris (PRP), though non-pathognomonic, are characterised by specific patterns in PLWHA. KS, with a blemish on face or other part of body is a typical neoplastic lesion that points to HIV infection. Certain types of non-Hodgkin’s lymphoma, albeit not diagnostic, should prompt the attending doctor to consider HIV infection particularly in high risk populations such as MSM. The patterns of inflammatory dermatoses and neoplasms are summarised in Box 18.6.
Diagnosis and Treatment
The drug history, morphology and clinical course of primary lesion, and immune status (CD4) are important clues to dermatological diagnoses. In many cases, HIV-associated skin diseases can be easily recognised on clinical grounds, especially in the early phase of HIV disease when clinical atypia is less frequent.
When diagnostic difficulty is encountered, skin biopsy should be considered for both histologic and microbiological evaluation. As HIV-infected persons frequently have more than one form of dermatoses, several biopsies may be necessary. Regardless, it would be too simplistic to consider skin biopsy as the definitive method of diagnosis. The histopathological pattern may not be specific to a particular diagnosis. The unusual clinical presentation of a dermatoses may also extend to its histological pattern, for instance granuloma is not well formed in advanced HIV disease. Despite the use of special stain and culture, immunohistochemical or molecular technique, clinico-pathological correlation is often required to arrive at the more likely diagnosis.
Although skin diseases in HIV patients are rarely life-threatening, many do severely hamper the quality of life by causing significant morbidity and affect drug adherence. Therefore, good management starts with effective communication with those affected. From another perspective, while the lifespan is prolonged by HAART, some PLWHA are troubled by drug-induced facial lipoatrophy which may affect the acceptability and adherence to HAART especially with the use of older generation of antiretrovirals. Not only can there be cosmetic concern, the intense pruritus due to eosinophilic folliculitis may severely impair the patients’ quality of life. Therefore, management of these seemingly minor conditions should not be overlooked.
A realistic therapeutic objective and expectation to outcomes should be considered and sensibly communicated with PLWHA. Therapeutic objectives may include:
- eradication or control of life threatening conditions,
- prevention of complications or disease progression,
- symptomatic relief,
- restoration of functional status,
- recovery of psychosocial well-being, and
- improvement in cosmesis.
In most cases, treatment modality of skin diseases in HIV-positive patients is similar to that in HIV-negative ones. However, the immunosuppressive state and concurrent medications should always be considered in formulating treatment strategy. For instance, prolonged high-dose systemic steroid should be used with caution because of the immunosuppressive effects. Nowadays, more advanced treatment has been used in inflammatory dermatoses like biologics in psoriasis. The use of these advanced treatment in HIV infected patient should be more judicious and cautious, balancing the immunodeficiency in HIV and efficacy of treatments as well as the drug-drug interaction with HAART.
Box 18.5. Selected pattern of endemic / opportunistic infections
| (a) Bacterial infection | |||||
| Disease | Typical Presentation | Atypical Presentation | Diagnosis | Treatment | Remark |
| Boils, folliculitis, impetigo and related conditions | Pustule as the primary skin lesion for boil and folliculitis; weeping macule or small patch with peripheral fine scale in impetigo; lesions commonly caused by Staphylococcus or Streptococcus or Pseudomonas | Botryomycosis in form of subcutaneous nodules or plaques with ulcer or fistulae discharging purulent materials on scalp, axillae or groins; associated with Staphylococcus | Clinical; swab for culture | Antibiotics, antiseptics +/- surgical drainage | Recurrent bacterial infection is a feature of HIV infection in children. |
| Mycobacteria including TB | Varying appearances – nodules, plaques or localised cutaneous abscess; suppurative lymphadenitis; non-specific ulcerations; reactive tuberculids such as papulonecrotic tuberculid, erythema induratum | Mainly by special culture or histopathology; supplemented by nucleic acid amplification tests | According to the type of mycobacterium isolated and immune status, similar as systemic infection | ||
| Bacillary angiomatosis (Bartonella spp.) | Vascular papules or nodules, distributed over face and upper trunk. (main ddx: KS and pyogenic granuloma) | Histopathology with special stain (eg Warthin Starry stain) | May include macrolide, doxycycline, ciprofloxacin, rifampicin and septrin | Seldom encountered in Hong Kong | |
| (b) Fungal infection | |||||
| Disease | Typical Presentation | Atypical Presentation | Diagnosis | Treatment | Remark |
| Superficial dermatophytosis | Annular lesion with active scaling margin and centre clearing in tinea corporis, faciei & cruris; diffuse hyperkeratosis or vesiculation in tinea pedis | Tinea faciei mimicking erythema multiforme or seborrhoeic dermatitis and tinea pedis presenting as keratoderma blenorrhagica like lesion; Majocchi’s granuloma; proximal subungual onychomycosis (PSO, uncommon in normal host) | Microscopy and fungal culture of skin scrapping, hair or nail obtained | Topical imidazoles or Whitfield ointment; systemic antifungal-griseofulvin, itraconazole, terbinafine, fluconazole, posaconazole | |
| Pityrosporum yeast | Pityriasis versicolor as classical lesion in form of hypopigmented macules with superficial fine powdery scale over upper trunk; pityrosporum folliculitis presented with itchy monomorphic folliculitis or inflammatory follicular papules over upper back, chest or face | Clinical; microscopy; histopathology | Topical or systemic imidazoles (or triazole) | Related to seborrhoeic dermatitis | |
| Candida spp | Oral thrush, angular cheilitis, intertrigo, balanitis, paronychia and vaginal thrush are common presentation | Median rhomboid glossitis | Clinical or microscopy; occasionally by culture | Topical or systemic imidazoles (or triazole) | Mucocutaneous candidiasis often by C albican, common in HIV infection |
| Penicilliosis | Umbilicated papules; simulating molluscum contagiosum | Ecthyma, folliculitis, subcutaneous nodule or morbilliform rash | Histopathology and/or culture the biopsy specimen | Amphotericin B or itraconazole | Skin involved in 75% of cases and common in Southeast Asia including Hong Kong |
| Cryptococcus | Molluscum contagiosum like lesions | May mimic HSV, cellulitis, KS or hypertrophic lesion like rhinophyma | Histopathology and/or culture the biopsy specimen | Amphotericin B or fluconazole + flucytosine, itraconazole and voriconazole | |
| (c) Viral infection | |||||
| Disease | Typical Presentation | Atypical Presentation | Diagnosis | Treatment | Remark |
| Acute retroviral syndrome / seroconversion | Systemic involvement like fever, lymphadenopathy, generalised viral exanthema occasional involved palm and sole | Clinical; HIV serology may need to be repeated after window period | Combined antiretroviral therapy according to prevailing guidelines | Symptomatic treatment | |
| Varicella zoster | Painful vesicles in crops along a single or multi dermatome; can be recurrent | Persistent non-healing ulcer; warty or molluscum like nodule, disseminated and generalised involvement | Clinical; viral culture; direct immunofluorescence study (DIF); histopathology may be needed especially in atypical presentation | Systemic acyclovir, valaciclovir, famciclovir | |
| Molluscum contagiosum | White or flesh colour papules or small nodules with or without umbilication | Large lesion may be warty like and multiple with predilection for face in adult | Clinical; histopathology may be needed in atypical presentation | Curettage and iodinisation commonly used; cryotherapy; spontaneous resolution after HAART reported | Off label use of imiquimod cream can be tried; topical cidofovir has been reported |
| Wart (refer to Chapter D29) | Common warts as warty papules, small plaques; plan warts as tiny flat papules | Extensive and thick; multiple; hyperkeratotic; may have ulceration | Clinical; histopathology may be needed especially when verrucous carcinoma is suspected in atypical cases | Cryotherapy; curettage and cauterisation; CO2 laser | Podophyllin, podophyllotoxin (not registered for such indication in some places); imiquimod mainly for anogenital wart |
Box 18.6. Selected pattern of other inflammatory dermatosis and neoplasm
| (a) Inflammatory dermatosis | |||||
| Disease | Typical Presentation | Atypical Presentation | Diagnosis | Treatment | Remark |
| Psoriasis | Well defined erythematous plaque with silvery scales and predilection to the extensor surfaces of limbs, body and scalp; may exacerbate in stable psoriasis patients once AIDS develops; may erupt spontaneously at some point of time after HIV seroconversion | Clinical; occasionally by histopathology | Topical treatment including tar, salicylic acid, steroid, vitamin D derivatives; phototherapy; systemic treatment including retinoid, methotrexate & cyclosporine (use with caution) | Use of biologics in people living with HIV/AIDS (PLWHA) reported but not adequately reviewed, need to balance risk and use with caution | |
| Seborrhoeic dermatitis | Poorly demarcated scaly erythematous patches involving glabella, nasolabial fold, external auditory canal, scalp and presternal area. | Unusual sites such as trunk, groins and extremities may be affected; can be extensive and resistant to conventional treatment | Clinical; occasionally by histopathology | As pityrosporum yeast is thought to play an important role, treatment is combination of topical imidazole and mild topical steroid | Probably one of the commonest skin conditions in PLWHA, occurring in 85% of PLWHA at some points of their disease course |
| Atopic dermatitis | Flares of pre-existing atopic dermatitis which may have been in remission for some years; erythroderma has been reported; typical itchy rash in form of poorly demarcated erythematous papulovesicular lesions with weeping, scale crust in characteristic distribution | Mainly by clinical | Emollient, topical steroid, phototherapy and occasionally systemic drug treatment such as short course of systemic steroid | A biologic has been introduced in HK; no data on its use in PLWHA with atopic eczema | |
| Xerosis, ichthyosis and asteatotic eczema | Dry skin is very common in PLWHA, typically dry and flaky with or without excoriation marks | Clinical; need to rule out other important conditions associated with generalised pruritus | Proper skin care and liberal use of emollient | Uncertain aetiology, probably the commonest cause of pruritus in PLWHA | |
| Pruritic dermatoses in HIV | Pruritus is common in PLWHA; eosinophilic pustular folliculitis is more specific and characteristic in HIV, presenting with widespread excoriated follicular papules involving mainly head and neck and upper truck, important to exclude other conditions that may cause pruritus such as scabies, non-Hodgkin’s lymphoma (NHL) or dermatitis herptiformis | Clinical and histopathology | WHO recommended to try oral antihistamine, topical steroids, oral itraconazole , topical 5% permethrin cream and other treatments reported but with variable efficacies include metronidazole, calcineurin inhibitor, UVB oral isotretinoin | Pruritic papular eruption originally described as a specific entity affecting PLWHA, now believed to be a feature of skin diseases of heterogeneous causes | |
| Cutaneous drug reaction | Common causes of drug hypersensitivity include septrin, anti-TB drugs, nevirapine, and abacavir; morbilliform rash probably the commonest type of drug rash; more serious reactions including SJS, TEN and DRESS | Clinical; supplemented by histopathology and by exclusion | Withdrawal of culprit drug and supportive treatment; systemic steroid may be used in DRESS, IVIG may be used in SJS and TEN | Abacavir hypersensitivity syndrome linked to HLA B5701, but is uncommon in Hong Kong | |
| (b) Neoplastic Diseases | |||||
| Disease | Typical Presentation | Atypical Presentation | Diagnosis | Treatment | Remark |
| Kaposi’s sarcoma (KS) | Asymptomatic bluish/ violaceous macules or papulonodules or plaque on any sites of body, more common in head and neck region and oral mucosa | Rarely hyperkeratotic KS | Clinical; confirmed by histopathology | Can be expectant after HAART, local destructive, local chemotherapeutic or radiotherapy; systemic chemotherapy depending on symptoms and internal organs involvement; HAART may sometimes induce remission of KS | [Chapter E30] |
| Non-Hodgkin’s lymphoma (NHL) | B-cell NHL occasionally presenting as fleshy skin papulonodules / plaques; T-cell lymphoma as bizarre shaped patches, plaque or nodule with superficial scaling and inter/intra-lesional morphology variation | Histopathology with immunohistochemical / molecular techiques | B-cell NHL mainly treated by systemic chemotherapy’ T-cell NHL treated by topical steroid, phototherapy, radiotherapy (including total body electron beam radiation), interferon and systemic chemotherapy | [Chapter E31] | |
| Cloacogenic carcinoma (or related dystrophic condition) | Lesions can present as wart like papules (Bowenoid papulosis / vulval dystrophy) or squamous carcinoma like exophytic growth involving anogenital area | Histopathology | As for non-HIV infected patients | Condition related to high risk HPV infection with pathogenesis similar to that for carcinoma of the cervix in female; disease incidence increased in HIV infected population; HPV vaccine is an effective way to prevent these cancers caused by vaccine related HPV | |
References
- Chan KWR, Chio TWM, Koh HY. Cutaneous Manifestations of HIV infection. In: Bolognia JL, Schaffer JV, Cerroni L. (eds) Dermatology 4th ed. St. Louis (MO): Mosby Elsevier; 2018.
- Raju PV, Rao GR, Ramani TV, Vandana S. Skin disease: clinical indicator of immune status in human immunodeficiency virus (HIV) infection. Int J Dermatol 2005;44:646-649. link
- Morar N, Willis-Owen SA, Maurer T, Bunker CB. HIV-associated psoriasis: pathogenesis, clinical features and management. Lancet Infect Dis 2010;10(7):470-8. link
- Sereti L, Sarlis NJ, Arioglu E, Turner ML, Mican JM. Alopecia universalis and Graves’ disease in the setting of immune restoration after highly active antiretroviral therapy. AIDS 2001;15:138-40. link
- Kigonya C, Lutwama F, Colebunders R. Extensive hypopigmentation after starting antiretroviral treatment in an HIV seropositive African woman. Int J Dermatol 2008;47:102-3. link
- Hardcastle NJ, Tunbridge AJ, Shum KM, Dockrell DH, Green ST. Alopecia in association with severe seborrhoeic dermatitis following combination antiretroviral therapy for acute retroviral syndrome. J Eur Acad Dermatol Venereol 2005;19:631-3 link
- Introcaso CE, Hines JM, Kovarik CL. Cutaneous toxicities of antiretroviral therapy for HIV: Part I and Part II. J Am Acad Dermatol 2010;63:549-569 link
- Borras-Blasco J, Navarro-Ruiz A, Borras C, Castera E. Adverse cutaneous reactions associated with the newest antiretroviral drugs in patients with human immunodeficiency virus infection. J Antimicrob Chemother 2008;62:879-888. link
- Luther J, Glesby MJ. Dermatologic adverse effects of antiretroviral therapy: recognition and management. Am J Clin Dermatol 2007;8(4):221-233. link
- Alexoudi I, Katsarou A, Paparizos V, Oikonomou K, Kourkounti S, Augerinou G, Antoniou C. Dermatological conditions associated with HIV medication in a cohort of Greek patients initiating antiretroviral therapy:1988-2013. J Virus Erad 2018;4:26-29. link
- Wu PY, Cheng CY, Liu CE, Lee YC, Yang CJ, Tsai MS, Cheng SH, Lin SP, Lin DY, Wang NC, Lee YC, Sun HY, Tang HJ, Hung CC. Multicentre study of skin rashes and hepatotoxicity in antiretroviral-naïve HIV-positive patients receiving non-nucleoside reverse transcriptase inhibitor plus nucleoside reserve transcriptase inhibitors in Taiwan. PLoS One 2017;12(2):e0171596. link
- Lin KY, Cheng CY, Yang CJ, Tsai MS, Hsieh SM, Sun HY, Sheng WH, Chen MY, Chang SY, Cheng SH, Hung CC. Skin rash related to once-daily boosted darunavir-containing antiretroviral therapy in HIV-infected Taiwanese: incidence and associated factor. J Infect Chemother 2014;20(8):465-470. link
- Nishijima T, Gatanaga H, Teruya K, Mizushima D, Aoki T, Watanabe K, Kinai E, Honda H, Yazaki H, Tanuma J, Tsukada K, Kikuchi Y, Oka S. Skin rash induced by ritonavir-boosted darunavir is common but generally tolerable in an observational setting. J Infect Chemother 2014;20(4):285-287. link
- Yee BE, Nyguyen NH, Lee D. Extensive pulmonary involvement with raltegravir-induced DRESS syndrome in a postpartum woman with HIV. BMJ Case Rep 2014 May 5;2014. pii: bcr2013201545. link
- Curtis L, Nichols G, Stainsby C, Lim J, Aylott A, Wynne B, Clark A, Bloch M, Maechler G, Martin-Carpenter L, Raffi F, Min S. Dolutegravir: clinical and laboratory safety in integrase inhibitor-naïve patients. HIV Clin Trials 2014;15(5):199-208. link