Serum galectin-3 levels be a marker in exudative -type age-related macular degeneration?

doi:10.21203/rs.3.rs-3570166/v1

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Serum galectin-3 levels be a marker in exudative -type age-related macular degeneration?

https://doi.org/10.21203/rs.3.rs-3570166/v1

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Background:To investigate the effect of serum galectin-3 on naive exudative AMD and its use as a serum marker by showing the variation of this molecule between patient and control groups. Methods:56 naive exudative AMD patients and 30 age-matched healthy controls were included in the prospective case-control study. Results:The average HsCRP level in the AMD group was significantly higher than that in the control group (p<0.001).The median leukocyte count was significantly higher in the AMD group than in the control group (p<0.001).The average NLR was not statistically significant between groups (p = 0.892).Total cholesterol, low-density lipoprotein (LDL), and triglyceride (TG) levels were statistically significant increases in the AMD group as compared to the control group (p<0.001,in all comparisons).The mean high-density lipoprotein (HDL) level showed a statistically significant decrease in the AMD group as compared to the control group (p<0.001). The mean galectin-3 level was 8.79 ± 0.55 in the AMD group and 6.55 ± 0.55 in the control group.There was a statistically significant increase in galectin-3 levels in the AMD group (p<0.001).There was a significant positive correlation between CMT and galectin-3 levels in the control (r = 0.495, p = 0.005) and AMD groups (r = 0.776, p<0.001). Conclusion:The increase of galectin-3 in serum and its positive correlation with CMT in the AMD group were remarkable. Although the role of galectin-3 in the pathogenesis of AMD is known, its correlation with the disease and its prognosis as a serum marker should be clarified in studies with a large number of patients.

Health sciences/Biomarkers/Prognostic markers

Health sciences/Diseases/Eye diseases/Retinal diseases

Age-related macular degeneration (AMD) is a common chronic and progressive retinal disease that affects older people and occurs as a result of damage to the retina, retinal pigment epithelium (RPE) and choriocapillaris, causing central visual impairment. [1]AMD is one of the leading causes of irreversible visual impairment in developed countries. [1–3]The overall prevalence is approximately 8.7%. In addition to genetic predisposition, oxidative stress, local inflammation and lipofuscin accumulation associated with neovascularisation are considered as pathogenetic processes in neovascular AMD. [2] Although many experimental and clinical studies have been performed to elucidate the pathogenesis, it is not fully understood due to its multifactorial nature. [3]

Human galectin‑3 is a 35‑kDa protein that is coded by a single gene named chimera‑type galectin based on domain organization. Galectin‑3 is widely expressed in human tissues, including all types of immune cells, epithelial cells, endothelial cells and sensory neurons. [4] It has a very important role in many biological activities such as cell growth, apoptosis, differentiation, transformation, angiogenesis, inflammation, fibrosis and host defense. Elevated serum galaectin 3 levels have been shown in many cardiovascular diseases associated with fibrosis and inflamation. [5–6] In terms of eye diseases, it is seen that the effect of galactin 3 on diabetic retinopathy, optic nerve damage and glaucoma has been investigated. Its effect on the fibrotic process of glaucoma, its role in retinal ganglion cell neuroprotection after optic nerve injury and its effect on neovascular processes in diabetic retinopathy have been demonstrated in studies. [7–8]

Due to the increase in life expectancy, it might be assumed that AMD will become more prevalent. [9] This situation increases the importance of early diagnosis of AMD and prevention of possible visual loss. In our study, we aimed to investigate the contribution of serum galectin-3 levels to the early recognition of wet AMD, the importance of this molecule in terms of disease progression and its variation between patient and control groups.

Study participants

This prospective case control study was conducted at the outpatient ophthalmology clinic in ophthalmology department of Recep Tayyip Erdogan University from July 2021 to September 2021 and was approved by the local human research ethics committee. ( 2021/166) All patients included in this study gave their informed consent, which adhered to the tenets of the Declaration of Helsinki.

Fifty-six patients, aged between 50 and 85 years, who applied to our clinic with the complaint of low vision, underwent a complete eye examination, and were diagnosed with wet AMD and thirty age-matched healthy controls subjects without any ocular pathologic features other than refractive errors. These were consecutive patients who applied to the same ophthalmology department for refractive complaints, and they also did not have the systemic exclusion criteria of the study. Data regarding age, sex, and detailed medical histories of hypertension, diabetes mellitus, peripheral coronary atherosclerotic disease, and cerebrovascular events were obtained.

All subjects underwent a complete ophthalmic examination, consisting of best corrected visual acuity; slit lamp biomicroscopy of the anterior segment; fundoscopic examination after dilation of the pupils with 0.5% tropicamide and 5% phenylephrine hydrochloride; and fundus photography with by optical coherence tomography (Spectral domain OCT, software version 5.6.3.0, Heidelberg, Germany) and fundus fluoroscein angiography( Topcon TRC 50DX Retinal Camera,FFA).The diagnosis was made using both clinical examination, optical coherence tomography and fundus fluorescein angiography by the same physician (FS).

AMD group was included in the study according to the clinical classification. As shown in Table 1, the severity stages (ie, early, intermediate, and late (exudative) AMD) were established according to drusen size and AMD pigmentary abnormalities. AMD pigmentary abnormalities were defined as hyperpigmentation or hypopigmentation present within 2 disc diameters of the center of the macula in eyes with drusen ≤ 63 µm in diameter and without known retinal disease entities or other reasons for such abnormalities Exudative type AMD was defined as the presence of choroidal neovascularization in patients older than 50 years of ageand without any other condition related to choroidal neovascularization, such as degenerative myopia, ocular histoplasmosis, or angioid streak. Dry-type AMD was defined as the presence of bilateral soft drusen with or without retinal pigment abnormalities or geographic atrophy. These patients were newly diagnosed naive patients who have not received any treatment before.

Table 1

Clinical classification of AMD based on phenotype characteristics
Classification	Characteristics
No abnormal fındings	No aging changes: •Absence of drusen •No pigmentary abnormalities Normal aging changes: •Drupelets only (small drusen ≤ 63 µm) •No pigmentary abnormalities
Early AMD	•Medium-sized drusen > 63 µm and ≤ 125 µm •No pigmentary abnormalities
İntermediate AMD	•Large drusen > 125 µm and/or pigmentary abnormalities
Late AMD- Exudative	•Neovascular AMD and/or any geographic atrophy
Abbreviation: AMD, age-related macular degeneration

Galectin-3 and other serum parameters

At the time of admission, venous blood samples were obtained from each sample included in the study. After blood collection for Galectin 3 (GAL 3) measurement, serum of all patients was immediately obtained by centrifugation, transferred into cryo tubes and stored at -20°C until assayed. Serum GAL 3 was measured using ELISA method (Human GAL 3 Elisa test kit, Elabscience, USA) according to the manufacturer’s protocol. Absorbance (OD) of each well determined at 450 nm with a microtiter plate reader (Multiskan GO, Thermo Scientific, Waltham, MA, USA) in the 5th minute. Standard curve was fitted using Titri ELISA software. The fitted curve was then used to convert sample absorbance readings to GAL 3 concentration. When blood samples were collected via venipuncture, serum triglyceride, total cholesterol, highdensity lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c) and the concentration of high-sensitivity CRP levels were measured with the Beckman Coulter (AU580, USA ) clinical chemistry analyzer. The hemogram, erythrocyte sedimentation rate (ESR),Leukocyte, monocytes, neutrophil, lymphocyte values were evaluated using an Mindray BC 6000-BC 6200 (China).

Statistical Analysis

All statistical analyses were performed using IBM SPSS 20.0 (SPSS, Chicago, IL, USA). Kolmogorov-Smirnov and Shapiro-Wilk’s tests were used to assess the assumption of normality. Numeric variables were presented depending on normal distribution with either mean ± standard deviation or (in case of no normal distribution) median (25th-75th percentile). Categorical variables were summarized as counts (percentages). Comparisons of numeric variables between groups were carried out using independent samples t test/Mann-Whitney U test, whichever was appropriate. Associations between numeric variables were determined by Pearson and Spearman correlation analyses. Association between two categorical variables was examined by Chi-square test. A p-value < 0.05 was considered as statistically significant.

In this prospective case control study, serum parameters of 56 AMD and 30 control subjects were compared. Baseline characteristics of patients were reported in Table 2. There were 25 female (44.6%) and 31 male (55.4%) patients in AMD group and 16 females (53.3%) and 14 males (46.7%) in control group (p = 0.587). The mean age was 65.25 ± 2.96 years in AMD group, 65.43 ± 2.75 years in control group (p = 0.780). None of the patients were smoking. There was no statistically significant difference between the groups in systolic (p = 0.209) and diastolic (p = 0.659) blood pressure and body mass index (p = 0.960) measurements.

Table 2

Demographic features of the AMD and control groups.
	AMD Group	Control Group	p value
Age (year)	65.25 ± 2.96	65.43 ± 2.75	0.780
Sex (female/male)	25 (%44.6)/31(%55.4)	16(%53.3)/14(%46.7)	0.587
BCVA (LogMAR)	0.33 ± 0.10	0.00
Smoking	56/0	30/0
Systolic blood pressure (mmHg)	120.0 (115.0/125.0)	120.0 (115.0/125.0)	0.209
Diastolic blood pressure (mmHg)	80.0 (80.0/85.0)	84.0 (80.0/85.0)	0.659
Body mass index	19.58 (19.43/19.76)	19.65 (19.43/19.73)	0.960
Central macular thickness (mm)	340.0 (312.75–375.50)	269.50 (265.0-285.25)	< 0.001
HbA1c (%)	4.89 (4.82–5.01)	4.93 (4.86–5.03)	0.247
AMD: Age related macular degeneration, BCVA:Best corrected visual acuity, LogMAR: logarithm of the minimum angle of resolution.

The average HsCRP level in the AMD group (3.89 mg/L (3.78–4.10)) was significantly higher than that in the control group (0.81 mg/L (0.75–0.85)), (p < 0.001). Besides that the median erythrocyte sedimentation rate (ESR) was statistically significant higher in AMD group than control group (p < 0.001). The median leukocyte count was significantly higher in AMD group (7.68 (7.36–7.98)) than that in the control group (6.98 (6.84–7.61)), (p < 0.001). The median lymphocyte count was significantly lower (p < 0.001) in AMD group according to the control group. The median neutrophil count was significantly lower in AMD group than that in the control group (p < 0.001). The average thrombocyte count was significantly lower in the patient group than that in the control group (p = 0.011). The average NLR was not statistically significant between groups (p = 0.892). The median homocysteine and HbA1c parameters had not shown statistically significant difference between groups (p = 0.799, 0.247, respectivelly).

Total cholesterol, low-density lipoprotein (LDL) and triglyceride (TG) levels were statistically significant increase in AMD group as compared to control group (p < 0.001, in all comparisons). The mean high density lipoprotein (HDL) level was statistically significant decrease in AMD group as compared to control group (p < 0.001). The results are shown in Table 3.

Table 3

Comparison of serum parameters between AMD and control groups.
	Patient	Control	P value
HsCRP (mg/L)	3.89 (3.78–4.10)	0.81 (0.75–0.85)	< 0.001
ESR (mm/hour)	22.18 (21.72–23.16)	18.50 (17.80–19.30)	< 0.001
LDH (U/L)	167.00 (152.50-177.25)	166.50 (152.0-173.75)	0.778
Leukocyte (× 109/L)	7.68 (7.36–7.98)	6.98 (6.84–7.61)	< 0.001
Monocytes (× 109/L)	0.52 (0.48–0.54)	0.53 (0.48–0.56)	0.131
Neutrophil (× 109/L)	3.78 (3.61–4.42)	4.13 (3.94–4.45)	0.009
Lymphocyte (× 109/L)	1.94 (1.80–2.02)	1.76 (1.69–1.98)	0.029
Thrombocyte (× 109/L)	198.0 (182.0-204.0)	204.0 (195.50–210.0)	0.011
Neutrophil / Lymphocyte ratio	2.12 (1.94–2.56)	2.11 (1.98–2.24)	0.892
Homocysteine (Mmol/L )	14.0 (13.12–14.77)	14.05 (13.50–14.80)	0.799
Total Cholesterol (mg/dl )	221.0 ± 9.43	212.0 ± 12.26	< 0.001
LDL(mg/dL)	179.18 ± 8.44	139.60 ± 6.44	< 0.001
HDL (mg/dL)	39.0 (38.0–42.0)	61.50 (56.0–63.0)	< 0.001
TG (mg/Dl)	176.0 (173.0-178.0)	166.0 (161.25–172.0)	< 0.001
Galectin-3 (ng/ml)	8.79 ± 0.55	6.55 ± 0.55	< 0.001
HsCRP : High sensitivity C-reactive protein,ESR: erythrocyte sedimentation rate,, LDH: lactate dehydrogenase, LDL: low-density lipoprotein, HDL: high density lipoprotein, TG: triglyceride

The mean galectin-3 level was 8.79 ± 0.55 in AMD group and 6.55 ± 0.55 in control group. There was a statisticlly significant increase in galectin-3 levels in AMD group (p < 0.001). There was a significant positive correlation between CMT and galectin-3 levels in control (r = 0.495, p = 0.005) and AMD group (r = 0.776, p < 0.001). The corelation conficient was remarkable in AMD group (Fig. 1). There was no statistically significant correlation between other parameters.

AMD is the leading cause of blindness in developed countries with its multifactorial nature [10]. Many multidimensional studies have been carried out to elucidate its etiology. Although biomarker studies, its relationship with systemic conditions, genetic studies and many other factors have been tried to reveal the relationship with the disease, it cannot be said that its etiology has yet been clarified and that a valid target molecule has not been found. In our study, we aimed to re-evaluate some parameters associated with the disease in previous studies with an easily accessible and low-cost research method such as serum and to reveal the relationship between the disease and galectin-3 molecule.

Obesity and hypertension are conditions considered in AMD risk factors research. The relative risk for AMD was reported 2.35 for those with a BMI over 30, and 2.32 for those with a BMI between 25 and 29 .[11] In a study examining risk factors in AMD, it was emphasized that obesity was associated with AMD, but it was emphasized that it was not clear whether there was a causal relationship between the two. [12] In our study, no significant change was observed between the AMD and control groups in BMI assessment. The BMI values of the patients in our study group are close to the normal range. The absence of patients with high BMI associated with AMD reported in the literature in our study group may have led to these results. Whether elevated blood pressure increases the risk of developing AMD is a matter of controversy. In our study, no change was observed between the groups in terms of systolic and diastolic blood pressure. HbA1c levels, which express the long-term results of the patients in terms of blood sugar, were found to be similar between the two groups.

Chronic low grade inflammation and hypoxia in AMD are believed to be responsible for the accumulation of ROs. The accumulation of oxidative stress products is thought to predispose to chronic parainflammation and prolonged tissue damage and the development of choroidal neovascularization. In this direction, many studies focuses on the relationship between hsCRP and AMD. [13] Besides that recent studies emphasize that the neutrophil lymphocyte ratio (NLR) can be a reliable marker of systemic inflammation. Studies have shown that NLR can be an indicator of prognosis in many diseases such as coronary artery disease, Behçet's disease and rheumatoid arthritis. [14–16] Many studies using CRP and NLR as inflammation markers have shown that these parameters are statistically significantly higher in AMD patients compared to controls and may be related to the disease. [17–19] A meta-analysis by Hong et al found that patients with serum CRP levels > 3 mg/L were twice as likely to have late-onset AMD as patients with serum CRP levels < 1 mg/L (35). On the other hand, there is a study reporting that inflammation markers such as NLR cannot be a reliable biomarker of AMD in men. [20] In our study, we found a significant increase in the CRP level, leukocyte and lymphocyte counts in the AMD group, and a significant decrease in the neutrophil and thrombocyte counts, but we did not observe a significant change in the NLR ratio between the groups. No significant change was observed in the correlation analysis performed with parameters that showed statistically significant changes.

One of the serum markers whose relationship with AMD has been investigated is serum homocysteine level. In general, there is no strong evidence that homocysteine can be a marker of AMD in the studies reported. [21] In our study, no significant change was observed between AMD and control groups associated with homocystein.

There are some studies reporting that cholesterol, apolipoprotein, and triglyceride levels may be related to AMD. [22–23] In a study comparing AMD and control groups, it was reported that LDL levels increased, HDL levels decreased, and total cholesterol level increased in AMD. [23] In our study, similar to the literature, an increase in LDL, TG, Total cholesterol levels and a decrease in HDL levels were detected in the AMD group. Hyperlipidemia states may be risk factors for AMD development and large-scale studies are needed to confirm these relationship.

Galectin‑3 is widely expressed in human tissues. Galectin‑3 is crucial in many conditions, including cell growth, apoptosis, transformation, angiogenesis, inflammation, fibrosis, and host defense. Many studies are being conducted on whether galectin 3 can be a prognostic marker for many diseases or whether it can be used as a target molecule in treatment. Cardiovascular diseases, renal diseases and some cancers are the areas where galectin 3 is most studied and it has been reported that galectin 3 reflects the inflammatory and fibrotic state in these conditions. [24] Some studies emphasize that galectin 3 accelerates the pathogenesis of some metabolic diseases by increasing inflammation. In a study evaluating serum galectin-3 levels in Type 2 Diabetes mellitus, it was reported that galectin-3 is highly predictive for vascular complications and increased levels of galectin-3 were associated with increased risk of vascular disease. These results were interpreted as the strong relationship between galectin-3 and diabetic vascular complications may be due to the effect of galectin-3 on proinflammatory mediators. [25] In another study, it was found that the decrease in galectin-3 levels reported to prevent diabetic retinopathy. [26] In a study examining the effect on the survival of retinal ganglion cells and the balance between axonal regeneration/degeneration after optic nerve injury, it was reported that the absence of galectin-3 improves neuroprotection. [27] In our study, it was observed that galectin 3 was significantly higher in the AMD group than the control group and showed a positive correlation with CMT in AMD patients.

Inflammation has an important place in the pathogenesis of AMD. The relationship between galectin 3 and inflammation has been shown in many studies as proteome methods and animal studies.⁽²⁷⁾The detection of galectin elevation in AMD patients in our study supports this relationship. The fact that this elevation can be detected by looking at the serum raises the hypothesis whether it can be used as a marker in the early diagnosis of the disease and monitoring the severity of the disease. The fact that it is cost-effective compared to other methods should also be considered as an advantage. Nowadays, as life expectancy increases, the need for early diagnosis of AMD disease and close follow-up to prevent possible blindness becomes even more important.

The limitations of our study include the need for studies including a large number of patients in order to comment on whether galectin-3 level can be used as a prognostic marker or a target molecule in AMD and the small number of patients and control groups due to the limited number of kits.

In conclusion, changes in AMD patients are not only limited to retina, vitreous and choroid, but also some serum parameters are altered in these patients. From this point of view, some serum values especially serum galectin-3 level can be used as a guide for diagnosis, follow-up and especially progression analysis of AMD. Positive correlation between serum galectin-3 and CMT may be a guide for the severity of the disease.

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

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There is no conflict of interest

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Serum galectin-3 levels be a marker in exudative -type age-related macular degeneration?

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Abstract

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Introduction

Methods

Study participants

Galectin-3 and other serum parameters

Statistical Analysis

Results

Discussion

Declarations

References

Additional Declarations

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