The study was performed in adherence to the tenets of the Declaration of Helsinki and the local ethics committee approved the methodology. Written informed consent was obtained from all of the subjects. Thirty-four obese subjects and 34 age-sex-matched healthy subjects (control group) with normal ophthalmological examination were enrolled in this prospective cross-sectional study. Exclusion criteria included smoking habits, history of any ocular disease or previous surgery, presence of systemic diseases such as diabetes mellitus, hypertension, renal or hepatic dysfunction and rheumatological diseases.

BMI was calculated as weight in kilograms divided by the height in meters squared (kg/m²). The participant's height was measured with a wall-mounted tape and weight was measured using a digital scale. Subjects with BMI within the 18.5 to 24.9 range were labeled as normal, while those with BMI higher than 30.0 were labeled as obese [16]. Systolic and diastolic blood pressures were taken with an automated sphygmomanometer.

All subjects underwent a comprehensive ophthalmic examination including medical history review, best-corrected visual acuity, slit-lamp biomicroscopy, tonometry, retinoscopy, biometry and topographic evaluation. IOP was measured with a Goldmann applanation tonometer (Haag-Streit, Koeniz, Switzerland). The anterior segment parameters were evaluated using the Scheimpflug camera with a Placido disc topographer (Sirius; Costruzione Strumenti Oftalmici, Florence, Italy). Measurements were conducted with undilated pupils under scotopic conditions by a single experienced technician. Scans were taken in automatic mode with proper quality. The following parameters were extracted from the obtained topographic and pachymetric maps for statistical analysis; CCT, ACD, ACV, and ACA. Furthermore, AL was measured with ocular biometry (LenStar LS900, Haag-Streit).

The mean age of the obese and control group was 49.3 ± 7.6 and 48.5 ± 9.4 years, respectively. Data on the age, sex and BMI of the subjects are presented in Table 1. There was a significant difference between the groups in terms of BMI (p < 0.01). As there were no significant differences between the measurements of right and left eyes, only the readings of the left eyes were used for analysis (Table 2).

The mean IOP was 15 mmHg (range, 10 to 22 mmHg) in the obese group and 13 mmHg (range, 8 to 20 mmHg) in the control group. IOP was significantly higher in the obese group (p = 0.003) (Table 3). The mean ACD in obese subjects was significantly lower than in control subjects (p = 0.036). AL, ACV, ACA, and CCT were not significantly different between the two groups. There was a positive correlation between BMI and IOP (r = 0.404, p < 0.001). ACD and ACA were negatively correlated with BMI (Table 4).

Results of correlation analysis for anterior chamber parameters revealed a strong positive correlation between ACD and ACA (r = 0.763, p < 0.001) (Fig. 1). A moderate but significant correlation was found between ACD and ACV (r = 0.647, p < 0.001) (Fig. 2), as well as between ACV and ACA (r = 0.531, p < 0.001) (Fig. 3).

To the best of our knowledge, this is the first study to evaluate anterior segment parameters in obese patients. This study demonstrated that IOP was significantly higher and ACD was significantly lower in obese patients. In addition, AL, ACV, ACA, and CCT values were similar in obese and healthy subjects.

Obesity occurs when energy intake exceeds energy consumption. In accordance with the definition of obesity, health risk is related to fat in relation to total body mass; so it is necessary to determine the total mass of fat and the ratio of fat to total body weight [17]. Fat storage varies based on obesity such that white adipose tissue can be found in many areas of the body, including the face, extremities, abdomen, omentum, intestines, thighs, bone marrow and retro-bulbar space [18,19]. Fat deposition in the orbita leads to orbital volume enlargement. Increased orbital pressure by mechanism of "mass effect" may cause a decrease in episcleral aqueous outflow, inducing elevated IOP [19,20]. This mechanism can be demonstrated by orbital space lesions, such as Graves' ophthalmopathy and carotid-cavernous fistula. In support of this theory, retrobulbar injection of anesthetics may lead to increased IOP [21]. The influence of BMI upon IOP has been reported in several studies. Stojanov et al. [19] showed obese subjects had significantly higher IOP than subjects with normal weight (15.96 vs. 12.99 mmHg, p < 0.01). Mori et al. [22] found elevated IOP in subjects with BMI over 25 in Japan. Zafra Perez et al. [23] suggested that elevated IOP is associated with obesity. In this study, we found IOP was significantly higher in the obese group compared to controls (15 vs. 13 mmHg, p = 0.003). Additionally, IOP was positively correlated with BMI (r = 0.404, p < 0.001), similar to the results of Jang et al. [24].

Elevated IOP in obese people may be facilitated by several mechanisms. One hypothesis asserts that increased orbital fat and blood viscosity increases the episcleral venous pressure and reduces the outflow of aqueous, which results in increased IOP [19,20]. The other theory is that obesity linked hyperleptinemia may cause oxidative damage to the trabecular meshwork [25].

Since increased IOP is the major risk factor for the development of glaucomatous optic neuropathy, it is important to assess how the structures of the anterior chamber and CCT affect IOP. Shallow ACD was reported as a strong risk factor for angle closure glaucoma [26,27]. In the obese group, we observed a significantly shallower anterior chamber (decrease in ACD) and narrower ACA as BMI increased. Increased retrobulbar fat volume also plays a critical role in elevated IOP in addition to other factors linked to IOP elevation in obesity such as increased episcleral venous pressure, increased blood viscosity and aqueous humor outflow disorders [28]. Retrobulbar fat is clearly limited by the orbital space. Due to this limitation there is no possibility of expansion, unlike other fat tissue depots in the body [19]. This limitation may cause a decrease in ACD and ACA depending on BMI and fat deposits. Although the relationship of obesity and biometry measurements such as ACD and ACA has not been well studied, obese individuals were noted to have more hyperopic vision and shorter vitreous chambers [29,30]. Moreover, obesity has been reported as a risk factor for cataracts [5,6]. Although a significant decrease in ACD was found with an increase in lens thickness [31], the complex relationship between obesity, cataract type and lens thickness is still controversial [8].

CCT is an important factor in the clinical evaluation of several eye disorders, especially glaucoma. In the current study, differences in CCT values between the groups were not statistically significant. Similarly, in a previous study, Turkish researchers did not find a significant difference in CCT of normal subjects and patients with metabolic syndrome [32]. Nonetheless, in contrast with our results, several studies have reported higher CCT readings with increasing BMI [33,34]. In the literature, there is a strong relationship between BMI and IOP, but the relationship between high BMI and glaucomatous optic neuropathy remains unclear [25]. Su et al. [33] explained this inconsistency with the impact of CCT on IOP measurements. People with high BMI have thicker corneas resulting in higher IOP readings. However, individuals with high CCT are less likely to develop glaucoma. We are unable to explain why CCT readings between our groups were not significant, though it may be related with sample size and nature. Still, we can conclude that we found a significant association between IOP and obesity, independent of the effect of CCT.

AL is the distance from the corneal surface to an interference peak corresponding to the retinal pigment epithelium [33]. In adults, AL remains practically unchanged but myopes tend to have a longer AL and hypermetropes tend to have shorter AL as compared to those with emmetropes [34]. Although AL was significantly associated with the higher body height [35], there is no clear data about the effect of obesity on the measurements of the AL. Previous studies have demonstrated that short AL is a strong risk factor for angle closure glaucoma [26,27]. In our study, we could not able to find a significant difference in AL between groups.

There are several limitations of the current study. It is a single-center study and has a relatively small sample size. Therefore, these findings need to be confirmed in a larger patient group.

In conclusion, IOP was significantly higher and ACD was significantly lower in obese subjects. AL, ACV, ACA and CCT were not significantly different between the groups. The impact of obesity on anterior chamber parameters should be further investigated.