becomes flatter and the iridocorneal angle widens. The area of iridolenticular contact increases, as aqueous flows through the iridotomy rather than the pupillary space (Foster et al., 2006).

Level II — ciliary body

Abnormal ciliary body position leads to anteriorly positioned ciliary processes, these force the peripheral iris into the angle causing angle closure. This is known as plateau iris. Examining the angle with gonioscopy will show the iris root angulated forward and centrally. Laser iridotomy partially opens or fails to open the angle. Therefore laser iridoplasty is the treatment of choice. Plateau iris syndrome occurs when angle closure develops, either spontaneously or after pupillary dilation, in an eye with plateau iris configuration despite a patent iridotomy. Other disorders of the ciliary body may mimic plateau iris configuration and include iridociliary cysts, tumors, or edema (Foster et al., 2006).

Level III — lens-induced glaucoma

A large lens (due to intumescence) may press against the iris and ciliary body, forcing them forward and therefore causing acute or chronic angle-closure glaucoma (phacomorphic glaucoma). This may also occur if there is anterior subluxation of the lens (Foster et al., 2006).

Level IV — malignant glaucoma

In this form of glaucoma, the pressure difference is created between the vitreous and aqueous compartments due to aqueous misdirection into the vitreous. This pushes the lens–iris diaphragm forward. Anterior rotation of the ciliary body with forward rotation of the lens–iris diaphragm and relaxation of the zonular apparatus causes anterior lens displacement causing angle closure by pushing the iris against the trabecular meshwork. A shallow supraciliary detachment maybe present and it is this effusion that is thought to cause the anterior rotation of the ciliary body (Foster et al., 2006).

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Other causes of angle closure

These include anterior subluxation of the lens, iris, or ciliary body cysts, ciliary body tumors or inflammation, as well as air or gas bubbles after intraocular surgery. PAS can be caused by iris and angle neovascularization, iridocorneal endothelial syndrome, or anterior uveitis. These disorders need to be identified and treated specifically (Foster et al., 2006).

Risk factors

A list of the common/important risk factors for angle-closure glaucoma are summarized in Table 2.

Age and gender

The prevalence of angle closure increases with age (Seah et al., 1997; Wong et al., 2000; Lai et al., 2001; Vijaya et al., 2007). The prevalence of narrow angles, PAC, and PACG is higher in females compared to males (Teikari et al., 1987; Seah et al., 1997; Wong et al., 2000; Lai et al., 2001; Ivanisevic et al., 2002; Vijaya et al., 2007).

Ethnicity

East Asian populations (Chinese from Singapore and Hong Kong) have the highest incidence rates of acute angle closure. Compared to East Asians, South and South East Asians (Indians, Thais, and Malays) have lower rates of angle-closure. It is noted that only 25–35% of angle closure in Asian people causes symptoms (Foster et al., 1996, 2000; Congdon et al., 1996; Yip and Foster, 2006). The highest rates of angle-closure glaucoma are found in the Inuits of Alaska, Canada, and Greenland (Alsbirk, 1976;

Table 2. Risk factors for angle closure

Increasing age

Female gender

Ethnicity: Inuits and East Asians

Shallow anterior chamber depth

Shorter axial length

Genetic factors

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Arkell et al., 1987). Studies from India show that PACG is more common in India than in Europeans and has a tendency to be asymptomatic (Jacob et al., 1998; Dandona et al., 2000). PAC is not a common condition in Europeans; its prevalence rate is 0.1% or less in people over 40 years old (Hollows and Graham, 1966; Coffey et al., 1993; Wensor et al., 1998). In the African population, a study has shown that the rate of PAC was equal among black and white populations in Johannesburg (Luntz, 1973); however, studies looking at people of Bantu ethnicity have shown a prevalence of PACG at 0.5% much lower then the prevalence of other glaucomas (Buhrmann et al., 2000).

Ocular biometry

Anterior chamber depth (ACD) is the most important anatomical risk factor for angle-closure (Yip and Foster, 2006). A shallower ACD leads to an increased risk of angle closure, and this collates to demographic factors. ACD is shallower in females and decreases with increasing age (Alsbirk, 1974; Foster et al., 1997). This age-related change is also more pronounced in women than men (Alsbirk, 1976; Foster et al., 1997).

As the position and thickness of the lens determines the ACD, these factors are the ultimate determinants of the risk of angle-closure. A study comparing normals with angle closure in Australians found the ACD to be 1.0 mm shallower in the PAC group. 66% of this difference was due to the more anterior positioning of the lens and 33% was due to the lens being thicker than normal (Lowe, 1969). A later study of Chinese people found lens thickness was the major determinant of a shallow ACD. The lens position only accounted for 4% of the difference between angle closure and normal eyes (Friedman et al., 2003).

Subjects with angle closure have shorter axial lengths (Lowe, 1977). Studies in both Chinese and Indian populations have shown that affected people have shorter axial lengths compared to those classified as normal. Also, eyes suffering from ‘‘acute’’ angle closure have shorter axial lengths than those affected by the ‘‘chronic,’’ asymptomatic angle closure (Lin et al., 1997; Sihota et al., 2000; George et al., 2003). Therefore in patients

with angle closure, the anterior segment is more crowded as the lens is thicker and more anteriorly located. This is confirmed by ultrasound biomicroscopy (UBM), which demonstrates forward rotation of the ciliary processes (Marchini et al., 1998).

Studies from Mongolia and Singapore clearly show PAS development increases with reduction in ACD (Aung et al., 2005a). Interestingly, in the Singaporean population there was a consistent increase in PAS across the range of ACD but in the Mongolian population there was a clear threshold (2.4 mm) at or above which PAS was very uncommon (Aung et al., 2005a).

Genetics

Relative to POAG, PACG has been poorly researched. A genetic locus for PACG has not been published and candidate-gene-association studies have not been reported. Tornquist first suggested that PACG was transmitted by a single dominant gene in 1953. Ocular characteristics related to angle-closure glaucoma, namely, the anterior positioning of the lens, increased lens thickness, and shallow anterior chambers are more common in close relatives of affected patients than in the general population (Lowe, 1964, 1972; Tomlinson and Leighton, 1973; Alsbirk, 1975).

Recently, a study into the heritability of ACD as an intermediate phenotype of angle closure found additive genetic effects appear to be the major contributor to the variation of ACD and relative ACD (ACD/axial length) in Chinese twins (He et al., 2008). Small studies have reported that PACG subjects may carry a mutation in the myocilin gene (MYOC) (Faucher et al., 2002; Vincent et al., 2002). It is thought that in POAG, mutant MYOC proteins accumulate in the trabecular meshwork, impairing aqueous humor outflow (Jacobson et al., 2001). However, molecular analysis of the MYOC gene in 106 Chinese patients with chronic PACG was negative and did not support the role of MYOC mutation in the pathogenesis of chronic PACG in the Chinese population (Aung et al., 2005b). An association between a single nucleotide polymorphism in matrix metallopeptidase 9 (MMP-9) gene and acute PAC has also been reported (Wang et al., 2006).