A Practical Approach to HIV/AIDS: Part 2

Authors: Kamoga Dickson, MD (EM Resident Physician, Makerere College of Health Sciences, Kampala, Uganda); Kakande Reagan (Senior Medical Student, Mbarara University of Science and Technology, Mbarara, Uganda); Akan Otu, MD (Senior Lecturer in Infectious Diseases, Department of Internal Medicine, University of Calabar, Calabar, Nigeria); Jessica Pelletier, DO, MHPE (APD/Assistant Professor of EM/Attending Physician, University of Missouri-Columbia) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case

A 25-year-old male presents to the emergency department (ED) of a teaching hospital in Nigeria with a fever of 4 weeks, persistent headache and vomiting for 1 week, and disorientation in time and place for 48 hours. Upon examination, he is febrile with a temperature of 40 °C, appears cachectic, and oral thrush is noted. Neck rigidity and Kernig’s and Brudzinski’s signs are present. He has diplopia and struggles to maintain his balance with closed eyes when the Romberg test is performed. There is no motor weakness, and both tendon reflexes and sensation are normal. His lymph nodes, liver, and spleen are not palpable.

On chart review, the patient was diagnosed with human immunodeficiency virus (HIV) 6 months prior,  when he presented with a multilobar pneumonia. At that time, his CD4 T-cell count was 80 cells/µl, and HIV RNA viral load was 380,200 copies/mL. He was offered therapy for HIV but did not keep subsequent hospital appointments. 

His blood tests today in the ED are as follows: White blood cells: 22,200/L, lymphocytes: 65%, normocytic anaemia, Platelets: 233,000 U, CRP (C‐Reactive Protein): 230 mg/L, blood culture: negative, CD4 count 15 cells/ µl and HIV RNA viral load was 880,200 copies/mL. A chest x-ray is normal. An urgent brain contrast-enhanced computed tomography (CT) and magnetic resonance imaging (MRI) are also normal. 

Initially, he is treated empirically with ceftriaxone and acyclovir for meningitis. Lumbar puncture reveals a raised opening pressure of 36 cmH20, a cell count of 120/µL (80 % mononuclear cells), protein 3.71 g/L, and glucose 1.3 mmol/L (serum glucose 8.7 mmol/L). CSF cultures are negative, as are polymerase chain reaction (PCR) tests for herpes simplex virus (HSV), Epstein-Barr virus (EBV), cytomegalovirus (CMV), and varicella-zoster virus (VZV) DNA. Cryptococcal antigen is detected in CSF and serum. India ink staining of the CSF reveals the presence of Cryptococcus neoformans (Fig. 1).

Figure 1. The yeast state of Cryptococcus neoformans. Photo Credit: Content Providers(s): CDC/Dr. Leanor Haley – This media comes from the Centers for Disease Control and Prevention’s Public Health Image Library (PHIL), with identification number #3771. This image is in the public domain and free of any copyright restrictions. https://phil.cdc.gov/details.aspx?pid=3771

After the CSF results are obtained, the patient is switched to induction therapy of liposomal IV amphotericin B 3 mg/kg once daily IV + oral flucytosine 25 mg/kg four times a day for 14 days. This is followed by consolidation therapy consisting of oral fluconazole 400 mg daily (single loading dose of 800 mg on the 1st day) for 8 weeks.

Unfortunately, the patient becomes delirious and repeat lumbar puncture reveals a raised opening pressure of 45 cmH20. Serial lumbar punctures are performed to reduce the CSF opening pressure to <20 cmH2O. The raised intracranial pressure persists despite repeated lumbar punctures,  and he is eventually referred to the neurosurgical team for ventriculoperitoneal shunt placement. Following this, his clinical condition steadily improves. Highly active antiretroviral treatment (HAART) (tenofovir disoproxil fumarate, emtricitabine, and dolutegravir) is started 6 weeks after the initiation of antifungal treatment. Primary prophylaxis with azithromycin for Mycobacterium avium complex (MAC), cotrimoxazole for Pneumocystis jirovecii (PJP), and secondary prophylaxis with fluconazole after completion of consolidation treatment are initiated. He is eventually discharged home after 6 weeks of hospitalisation with no neurological sequelae. 

Background

HIV patients are at higher risk than the general population for a multitude of infectious diseases and chronic conditions impacting every organ system of the body. HIV itself, as well as the drugs used to treat it, are associated with a wide variety of pathologies, which the emergency clinician must be aware of. Patients with HIV are considered to have acquired immune deficiency syndrome (AIDS) when the CD4 count is <200 cells/µl or patients present with AIDS-defining illnesses (Table 1).1 Those with CD4 count 200–500 cells/μL are at higher risk than the general population for bacterial pneumonia, tuberculosis, and certain malignancies.2,3 Though the risk for opportunistic infections is low in patients with CD4 count >500 cells/μL, invasive pneumococcal disease, tuberculosis, and some malignancies are still more likely than in patients without HIV.2 It is critical to note that even HIV patients with normal CD4 counts who are on HAART are not fully immunocompetent.4 In the era of HAART, HIV patients are living longer, and are experiencing more non-communicable diseases that need to be on our differential for this population.1

Table 1. AIDS-defining illnesses. Adapted from: Centers for Disease Control and Prevention (CDC). Appendix A AIDS-Defining Conditions; 2008. https://www.cdc.gov/mmwr/preview/mmwrhtml/rr5710a2.htm

For details on the epidemiology, risk factors, pathophysiology, and clinical manifestations by stage of HIV infection, please check out Part 1 of this multi-part post: https://www.emdocs.net/a-practical-approach-to-hiv-aids-part-1/

We will cover opportunistic infections in Part 3 of this post. This article will focus on the most common manifestations of HIV/AIDS by organ system and their specific management.  

Organ System Manifestations & Management

Cardiovascular System

The risk for cardiovascular diseases (CVDs), including myocardial infarction (MI), heart failure, stroke, and pulmonary hypertension, is higher in individuals with HIV than in those without the disease.⁵ The risk for MI is found to be 50% higher among individuals with HIV compared to non-HIV individuals, according to multiple large cohort studies.^6,7 This is attributed partly to increased life expectancy for persons living with HIV (PLHIV) as a result of effective antiretroviral therapy (ART) usage, which heightens their risk for age-related diseases such as CVDs.⁸ The PLHIV also face an elevated risk of CVDs from both traditional and HIV-specific factors. The traditional risk factors include smoking, hypertension, diabetes, and dyslipidemia, and these are more prevalent among PLHIV. The HIV-related mechanisms include chronic inflammation, immune activation, and exposure to certain ART.⁹ Other factors driving up the risk for CVDs among PLHIV include the high viremia, low CD4 count, dyslipidemia associated with HIV, coinfection with hepatitis, and CMV.¹⁰

HIV induces widespread chronic systemic and vascular inflammation, which contributes to endothelial damage.  This chronic inflammation may be mediated by the HIV reservoir, coinfections, microbial translocation, clonal hematopoiesis of indeterminate potential (CHIP), and ART.¹¹ This vascular inflammation triggers platelet activation and aggregation, which promotes the development of atheromatous plaques and thrombus formation.¹² Plaque buildup within the coronary arteries can lead to ischemic heart disease and myocardial infarction. Additionally, chronic systemic inflammation in HIV, combined with abnormal fat distribution, contributes to the development of atherosclerosis and hypertension, further increasing the risk of ischemic heart disease.

Through complex pathophysiological mechanisms, including the direct effects of HIV on cardiac myocytes, immune dysregulation, and certain opportunistic infections, HIV can cause dilated cardiomyopathy characterized by severe systolic dysfunction in the absence of obstructive coronary artery disease.¹³

These CVDs culminate in heart failure, and below is a conceptual model of the proposed mechanisms of heart failure in HIV.

Figure 1. Pathophysiology of HIV-related CVD. Adapted from: M. J. Feinstein et al., “Characteristics, Prevention, and Management of Cardiovascular Disease in People Living With HIV: A Scientific Statement From the American Heart Association,” Circulation, vol. 140, no. 2, pp. e98–e124, Jul. 2019, doi: 10.1161/CIR.0000000000000695.

Management of HIV associated CVDs involves:¹³

• Use of effective ART to control HIV replication and reduce systemic inflammation.
• Regular cardiovascular risk assessment, including monitoring blood pressure, lipid profiles, and glucose levels.
• Lifestyle modifications: smoking cessation, healthy diet, and regular exercise.
• Pharmacologic interventions: statins for dyslipidemia, antihypertensives for blood pressure control, and antiplatelet agents as indicated.

Central Nervous System (CNS)

Despite advances in ART, a significant number of individuals with HIV experience nervous system complications.¹⁴ These complications affect both the central and peripheral nervous system (PNS), and these can present in an acute or chronic state.

The cause of HIV associated CNS complications is multifactorial, ranging from the direct effect of the virus on neuronal cells, CNS opportunistic infections (OIs), due to dysregulated immune function, and neurotoxic effects of ART. Furthermore, the increased life expectancy of individuals with HIV on long-term ART has increased the incidence of age-related neurological conditions such as cerebrovascular diseases and cognitive impairment.^9,10 This is exacerbated by HIV’s impact on the brain, resulting in a complex interplay between HIV-related and age-related neurological change.

HIV enters the CNS as early as 1 to 2 weeks when infected CD4 T lymphocytes cross the blood–brain barrier using a “Trojan Horse” mechanism.^17,18 HIV viral particles are then released into perivascular macrophages and microglia, where they disrupt normal neuronal function by directly releasing neurotoxic viral proteins or indirectly by causing release of inflammatory cytokines, which damage the surrounding neurons.¹⁹

HIV sets up a reservoir in the CNS that contributes to ongoing neuroinflammation and immune activation in the CNS even after ART initiation and viral suppression in PLHIV. As a result, HIV patients continue to experience a wide range of neurologic complications despite systemic viral suppression.^20,21

Changes in memory, attention, concentration, and motor skills occur commonly in PLHIV and present a diagnostic dilemma to the clinician.²² HIV-associated neurocognitive disorders (HAND) is the overarching term for the range of neurocognitive impairments associated with HIV infection when not clearly attributable to an alternate cause other than HIV infection. Clinical manifestations of HAND vary greatly depending on the particular disorder and whether it is chronic or acute. Symptoms include headache, convulsions, altered mental status, and intellectual disability. The Figure below provides an overview of these HIV-associated neurologic manifestations and their risk factors.

Figure 2. Neurologic manifestations of HIV and the underlying risk factors. Image created using BioRender. Abbreviations: cART, combination antiretroviral therapy; CNS, central nervous system; HIV, human immunodeficiency virus.

HIV-associated neurocognitive disorders range from asymptomatic neurocognitive impairment to HIV-associated dementia. Symptoms include memory loss, difficulty concentrating, and motor dysfunction.

Opportunistic infections include cryptococcal meningitis, toxoplasma encephalitis, and progressive multifocal leukoencephalopathy (PML).

Management:

Involves early initiation of ART to prevent or mitigate neurological complications and specific treatments for opportunistic infections:

• Cryptococcal meningitis: Antifungal therapy with either liposomal amphotericin B + flucytosine or amphotericin B deoxycholate + flucytosine or single-dose liposomal amphotericin B + flucytosine + fluconazole for two weeks, followed by fluconazole maintenance (for 8 weeks).²³ Repeated lumbar punctures are often necessary for managing cryptococcal meningitis, specifically to reduce elevated intracranial pressure.
• Toxoplasma encephalitis: Combination therapy with pyrimethamine, sulfadiazine, and leucovorin or trimethoprim and sulfamethoxazole (TMP-SMX).
• PML: No specific antiviral treatment; management focuses on restoring immune function through ART.

Supportive care and rehabilitation for neurocognitive and motor deficits.

Gastrointestinal System

Gastrointestinal (GI) diseases are common in HIV patients and affect the entire GI tract (GIT) from the mouth to the rectum. The spectrum of gastrointestinal symptoms in HIV ranges from odynophagia and dysphagia to nausea and vomiting, to abdominal pain, and finally diarrhea and tenesmus. These disorders are mainly caused by opportunistic infections, but can also be due to the direct effect of the virus on the gastrointestinal tract (GIT) or from neoplasms or medication side effects.²⁴

Due to widespread use of ART, there has been a drastic fall in the incidence of HIV associated GI tract disorders. However, these do still occur in patients with high viremia and viral loads.²⁵ Table 1 highlights some of the common GI diseases that occur among HIV patients. It should be noted that the evaluation of HIV patients with GI complaints requires a thorough history and physical exam, as well as selected studies such as endoscopy and biopsy to diagnose the correct disease and treat accordingly.

Table 2. GI pathology affecting HIV patients.

Ophthalmologic System

Ocular manifestations are a common occurrence in HIV patients. These are caused by either opportunistic infections, vascular pathologies, neoplasms, neuro-ophthalmic conditions, or adverse effects of ART. This section provides an overview of the different forms of HIV associated ocular manifestations, their clinical presentation, diagnosis, and management.³⁰

Studies have found that about three-quarters of patients with HIV develop ocular disease, and 5 to 25% become blind in their lifetime. Retinal microvasculopathy and CMV retinitis account for almost 30% to 40% of ocular disease in HIV patients.³¹ Low CD4 count is the most critical risk factor for HIV ocular disease.³² The advent of ART has caused improvement in the immune status of HIV-infected persons and a drastic fall in opportunistic infections, hence ocular pathology. However, the improvement in immunity may be associated with an immune reconstitution inflammatory syndrome (IRIS) called immune recovery uveitis.

Table 3. Ocular emergencies in HIV patients.

Pulmonary Manifestations

Pulmonary complications are a leading cause of hospitalization, morbidity, and mortality in PLHIV, and the lungs are the most common organ system affected by HIV/AIDS.³⁸

Bacterial Pneumonia

Bacterial pneumonia is highly prevalent in PLHIV and can occur at any CD4 level.³⁹ Pneumonia is the most common pulmonary complication of HIV in developed countries.³⁸ Recurrent pneumonia (two or more episodes in one year) is an AIDS-defining condition.⁴⁰ Common pathogens include Streptococcus pneumoniae and Haemophilus influenzae,⁴¹ while Staphylococcus aureus, Pseudomonas aeruginosa, and atypicals (e.g., Legionella, Mycoplasma, Chlamydophila) are less frequent but more common than in HIV-negative populations.^42,43

Typical presentation includes acute onset of fever, chills, pleuritic chest pain, purulent sputum, and dyspnea.⁴⁴Physical signs include focal crackles, egophony, or pleural effusion. Labs often show elevated WBC counts with neutrophilic predominance. Radiographs typically reveal lobar or segmental consolidation; cavitary lesions suggest more virulent organisms.⁴⁵

Empiric outpatient treatment includes a beta-lactam (e.g., high-dose amoxicillin or amoxicillin-clavulanate) plus a macrolide (azithromycin or clarithromycin) or a respiratory fluoroquinolone in penicillin-allergic patients.⁴⁶Inpatients with non-severe community-acquired pneumonia (CAP) should receive IV beta-lactam plus a macrolide or a respiratory fluoroquinolone. For severe CAP or suspected Pseudomonas infections, broader-spectrum IV agents, such as piperacillin-tazobactam, are recommended in combination with fluoroquinolones or aminoglycosides. Cotrimoxazole remains important for prophylaxis, but rising resistance has been documented.^47,48 Pneumococcal vaccination is crucial for reducing the disease burden.⁴⁹

 Pneumocystis jirovecii pneumonia (PCP)

Among them, PCP remains a hallmark opportunistic infection, occurring in approximately 90% of PCP cases in HIV-positive individuals with CD4 counts <200 cells/mm.³ PCP is caused by Pneumocystis jirovecii, a ubiquitous fungus to which most children are exposed early in life.⁵⁰

PCP often presents subacutely with progressive dyspnea, non-productive cough, fever, and chest discomfort that worsen over days to weeks.⁵¹ On physical exam, tachypnea, tachycardia, and diffuse dry (“cellophane”) rales may be observed.⁴⁴ Hypoxemia is the most characteristic laboratory abnormality, ranging from mild (PaO2 ≥70 mmHg) to severe.⁵² Chest radiographs typically show bilateral, symmetrical “ground-glass” infiltrates in a perihilar butterfly pattern,⁴⁴ though they may be normal early in the disease.⁵³ Atypical radiographic findings include cysts, nodules, asymmetric infiltrates, and spontaneous pneumothorax, which should prompt suspicion for PCP.⁵⁴ High-resolution chest computed tomography (CT) is often abnormal even when radiographs are not, and has a high negative predictive value.⁵⁵  Pneumocystis jirovecii cannot be cultured in routine clinical laboratories; thus, diagnosis relies on microscopy, histology, serology, and/or PCR of the Pneumocystis DNA.⁵⁶

Empiric treatment should begin promptly with trimethoprim-sulfamethoxazole (TMP-SMX) and adjunctive corticosteroids if A-a gradient >35 mmHg or PaO2 <70 mmHg. Moderate-to-severe cases may require IV dosing. Alternatives include primaquine plus clindamycin or IV pentamidine. ART initiation is recommended within two weeks of PCP diagnosis. Prophylaxis with TMP-SMX is essential in patients with CD4 <200 cells/mm.^{3 57}

Pulmonary Kaposi Sarcoma

Pulmonary Kaposi sarcoma (KS) is the most common AIDS-associated malignancy and is caused by human herpesvirus 8 (HHV-8).^58,59 It is often indistinguishable from opportunistic lung infections, especially in the absence of cutaneous findings. Clinical features include a non-productive cough, hemoptysis, fever, and weight loss. Approximately 90% of pulmonary KS cases are associated with concurrent skin lesions.^57,60

Radiographs and CT may show perihilar infiltrates, nodular or reticulonodular opacities, pleural effusions, and hilar adenopathy. Bronchoscopy may reveal violaceous endobronchial lesions, though findings can be subtle or absent.⁶¹

Treatment centers on ART initiation. Advanced cases may require chemotherapy (e.g., liposomal anthracyclines (first line), taxanes like paclitaxel) or immunotherapy.⁶² Be cautious of immune reconstitution inflammatory syndrome (IRIS) following ART, particularly in patients with higher CD4 counts.⁶³

Tuberculosis (TB)

Tuberculosis (TB) remains the leading cause of death among PLHIV worldwide.⁶⁴ Infection begins via inhalation of Mycobacterium tuberculosis, leading to latent TB infection (LTBI) or active disease.⁶⁵ Active TB may follow primary infection or reactivation of LTBI, and is more likely with CD4 counts <350 cells/mm.^{3 66}

Pulmonary TB should be suspected in PLHIV presenting with cough, fever, night sweats, and weight loss, particularly in endemic regions. Even one of these symptoms has high sensitivity but low specificity for TB diagnosis in resource-limited settings.⁶⁷ Radiographic findings vary with immune status; those with higher CD4 counts often show apical infiltrates with cavitation, while advanced HIV may show lower or mid-lung infiltrates or miliary patterns.⁶⁸

Treatment of latent TB includes once weekly isoniazid plus rifapentine for 3 months, daily isoniazid and rifampin for 3 months, or daily rifampin for 4 months. Daily isoniazid for 6–9 months is a second-line option due to increased toxicity.⁶⁹

Infection with multi-drug resistant strains of Mycobacterium tuberculosis can occur and carries an exceptionally high mortality.⁷⁰ It is therefore critical to test for resistance before starting medical therapy for active TB. For active TB, the standard regimen includes an intensive 8-week phase with isoniazid, rifampin or rifabutin, pyrazinamide, and ethambutol, followed by a continuation phase lasting 4 months. ART should be initiated 2-4 weeks after starting anti-TB therapy.⁵⁸ Treatment for drug-resistant tuberculosis and HIV, when co-administered, can lead to overlapping toxicities due to the shared adverse effects of ART and anti-tuberculosis drugs. The initiation of ART in individuals with CNS TB can be delayed for 8 weeks, as early initiation is associated with an excess of serious adverse events and no survival benefit.⁷¹ Corticosteroids should be used as an adjunct to TB therapy to reduce the immune/inflammatory response to M. tuberculosis in those with meningitis.

Table 4. Pulmonary manifestations of HIV/AIDS.

Renal Manifestations

Several mechanisms may contribute to kidney disease in people living with HIV (PLWH), including direct renal damage resulting from intrarenal HIV infection and gene expression, immune dysregulation, treatment toxicity, comorbidities, and co-infections.⁷² Renal disease is a significant complication of HIV infection, with a prevalence of 2.4-17%.⁷³

These disease entities result directly from viral nephrotoxic effects, leading to the histologic features of HIV-associated nephropathy (focal collapsing glomerulosclerosis), thrombotic microangiopathy, and immune complex glomerulonephritis, or indirectly due to antiretroviral medications such as indinavir, atazanavir, and tenofovir, which have a nephrotoxic effect.⁷⁴ These, in turn, cause acute or chronic kidney disease (CKD). Acute renal failure is often a characteristic finding in HIV-infected patients. It is usually seen in advanced stages of HIV infection (i.e., CD4 cell count of <200 cells/mm³ and HIV RNA level of >10,000 copies/mL), hepatitis C virus co-infection, and a history of antiretroviral treatment.⁷⁴

Renal diseases such as diabetic nephropathy and arterionephrosclerosis may occur in PLWH due to multiple risk factors. T2DM can increase the risk and severity of renal manifestations in PLWH.⁷⁵ Several renal complications occur with HIV infection, such as HIV-associated nephropathy (HIVAN), HIV-associated thrombotic microangiopathy (TMA), and HIV-associated immune-mediated glomerulonephritis.⁷⁶

HIVAN

HIVAN is one of the major causes of end-stage renal disease (ESRD) in HIV seropositive patients, often progressing to ESRD without combined antiretroviral therapy (cART). Its clinical presentation is characterized by azotemia and proteinuria without significant peripheral edema in patients with advanced HIV infection. At the same time, the kidneys have a characteristic enlargement with loss of corticomedullary differentiation on ultrasound scans.⁷⁷

HIV-Associated TMA

This includes the clinical findings of hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP). Clinical features include microangiopathic hemolytic anemia, microangiopathic hemolytic thrombocytopenia, reduced haptoglobin, and schistocytes seen in peripheral blood smear. Clinical presentation is proteinuria and hematuria, complicated by rapid onset renal failure and damage, and multi-system organ dysfunction ⁷⁸

HIV-Associated Immune-Mediated Glomerulonephritis

More common in Caucasian populations than African American populations possess similar characteristics with lupus nephritis, including immunologic, histologic, and ultrasonographic features such as immunoglobulin (IgG, IgA, and IgM) and complement (C3 and C1q) mesangial deposits; however, it occurs in patients without negative serological findings and no clinical evidence of systemic lupus erythematosus (SLE).^79,80

Other causes of acute kidney injury (AKI) include volume depletion due to diarrhea, sepsis, and nephrotoxic medications such as tenofovir or amphotericin B. Electrolyte disturbances (e.g., hyponatremia, hyperkalemia) may be seen in adrenal insufficiency or due to gastrointestinal losses.⁸¹

Management

In the ED, management should include basic renal function assessment (serum creatinine, electrolytes), urinalysis, and cautious fluid resuscitation. Avoid further nephrotoxins and consider renal dosing for all medications to minimize potential renal toxicity.⁸²

HIVAN is an indication for the initiation of ART, regardless of CD4 cell count. The guidelines also recommend adjunctive therapy with ACE inhibitors or angiotensin receptor blockers as tolerated.⁸³ The addition of corticosteroids may be considered in patients with aggressive disease or a prominent interstitial inflammatory component.⁸⁴ Patients with HIVAN who are approaching ESRD should be offered a choice between hemodialysis and peritoneal dialysis, which offer similar survival in adults with HIV infection.⁸⁵ Selected patients with remote HIVAN and well-controlled HIV infection may also be candidates for kidney transplantation.⁸⁶

Table 5. Renal manifestations of HIV/AIDS.

Skin and Soft Tissue Manifestations

Cutaneous signs may be the initial manifestation of HIV-related immunosuppression. Skin diseases in HIV patients are rarely fatal, but they have a significant effect on the quality of life (51). They could be HIV specific dermatoses, such as papular pruritic eruption, xeroderma, eosinophilic folliculitis, prurigo nodularis, or could be opportunistic skin dermatoses such as Kaposi sarcoma, Molluscum contagiosum, Histoplasmosis, bacillary angiomatosis, etc.⁸⁷

Papular pruritic eruption (PPE), which is the most prevalent dermatologic manifestation in HIV-infected patients, is characterized by chronic symmetric papular eruptions on the limbs, trunk, and sometimes face. It has been demonstrated that lower CD4 cell counts are correlated with more intense pruritus and increased rash severity.⁸⁸

Xeroderma or xerosis, this dermatologic condition is the main cause of premature skin ageing in HIV patients and one of the reasons for pruritus in these patients.⁸⁹

Any type of acne, including vulgaris, rosacea, and conglobata (a cystic form), can occur in the setting of IRIS after starting a patient on ART.⁹⁰

Some common dermatologic disorders, such as seborrheic dermatitis, are reported with a higher frequency in HIV patients than in the general population. Some others, including atopic-like dermatitis, psoriasis, pityriasis rubra pilaris (PRP), reactive arthritis, and hidradenitis, have also been demonstrated to be related to AIDS.⁸⁷

In advanced stages of HIV infection with lower CD4 counts and higher viral loads, most of the patients develop opportunistic infections, including herpetic and mycobacterial infections, cryptococcosis, histoplasmosis, molluscum contagiosum, and bacillary angiomatosis (BA). It is essential to know that these opportunistic infections may present differently in the setting of AIDS.⁸⁷

Cryptococcus skin involvement usually presents with umbilicated papules, acneiform pustules, or papulonodular necrotizing skin lesions such as molluscum contagiosum.⁹¹

Cutaneous TB presents with papulonecrotic tuberculid, tuberculous chancre, lupus vulgaris, tuberculosis verrucosa cutis, orificial tuberculosis, scrofuloderma, lichen scrofulosorum, erythema induratum of Bazin, nodular granulomatous phlebitis, miliary tuberculosis, and metastatic tuberculosis abscess (gummatous tuberculosis).⁹²

Cellulitis, abscesses, necrotizing fasciitis, granulomas, phlegmons, nonhealing ulcers, purpura, microemboli, and leukocytoclastic vasculitis occur commonly in IV drug users among PLHIV.⁹³

Cutaneous malignancies in HIV include cutaneous Kaposi sarcoma, cutaneous lymphomas such as B-cell non-Hodgkin lymphoma and cutaneous T-cell lymphoma, and melanoma.

Kaposi sarcoma, caused by human herpesvirus 8 (HHV-8), appears as violaceous, non-blanching macules or nodules, often on the face, oral mucosa, and extremities. Kaposi sarcoma usually occurs in late stages of HIV infection, but it can happen at any CD4 count or HIV viral load. Skin lesions are composed of a combination of abnormal vascularity, inflammation, and fibrosis with hemosiderin deposits.⁸⁷

HIV patients are generally at increased risk of herpes zoster infection with atypical presentations such as necrotic or verruciform hyperkeratotic lesions.⁹⁴

Molluscum contagiosum presents with multiple, small, umbilicated papules. In immunocompetent individuals, it is self-limited, but in advanced HIV, it may be disfiguring and resistant to treatment.⁸⁷

Table 6. Skin and soft tissue manifestations of HIV/AIDS.

Disposition

Patients with serious, life-threatening complications of HIV, such as acute coronary syndrome (ACS), stroke, and acute renal failure, necessitate admission to the hospital. Those presenting with AIDS-defining illnesses or opportunistic infections need admission to the hospital with infectious disease consultation. Patients with non-emergent conditions that tend to present in patients with HIV, such as chronic ophthalmologic or dermatologic conditions, may follow up with appropriate consultants in the outpatient setting.

Pearls and Pitfalls

• All HIV patients have immune dysfunction, even with normal CD4 counts and ART compliance, which makes them susceptible to infection
• HIV is associated with infectious and non-infectious comorbidities involving the cardiovascular, central nervous, pulmonary, ocular, renal, and , dermatologic systems
• Clinicians must be aware of these possible co-morbidities and be ready to pursue work-up and management where needed

Further Reading

Further FOAMed:

References

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