Ocular Manifestations of HIV

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Dr. Sharanya Abraham, DO DNB FICO Consultant, Department of Uvea , Sankara Nethralaya

Published Online: November 30th, 2021 | Read Time: 42 minutes, 56 seconds

Human immunodeficiency virus (HIV) disease is a pandemic of global concern, not only due to serious health issues affecting all organs of the body but also due to its huge economic burden.(1) The diagnosis is often associated with social stigma that includes changing sexual practices, lack of availability of a vaccine and the chronicity of the disease requiring lifelong treatment.(2) The disease runs a severe course, involving multiple organs. Ocular lesions are varied and can affect any structure, usually in the late phase of HIV infection. Rarely, these lesions can be the presenting manifestations of the disease.

While a variety of cell types may be infected by HIV, the immunologic hallmark is the selective loss of the CD4+ T cells. CD4 is a cell surface marker that identiﬁes the helper/inducer subset of T cells. During the initial phases of infection, a majority of patients remain asymptomatic. With a decrease in the CD4+ T cell count (< 500 cells/µL) the immune system shows evidence of impairment, in the form of mild symptoms, such as fever, loss of weight and thrush. Further reduction in the CD4+ T cell count (< 200 cells/μL) leads to signiﬁcant impairment of the immune system, characterized by a series of opportunistic infections or unusual neoplasms.(3) This chapter aims to review the characteristic ocular manifestations in HIV and briefly describe the phenomenon of immune recovery uveitis (IRU) in the highly active antiretroviral therapy (HAART) era.

HIV-associated ocular tumours

Kaposi Sarcoma

Ocular surface squamous neoplasia (OSSN)

Ocular adnexal lymphoma and intraocular lymphoma

HIV-associated ocular lesions

Microangiopathy

Uveitis

Opportunistic infections

Although transmission of the infection through ocular fluids such as tears (4)is not established, it is important to know that transmission can occur through corneal transplantation² or contact with other intraocular fluids such as aqueous or vitreous fluids. (5) Morbidity and quality of life (QOL) are indicators of rehabilitation and are altered irreversibly if the ocular lesions are not detected early and appropriately managed. HAART has reduced AIDS-related mortality, but insufficient or improper management can affect the rehabilitation process.

Ocular lesions In AIDS:

Ophthalmic manifestations of AIDS were described as early as 1982 in the United States.(1) In India, these lesions were first reported in 1995, and later in 2000.(6,7) In this chapter, the ocular lesions will be described under the following headings:

Ocular adnexal
Anterior segment
Posterior segment and neuroophthalmic
Neoplasms
Drug-induced (Iatrogenic)
Immune Recovery Uveiits (IRU)

The ocular lesions in AIDS in the HAART era have varied manifestations and are marked by atypical presentations of known diseases. The immune status of a patient with HIV is determined by the CD4 T cell counts, and various studies demonstrate that a definite pattern of ocular complications is associated with various levels of CD4 cell counts (Table 1) (8)

CD4 counts (cells/ mm³)
1000	Normal
<500	Kaposi sarcoma Lumphoma Tuberculosis
<250	Pneumocytosis Toxoplasmosis Retinal/ conjunctival microvasculopathy
<100	Keratoconjunctivitis sicca VZV retinitis CMV retinitis

Table 1 – Pattern of ocular complications with various levels of CD4 counts

Anterior segment lesions are seen in more than half of all HIV-infected patients, and almost one-third have ocular adnexal complications (Table 2) (9), which can be a sign of severe systemic immunosuppression. The anterior and posterior segment manifestations of HIV are listed in Tables 3 and 4 respectively.

Ocular adnexal manifestations

Clinical characteristics

Preseptal cellulitis

Caused by Staphylococcus aureus, a commensal in the nasal mucosa

Results in systemic and cutaneous infections

Bacillary angiomatosis

Caused by Bartonella

Occurs when CD 4 counts ≤ 200 cells/µL

Similar to Kaposi sarcoma

Table 2: Ocular adnexal manifestations of opportunistic infections

Anterior segment manifestations	Clinical Characteristics
Herpes zoster ophthalmicus (HZO)	Incidence: 10% - 20% of HIV positive patients (10,11) Risk of HZO: 6.6 times higher Characteristic feature: vesiculobullous rash along withthe distribution of the ophthalmic branch of the trigeminal nerve with necrotic skin lesions Signs: dendriform and stromal keratitis, conjunctivitis, blepharitis, uveitis (often with secondary glaucoma), hemorrhagic hypopyon, scleritis, retinitis, and encephalitis. Diagnosis: mainly clinical, viral culture, Tzanck smear, and polymerase chain reaction (PCR)
Molluscum contagiosum	Causative organism: large DNA pox virus Incidence: 5% - 18% of HIV infected patients (11,12) Pathogenesis: profound dysfunction of T lymphocyte mediatedlymphocyte-mediatedimmune response Characteristic feature: pink or pearly white wart-like umbilicated nodules on the skin (Figure 1) Aggressive presentation in children and young adults, involving the eyelid and conjunctiva, larger in number and size, often conﬂuent, bilateral, and resistant to therapy Diagnosis: clinical examination of the lash line (13) Management: HAART, topical phenol, liquid nitrogen, lesion excision and cryotherapy
Bacterial and viral keratitis	Bacterial keratitis Causative organisms: Staphylococcus aureus, Staphylococcus epidermidis, and Pseudomonas aeruginosa, Klebsiella oxytoca, Streptococcus, Bacillus, Micrococcus, Capnocytophaga and Acanthamoeba species (10,11) Characteristic feature: bilateral corneal ulcerations, polymicrobial and with a higher risk of perforation Microsporidial keratitis Presentation: bilateral superﬁcial punctate epithelial keratitis, white intraepithelial inﬁltrates and follicular conjunctivitis with minimal anterior chamber reaction Diagnosis: Masson trichrome or Giemsa stain from conjunctival scrapings or corneal biopsy Treatment: fumagillin eye drops and oral albendazole are eﬀective Viral keratitis Causative organisms: Varicella zoster virus (VZV), Herpes simplex virus (HSV), and Cytomegalovirus (CMV) Presentation: corneal scarring, iritis and raised intraocular pressure (14)

Table 3: Anterior segment manifestations of opportunistic infections

Figure1: Pink or pearly white wart-like umbilicated nodules on the skin of upper and lower eyelids (Photo courtesy: Dr. Rohit Rao)

Posterior segment manifestations	Clinical characteristics
Cytomegalovirus (CMV) retinitis	Incidence: 15% - 40% of ocular lesions in HIV (15,16) Risk factors: genetic susceptibility (haplotypes of interleukin 10 receptor (IL 10R1), chemokine receptor 5 (CCR5) and stromal derived factor 1 (SDF 1) and retinal microinfarctions (17) Presentation: unilateral or bilateral lesions with hematological spread At low CD4 counts: classical ‘pizza pie’ appearance with retinal hemorrhages and/or the yellow white necro- tizing granular type retinitis with or without minimal vitri- tis (Figure 2) At moderate CD4 counts: vitreous or vascular inflamma- tion. Retinal necrosis with superimposed IRIS in cases re- cently started on HAART In the active stage: lesions may be fulminant, indolent (granular CMV) or exudative with extensive perivascular sheathing or frosted branch angiitis (FBA). These le- sions may progress to retinal necrosis and multiple tears leading to subsequent retinal detachment or they may heal, leaving behind an atrophic retina with fibrosis, calcification, and sclerotic retinal vessels Diagnosis: clinical examination, intraocular fluid PCR for CMV Immune status of the patient must be reconstituted with HAART (18)
*Acute retinal necrosis (ARN)*	Causative organism: Herpes simplex virus (HSV-1 and HSV-2); Varicella zoster virus (VZV) Characteristic feature: peripheral confluent lesions spreading circumferentially (Figure 3) Presentation: necrotizing herpetic retinitis with char- acteristic well-demarcated, multifocal, coalescing, and deep or full thickness areas of retinal necrosis; Vitritis is seen in severely compromised patients (19)\ Diagnosis: clinical examination and PCR of intraocular sample Treatment: systemic antivirals, prophylactic laser barrage or vitrectomy
Progressive outer retinal necrosis (PORN)	Causative organism: Varicella zoster virus (VZV) Characteristic feature: outer retinal whitening (cracked mud appearance) Presentation: posterior lesions; full thickness retinal necrosis with minimal or no other signs of in- traocular inflammation; vitritis is absent or minimal Treatment: antivirals with HAART (20)
Ocular toxoplasmosis	Presentation: Focal, multifocal or diffuse necrotizing retinitis with indistinct borders with or without he- morrhages. I t can also present with active retinochoroiditis adjacent to a retinochoroidal scar Adjacent retinal vasculitis (Kyrieleis’ arteriolitis) with varying amounts of vitreal inflammation (mild to exten- sive) due to low CD4+ T cell counts May follow a fulminant course with good response to early treatment Diagnosis: clinical examination, raised serum IgM and IgG titres in atypical cases and PCR Seroprevalence of toxoplasmosis is 67.4% in HIV/ AIDS patients (21) Goldmann–Witmer coefficient which compares the level of intraocular antibody (IgG) production to that in serum as measured by ELISA, is less sensitive than PC, R in patients with advanced immunosuppression (22,23)
Ocular tuberculosis (OTB)	Incidence: 3.8% of patients with HIV, can occur in all ranges of CD4+ counts (16, 24) Presentation: asymptomatic choroidal tubercles, subretinal abscess, conjunctival tuberculosis and panophthalmitis (25) Diagnosis: disseminated systemic disease may be a clue to diagnose a miliary form of the disease Treatment: systemic antitubercular therapy (ATT) along with HAART Paradoxical worsening of tubercular infection may follow the initiation of HAART due to the improvement of the host’s immune response to Mycobacterial antigens with devastating complications including Immune Reconstitution Inflammatory Syndrome (IRIS) (26-28) HIV positive patients may be 10 times at greater risk of multidrug resistant (MDR) TB than HIV negative patients (29)
Ocular syphilis	Presentation: anterior uveitis, significant vitritis, diffuse retinitis, placoid chorioretinitis, panuveitis and optic neuropathy (30) Jarisch–Herxheimer reaction may present as worsening of ocular signs following anti-syphilitic treatment (31) Diagnosis: clinical examination and positive serology with serum nontreponemal tests (VDRL, RPR), treponemal tests (FTA ABS, TPHA), PCR from ocular fluids, lumbar puncture (LP) and CSF antibody testing (CSF– VDRL/ TPHA) for neurosyphilis (32)
Neuro-ophthalmic manifestations	Presentation - optic atrophy, disc edema, optic neuritis, cranial nerve palsies and retrobulbar neuritis, progressive multifocal leukoencephalopathy (PML) and cortical blindness (33)

Table 4: Posterior segment manifestations of opportunistic infections

Figure 2: Fundus photograph of Acute Retinal Necrosis in a patient with HIV

Figure 3: Ocular toxoplasmosis in HIV

The treatment of the above described anterior and posterior segment opportunistic infections is outlined in table 5.

Opportunistic infection	Treatment of choice	Alternate therapy	Adverse effects
HZO	Oral acyclovir 800mg five times a day or oral valacyclovir 1g thrice daily	Oral famciclovir or foscarnet- in resistant cases	Nephrotoxicity


Viral Keratitis	Topical therapy VZV and HSV: Acyclovir eye ointment five times daily CMV: Ganciclovir gel 0.15% five times daily until healing occurs followed by thrice daily for 7 days Systemic therapy VZV and HSV: Acyclovir 400 mg 5 times a day or valacyclovir 500mg twice a day CMV: Valganciclovir 900 mg twice daily for 21 days, fol- lowed by 900 mg once a day	Vidarabine 3% ointment five times daily or Famciclovir (125-500 mg three times daily) Long-term prophylaxis for recurrent cases - oral acyclovir 400 mg twice a day for one year	Nephrotoxicity, Myelosuppression
CMV retinitis	Ganciclovir (IV) induction: 5mg/kg twice daily for 14-21 days maintenance: 5mg/kg/day or Oral Valganciclovir induction: 900 mg twice daily maintenance: 900 mg once daily Intravitreal Ganciclovir induction: 2 mg/0.1 mL as needed (1-4 times) maintenance: 2 mg/0.1 mL weekly	Foscarnet (IV) induction: 90 mg/ kg twice daily for 14 days maintenance:120mg/kg/day Cidofovir (IV) induction: 5 mg/ kg weekly for 3 weeks maintenance: 5 mg/kg every 2 weeks Intravitreal foscarnet induction: 1.2-2.4 mg 1-2 times weekly maintenance:1.2 mg weekly Cidofovir induction: 20 µg 1-8 times, as needed to halt retinitis, maintenance: 20 µgevery 5-6 weeks	Ganciclovir/ valganciclovir: myelosuppression Foscarnet: nephro- toxicity, electrolyte disturbance, nausea and vomiting CidofovirNephrotoxicity Intravitreal cidofovir - anterior uveitis and hypotony CMV mutations in UL54 or UL97 genes cause ganciclovir resistance
Ocular toxoplasmosis	Pyrimethamine: 200 mg on the first day followed by 75- 100 mg daily Sulfadiazine: 1-1.5 g four times daily Folinic acid: 10-50 mg daily Trimethoprim 160mg + sulphamethoxazole 800 mg with/or (in sulpha allergy) Oral clindamycin: 300 mg 4 times a day	Atovaquone, azithromycin 500 mg followed by 250 mg once a day	Myelosuppression,leukopenia,pseudomembranous colitis
Ocular TB	H - isoniazid R - rifampicin Z - pyrazi- namide E - ethambutol S - streptomycin New case (never had treatment or less than 1 month of ATT): 2 HRZE + 4 HRE Previously treated (one month or more of ATT): 2 HRZES + 1 HRZ E + 5 HRE	Multidrug resistant (MDR) TB: aminoglycosides (kanamycin, amikacin) fluoroquinolones (ofloxacin, levofloxacin) linezolid, bedaquiline	Hepatotoxicity, peripheral neuropathy, optic neuropathy
Ocular syphilis	Aqueous crystalline peni- cillin G: 18-24 million units/ day administered as 3-4 mil- lion units IV every 4 hours or continuous infusion for 10-14 days	Procaine penicillin G: 2.4 mil- lion units/ day IM+ probenecid 500mg orally four times a day for 10-14 days Penicillin allergy: ceftriaxone 2g daily either IM or IV for 10 to 14 days or doxycycline 100 mg orally twice daily for 14 days	Jarisch-Herxheimer reaction
ARN/ PORN	Acyclovir induction: intra- venous acyclovir 500 mg every 8 hours for 2 to 3 weeks maintenance: oral acyclovir 800 mg 5 times daily (15 mg/kg in three divided dos- es) for 6 weeks to 3 months or oral valacyclovir 1 gram three times daily		Nephrotoxicity

Table 5 : Recommended treatment guidelines for various opportunistic infections

Neoplasms

(i) Kaposi sarcoma

It is a highly vascular mesenchymal tumor characterized by the presence of multiple purple‐to‐red nodules on the skin and mucous membrane. It is caused by human herpesvirus-8 (HHV‐8) or KS herpesvirus (KSHV), and occurs when CD4+ cells are ≤150 cells/μL.(34) Approximately, 10% to 20% of HIV-infected individuals are affected with Kaposi sarcoma (KS), involving the eyelids, conjunctiva, and, rarely, the orbit. The tumor is relatively rare in India. When present on the lids, the tumour can mimic a chalazion, while in the conjunctiva it can be mistaken for a subconjunctival hemorrhage or a pyogenic granuloma. For the purpose of prognosis, the tumor is staged as follows:

Stages I and II lesions are flat (less than 3 mm in height), patchy, and of up to 4 months duration
Stage III lesions are nodular (greater than 3 mm in height) and greater than 4 months duration
Accurate staging determines response to therapy.(35)

Treatment depends on the site and extension of KS and includes radiotherapy, cryotherapy, surgical excision and systemic chemotherapy. Localized lesions can be surgically excised with or without adjunctive cryotherapy to the margins. Systemic agents are warranted for patients with advanced disease, such as extensive cutaneous disease, visceral disease, or lymphedema. HAART has been successful in treating AIDS-related primary KS and has reduced the need for other methods such as chemotherapy or damaging radiation to control the disease.(36)Chemotherapy with pegylated liposomal doxorubicin, paclitaxel, bleomycin, lenalidomide, interferon α, and immune checkpoint inhibitors (nivolumab, pembrolizumab) are under investigation.(37)

(ii) Ocular surface squamous neoplasia (OSSN)

It is a common primary malignancy of the eye. Risk factors include exposure to ultraviolet (UV) rays, human papillomavirus (HPV) infection, and chemicals such as arsenic and hydrocarbon. Increased incidence of OSSN is reported in HIV patientsand is a presenting sign in more than two-thirds of patients. In individuals with HIV, it can occur at an earlier age (3^rd/4^th decade) and aﬀects both the cornea and the conjunctiva. (38) It may present with unilateralorbilateral, pigmentedor non‐pigmented papillary lesions with intra‐lesional blood vessel (feeder's vessel) and fronds, raised plaque with keratinization, or as a diﬀuse gelatinous form. Patients may be asymptomatic or have mild symptoms such as foreign body sensation, irritation, or mild pain. HIV‐infected patients have larger, more aggressive tumors, higher‐grade malignancy with a higher incidence of corneal, scleral, and orbital invasion. Diﬀerential diagnoses include pinguecula, pterygium, and papilloma. Diagnosis is by an incision or excision biopsy. Surgical treatment options include tumor excision with amniotic membrane grafting with adjunctive cryotherapy or chemotherapy; while medical management involves topical mitomycin‐C (MMC) or 5‐ﬂurouracil (5-FU) for a week, followed by a drug holiday, and repetition of the cycle until regression ofthelesion. Monitoring for side eﬀects such as epithelial toxicity is recommended. Since interferon is better tolerated, it can be administered either as eye drops or weekly subconjunctival injections. Recently, a possible role of HPV vaccination in the prevention of OSSN is under consideration.(38)

(iii) Ocular adnexal lymphoma and intraocular lymphomas

These are the B‐cell non‐Hodgkins lymphomas (NHL) seen in HIV/AIDS with a poor prognosis.(39) They appear as erythematous lesions aﬀecting the orbit, lacrimal glands, conjunctivae,and eyelids. The management of low-grade tumors includes chemotherapy with chlorambucil or ﬂudarabine and that of high-grade lymphomas include, CHOP (cyclophosphamide, vincristine, doxorubicin and prednisolone) or radiotherapy. Novel treatments under investigation are monoclonal antibodies targeted against CD40 and bortezomib, a proteasome inhibitor that targets the intracellular pathways involved in tumor cell survival and growth.(40)

Diagnosis and Management in the HAART era

One of the hallmarks of progressive immune deficiency is a steady decline in the absolute number of CD4+ T-lymphocytes.(7) In the pre-HAART era, the lifetime cumulative risk for developing at least one abnormal ocular lesion in those with HIV, ranged from 52% to 100%.(41) Treatment of HIV infection with the HAART regimen aims to inhibit progression to full-blown AIDS (defined by a CD4+ cell count of < 200 cells/μL), or death. This is achieved by reduction in plasma HIV RNA to permanently low levels, reduction in the viral load and an increase in CD4+ cell counts which improve the immune status of the individual. Those on HAART are less likely to be affected by blinding posterior segment infections, and there has even been a marked reduction in the occurrence of anterior-segment and adnexal lesions in patients who received treatment.

Patients with HIV/AIDS can develop ocular lesions from the drugs used for treatment of the immunocompromised state or from those used in the management of opportunistic infections.

HAART-induced immune recovery has its own merits and demerits, with 10% to 25% of patients experiencing immune recovery problems or immune reconstitution inflammatory syndrome (IRIS).(11,42)

Drug-induced Uveitis

Careful monitoring is advocated during treatment with HAART, especially in elderly patients due to the high degree of concurrent medication use and, the greater potential for harmful drug interactions, as well as age-related changes in renal and hepatic function that could affect drug clearance.(43) Similar complications may be seen in the eye, presenting as uveitis, following systemic and intraocular therapies. Most commonly implicated drugs are cidofovir and rifabutin. Cidofovir is a nucleotide analog that acts against CMV. It has been associated with side effects such as granulomatous anterior uveitis with both intravenous and intravitreal routes of administration.(44) The increased number of CD4+ T cells following HAART can lead to an inflammatory response resulting in uveitis.(45) Co‐administration of probenecid, a competitive inhibitor of organic anion transport in epithelial barriers reduces the chance of anterior uveitis by almost 50%. Rifabutin is commonly used in the treatment of pulmonary tuberculosis and for prophylaxis of Mycobacterium avium complex (MAC) in patients with AIDS and low CD4+ T‐cell counts. It is a less potent inducer of the cytochrome P450 drug metabolizing enzymes than rifampicin and is often used as a replacement drug. Its use can commonly cause hypopyon uveitis, intermediate uveitis or posterior uveitis.(45) The pathogenesis for uveitis is correlated to both direct chemical drug toxicity and immune complex deposition. While the long duration of treatment associated with the development of uveitis supports the immunological model of inflammation, short-term drug exposure would be expected to cause drug toxicity reaction.Other HAART drugs with ocular side effects include nevirapine, didanosine, ritonavir,indinavir, efavirenz and newer elvitegravir-based combination therapies.(45-49) Most cases of drug-induced uveitis respond well to topical corticosteroid and cycloplegic agents. Discontinuation of the inciting drug is required in refractory uveitis that does not respond to conventional treatment or in case of recurrences or other complications.(45)

Immune Recovery Uveitis

Before the introduction of protease inhibitors in the treatment of HIV, patients with CMV retinitis typically had CD4+ T lymphocyte counts <50 cells/μL, with minimal intraocular inflammation. Partial recovery of immune responses specific to residual CMV antigen located in the eye results in Immune recovery uveitis (IRU). It affects the anterior uvea and vitreous, and is associated with visual impairment. IRU is part of the immune reconstitution inflammatory syndrome (IRIS). These reactions may either worsen the clinical manifestations of the opportunistic infection (paradoxical reaction), or develop new manifestations shortly after the initiation of HAART (unmasking syndromes).(27)

The AIDS Clinical Trial group defined IRU as

decrease in vision accompanied by at least 2 of the following signs in the absence of active CMV retinitis: presence of >2+ inflammatory cells in the vitreous; cystoid macular edema (CME); or epiretinal membrane (ERM) formation in patients receiving antiretroviral therapy with evidence of immune reconstitution.(50)
Immune reconstitution, in turn, was defined as a CD4+ count of 100 cells/μL or more.

It is estimated that IRIS develops in 15-25% of HIV-positive patients receivingHAART, with the highest incidence during 8-16 weeks following the initiation oftreatment.(51,52) Therefore, to prevent the occurrence and severity of IRU, it may be advised to delay initiation of HAART, until CMV retinitis is managed with treatment. However, careful clinical judgment and close monitoring of the patient are optimal to prevent mortality.

The pathogenic mechanism in IRU is an inflammatory response mediated by CD8+ T-cellcytokine to the presence of CMV antigens in the retina.

Reported risk factors for IRU include (27):

• Presence of HLA-8–18 (genetic risk factor)

• Very low CD4+ T-cell count at the time of initiation of HAART (≤ 50 cells/μL)

• Larger retinitis lesions (≥25 - 30%), due to higher antigen load

• Use of intravitreal injections of cidofovir

• Use of boosted protease inhibitors and a fast onset of retroviral suppression

IRU has varying clinical presentations. It may be symptomatic or asymptomatic, with a self-limiting or chronic inflammatory course. Visual loss or floaters arethe most common features of symptomatic IRU. IRU-induced vision loss is generallymoderate, which typically results from complications of the intraocular inflammation.However, occasionally it may result in severe visual loss (visual acuity 20/200 orworse).(53,54) The most common inflammatory complications of IRU are CME and ERM, followed by preretinal neovascularization, papillitis, proliferative vitreoretinopathy and anterior segment inflammation that leads to iris synechiae and cataract.(27,54,55)

A thorough clinical and ancillary examination must be carried out in patients withmanifestations of ocular inflammation undergoing HAART, to exclude co-infectionssuch as syphilis, drug toxicity or interactions, and primary manifestations of ocularopportunistic infections. PCR of intraocular fluids can be used as a confirmatory test.Aqueous or vitreous aspirate PCR may be used to rule out co-existing causes of uveitis,when available.(56) The CMV Pp65 antigenemia assay quantitates the number ofCMV-infected leukocytes in peripheral blood. It has proven efficacy in the detection and monitoring of CMV infection in immunocompromised patients.(57)

In cases of mild and more advanced IRU, topical or periocular corticosteroids may be sufficient to control inflammation and CME.(27) The use of intravitreal triamcinolone acetonide (IVTA) injections has been reported.(58, 59) Long-term intravitreal implanted corticosteroid depot has been proven effective.(60) Oral valganciclovir has been observed to show a reduction in CME following treatment.(61)

Tips in the management of a patient with suspected ocular HIV

Do’s (when to suspect and test for HIV)

Younger patients (<45 years) with HZO or typical ocular manifestations
Corneal perforation in a patient with HZO infection
Molluscum lesions in a young adult
Atypical presentations of ocular disease

Don’t’s (pertaining to careful systemic and treatment history)

Overlook early HIV microangiopathy
Treat IRU with aggressive steroid therapy without monitoring for signs of CMV retinopathy (CMVR) reactivation
Consider all CMVR to be HIV-related. Rule out other causes of immunosuppression, organ transplantation, diabetes mellitus, local steroid therapy (intra/ periocular)
Overlook patient’s CD4+ counts and HIV treatment regime

Conclusion

Ocular complications of HIV are numerous and can be sight-threatening. The presence of multiple but distinct pathogens from the eye provides a definitive clue to HIV-related systemic disorders. HAART has remarkably reduced the frequency of rare malignancies and severe immunosuppression. Patients on HAART can develop severe inflammatory reaction due to the immune recovery phenomenon, which in itself may be a source of severe ocular morbidity.

Patient awareness about the signs and symptoms of ocular complications of HIV is an important part of their management. Routine monitoring is also an essential tool in the management of these patients, including those with immune

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Articles Uvea & Inflammatory Diseases Cornea and External Eye Diseases Anterior Segment Uvea and Intraocular Inflammation Review Made Easy

Dr. Sharanya Abraham, DO DNB FICO

Consultant, Department of Uvea , Sankara Nethralaya

Sharanya Abraham is a Consultant in the Uveitis department at Sankara Nethralaya, Chennai. She completed her ophthalmic training in Aravind Eye Hospitals, Madurai and Sankara Nethralaya, Chennai. She has presented at national conferences and published in national and international journals. She has an interest in intraocular infections.