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Ординатура / Офтальмология / Английские материалы / The Sclera 2nd edition_Sainz de La Maza, Tauber, Foster_2012.pdf
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7.3 Viral Scleritis

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The role of systemic steroids in preventing postherpetic neuralgia is controversial [195Ð197]; however, they reduce the incidence and severity of ocular complications, such as scleritis, keratitis, anterior uveitis, or glaucoma [169, 197], Systemic steroids may be reserved for immunocompetent adults over age 60 years because they are at greatest risk for severe or permanent pain. The suggested dosage is 40Ð60 mg/day for 5Ð7 days, 30Ð40 mg/day for 5Ð7 days, and 20 mg for 5Ð7 days.

Capsaicin (a 0.025% topical skin cream applied 3Ð6 times daily in the involved dermatome after the skin has healed) relieves pain in 75% of patients (after 2Ð6 weeks of treatment) through depletion of substance P from the sensory peripheral neurons [198, 199]. Tricyclic antidepressants, especially amitriptyline hydrochloride, may also relieve postherpetic neuralgia [200Ð203].

Systemic nonsteroidal anti-inßammatory drugs may be helpful in patients with immunemediated ophthalmic complications, such as scleritis (diffuse or nodular) with or without keratitis or anterior uveitis. If systemic nonsteroidal anti-inßammatory agents are not effective in diffuse or nodular scleritis, systemic steroids may be used. Oral acyclovir, famciclovir, or valaciclovir should be added for prevention of acute VZV infection or if the diagnosis is not completely clear in terms of differentiating herpes zoster from herpes simplex. Topical steroid therapy has little effect on scleral inßammation. Immunosuppressive agents (alone or in combination with systemic steroids) are indicated if there is a necrotizing scleritis, if the scleritis is steroid unresponsive, or if the scleritis is steroid responsive but requires prolonged toxic doses of systemic steroids. Addition of oral acyclovir, famciclovir, or valaciclovir is recommended for prevention of recurrent VZV infection or if the diagnosis is not completely clear in terms of differentiating herpes zoster from herpes simplex.

7.3.1.2 Herpes Simplex Scleritis

HSV may occasionally cause episcleritis and scleritis. Episcleritis most often occurs as a result

of direct viral invasion during the active HSV infection. Scleritis may occur during the active HSV infection as a result of direct viral invasion, or months after the initial viral encounter as a result of an immune-mediated reaction induced by the virus.

Epidemiology

HSV is ubiquitous and primary infection usually occurs between 6 months and 5 years of age. More than 70% of individuals have been infected with HSV by age 15Ð25 years and, therefore, have HSV antibodies; this percentage progressively increases with age to about 97% of individuals 60 years of age being infected [204]. Because only about 1Ð6% of patients with primary HSV infection experience some form of clinical disease [205], most primary HSV infections are subclinical and, therefore, more than 95% of HSV-related clinical manifestations are the result of recurrences that develop long after a primary infection [206].

Pathogenesis

Viral transmission in primary HSV seems to be by direct contact from infected individuals. The virus infects a peripheral end organ and travels to the ganglia, where it becomes latent. The virus may be reactivated by different stimuli, such as fever, sunlight, trauma, or stress, presumably through cyclic nucleotide concentration changes [207]; it travels to the peripheral end organ via the neuronal network and produces recurrent HSV disease. Immunosuppressed individuals, such as patients with leukemia, malignancies, or transplanted organs, are at high risk for reactivation of latent HSV [208, 209].

Clinical disease and frequency of recurrences seem to depend on the type of virus strain (viral genome) of the primary HSV infection [210, 211]: although most people are colonized by a ÒgoodÓ virus incapable of producing disease except under extreme conditions (leukemia, malignancies, etc.), some patients are colonized by a more virulent virus that causes clinical manifestations with varying frequencies of recurrence [206]. Viral genome and neuronal stimuli, therefore, are important factors in the development of

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