¹Center for Clinical Studies, Houston, TX, USA
²University of Texas School of Medicine at San Antonio, San Antonio, TX, USA
³Department of Dermatology, University of Texas Health Science Center at Houston, Houston, TX, USA

ABSTRACT
Human papillomavirus (HPV) has a predilection for infecting epidermal and mucosal surfaces such as those of the anogenital region. HPV causes substantial pre-malignant, malignant, and benign disease in both women and men, ranging from cervical, vulvar, penile, and anal cancers to condyloma acuminata (genital warts). Although HPV vaccination is becoming more common, infection rates remain high in both genders. Perception of HPV vaccine has largely centered on its ability to prevent cervical cancer in women, though indication for its use in men is expanding. The benefits to men include prevention of genital warts and, more recently, regulatory approval was expanded in the US for prevention of anal cancer. Herein, we review HPV vaccine with a focus on its new indication in men and existing controversies.

Key Words:
cancer, HPV, human papillomavirus, vaccine, warts, Gardasil®, Cevarix®

Background

Genital human papillomavirus (HPV) is the most common sexually transmitted infection (STI) in the US.¹ An estimated 20 million Americans are currently infected, with 6.2 million new cases occurring each year in people 14-44 years of age. Seventy-four percent of new cases occur in persons aged 15-24 years, and it is suggested >80% of sexually active women will acquire genital HPV by age 50. The majority of infections are asymptomatic and self-limited; however, persistent HPV infection with an oncogenic type can cause cervical cancer. HPV infection is also common among men. Approximately 1 million American men have genital warts caused by HPV, with 2 of every 1,000 men newly diagnosed.²

More than 130 HPV types have been identified, with greater than 40 causing genital infection. Genital HPV is divided into two groups based on potential to cause cancer: high-risk or oncogenic types and low-risk or nononcogenic types. High-risk types (such as 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 69, and 73) can cause low-grade and high-grade cervical cell abnormalities as well as anogenital carcinoma. Together HPV-16 and 18 account for about 70% of cervical cancers.³

Low-risk types (mainly 6 and 11) cause most (90%) of the genital warts in males and females, recurrent respiratory papillomatosis, and nasopharyngeal papillomas, as well as low-grade disease of the cervix in women.²

HPV Vaccines

Two HPV vaccines are currently available in the US, quadrivalent (Gardasil®) and bivalent (Cevarix®) vaccines. The Food and Drug Administration (FDA) approved the quadrivalent vaccine in 2006 and bivalent vaccine in 2009.²

The quadrivalent vaccine is composed of four HPV type-specific virus-like particles (VLPs) prepared from the capsid protein of HPV-6, 11, 16, and 18 combined with aluminum adjuvant. This vaccine is recommended for females 9-26 years (in Canada the approved indication includes girls and women 9-45 years of age) and is administered intramuscularly according to a 3-dose schedule at 0, 2, and 6 months. The bivalent vaccine is composed of two VLPs of HPV-16 and 18 and is recommended for females 10-25 years through intramuscular injection according to a 3-dose schedule at 0, 1, and 6 months.^2,4

The efficacy of quadrivalent vaccine is well established. In a per-protocol analysis (two Phase III trials), vaccine efficacy was 100% (95% CI, 80.9-100) for prevention of HPV-16 or 18 related cervical intraepithelial neoplasia (CIN) grades 2/3. In Protocol 013, which included 5,442 females aged 16-23 years, vaccine efficacy was 100% (95% CI, 89.5-100) for prevention of any grade CIN related to the vaccine types. The three studies (Protocol 007, 013, and 015) demonstrated vaccine efficacy of 98.9% (95% CI, 93.7-100) for prevention of HPV-6, 11, 16, and 18 related genital warts and 100% (95% CI, 55.5-100) for prevention of HPV-16 or 18 related vulvar intraepithelial neoplasia (VIN) 2/3 or vaginal intraepithelial neoplasia (VaIN) 2/3.^5,6

The efficacy of bivalent vaccine is also well established. In a Phase III trial, which included 18,644 females aged 15-25 years, perprotocol cohort vaccine efficacy was 98.1% (96.1% CI, 88.4-100) for prevention of HPV-16 or 18 related CIN 2/3.⁷

New Indications

Although < 25% of all HPV-related cancers occur in men, specific groups, such as men who have sex with men, have significantly higher rates of HPV-related diseases, including anal cancer. HPV- 16 and 18 cause approximately 90% of anal cancers. Around 340,000 new cases of genital warts are reported in the US each year.⁸ In 2009, the FDA approved the quadrivalent vaccine for prevention of genital warts in young men. The Advisory Committee on Immunization Practices (ACIP) recommended permissive use but not routine use of the vaccine for males aged 9-26 years.⁹ More recently, regulatory approval was expanded in the US for prevention of anal cancer.

Recent data has demonstrated the quadrivalent vaccine to be effective in preventing anal intraepithelial neoplasia in males. A randomized, placebo-controlled, double-blind study conducted by Guiliano et al.¹⁰ included 4,065 males aged 16-26 years from 71 sites throughout 18 countries. Of these participants, 3,463 were heterosexual. At screening, subjects who had clinically detectable anogenital warts or genital lesions suggestive of existing HPV infection were excluded from the study. The participants were followed for 2.9 years.

Guiliano’s study showed prophylactic administration of quadrivalent vaccine to be efficacious in the prevention of genital lesions associated with HPV-6, 11, 16, and 18 in males aged 16-26 years. In the intention-to-treat population, vaccine efficacy was 65.5% (95% CI, 45.8-78.6) for prevention of vaccine type lesions and 60.2% (95% CI, 40.8-73.8) for prevention of any external genital lesion regardless of HPV type. When the per-protocol population was analyzed, vaccine efficacy for prevention of external genital lesions related to HPV-6, 11, 16, and 18 was 90.4% (95% CI, 69.2-98.1) and the efficacy against condyloma acuminata was 89.4% (95% CI, 65.5-97.9). No cases of PIN (penile, perianal, or perineal intraepithelial neoplasia) lesions were observed in the perprotocol vaccine group, however, this finding was not statistically significant in the study. Limitations of the study include the narrow age-range of the subjects and the relatively short followup period. Additionally, subjects had no more than five lifetime sexual partners, which could result in overrepresentation of subjects with a low likelihood of HPV exposure at baseline and subsequent exposure.¹⁰

Controversies

Several questions have arisen concerning the use of HPV vaccine in females, which have further expanded with approval of the vaccine for males.

Will the vaccine prevent not only genital lesions, but also cervical and anal cancer and ultimately death?
An answer to this question will likely depend on decades of observation. However, benefits of the quadrivalent and bivalent vaccines have been consistently reported. HPV vaccine also has other early benefits. As reported in end-of-study data from Phase IIB and Phase III (FUTURE I and II) trials, vaccination in the negative to 14 HPV types population reduced the proportion of women who experienced a cervical therapy by 42% (95% CI, 28-54), which may reduce adverse pregnancy outcomes related to these procedures.¹¹ HPV vaccine may also reduce the number of preterm deliveries due to cervical therapies.¹²

The probability of infection with HPV-6, 11, 16, and 18 in young women pre-sexual debut is very low, however, almost all women will come into contact with at least one type with only 0-4 sexual partners, thus, almost all young women may benefit from the vaccine. Studies have also shown that in women with evidence of current infection with at least one HPV vaccine type, quadrivalent vaccine may prevent disease caused by the remaining nonexposed vaccine types. Further, in women with cleared infections by an HPV vaccine type, quadrivalent vaccine has been shown to prevent recurrent disease caused by the same type.^13,14

Australia is the first country to mount a fully funded HPV immunization program for all females 12-26 years of age. Within the first two years the country witnessed a 59% (95% CI, 54-61) reduction in genital warts in this age group of females, with the proportion of women diagnosed declining from 11.7% to 4.8%. In heterosexual males aged 12-26 years, a 39% (95% CI, 33-46) reduction in men diagnosed with genital warts from 17.3% to 10.5% was observed within the same two-year period. This finding in men is suggestive of herd immunity attributable to reduced exposure to HPV in vaccinated women.¹⁵

How long will protection conferred by the vaccine last?
Antibody titers reach their peak after the third dose, then decline gradually until month 24 and remain higher than those naturally infected. Phase IIB trials showed complete protection for the monovalent HPV-16 vaccine after 9.5 years, 6.4 years for the bivalent vaccine, and 4 years for the quadrivalent vaccine.¹⁶ HPV vaccine follow-up continues, with recent data indicating a rapid and strong anamnestic response induced by a fourth dose of HPV vaccine 6.8 years after the initial 3-dose vaccination course; all subjects demonstrated an approximate eight-fold increase in HPV-16 and 18 antibody titers 7 days after the fourth dose and a >16-fold increase after 1 month.¹⁷

Since most HPV infections are easily cleared by the immune system, how will vaccination affect natural immunity against HPV, and with what implications?
Although most HPV infections are easily cleared by the immune system, interim lesions represent a substantial burden on the health care system and can cause psychosexual distress in patients. As well, persistent infections have significant implications as a cause of cervical cancer. Antibody response to HPV, in general, is specific for the HPV type; however, cross-reactivity has been noted. Recent studies suggest that the quadrivalent vaccine may also provide cross-protection against HPV strains not contained in the vaccine, but are closely related.^18,19 Notwithstanding, the durability of immunity and the importance of these findings remain to be established.

Will type replacement be seen?
With the introduction of HPV vaccines, “type replacement” is a concern. Type replacement is a viral population dynamics phenomenon defined as elimination of some types causing an increase of others. It occurs when partial competition exists among different types during natural infection and the vaccine does not provide cross-protection against competing types. In HPV, natural competition does not appear to exist, therefore type replacement is unlikely.⁴

How will the vaccine affect other oncogenic strains of HPV?
There is risk of change in population dynamics for existing HPV types and viral mutations may occur to generate new variants that are equally oncogenic but not recognized by vaccine-induced antibodies. However, HPV uses host cell DNA polymerases, and thus, has a very slow mutation rate, suggesting this risk is very low.⁴

How will vaccination affect screening practices?
Cytological screening practices should not be modified since the endpoint of the vaccine (cervical cancer) may take decades before incidence change can be measured. It has been suggested by HPV vaccine biologic models that the vaccine may increase the screening intervals.⁴ Positive predictive value will drop, making viral testing more appealing.

Other Vaccine Benefits

All HPV lesions, including genital warts, are associated with significant physical and psychological morbidity, high treatment failure and recurrence rates, as well as substantial cost.

The incidence of HPV infection is similar among both males and females, however, prevalence of infections is higher in males. Differences in immune response to HPV between genders have been described. A US study found HPV-seropositivity was higher in females than males (17.9% vs. 7.9%, respectively).²⁰ The higher prevalence of HPV infections in men may be explained in part by the lower immune response to natural infection.

The ACIP recommends routine vaccination of females aged 11-12 years (the vaccination series may be started as early as 9 years) and catch-up vaccination for females aged 13-26 years. Similarly, the European Centre for Disease Control and Prevention recommends that the primary target population for HPV vaccination should be young girls before they become sexually active, with catch-up vaccination administered in older girls and young women. These measures will likely accelerate the public health impact of vaccination while also increasing short-term benefits.

Conclusion

HPV vaccination represents an important approach in cancercontrol strategies aimed at reducing the global incidence of cervical cancer. Routine vaccination of girls is already recommended and catch-up immunization programs have also been instituted for older girls not yet vaccinated in order to complete the schedule. The increasing prevalence of HPVrelated cancers in males coupled with a lack of anal cancer screening underscores the importance of routine vaccination of boys, not only to benefit the boys themselves but also to reduce transmission to unvaccinated girls, thus further widening the impact of HPV vaccination.

References

1. Nandwani MC. Men’s knowledge of the human papillomavirus vaccine. Nurse Pract 35(11):32-9 (2010 Nov).
2. Markowitz LE, Dunne EF, Saraiya M, et al. Quadrivalent human papillomavirus vaccine. Recommendations of the Advisory Committee on Immunization Practices (ACIP). Centers for Disease Control and Prevention 2007.
3. Monsonego J, Cortes J, Greppe C, et al. Benefits of vaccinating young adult women with a prophylactic quadrivalent human papillomavirus (types 6, 11, 16 and 18) vaccine. Vaccine 28(51):8065-72 (2010 Nov).
4. Dillner J, Arbyn M, Unger E, et al. Monitoring of human papillomavirus vaccination. Clin Exp Immunol 163(1):17-25 (2011 Jan).
5. Kjaer SK, Sigurdsson K, Iversen OE, et al. A pooled analysis of continued prophylactic efficacy of quadrivalent human papillomavirus (Types 6/11/16/18) vaccine against high-grade cervical and external genital lesions. Cancer Prev Res (Phila) 2(10):868-78 (2009 Oct).
6. Munoz N, Manalastas R, Jr., Pitisuttithum P, et al. Safety, immunogenicity, and efficacy of quadrivalent human papillomavirus (types 6, 11, 16, 18) recombinant vaccine in women aged 24-45 years: a randomised, double-blind trial. Lancet 373(9679):1949-57 (2009 Jun).
7. Paavonen J, Naud P, Salmeron J, et al. Efficacy of human papillomavirus (HPV)- 16/18 AS04-adjuvanted vaccine against cervical infection and precancer caused by oncogenic HPV types (PATRICIA): final analysis of a double-blind, randomised study in young women. Lancet 374(9686):301-14 (2009 Jul).
8. Barroso LF, 2nd, Wilkin T. Human papillomavirus vaccination in males: the state of the science. Curr Infect Dis Rep 13(2):175-81 (2011 Apr).
9. FDA licensure of quadrivalent human papillomavirus vaccine (HPV4, Gardasil) for use in males and guidance from the Advisory Committee on Immunization Practices (ACIP). Centers for Disease Control and Prevention 2010.
10. Giuliano AR, Palefsky JM, Goldstone S, et al. Efficacy of quadrivalent HPV vaccine against HPV Infection and disease in males. N Engl J Med 364(5):401-11 (2011 Feb).
11. Munoz N, Kjaer SK, Sigurdsson K, et al. Impact of human papillomavirus (HPV)-6/11/16/18 vaccine on all HPV-associated genital diseases in young women. J Natl Cancer Inst 102(5):325-39 (2010 Mar).
12. Sjoborg KD, Eskild A. Vaccination against human papillomavirus–an impact on preterm delivery? Estimations based on literature review. Acta Obstet Gynecol Scand 88(3):255-60 (2009).
13. Mariani L, Venuti A. HPV vaccine: an overview of immune response, clinical protection, and new approaches for the future. J Transl Med 8:105 (2010 Oct).
14. Olsson SE, Kjaer SK, Sigurdsson K, et al. Evaluation of quadrivalent HPV 6/11/16/18 vaccine efficacy against cervical and anogenital disease in subjects with serological evidence of prior vaccine type HPV infection. Hum Vaccin 5(10):696-704 (2009 Oct).
15. Donovan B, Franklin N, Guy R, et al. Quadrivalent human papillomavirus vaccination and trends in genital warts in Australia: analysis of national sentinel surveillance data. Lancet Infect Dis 11(1):39-44 (2011 Jan).
16. Stanley M. Potential mechanisms for HPV vaccine-induced long-term protection. Gynecol Oncol 118(1 Suppl):S2-7 (2010 Jun).
17. Moscicki A-B, Wheeler CM, Romanowski B, et al. Anamnestic response elicited by a fourth dose of the HPV-16/18 ASO4-adjuvanted vaccine in young women. Abstract presented at: European Research Organization on Genital Infection and Neoplasia 2010 (EUROGIN). Monte Carlo, Monaco, 17-20 February 2010.
18. Brown DR, Kjaer SK, Sigurdsson K, et al. The impact of quadrivalent human papillomavirus (HPV; types 6, 11, 16, and 18) L1 virus-like particle vaccine on infection and disease due to oncogenic nonvaccine HPV types in generally HPV-naive women aged 16-26 years. J Infect Dis 199(7):926-35 (2009 Apr).
19. Wheeler CM, Kjaer SK, Sigurdsson K, et al. The impact of quadrivalent human papillomavirus (HPV; types 6, 11, 16, and 18) L1 virus-like particle vaccine on infection and disease due to oncogenic nonvaccine HPV types in sexually active women aged 16-26 years. J Infect Dis 199(7):936-44 (2009 Apr).
20. Stone KM, Karem KL, Sternberg MR, et al. Seroprevalence of human papillomavirus type 16 infection in the United States. J Infect Dis 186(10):1396- 402 (2002 Nov).

¹Center for Clinical Studies, Houston, TX, USA
²The Institute of Human Virology, University of Maryland, Baltimore, MD, USA
³Department of Dermatology, University of Texas Health Sciences Center,
Houston, TX, USA

ABSTRACT

Atypical presentations of typical dermatological conditions are common in human immunodeficiency virus (HIV). This article will focus on three specific topics: eosinophilic folliculitis, psoriasis, and cutaneous mycoses. Their unique presentations in HIV and treatments are discussed.

Key Words:
HIV, eosinophilic folliculitis, psoriasis, cutaneous mycoses

Despite attempts at increasing awareness of HIV and its transmission, this infection continues to spread and remains a significant cause of morbidity and mortality worldwide. As of 2003, there were an estimated 1 million people living in the US with HIV infection, and nearly 40,000 cases were diagnosed in 2005.¹ HIV infection affects nearly every organ system in the body, including the skin. HIV-infected patients can pose diagnostic challenges, as their altered immune status may lead to atypical presentations of common cutaneous diseases, as well as the occurrence of uncommon or opportunistic skin disorders. Management of cutaneous disease in sero-positive patients can also be challenging, as the dermatological manifestations may be more severe, may recur with greater frequency, and may be refractory to standard treatment. The addition of highly active antiretroviral therapy (HAART) further complicates the picture as other dermatologic manifestations may arise as part of the immune reconstitution phenomenon. The scope of issues encountered in HIV positive patients is too broad to discuss in its entirety. This article will focus on three diseases and their management: eosinophilic folliculitis, psoriasis, and cutaneous mycoses.

Eosinophilic Folliculitis

Eosinophilic folliculitis (EF) is seen commonly in HIV with CD4 cell counts of <250-300/mm3.2,³ It presents as recurrent, pruritic, erythematous papules and pustules that are usually distributed on the face, shoulders, upper back, and upper extremities.³ The pruritus associated with EF can be severe and debilitating. Its etiology is not well elucidated, but some theories propose an infectious derivation. EF is an example of a dermatosis that is associated with immune-reconstitution.³ It is described as a phenomenon wherein HAART triggers a generalized immune activation as viral loads decrease and CD4 lymphocytes increase.^{4, 5} Studies have shown that EF typically flares shortly after starting antiretroviral therapy, but will resolve from 3 weeks to several months later.³ Clinicians should warn patients with EF that after starting HAART, their skin will likely worsen initially, then improve.
EF can be difficult to manage, as response to treatment is variable and it tends to recur once treatment is discontinued. Various treatments have been employed, including: isotretinoin, UVB phototherapy, itraconazole, and metronidazole, among others, with contrasting results.² The treatment of EF with potent topical corticosteroids is reportedly effective, but is accompanied by skin atrophy and hypopigmentation. This can be a problem given the distribution of EF on the face, and can be especially challenging in dark-skinned individuals.⁶ A relatively recent case study showed promising results with topical tacrolimus. Subjects who applied daily topical tacrolimus 0.1% to the face had an average lesion clearance time of 2.6 months with an absence of residual scarring. The average remission of 12.3 months was seen in subjects with well controlled viremia on HAART. The associated pruritus subsided within days.² Given these promising results and the relative safety of topical tacrolimus, clinicians may want to consider this as an alternative to corticosteroids, which can cause hypopigmentation and scarring in dark skinned patients, resulting in potential disfigurement.

Psoriasis

The prevalence of psoriasis in HIV-infected individuals is the same or slightly higher than that seen in noninfected individuals, but its clinical presentation can be more severe.^{7, 8} The severity of presentation often correlates with the degree of immunosuppression. HIV-positive patients with pre-existing psoriasis may see a flare of lesions as their CD4 count decreases and their viral load increases. A higher frequency of guttate and inverse psoriasis, as well as cases of generalized erythrodermic type psoriasis, has been reported in HIV-positive patients.⁹ Psoriasis has been the presenting manifestation of HIV in some individuals, thus HIV testing should be considered in patients that present with de novo psoriasis.⁸

Treatment of psoriasis in HIV-positive patients can be challenging, as it is often refractory to standard psoriasis treatments.⁷ When started on HAART, patients’ psoriasis tends to improve as the immune system is reconstituted.¹⁰ Case reports have shown a dramatic and rapid improvement of psoriasis in HIV-positive patients who have been either started or restarted on HAART.^{7, 10} Consequently, these reports emphasize the importance of strict adherence to antiretroviral regimens. This response is paradoxical, as drugs effective at treating psoriasis are targeted at Tlymphocytes, yet a low CD4 cell count causes worsening of the psoriasis. Although still unclear, the development of psoriasis is postulated to be an expression of the disease, which depends on the ratio of CD4 to CD8 cells. This ratio decreases in advanced HIV.11 It is also thought that TNF-á, an inflammatory cytokine associated with both psoriasis
and HIV replication, may play a role.¹⁰ Subjects on HAART should have lower viral replication and therefore, reduced levels of TNF-á. The regulatory T-cell subpopulation may also play a role, as this dedicated population is deficient in psoriasis, but expanded in the peripheral blood of HIV patients on HAART.¹⁰ Additional research will need to be conducted to further elucidate this phenomenon. Regardless, strict adherence to an antiretroviral treatment regimen is an important point to remember and to relay to patients.

Cutaneous Mycoses

Cutaneous dermatophytosis is generally more varied, extensive, and atypical in HIV than in immunocompetent hosts. As with psoriasis, the frequency of cutaneous dermatophytosis in the HIV population is not significantly greater than in noninfected individuals. Involvement of the nails is seen as proximal, subungual onychomycosis. Often the majority of the toenails are involved, which is a classic sign in HIV-infected patients.¹² Extensive lesions refractory to treatment are typical.¹³ Pruritus and pain are not always present in this population despite the potential for extensive involvement.¹²

The most common etiologic organism of cutaneous fungal infection is Trichophyton rubrum, which generally inhabits the cornified layer of the dermis. Deeper penetration into the stratum corneum occurs after the dermatophyte releases enzymes, such as keratinase.¹⁴ The skin has a number of defense mechanisms in place to prevent penetration below the epidermis, including a cell-mediated response.¹⁵ In the immunocompromised population, however, invasive fungal infections can be identified, although they are rare. It is important to recognize and treat cutaneous fungal infections early, as delay of treatment allows for the
infection to become more deeply invasive. Deep or locally invasive dermatophyte infection will typically present as nodular eruptions near the initial site of infection. Abscesses, mycetomas, and atypical lesions may also occur.¹⁴

Treatments used for various mycoses in immunocompetent individuals may not be sufficient to treat the same infections in the immunocompromised. For example, systemic therapy may be necessary even for superficial infections, whereas topicals alone would likely be adequate to treat the same infection in immunocompetent patients.¹² Resistance to oral antifungals, such as fluconazole, is a problem when it is used long-term as prophylaxis or for frequent short-term exposures. These drugs are used to treat candidal infections. In addition, immunosuppressed patients are more likely to be infected with atypical fungi.¹² Oral antifungals such as ketoconazole, fluconazole, and griseofulvin are usually effective in treating superficial and deep dermatophyte infections in this population.¹⁴ However, when systemic therapy fails to be curative, surgery may be required. Failure to eradicate the infection has led to death in patients due to septicemia and systemic dissemination.^{16, 17} In order to make a proper diagnosis and prescribe an appropriate treatment regimen, it is important that, in addition to potassium hydroxide (KOH) mounts, cultures be performed on Sabouraud’s agar to allow for specific species identification.¹⁴

In some cases, antiretroviral therapy alone is sufficient to clear dermatophyte infections in immunosuppressed patients. However, it is important to consider possible interactions between antiretrovirals and antifungals, particularly ketoconazole. Although not contraindicated, it is advisable to use the medications concomitantly with close observation, as both ketoconazole and certain antiretrovirals have an effect on cytochrome P-450, leading to increases or decreases in either ketoconazole levels and/or antiretroviral levels.¹⁸ Other antifungals such as griseofulvin and terbinafine have not been shown to interact with HIV medications, and no specific warnings exist.¹⁴ Amphotericin B, a potent broad spectrum antifungal agent is still used in certain cases. However, this drug has substantial toxicity and must be used with caution. The development of an entirely different class of antifungals, echinocandins, has had a significant impact on the therapeutic approach to fungal infections. Drugs in this class, such as caspofungin, have few side-effects and few drug interactions. However, this drug does not have an oral preparation and has a relatively narrow spectrum of activity when compared with amphotericin B.¹² The choice of an antifungal agent will depend on the patient, the organism being treated, and the severity of the infection.

Conclusion

HIV infection can lead to a myriad of dermatoses with complicated clinical presentations. The altered immune status of HIV-infected individuals leads to diagnostic and therapeutic challenges. As dermatologists, it is important to be aware of the varied dermatoses associated with HIV, as well as their management. Knowledge of HIV-associated dermatologic manifestations may be useful in helping to make the diagnosis of HIV. Additionally, recognition of the need for more intensive therapy in these patients can provide improved care, and ultimately, improved patient outcomes.

References

1. Department of Health and Human Services. Center for Disease Control Cases of HIV infection and AIDS in the United States and dependent areas, 2005.
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3. Rajendran PM, Dolev JC, Heaphy MR, et al. Eosinophilic folliculitis: before and after the introduction of antiretroviral therapy. Arch Dermatol 141(10):1227-31 (2005 Oct).
4. Lawn SD, Wilkinson RJ. Immune reconstitution disease associated with parasitic infections following antiretroviral treatment. Parasite Immunol 28(11):625-33 (2006 Apr).
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6. Grange F, Schoenlaub P, Tortel MC, et al. AIDS-related eosinophilic folliculitis: efficacy of high dose topical corticotherapy. Ann Dermatol Venereol 123(8):456-9(1996).
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15. Chastain MA, Reed RJ, Pankey GA. Deep dermatophytosis: report of two cases and review of the literature. Cutis 67(6):457-62 (2001 Jun).
16. Hironaga M, Okazaki N, Saito K, et al. Trichophyton mentagrophytes granulomas: unique systemic dissemination to lymph nodes, testes, vertebrae, and bone. Arch Dermatol 119(6):482-90 (1983 Jun).
17. Rinaldi MG. Dermatophytosis: epidemiological and microbiological update. J Am Acad Dermatol 43(5 suppl1):S120-4 (2000 Nov).
18. Bartlett JG, Gallant JE. Medical Management of HIV Infection. 2007 ed. Baltimore (MD): Johns Hopkins University, Division of Infectious Diseases (2007).