To data, CMV can cause an acute, recurrent, or chronic hypertensive anterior uveitis, particularly in the middle aged Asian male populations [3, 5, 6]. In acute CMV-AU, it often been clinical diagnosed as PSS or glaucomatocy clitic crisis, which typically characterized by recurrent pathological ocular hypertension with mild anterior segment inflammation [5,6,7,8,9]. And in chronic course, the manifestations were insidious persistent, with slightly elevated IOP, lower aqueous flare counts and mild ocular blurring [2, 9]. Though there were no definite clinical manifestations that enabled us to distinguish the eyes with CMV infected or not, there are some characteristic features indicated CMV infection: coin-shaped KPs, nodular endothelial lesions and patched or diffused iris atrophy [3, 5, 9,10,11,12,13]. Meanwhile, Posner-Schlossman syndrome (PSS) was described as acute attacks of unilateral, nongranulomatous, mild anterior uveitis that accompanied by markedly elevated IOP and opened anterior chamber [14]. Usually, it always a benign disease and rarely causes intractable glaucoma and glaucomatous optic neuropathy [15]. Thus, it is important to note that any eye with hypertensive anterior uveitis exhibits endotheliitis, KPs or iris atrophy, especially with optic nerve damage, qualitative PCR analysis of aqueous for viruses DNA should be performed as the presumptive evidence of viral infection.
CMV-AU treatment should be customized due to the severity of the disease. The common management focused on anti-virus and control elevated IOP [3, 5, 6]. Topical use of ganciclovir gel is well responded with minimal side effect and economized in CMV infections. But the ocular hypertension with inflammation often recurred frequently. Various modalities of ganciclovir (or its prodrug valganciclovir) including oral application and intravitreal implantation/injection were used [5,6,7,8,9]. Most studies recommend a 3-month course of oral anti-viral treatment [3, 5, 6, 16]. Nevertheless, some studies reported that the relapse rate in patients with CMV were high regardless of treatment regimen [6, 17]. It was anticipated that antiviral medicines like ganciclovir are virostatic. It could reduce viral replication but could not eradicate it [3, 6, 16, 18]. For this reason, a prolonged course of systemic antivirals was reported [3, 16, 18].
The virus load in aqueous humor maybe one of the reasons for the relapse of CMV induced hypertensive AU. In our case, after 14 days systemic using of ganciclovir combined with topical ganciclovir gel four times a day consistently, the CMV DNA copies from the aqueous humor was much lower than that in the first time when uncontrolled IOP relapsed with little aqueous flare. Some studies presumed that the impairment of trabecular meshwork function was involved [7,8,9, 16, 19]. A study proved that human TM cells can support CMV replication in vitro effectively and the active CMV viral infection in TM cells which may be the key mechanism for the elevation of IOP in anterior viral uveitis [20]. Other than that, ocular immune response may also play a role in the relapse of ocular hypertension [19]. The duration of systemic and topical antiviral therapy should be reconsidered. Further studies are needed to investigate detail mechanisms.
Glaucoma surgery is preferable for patients with consecutive uncontrolled IOP. Pathological IOP elevation is the main reason for vision loss in CMV infection cases [6,7,8]. Studies show that CMV associated AU is particularly at risk for the frequent attacks of high IOP [7,8,9, 18], which leads to a series of secondary glaucomatous damages. Hence, treatment may be initiated with anti-glaucoma agents as a supplement. But considering the toxicity of long-term use of topical medicines, advanced surgical treatment, such as trabeculectomy, is required to protect progressive visual field defects in patients with refractory ocular hypertension [4,5,6,7,8,9, 16, 18]. On the other hand, consistent with our study, a number of studies have shown that CEC loss appears to be significantly correlated with CMV viral load [4, 10, 12]. Meanwhile, repeated relapse of IOP leads to CEC decrease [7]. Glaucoma surgery could irrigate CMV in aqueous humor and stabilize IOP, which prevents CEC dysfunction and glaucomatous optic nerve damage.
