Mucocutaneous manifestations of human immunodeficiency virus (HIV) are commonly seen in clinical practice; at least 90% of patients living with HIV (PLWHs) will develop some type of skin condition over the course of their lifetime. Skin is oftentimes the first organ affected by HIV and is a useful clinical marker of HIV disease progression (Basida et al., 2021). Mucocutaneous manifestations may include inflammatory conditions such as seborrheic dermatitis, pruritus, or psoriasis; viral, bacterial, and fungal infections; and HIV-associated malignancies like Kaposi sarcoma (KS; Chelidze et al., 2019). This article will review the most common dermatological conditions in PLWHs, as well as how they typically present in clinical practice, and discuss current evidence for treatment.

EPIDEMIOLOGY

Almost every PLWH will present with dermatological complaint at some point during their care. Compared with people living without HIV, PLWHs have a greater likelihood of skin eruptions because of dysregulation of the skin immune system or drug reactions (Ramos-e-Silva et al., 2020). A common skin condition that afflicts PLWHs is seborrheic dermatitis, which affects 30%–83% of patients (Adalsteinsson et al., 2020). Another common skin manifestation is methicillin-resistant Staphylococcus aureus (MRSA) infection; PLWHs have a 6- to 18-fold higher rate of infection with a recurrence rate of 27% within 6 months of treatment (Skiest et al., 2006). Mucocutaneous manifestations are typically more common as CD4 cell count drops, HIV RNA level increases, and immune function decreases. Studies found that pruritic papular rashes, psoriasis, and drug-induced reactions were more likely among PLWHs with CD4 < 200 (Esser & Sammet, 2021; Mirnezami et al., 2020). Some other conditions, such as varicella-zoster, may occur at any stages of HIV regardless of CD4 cell count; however, the manifestation may be more severe and extensive than compared with someone living without HIV (Chelidze et al., 2019).

PATHOGENESIS

The skin's immune system maintains homeostasis of the body's internal operations by preventing and eliminating invasions from external pathogens, toxins, allergens, and neoplastic disorders (Barroca et al., 2014). This is accomplished through an immunological response process that involves the resident cells (kerantinocytes, lymphatic and capillary endothelial cells), antigen-presenting cells (Langerhans cells and dermal dendritic cells), and T-lymphocytes (Barroca et al., 2014). HIV infection disrupts this process, resulting in decreased numbers of Langerhans cells and dermal dendritic cells as well as CD4 T-lymphocytes, natural killer cells, macrophages, and monocytes. Any loss of immune cells allows the skin to become more vulnerable to opportunistic infections, inflammatory processes, and neoplastic disorders (Barroca et al., 2014). Clinically, the CD4 count is a frequently used parameter to determine HIV stage and aid in its management because HIV targets these cells. Although multiple variables can affect its count, a normal adult CD4 count, when taking in laboratory variations, may range from 500 to 1400 cells/μL (Sax, 2021). A CD4 count lower than 200 cells/μL is the clinical definition of acquired immunodeficiency syndrome and could aid in the clinical assessment of skin-related opportunistic infections (Sax, 2021).

CUTANEOUS MANIFESTATIONS/CLINICAL FEATURES MRSA and Soft Tissue Infections

Although there has been a decreased incidence of MRSA bacteremia with the introduction of antiretroviral therapy (ART), PLWHs are still at a higher risk of severe infection compared with those living without HIV, with lower CD4 count being one of the risk factors for MRSA (Lopez & Sanders, 2021; Shadyab & Crum-Cianflone, 2012). A review of literature found that the most common type of MRSA infections among PLWHs was soft tissue infections caused by the community strain USA300 (Shadyab & Crum-Cianflone, 2012). Localized skin and soft tissue infections are common and may present as abscesses, cellulitis, furuncles, folliculitis, ulcerations, and impetigo (Shadyab & Crum-Cianflone, 2012). Lesions are typically found on the lower and upper extremities, followed by the trunk, axillae, face, and neck with increased incidences found in the genital region (Shadyab & Crum-Cianflone, 2012). Risk factors to note in the clinical setting are poor immune status/lower CD4 count, high-risk sexual behaviors, illicit drug use, recent sexually transmitted infections, prior incarceration, and prior hospitalization, all of which require further interventions (Lopez & Sanders, 2021; Shadyab & Crum-Cianflone, 2012). Without treatment, localized skin infections in PLWHs may result in severe bacteremia, which may consequently lead to complications such as pneumonia, septic pulmonary emboli, osteomyelitis, meningitis, and endocarditis (Shadyab & Crum-Cianflone, 2012).

Bacillary Angiomatosis

This condition occurs because of infection by the bacteria Bartonella, with the species Bartonella henselae and Bartonella quintana affecting PLWHs more severely (Mosepele et al., 2012). Providers should be prompted to consider Bartonella infection if patients report being scratched by a cat, have lice, or may have experienced homelessness. Bacillary angiomatosis are typically seen in PLWHs with a CD4 cell count of <100 (Mosepele et al., 2012). Lesions may appear as reddish or purplish vascular nodules on the skin and are typically found in the upper extremities in clusters (Akram et al., 2022). PLWHs typically present with fever of unknown origin (≥38°C), osteomyelitis, and angioproliferative lesions affecting primarily the skin, liver, and spleen (Mosepele et al., 2012). Differential diagnoses to consider are KS, cherry angioma, or dermatofibroma given the similar presentation of these lesions to bacillary angiomatosis (Spach, 2022). It is important to note that bacillary angiomatosis, if misdiagnosed and treated with chemotherapy for presumed KS, can disseminate to the bone and viscera and become life-threatening (Forrestel et al., 2015). Histology should be performed to confirm diagnosis before beginning treatment (Forrestel et al., 2015).

Molluscum Contagiosum

This infectious viral condition manifests as discreet, skin-colored papules with a central umbilication measuring 2–5 mm (Chelidze et al., 2019; Spach, 2022). As HIV progresses and immune status weakens, these discreet lesions increase in numbers and become irregular in shape with loss of the umbilicated center; they may spread to the face and merge into larger lesions (“giant molluscum”) and may appear as disfiguring papular lesions similar to the morphology of warts (Chelidze et al., 2019).

Herpes Zoster

The highest risk for reactivation of varicella-zoster virus among PLWHs is in those with CD4 cell counts of less than 200 cells/mm3 and in those who started ART within the first 4 months because of immune reconstitution inflammatory syndrome (IRIS; Chelidze et al., 2019). Physical manifestations are usually preceded by prodrome of tingling/numbness. Lesions appear in clusters of vesicles on an erythematous base distributed on dermatomes but may also appear as chronic, ulcerative, bullous, or verrucous lesions (Chelidze et al., 2019). Once healed, PLWHs are at a higher risk of developing postherpetic neuralgia compared with those without HIV (Forbes et al., 2016). Those with severely immunocompromised status, including PLWHs, have a higher likelihood of developing disseminated infection to the eyes, central nervous system, or visceral organs (Spach, 2021).

Seborrheic Dermatitis

Skin biopsies showed a different histology in seborrheic lesions among PLWHs and those in the general population (Cedeno-Laurent et al., 2011; Mirnezami et al., 2020). In the general population, seborrheic lesions may present initially on the scalp, resulting in dandruff, or on the back or shoulder; clinical findings may show greasy scales above discreet, well-approximated erythematous patches. For PLWHs, erythema is more widespread, lesions are more extensive and may be found in areas beyond the face, scalp, shoulder, and back; and a biopsy of lesions shows proteins otherwise not seen in those without HIV (Adalsteinsson et al., 2020; Cedeno-Laurent et al., 2011).

Scabies is a parasitic condition that is transmitted by skin-to-skin contact and results in intense pruritus for the patient. It may appear initially as small erythematous papules and turn to vesicular lesions (Chosidow, 2006). The hallmark of scabies is thin, short, wavy burrows in the spaces between fingers, wrist flexors, axillae, feet, genitalia in men, areola in women, and inner thighs (Thomas et al., 2020). Crusted scabies, on the other hand, differ from common scabies in that they are often seen in PLWHs with severe immunodeficiency and have a hyperkeratotic scaly appearance on the buttocks (Spach, 2021; Tolkachjov et al., 2018).

Herpes Simplex Virus

PLWHs with herpes simplex virus (HSV) frequently present with atypical lesions that are extensive, painful, and prolonged, especially among those with severe immunosuppression (Chelidze et al., 2019). Lesions may appear on the lips or mouth with HSV-1 and around the genitalia region if patients have HSV-2, although location is not definitive of HSV type (Burke & Lopez, 2017). HSV typically presents initially with prodromal sensory symptoms, progressing to physical manifestation of papular and then vesicular lesions, followed by the crusting stage (Burke & Lopez, 2017). Clinicians should be aware that chronic, painful, nonhealing ulcers are hallmarks of severe immunodeficiency (CD4 cell count below 100 cells/mm3) and can occur anywhere on the body aside from the lips, mouth, or genitals (Chelidze et al., 2019). One study found that although the frequency of lesions did not change ART initiation, long-term ART use reduced both HSV shedding and recurrence of lesions (Ford et al., 2018).

Syphilis

The cutaneous manifestations of syphilis are similar among PLWHs and those without HIV (Chelidze et al., 2019). In PLWHs, primary syphilis may manifest as many large, slow-healing chancres compared with those without HIV and may be atypical or painful (Chelidze et al., 2019; Workowski et al., 2021). Secondary syphilis on examination may reveal maculopapular lesions on the trunks and extremities with palm and sole involvement, as well as uncommonly seen cutaneous manifestations such as annular plaques with hypopigmented centers, or necrotic, crusty, and scaly plaques (Chelidze et al., 2019). Clinicians should recognize that PLWHs may present with both primary and secondary syphilis and may quickly progress to tertiary syphilis (Chelidze et al., 2019). Clinicians should also conduct a thorough ocular examination as ocular syphilis and associated neurosyphilis have been rising in recent years (Chelidze et al., 2019).

Human Papillomavirus

Compared with those living without HIV, PLWHs are more likely to present with human papillomavirus (HPV) infection (Chelidze et al., 2019). The etiology has been suggested to relate to the dysregulation of p27 expression and proliferation of cutaneous cells (Chelidze et al., 2019). Warts may appear in genital or sun-exposed areas of the body and present with more severity and with a higher frequency than those living without HIV (Coates & Leslie, 2019). In women, HPV infection and progression of HPV-associated cervical lesions are highly associated with an immunodeficient status (G. Liu et al., 2018).

Psoriasis

Although the prevalence of psoriasis among PLWHs and those in the general population is similar, lesions among PLWHs are typically more severe, destructive, and resistant to treatment (Ceccarelli et al., 2019; Cedeno-Laurent et al., 2011). Psoriasis lesions among PLWHs tend to present as extensive lesions of guttate, inverse, and erythrodermic subtypes as well as those affecting the extremities, fingers, or ears (Ceccarelli et al., 2019; Cedeno-Laurent et al., 2011; Spach, 2021). Clinicians should also assess for psoriatic arthritis among those who are severely immunocompromised, including PLWHs, as it is common in this population (Cedeno-Laurent et al., 2011). Psoriatic arthritis in PLWHs may present as joint pain, stiffness, and effusion in the finger joints and spine (Spach, 2021).

Eosinophilic Folliculitis

The condition is typically seen in PLWHs and more often in those with advanced disease (Cedeno-Laurent et al., 2011). Eosinophilic folliculitis usually presents as a papular rash on an erythematous base with scattered vesicular or pustular lesions on the face, neck, chest, and back, primarily above the nipple line (Afonso et al., 2012; Cedeno-Laurent et al., 2011). Laboratory findings reveal elevated serum immunoglobulin E levels, eosinophilia, and peripheral leukocytosis (Cedeno-Laurent et al., 2011).

Prurigo Nodularis

This is a cutaneous manifestation that occurs in both PLWHs and those without HIV. The lesions commonly present as nodular or papular hyperkeratotic lesions approximately 3–5 mm in size with associated crusting in a symmetrical distribution (Garg & Sanke, 2017; Matthews & Cockerell, 1998). Lesions are typically seen on the trunk and extremities without face or scalp involvement (Whang et al., 2019). The patient will typically complain of generalized, intense pruritus that causes scratching to relieve symptoms (Whang et al., 2019). It is important for clinicians to distinguish this condition from other similar skin manifestations such as eosinophilic folliculitis given similar presentation to the affected areas.

Drug-Induced Reactions

PLWHs are at a higher risk of cutaneous reactions to medications compared with the general population (Cedeno-Laurent et al., 2011; Chelidze et al., 2019). These reactions may include mild and more common cases such as morbilliform exanthematous reactions or more severe cases such as Stevens–Johnson syndrome and toxic epidermal necrolysis (Cedeno-Laurent et al., 2011). Mucocutaneous presentations may include pruritic maculopapular eruptions, generalized urticaria or angioedema, acute generalized erythematous pustulosis, drug rashes with eosinophilia and systemic symptoms, and xerosis. Clinicians should be aware that certain ART medications, including protease inhibitors, efavirenz, nevirapine, and abacavir, are more likely to cause reactions (Cedeno-Laurent et al., 2011). PLWHs with a CD4 cell count below 200 cells/mm3 are typically placed on sulfamethoxazole/trimethoprim for opportunistic infection prophylaxis, which may also induce a cutaneous reaction (typically a maculopapular rash with or without a fever) and require further evaluation (Cedeno-Laurent et al., 2011; Giles et al., 2019). Compared with the 3%–8% rate of sulfa hypersensitivity in the general population, a study found that 27% of PLWHs developed drug-induced reactions when taking sulfamethoxazole/trimethoprim for the treatment of pneumocystis pneumonia (Giles et al., 2019). It is important to perform a thorough history to differentiate between drug-induced reactions from other causes, such as IRIS. IRIS is a hyperinflammatory response to latent infections after patients initiate ART and their CD4 count improves; these infections may include pneumocystis pneumonia, cryptococcal meningitis, or Hepatitis B or C (Thapa & Shrestha, 2022).

Kaposi Sarcoma

KS is a vascular malignancy caused by the oncovirus human herpes virus 8 and primarily affects PLWHs who are severely immunosuppressed and may also present in older men and transplant patients (Cesarman et al., 2019; Coates & Leslie, 2019). Since the initiation of ART in the 1990s, there has been a reduction of incidence in KS among PLWHs in the United States. However, the risk of KS remains extremely high among PLWHs compared with those who do not have HIV (Coates & Leslie, 2019). KS can present as violaceous macular, papular, or plaque lesions. KS affects the skin but can also involve other organs such as the lungs and gastrointestinal tract (Ramos-e-Silva et al., 2020). Recent research suggested that cumulative viral load level may trigger early development of KS independent of CD4 cell count; therefore, clinicians should be concerned of KS regardless of CD4 cell count and perform a thorough physical examination at every patient encounter (Dubrow et al., 2017). For confirmatory diagnosis of KS, a biopsy of the lesion should be sent for pathology (Dubrow et al., 2017).

DIFFERENTIAL DIAGNOSES OF SKIN MANIFESTATIONS

Given the numerous expressions of skin lesions that present in clinical practice among PLWHs, it may be appropriate to break down the differential diagnoses by categorizing skin manifestations based on their morphological appearances. Given that PLWHs have higher incidence of bacterial infections, providers should consider soft tissue and Staphylococcus aureus infections if lesions appear to be purulent or are abscess forming (Lopez & Sanders, 2021). Macular lesions may suggest cutaneous drug eruption, acute HIV infection, or primary and secondary syphilis infection (Spach, 2021). Papular lesions may include differential diagnoses of molluscum contagiosum, eosinophilic folliculitis, warts, and scabies (Spach, 2021). Clinicians should be prompted to consider KS, bacillary angiomatosis, or prurigo nodularis when encountering nodular lesions (Spach, 2021). Scaling of the skin may indicate seborrheic dermatitis or psoriasis as well as the final stage of HSV infection (Spach, 2021). Vesicular lesions may indicate HSV or varicella-zoster virus (Spach, 2021). Providers should further narrow down their differential diagnoses by pattern of lesions, onset, location, symptomology, patient's immune status, and laboratory testing or biopsy, as appropriate.

It is important to recognize that certain mucocutaneous lesions present differently in PLWHs versus the general population. For example, the subtypes of psoriasis that are commonly noted in PLWHs are inverse, guttate, erythrodermic, and acral lesions with associated symptoms of joint pain, versus the classical presentation of plaque-like lesions (Cedeno-Laurent et al., 2011). HSV lesions may be extensive, ulcerative, painful, and refractory to treatment, especially if patients are immunocompromised and/or not on ART (Chelidze et al., 2019). Understanding the unique presentations of these mucocutaneous conditions may aid the clinicians in the development of an appropriate care plan (e.g., initiating ART, supportive management).

Recognizing the patient's immune status is also critical in understanding how mucocutaneous lesions may present and where. For example, psoriasis is a T-lymphocyte-mediated disease that improves or worsens based on immune status; therefore, initiation of ART and return of CD4 cells among PLWHs with psoriasis will show most significant improvements in psoriasis eruptions (Menon et al., 2010).

Once a diagnosis is established, clinicians may continue with treatment of the skin condition per the most recent, evidence-based guidelines.

TREATMENT OF SKIN MANIFESTATIONS

Table 1 below summarizes the treatments for common mucocutaneous conditions described in this article and may be utilized as a quick guide in the clinical setting. CD4 count should be used as a guide but not a definitive approach when diagnosing a dermatological condition, as CD4 count may fluctuate depending on other comorbidities or conditions and not a true marker of HIV progression (Sax, 2021). For many dermatological conditions related to HIV, initiation and continuation of ART should be considered as the first line of treatment in conjunction with other measures as many skin conditions are associated with poor prognosis and a faster progression to acquired immunodeficiency syndrome (Lopez & Sanders, 2021).

TABLE 1 - Summary of Treatments for Common Mucocutaneous Conditions Cutaneous Manifestation Immune Status (CD4 Cells/mm 3) Treatment Clinical Practice Guidelines or Evidence-Based Practice Bacterial  MRSA and soft tissue infections Any CD4 count In the outpatient setting: incision and drainage of abscess and addition of antibiotics if: Patients have an extensive disease with evidence of cellulitis Systemic illness Comorbidities and immunosuppression Patients are older adults Lack of response to incision and drainage or area difficult to drain For purulent cellulitis, cover for community-acquired MRSA with any of the following antibiotics, and duration may last 5–10 days: Clindamycin 300–450 mg PO TID
Trimethoprim–sulfamethoxazole DS PO BID
Doxycycline 100 mg PO BID Minocycline 200 mg × 1 and then 100 mg PO BID Linezolid 600 mg PO BID For nonpurulent cellulitis, cover for beta-hemolytic streptococci and community-acquired MRSA if no response to beta-lactam therapy, with any of the following antibiotics, and duration may last 5–10 days: Beta-lactam (e.g., cephalexin and dicloxacillin) 500 mg PO QID Clindamycin 300–450 mg PO TID
Beta-lactam (e.g., amoxicillin 500 mg PO TID) and/or trimethoprim–sulfamethoxazole (DS PO BID) or a tetracycline (e.g., doxycycline 100 mg PO BID) Linezolid 600 mg PO BID Infectious Diseases Society of America (C. Liu et al., 2011)  Bacillary angiomatosis CD4 < 100 Preferred therapy: Doxycycline 100 mg PO/IV q12h for at least 3 months or Erythromycin 500 mg q6h for at least 6 months Alternative therapy: Azithromycin 500 mg PO daily or
Clarithromycin 500 mg PO BID Spach (2022) Viral  Molluscum contagiosum Seen in about 35% of patients with CD4 < 200 Patients should be started on ART immediately; lesions should recede once viral suppression is achieved (IRIS can cause a temporary worsening of the lesions). For persistent lesions, localized treatment may include cryotherapy, curettage, pulsed dye laser therapy, or immune modulators. Chelidze et al. (2019), Spach (2021)  Herpes zoster Highest risk among those with CD4 < 200 Acute localized lesions: Valacyclovir 1000 mg TID 7–10 days Famciclovir 500 mg PO TID 7–10 days Alternatively: acyclovir 800 mg PO 5 times daily 7–10 days Extensive, widespread lesions or visceral involvement: Acyclovir 10 mg/kg IV q8h until clinical improvement; may switch to PO antivirals 10–14 days once no more new lesions are seen Prevention with the varicella vaccine is indicated for those without documented immunity and whose CD4 > 200.
Prevention with the zoster vaccine is indicated for those >50 years old regardless of CD4 count. Spach (2021), Panel on Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV (2022) Fungal  Seborrheic dermatitis CD4 200–500 (Nnoruka et al., 2007) Initiation of ART will provide the most significant improvement of lesions (Spach, 2021).
Initial approach the same as patients without HIV; sulfur-containing soap may not be as effective in PLWHs (Gupta & Bluhm, 2004). Antifungal drugs via shampoos, creams, or oral medications (ketoconazole 2%, miconazole 2%, or terbinafine 1%) Topical steroids for symptom management of pruritus and erythema for short-term therapy (low-to-mild potency) Nonsteroidal anti-inflammatory agents are helpful and well tolerated to treat inflammation. 8% lithium succinate plus 0.05% zinc sulfate ointment to areas other than the scalp, BID for up to 8 weeks (Naldi & Rebora, 2009) In severe or refractory cases to topical medications, patients may use itraconazole 200 mg PO daily ×7 days (Sasseville, 2022). Borda et al. (2019) Parasitic  Scabies Any CD4 count, but typically seen in those
with advanced disease Recommended regimens for uncomplicated disease: Topical permethrin 5% cream, one-time application for patients and household and sexual contacts treated at the same time or Ivermectin 200 mcg/kg PO one-time dose with repeated dose 10–14 days later For crusted scabies: use topical scabicide (topical permethrin 5% cream daily ×7 days and then ×2 weekly until cured or 25% topical benzyl benzoate) and ivermectin 200 mcg/kg PO on Days 1, 2, 8, 9, and 15, with additional doses required on Days 22 and 29 for severe cases. Avoid lindane. Workowski et al. (2021) Sexually transmitted infections  Herpes simplex virus Any CD4 count In addition to ART, which can reduce the frequency and severity of symptoms,a treatment for cutaneous outbreak includes 5–10 daysb of: Valacyclovir 1 g PO BID or Famciclovir 500 mg PO BID or Acyclovir 400 mg PO TID for 5–10 days Suppressive therapy is indicated if (a) the patient has severe recurrent HSV outbreaks, (b) the patient would like to reduce HSV outbreaks, (c) CD4 < 200 and the patient is initiating ART ×6 months to decrease risk of genital ulcer disease: Valacyclovir 500 mg PO BID or Famciclovir 500 mg PO BID or Acyclovir 400 mg PO BID Workowski et al. (2021)  Syphilis Any CD4 count Primary and secondary syphilis: Benzathine penicillin G 2.4 million units IM in a single dose Latent syphilis: Early latent: benzathine penicillin G 2.4 million units IM in a single dose Late latent: benzathine penicillin G 7.2 million units in total, administered as three doses of 2.4 million units IM each week at 1-week intervals Tertiary syphilis: benzathine penicillin G 7.2 million units in total, administered as three doses of 2.4 million units IM each week at 1-week intervals Workowski et al. (2021)  HPV Any CD4 count External anogenital warts: Imiquimod 3.75% (once at bedtime every night for up to 8 weeks) or 5% cream (once at bedtime, 3×/week for up to 16 weeks) or Podofilox 0.5% solution or gel (2× daily for 3 days and then 4 days of no therapy, repeated as needed up to four cycles) or Sinecatechins 15% ointment (3× daily for <16 weeks) Alternatively: cryotherapy with liquid nitrogen or cryoprobe, or Surgical removal, or Trichloroacetic acid or bichloroacetic acid 80%–90% solution Prevention is indicated with HPV vaccines. Workowski et al. (2021) Inflammatory conditions  Psoriasis Any CD4 count Initiation of ART; zidovudine-inclusive regimens have also shown significant improvement Mild-to-moderate disease: Topical steroids (calcipotriene, corticosteroids, tazarotene, calcipotriol–betamethasone dipropionate) Other treatments with some skin improvement include UVB phototherapy and psoralen with UVA. Moderate-to-severe disease: Phototherapy (first-line therapy) Oral retinoids (second-line therapy) Refractory disease: Cyclosporine, methotrexate, hydroxyurea (evidence in either PLWHs or those with psoriasis), and tumor necrosis factor-alpha may be considered. National Psoriasis Foundation (Menon et al., 2010)  Eosinophilic folliculitis CD4 typically <300 Initiation of ARTc with moderate-potency topical steroids Second-line treatment: phototherapy
Third-line treatment: itraconazole PO, isotretinoin PO, macrolides Chelidze et al. (2019)  Prurigo nodularis CD4 typically <50 Moderate- or high-potency topical corticosteroids or systemic corticosteroids and antihistamines for symptom management Phototherapy, benoxaprofen, or direct injection of steroid to the nodules may be considered. Workowski et al. (2021), Maurer (2005)  Drug-induced reactions Any CD4 count Patients should be discontinued on the suspected drug after a thorough history to rule out other causes of rash. Management may range from controlling symptoms such as pruritus with antihistamines to inpatient admission for intravenous fluids for Stevens–Johnson syndrome. For mild reactions, clinicians may reintroduce the drug back into the ART regimen with symptom management at initiation. If the patient is still unable to tolerate the drug, consider an alternative ART regimen. Chelidze et al. (2019) Neoplastic malignancies  Kaposi sarcoma Commonly seen among those with CD4 < 300; however, cases have been noted for those with CD4 > 350 ART alone for mild/moderate disease per current WHO guidelines For severe disease: systemic cytotoxic chemotherapy in addition to ART Local treatments may also be used for specific lesion control. Chelidze et al. (2019)

Treatments listed in this table do not address treatment for pregnant women or children; refer to the clinical guidelines for specific treatment recommendations for these populations. In addition, this table is not all-encompassing of treatments for various skin manifestations of HIV; therefore, providers should refer to clinical guidelines for full treatment information. MRSA = methicillin-resistant Staphylococcus aureus; ART = antiretroviral therapy; IRIS = immune reconstitution inflammatory syndrome; HIV = human immunodeficiency virus; PLWHs = patients living with HIV; HSV = herpes simplex virus; HPV = human papillomavirus.

aSubclinical shedding may still occur; symptoms may worsen early after initiation of ART.

bTreatment courses may need to be extended.

cSymptoms may worsen early after initiation of ART in the setting of IRIS.

CONCLUSION

There are over 50 dermatological conditions found to be associated with HIV infection (Cedeno-Laurent et al., 2011). The mucocutaneous clinical presentation for PLWHs is diverse and may vastly vary from the general population. Nurses and nurse practitioners providing care to this population should be well versed in the most common types of dermatological conditions with which patients may present. Furthermore, providers should be aware of how a patient's immune status plays a role in the mucocutaneous manifestations of various skin conditions as well as course of treatment. It is imperative that patients who are newly diagnosed with HIV are immediately started on ART, as viral suppression and immune function recovery are paramount to alleviating many skin conditions discussed in this article.

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