Evaluation of the Relationship Between Retinopathy and Serum Magnesium Levels in Patients with Type 2 Diabetes Mellitus

doi:10.21203/rs.3.rs-4956540/v1

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Evaluation of the Relationship Between Retinopathy and Serum Magnesium Levels in Patients with Type 2 Diabetes Mellitus

https://doi.org/10.21203/rs.3.rs-4956540/v1

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Objective: Diabetic retinopathy, a severe complication of Type 2 Diabetes Mellitus, can lead to vision loss and blindness. Magnesium, a vital intracellular cation, plays a key role in insulin and glycaemic regulation. This study investigates the relationship between serum magnesium levels and diabetic retinopathy in T2DM patients.

Methods: A total of 118 patients who visited the Family Medicine Clinic of a tertiary hospital, were included in the study. Routine diabetes follow-up examinations and tests (blood pressure measurement, complete blood count, blood biochemistry, electrolytes, HbA1c, cholesterol panel, urinalysis, urine protein/creatinine ratio) were conducted. Retinopathy presence was determined through ophthalmologist consultations, identifying proliferative and non-proliferative diabetic retinopathy.

Results: The mean age of patients was 57.1 (10.3) years, with an average diabetes duration of 5.8 ( 4.2) years. Hypomagnesemia was observed in 19.49% of patients. Proliferative retinopathy was present in 7.63%, and non-proliferative retinopathy rate was 15.25%. Diabetes regulation status was well in 59.32%, moderate in 27.97%, and poor in 12.71% of cases. HbA1c values were significantly higher in those with hypomagnesemia (8.73±1.69) compared to those with normal magnesium levels (7.59±1.57) (p<0.05). There was a significant link between retinopathy and T2DM regulation status (p=0.009) and between hypomagnesemia and retinopathy (p<0.001). Retinopathy was found in 43.48% of patients with magnesium deficiency compared to 14.74% without it. Proliferative retinopathy risk increased 6.3 times, and non-proliferative retinopathy risk increased 5.8 times with hypomagnesemia.

Conclusion: The risk of developing retinopathy in patients with Type 2 DM increases with magnesium deficiency, and glycemic control is linked to both magnesium deficiency and retinopathy presence. It is concluded that magnesium supplementation may reduce the risk of retinopathy in DM patients with hypomagnesemia.

“This study has been presented as an oral abstract in 17th Family Medicine Autumn School, 20-24 September 2023, Concorde Congress Center, Bafra, Cyprus.”

Diabetes

Magnesium

Retinopathy

In 2017, an estimated 451 million people aged 18 to 99 had diabetes globally, with this number projected to rise to 693 million by 2045. Nearly half (49.7%) of these cases are undiagnosed [1]. Proliferative diabetic retinopathy (DR), a severe diabetes complication, is the leading cause of blindness in working-age adults. Current DR screenings often miss the disease until irreversible damage occurs. Proliferative DR stems from exacerbated DR due to small vessel disease and neuroretinal changes, leading to cell damage, inflammation, neovascularization, and reduced vision. It also predicts other severe diabetic complications like ischemic stroke, creating a "domino effect" in diabetes progression [2]. The global prevalence of DR has been detected at 22.27% and has different rates: 35.90% in Africa, 33.30% in North America and the Caribbean and 13.37% in South and Central America [3]. As life expectancy continues to rise and the prevalence of diabetes increases, the prevalence of DR is expected to rise alongside [3]. Observations in Caucasian diabetics have linked hypomagnesemia as being an additional risk factor for the development of DR, but this correlation is not observed in black African diabetics [4].

Magnesium (Mg) is the fourth most abundant cation in the human body, and hypomagnesemia is common in patients with type 2 diabetes mellitus (T2DM), particularly those with poor metabolic control. Lower serum magnesium levels correlate with higher HbA1c levels in T2DM patients. Increasing dietary magnesium intake can improve HOMA-IR scores and elevate serum magnesium levels in individuals with T2DM [5]. Magnesium deficiency is common in diabetic patients, 25–39% of diabetics have low serum magnesium concentrations, compared to rates ranging from 2.5–18% in the normal population [6, 7].

Primary care is essential for managing chronic diseases in the health system, with extensive lab facilities, including magnesium testing. Although retinopathy cannot be directly assessed in primary care, its risk factors can be mitigated. This study aimed to determine the relationship between retinopathy and serum magnesium deficiency in patients with type 2 diabetes mellitus.

2.1. Study Design

In this single-center, cross-sectional study conducted between October 30, 2021, and December 30, 2021, T2DM patients aged 18 years and older were included. Written informed consent was obtained from each participant. All fundus examinations were conducted by the same ophthalmologist with the patient's consent. Sociodemographic data (age, education, marriage, occupation), anthropometric measurements (height, weight, and body mass index), general health status (arterial blood pressure, DM disease duration, additional disease such as hypertension, drug use list), and laboratory assessments included complete fasting blood glucose, blood count, blood biochemistry, electrolytes, glycated hemoglobin (HbA1C HPLC), cholesterol panel, urinalysis, and urine protein/creatinine ratio were collected through face-to-face interviews using a custom-designed Patient Information Form. A sample of about 5 mL of venous blood was taken after 12 h of fasting. A urine sample of about 10 mL was collected from the patients. The samples were run in a fully automated clinical chemical analyzer.

2.2. Study Sample Size

The prevalence of diabetic retinopathy in Type 2 Diabetes Mellitus (T2DM) was considered to be 28.5% in accordance with the literature [8], and the average number of patients visiting the clinic over two months was taken as 800. Using a two-sided Type 1 (alpha) error of 5% and a power (1-beta) of 80%, the analysis determined that at least 114 patients should be included in the study for diabetic retinopathy screening.

2.3. Patient selection and data collection

Patients under the age of 18, pregnant women, breastfeeding women, those with a history of sepsis, those who did not volunteer to participate in the study, those using drugs that may affect magnesium levels (Aminoglycan, Amphotericin B, Cetuximab, Cyclosporine, Digoxin, Diuretics), those with acute or chronic diarrhoea/malabsorption, those taking magnesium-containing supplements and those having a history of eye surgery were not included. Magnesium levels below 1.7 mg/dL are considered hypomagnesemia. All had normal serum creatinine concentrations (below 1.2 mg/dL for men, 1.1 mg/dL for women) and none had other diseases or received drugs known to interfere with mineral metabolism.

2.4. Statistical Analysis

SPSS (Statistical Package for Social Sciences for Windows, Armonk, NY, IBM Corp) 22.0 program was used in the analysis. The Kolmogorov-Smirnov test, skewness, and kurtosis values were applied to evaluate the normality of the data distribution. Continuous variables were summarized using mean, median, minimum, maximum, and standard deviations, whereas categorical variables were reported as frequencies and percentages. Logistic regression analysis identified independent risk factors for retinopathy in patients with T2DM. For all statistical tests, a P value < 0.05 was a significant difference level.

Interrelations between magnesium and glucose metabolism were studied in 118 diabetic outpatients aged 57.1 (10.3) years who applied to family medicine clinics. Prevalence of hypomagnesemia was observed among 23 participants out of 118 (19.5%). The frequency of retinopathy was 22.9% (n = 27), of which 7.6% (n = 9) were proliferative retinopathy and 15.3% (n = 18) were nonproliferative retinopathy.

Table 1 compares sociodemographic characteristics, diabetes medications, diabetes regulation status, and retinopathy between the groups with normal Mg levels and hypomagnesemia. The rate of insulin use and the frequency of hypertension comorbidities were higher in the group with hypomagnesemia than in the group with normal Mg levels (p = 0.004; p = 0.035, respectively). In the group with normal Mg levels, patients with the HbA1c level below 6% and the well-regulation rate were higher than that of the hypomagnesemia group (p = 0.015; p = 0.006, respectively). Proliferative or non-proliferative retinopathy was observed more frequently in the hypomagnesemia group than in the group with normal Mg levels (p < 0.001).

Table 1

Comparison of sociodemographic characteristics, diabetes medications, diabetes regulation status, and presence of retinopathy between normal and deficient groups
Variables		Groups with normal and hypomagnesemia levels
		Normal	Hypomagnesemia	X²	P value
		n (% )	n (% )	X²	P value
Diabetes Medications	Oral Antidiabetic Drugs (OAD)	65 ( 68.42)	8 ( 34.78)	8.881	0.004*
Diabetes Medications	OAD + Insulin	30 ( 31.58)	15 ( 65.22)	8.881	0.004*
Hypertension	No	54 ( 56.84)	7 ( 30.43)	5.171	0.035*
Hypertension	Yes	41 ( 43.16)	16 ( 69.57)	5.171	0.035*
Marital Status	Single	18 ( 18.95)	10 ( 43.48)	6.157	0.017*
Marital Status	Married	77 ( 81.05)	13 ( 56.52)	6.157	0.017*
Education Level	Primary Education	64 ( 67.37)	19 ( 82.61)	2.061	0.205
Education Level	More than high school	31 ( 32.63)	4 ( 17.39)	2.061	0.205
Occupation	Unemployed	59 ( 62.11)	19 ( 82.61)	3.474	0.085
Occupation	Employed	36 ( 37.89)	4 ( 17.39)	3.474	0.085
Body Mass Index (BMI)	< 18.5	1 ( 1.05)	1 ( 4.35)	1.622	0.673
	18.5–24.9	36 ( 37.89)	8 ( 34.78)
	25-29.9	36 ( 37.89)	10 ( 43.48)
	≥ 30	22 ( 23.16)	4 ( 17.39)
HbA1c (%)	< 6	17 ( 17.89)	1 ( 4.35)	10.184	0.015*
	6-7.9	46 ( 48.42)	6 ( 26.09)
	8–10	22 ( 23.16)	11 ( 47.83)
	≥ 10	10 ( 10.53)	5 ( 21.74)
DM Regulation Status	Good	63 ( 66.32)	7 ( 30.43)	9.879	0.006*
	Moderate	22 ( 23.16)	11 ( 47.83)
	Poor	10 ( 10.53)	5 ( 21.74)
Retinopathy	No Retinopathy	81 ( 85.26)	10 ( 43.48)	21.272	< 0.001*
	Proliferative Retinopathy	3 ( 3.16)	6 ( 26.09)
	Non-Proliferative Retinopathy	11 ( 11.58)	7 ( 30.43)
*significant p < 0.05

Insert Table 1 here

Table 2 compares age, disease duration, anthropometric measurements, and laboratory test results between groups with normal Mg levels and groups with hypomagnesemia. The age and duration of T2DM disease in the group with hypomagnesemia were higher than the others (p = 0.009; p = 0.003, respectively). Fasting blood glucose, HbA1c and Thyroid-Stimulating Hormone (TSH) levels were higher in the group with hypomagnesemia than those without (p = 0.003; p = 0.003; p = 0.016, respectively).

Table 2

Comparison of age, disease duration, anthropometric measurements, and laboratory test results between groups with normal Mg level and groups with hypomagnesemia
	Groups with normal and low magnesium levels
	Normal	Hypomagnesemia	t/U	p
	mean ± SD	mean ± SD
Age	55.93 ± 10.02	62.17 ± 10.17	t=-2.675	0.009*
Duration of Diabetes	5.24 ± 3.91	8.09 ± 4.76	t=-2.997	0.003*
BMI (Body Mass Index)	26.83 ± 5.14	26.76 ± 7.43	U = 1078.0	0.922
Systolic Blood Pressure	130.79 ± 10.7	135.22 ± 8.98	t=-1.833	0.069
Diastolic Blood Pressure	82.16 ± 5.24	82.83 ± 4.22	t=-0.568	0.571
Fasting blood glucose	154.66 ± 50.35	191.04 ± 52.85	t=-3.080	0.003*
HbA1c	7.59 ± 1.57	8.73 ± 1.69	t=-3.062	0.003*
Sodium (Na)	140.05 ± 2.06	139.57 ± 2.06	U = 1002.0	0.532
Potassium (K)	4.4 ± 0.48	4.51 ± 0.58	t=-0.926	0.356
Calcium (Ca)	9.39 ± 0.47	9.24 ± 0.53	t = 1.319	0.190
LDL (Low-Density Lipoprotein)	107.08 ± 36.02	99.78 ± 37.93	t = 0.863	0.390
HDL (High-Density Lipoprotein)	48.15 ± 14.81	43.87 ± 6.25	U = 843.0	0.090
Triglycerides (TG)	231.81 ± 202.91	195.83 ± 82.61	U = 953.5	0.345
Total Cholesterol	199.63 ± 39.02	187.13 ± 37.26	t = 1.39	0.167
Glomerular Filtration Rate (GFR)	91.84 ± 17.4	85.04 ± 19.36	t = 1.645	0.103
Protein/Creatinine Ratio	127.07 ± 54.76	176.35 ± 136.58	U = 844.5	0.092
Thyroid-Stimulating Hormone (TSH)	2.19 ± 1.59	3.31 ± 2.59	U = 737.5	0.016*
Thyroxine (T4)	11.61 ± 3.72	10.52 ± 3.07	U = 1043.0	0.737
Alanine Aminotransferase (ALT)	23.14 ± 12.31	22.96 ± 10.78	U = 1092.0	0.997
Aspartate Aminotransferase (AST)	22.72 ± 11.93	22.74 ± 10.43	U = 1071.0	0.884
Urea	30.15 ± 10.81	33.91 ± 10.83	t=-1.498	0.137
Creatinine	0.85 ± 0.22	1.03 ± 0.76	U = 951.0	0.336
*significant p < 0.05

Insert Table 2

Table 3 compares groups with proliferative or non-proliferative retinopathy and without retinopathy. The proliferative retinopathy group showed higher age, diastolic blood pressure, fasting blood glucose, HbA1c, and Protein/Creatinine Ratio levels than the non-retinopathy group ( p = 0.015, p = 0.020, p = 0.019, p = 0.035, p = 0.024, respectively). The mean Mg and glomerular filtration rate (GFR) levels in the group without retinopathy were higher than in the non-proliferative retinopathy group (p = 0.018; p = 0.007, respectively).

Table 3

Comparison of groups with proliferative retinopathy or non-proliferative retinopathy and without retinopathy
Groups	Groups with and without retinopathy
	^aNo Retinopathy	^bProliferative Retinopathy	^cNon-Proliferative Retinopathy	F/X²	p
	mean ± SD	mean ± SD	mean ± SD	F/X²	p
Age	55.88 ± 10.23	65.78 ± 9.81	59.22 ± 8.93	F = 4.455	0.014* p^ab=0.015*
Duration of Diabetes	5.34 ± 4.01	8.22 ± 4.35	6.89 ± 4.80	F = 2.695	0.072
BMI (Body Mass Index)	26.61 ± 4.86	30.53 ± 8.64	26.01 ± 7.02	X² = 0.890	0.641
Systolic Blood Pressure	130.77 ± 10.95	139.44 ± 7.26	132.22 ± 7.90	F = 2.919	0.058
Diastolic Blood Pressure	81.98 ± 5.21	86.67 ± 4.33	81.67 ± 3.43	F = 3.874	0.024* p^ab=0.020* p^bc=0.038*
Fasting blood glucose	153.6 ± 49.44	202.22 ± 39.91	182.72 ± 60.80	F = 5.583	0.005* p^ab=0.019
HbA1c	7.55 ± 1.48	8.94 ± 1.46	8.58 ± 2.08	F = 5.665	0.005* p^ab=0.035* p^ac=0.034*
Sodium (Na)	140.09 ± 2.09	140.11 ± 1.76	139.22 ± 2.05	X² = 1.642	0.440
Potassium (K)	4.41 ± 0.49	4.54 ± 0.56	4.46 ± 0.55	F = 0.327	0.722
Calcium (Ca)	9.41 ± 0.46	9.10 ± 0.49	9.22 ± 0.52	F = 2.745	0.068
Magnesium (Mg)	1.88 ± 0.20	1.72 ± 0.21	1.73 ± 0.26	X² = 13.636	0.001* p^ac=0.018*
LDL (Low-Density Lipoprotein)	108.99 ± 34.48	95.44 ± 46.01	93.91 ± 39.28	F = 1.697	0.188
HDL (High-Density Lipoprotein)	46.63 ± 13.52	48.56 ± 17.47	50.17 ± 12.63	X² = 2.157	0.340
Triglycerides (TG)	234.93 ± 207.08	243.22 ± 71.61	164.33 ± 62.13	X² = 9.345	0.009* p^ac=0.025* p^bc=0.039*
Total Cholesterol	201.49 ± 37.09	192.78 ± 40.95	177.67 ± 42.43	F = 2.988	0.054
Glomerular Filtration Rate (GFR)	92.49 ± 16.76	73.78 ± 23.84	88.89 ± 16.81	F = 4.856	0.009* p^ab=0.007*
Protein/Creatinine Ratio	125.43 ± 54.97	189.33 ± 92.08	167.19 ± 142.29	X² = 6.235	0.044* p^ab=0.024*
*significant p < 0.05

Insert Table 3 here

Table 4 presents a logistic regression analysis of factors increasing the hypomagnesemia in diabetes patients. The presence of proliferative retinopathy increased 6.3 times (odds ratio (OR) = 6.286, 95% Confidence Interval (CI) = 1.067–37.016), and non-proliferative retinopathy increased 5.8 times (OR = 5.778, 95% CI = 1.477–22.609), in cases of magnesium deficiency.

Table 4

Logistic Regression Analysis of Factors Increasing the Hypomagnesemia in Diabetes Patients
Variables		O.R.	95% CI (lower-upper limits)	p
Diabetes Medications	Oral Antidiabetic Drugs (OAD)	1	-	-
Diabetes Medications	OAD + Insulin	2.537	0.692–9.296	0.160
Hypertansion	No	1	-	-
Hypertansion	Yes	1.051	0.305–3.621	0.937
Marital Status	Single	1	-	-
Marital Status	Married	0.530	0.164–1.710	0.288
Employment Status	Unemployed	1	-	-
Employment Status	Employed	1.265	0.276–5.805	0.762
Income Level	Income less than expenses	-	-	0.536
	Income equal to expenses	0.581	0.157–2.150	0.416
	Income greater than expenses	0.261	0.020–3.337	0.302
HbA1c	< 6	1	-	-
	6-7.9	1.002	0.096–10.428	0.999
	8–10	2.146	0.197–23.403	0.531
	≥ 10	0.919	0.060-14.036	0.951
Retinopathy	No Retinopathy	-	-	0.014*
	Proliferative Retinopathy	6.286	1.067–37.016	0.042*
	Non-Proliferative Retinopathy	5.778	1.477–22.609	0.012*
*significant p < 0.05

Insert Table 4 here

This present study explored the association between serum magnesium levels and the presence of diabetic retinopathy in patients with T2DM. Findings demonstrated a significant relationship between hypomagnesemia and the presence of diabetic retinopathy (DR). Hypomagnesemia was prevalent in 19.5% of the T2DM patients, while 22.9% exhibited DR. Notably, the likelihood of the presence of proliferative retinopathy was 6.3 times higher, and non-proliferative retinopathy was 5.8 times higher in T2DM patients with hypomagnesemia compared to those with normal magnesium levels.

A rapid disease progression and an elevated risk of diabetes complications are observed in patients with hypomagnesemia [9]. Clinical research shows that T2DM patients with hypomagnesemia have decreased activity of pancreatic β-cells and are more insulin resistant. Additionally, dietary supplementation for these patients enhances glucose metabolism and improves insulin sensitivity [9]. In Turkey, Mısırlıoğlu et al. reported a hypomagnesemia rate of 34% [10]. However, there are also different studies, such as the study by Erasmus et al. in Nigeria, in which magnesium levels were not found to be significantly lower in diabetic patients [4]. In our study, 19.5% of T2DM patients had low serum magnesium levels, which correlated with poor glycemic control, as indicated by HbA1C and fasting blood glucose levels. This finding aligns with a meta-analysis by Ana Kelen Rodrigues et al., which identified a link between glycemic control and low serum magnesium levels [11]. Similarly, Daya Ram Pokharel et al. in Nepal observed that patients with low serum magnesium had higher HbA1C levels [12]. Another study found an inverse relationship between serum magnesium levels and glycemic parameters (HbA1C and fasting blood glucose) in T2DM patients [13]. Kumar et al. also noted that 44% of diabetic patients had hypomagnesemia, which was associated with poor glycemic control and DR.[14].

Elevated magnesium retention in the elderly indicates a significant subclinical magnesium deficit that routine serum magnesium measurements may not detect. Limited data exist on the relationship between magnesium levels and the duration and severity of diabetes. A 2021 study by Paladiya et al. found that hypomagnesemia was significantly lower in patients with a diabetes duration of more than 10 years compared to those with a duration of less than 10 years [15]. Moreover, this group exhibited poorer glycemic control, evidenced by higher fasting blood glucose and HbA1c levels. The wide range of reported hypomagnesemia incidence likely results from variations in the definition of hypomagnesemia, magnesium measurement techniques, and patient age heterogeneity related to renal function.

In a study by Sjögren et al., muscle and plasma magnesium levels in insulin-dependent diabetes patients were significantly lower compared to the general population and correlated with glycemic control [16]. In our study, 68.42% of patients without low Mg levels were using only oral antidiabetic drugs (OAD), compared to 34.78% who were using insulin plus oral antidiabetic drugs. These data suggest a potential relationship between glycemic control, insulin use, and magnesium levels. As reported by prior studies, hyperglycemia is a possible factor contributing to DR [17]. This association may be related to the longer duration of diabetes, a history of poorer glycemic control, and increased complications observed in patients using insulin.

The Turkish Ophthalmologic Society's Medical Retina Division found that the prevalence of DR was 30.5% based on results from 14 different centers in the country [18]. The United Kingdom Prospective Diabetes Study (UKPDS) reported that the prevalence of DR was 37% [19]. In newly diagnosed Type 2 DM patients, Svah et al. found a retinopathy prevalence of 18%. [20]. A study by Zhang X et al. in the United States found that DR prevalence was 28.5% [8]. Our study found DR representing a rate of 22.88%, which is consistent with the literature.

In a retrospective cohort study by Voigt M et al. analyzing 17461 consultations of 4513 patients from 1987 to 2014, the prevalence of retinopathy was 1.1% at diagnosis, 6.6% after 0–5 years, 12% after 5–10 years, 24% after 10–15 years, 39.9% after 15–20 years, 52.7% after 20–25 years, 58.7% after 25–30 years, and 63% after more than 30 years of disease duration [21]. In our study, the ages of patients without DR were 55.88 (10.23) years, those with non-proliferative retinopathy were 59.22 (8.93) years, and those with proliferative retinopathy were 65.78 (9.81) years. Our findings were consistent with those of the literature.

In the UKPDS study, patients under tight blood pressure control found a 34% reduction in the risk of DR development over 9 years [22]. Epidemiological studies have shown that hypertension is a risk factor for DR [23]. A study by Hans U Janka et al. found a relationship between retinopathy development and particularly high diastolic blood pressure [24]. Our study also found a significant relationship between high diastolic blood pressure and retinopathy, while no significant relationship was found with systolic blood pressure, supporting this study.

ACCORD study found that intensive blood glucose control with a target HbA1c level below 6.0% significantly reduced the progression rate of DR compared to a target HbA1c level of 7.0-7.9% [25]. A Cochrane review has confirmed these findings. In the CURES study by Pradeepa et al., HbA1C levels were significantly higher in retinopathy patients [26]. In our study, serum glucose levels and HbA1C were significantly higher in DR patients, consistent with the literature. Meah et al. demonstrated that hypomagnesemia is associated with poorly controlled diabetes and worsening fasting blood glucose levels [27]. Zhang et al. found that low serum magnesium concentrations are linked to DR and other diabetic complications [28]. Similarly, our results support the assosiations of hypomagnesemia, presence of DR and poor controlled T2DM.

Limitations

There are some limitations in this study. First, serum magnesium might not fully reflect intracellular magnesium status. Secondly, while adequate for detecting significant associations, it may still be insufficient to generalize the findings to all T2DM patients.

The results of this study demonstrate a significant association between serum magnesium levels and DR in patients with T2DM, with those with hypomagnesemia showing a markedly higher likelihood of both proliferative and non-proliferative retinopathy. This reinforces the need for vigilant management of serum magnesium, blood pressure, and glycemic control to prevent and manage diabetic retinopathy in T2DM patients.

Author Contributions

The authors declare that:

● All the authors have made substantive contributions to the article and assume full responsibility for its content;

● All those who have contributed substantially to the article have been named authors.

Conceptualization, I.S.A., E.E., M.M.B, and O.B.; methodology, I.S.A., M.M.B.; formal analysis, I.S.A., M.M.B, and O.B; investigation, I.S.A., M.M.B.; resources I.S.A.,E.E., M.M.B, and O.B.; data curation, I.S.A., E.E. ; writing—original draft preparation, I.S.A., M.M.B.; writing—review and editing, I.S.A.,E.E., M.M.B, and O.B.; visualization, I.S.A., E.E., M.M.B, and O.B.; supervision, I.S.A., E.E., M.M.B, and O.B.; All authors have read and agreed to publish version

Funding

This research received no external funding.

Institutional Review Board Statement

The Clinical Research Ethics Committee of Gaziosmanpaşa Training and Research Hospital accepted the study protocol by date 20.10.2021- No:349.

Informed consent

Informed consent was obtained from all subjects involved in the study.

Data Availability Statement

The data presented in this study are available on request from the corresponding author.

Acknowledgements

Thanks to all the participants in this study.

Conflict of interest

The authors declare no competing interests.

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Evaluation of the Relationship Between Retinopathy and Serum Magnesium Levels in Patients with Type 2 Diabetes Mellitus

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Abstract

1. Introduction

2. Methods

2.1. Study Design

2.2. Study Sample Size

2.3. Patient selection and data collection

2.4. Statistical Analysis

3. Results

4. Discussion

5. Conclusions

Declarations

Author Contributions

Funding

Institutional Review Board Statement

Informed consent

Acknowledgements

Conflict of interest

References

Additional Declarations

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