European Journal of Cardiovascular Medicine

Meibomian gland dysfunction (MGD) is the principal cause of evaporative dry-eye disease, arising when the lipid-secreting glands embedded in the eyelids become obstructed or produce secretions of abnormal quality. The consequent collapse of the tear-film lipid layer accelerates evaporation, destabilises the ocular surface and triggers symptoms ranging from foreign-body sensation to fluctuating vision. Histopathological and imaging studies highlight the indispensable role of meibomian lipids in preserving tear-film integrity and ocular comfort. [1]

Epidemiological surveys estimate that one-third to two-thirds of adults exhibit clinical signs of MGD, with prevalence highest in Asia where dusty climates, prolonged screen exposure and ageing demographics converge. [2] Yet the disorder is frequently under-recognised, allowing chronic inflammation and gland atrophy to progress silently. Early Indian observations noted that many patients with moderate or severe MGD also had unrecognised serum lipid abnormalities, hinting at a systemic metabolic contribution to gland pathology. [3]

The biological rationale for this link is compelling. Meibum is rich in cholesterol esters and triglycerides; disturbances in circulating lipid fractions can raise its melting point, increase viscosity and precipitate ductal stasis. A 2023 systematic review pooling more than 4,000 participants confirmed that individuals with MGD harbour significantly higher pooled total cholesterol and triglyceride concentrations than controls, strengthening the hypothesis that dyslipidaemia is a modifiable driver of gland dysfunction. [4]

Recent clinic-based studies provide convergent evidence. A Mediterranean outpatient cohort showed that subjects with elevated total cholesterol and low-density lipoprotein (LDL) levels reported worse symptom scores, thicker tear menisci and greater gland dropout than lipid-normal peers. [5] Similarly, a hospital study in Nepal demonstrated a clear stepwise rise in MGD grade across cholesterol quartiles, independent of age or sex. [6] Meta-analytic pooling of case–control and cohort datasets estimated that hypercholesterolaemia confers approximately five-fold higher odds of developing MGD, underscoring its clinical relevance. [7]

Age-stratified Asian data further reveal that total cholesterol above 200 mg/dL and triglycerides above 150 mg/dL markedly amplify both prevalence and severity of MGD, emphasising the public-health importance of lipid screening in ophthalmic clinics. [8] Indian research mirrors these trends. A tertiary-care case–control investigation documented mean total cholesterol nearly 40 mg/dL higher in MGD cases than controls, with dyslipidaemia present in 57 % of affected individuals. [9] Subsequent cohorts confirmed that exceeding a 200 mg/dL cholesterol threshold independently predicts advanced gland obstruction and dropout, even in patients without previously diagnosed lipid disorders. [10]

Despite this mounting evidence, serum lipids are not routinely assessed in patients presenting with lid-margin disease, and the predictive performance of individual lipid fractions remains incompletely defined. Total cholesterol is, however, a cost-effective and widely available biomarker that could bridge ophthalmic and primary-care practice, enabling early metabolic counselling while informing tailored MGD management strategies. The present study therefore focuses on delineating the correlation between serum total cholesterol levels and the presence and severity of MGD in adults attending a tertiary eye hospital. By quantifying the strength of this association and assessing the diagnostic utility of total cholesterol, we aim to generate actionable evidence for integrated ocular–systemic health promotion.

Study design and setting A hospital-based, age- and sex-matched case–control study was conducted in the outpatient Ophthalmology department of a tertiary teaching centre in Chengalpet District over an 18-month period (January 2023 – June 2024). The protocol adhered to the tenets of the Declaration of Helsinki and received prior approval from the Institutional Ethics Committee (IEC/2022/-017). Written informed consent was obtained from every participant before enrolment. Participants Adults aged 30–80 years attending the eye clinic were screened. Cases were defined as patients with clinical evidence of Meibomian gland dysfunction (MGD) but no previously diagnosed dyslipidaemia. Controls were individuals without MGD and without a history of dyslipidaemia, matched 1:1 to cases for age (±3 years) and sex. Exclusion criteria comprised: (i) known hyperlipidaemia or current lipid-lowering therapy, (ii) infectious kerato-conjunctivitis or other ocular surface inflammatory diseases, (iii) ocular surgery within the preceding three months, (iv) topical corticosteroid use within four weeks, (v) Sjögren syndrome, systemic autoimmune disease, pregnancy, or lactation. Sample size A minimum of 62 subjects per group was required to detect a 20 mg/dL inter-group difference in mean total cholesterol with 80 % power and α = 0.05. Allowing for 10 % attrition, 70 cases and 70 matched controls (total = 140) were recruited. MGD assessment All participants underwent slit-lamp examination by a single masked ophthalmologist. Diagnostic criteria followed the International Workshop on Meibomian Gland Dysfunction definitions: lid-margin telangiectasia, gland orifice plugging, and altered expressibility or quality of meibum. Severity was staged 0–4 using expressibility (0–3) and secretion quality (0–3) scores, with composite grades adapted from the Japanese and Indian preferred-practice guidelines. Laboratory evaluation After an overnight (≥8 h) fast, 5 mL of venous blood was drawn and analysed within two hours on an automated enzymatic analyser (Beckman Coulter AU2700). Serum total cholesterol (TC), high-density lipoprotein (HDL-C), low-density lipoprotein (LDL-C) and triglycerides (TG) were reported in mg/dL. Internal and external quality controls were performed daily. Hypercholesterolaemia was defined as TC ≥ 200 mg/dL, elevated LDL-C as ≥130 mg/dL, hypertriglyceridaemia as TG ≥ 150 mg/dL, and low HDL-C as <40 mg/dL in males or <50 mg/dL in females, according to the National Cholesterol Education Program Adult Treatment Panel III cut-offs. Outcome measures The primary outcome was the association between total serum cholesterol and the presence of MGD (Table 5). Secondary analyses evaluated relationships between HDL-C, LDL-C, TG and MGD severity, together with the diagnostic utility of individual lipid fractions. Statistical analysis Data were entered into Microsoft Excel and analysed with IBM SPSS Statistics v27. Continuous variables are presented as mean ± SD and categorical data as frequencies or percentages. Inter-group differences in lipid parameters were compared using independent-samples t-test. Point-biserial correlation quantified the strength of association between each lipid index and MGD status. Receiver-operating-characteristic (ROC) curves with area under the curve (AUC) were plotted to determine the discriminative performance of total cholesterol, HDL-C, LDL-C and TG. Statistical significance was set at p < 0.05. Ethical considerations Participants could withdraw at any stage without prejudice to clinical care. Data were anonymised, encrypted, and stored on password-protected hospital servers accessible only to the research team.

The mean lipid profile values among MGD cases and controls revealed statistically significant differences. MGD patients had markedly higher mean total cholesterol (228.26 ± 34.72 mg/dL) compared to controls (172.43 ± 36.68 mg/dL), with a p-value < 0.001. Similarly, LDL levels were significantly elevated in the case group (154.41 ± 32.47 mg/dL) versus controls (104.81 ± 31.99 mg/dL), also with p < 0.001. Triglyceride levels were higher in MGD cases (186.74 ± 51.26 mg/dL) than in controls (133.14 ± 51.42 mg/dL), with a significant p-value < 0.001. HDL levels were significantly lower in cases (37.27 ± 6.27 mg/dL) than in controls (49.56 ± 8.76 mg/dL), suggesting an adverse lipid profile in MGD patients. [Table 1]

A significant positive correlation was observed between total serum cholesterol levels and the presence of MGD. The Pearson correlation coefficient (r) was 0.637, indicating a moderate to strong relationship, and the p-value was < 0.001, confirming statistical significance. This suggests that as total cholesterol increases, the likelihood of having MGD also rises. The association underscores the potential role of systemic hypercholesterolemia in the pathogenesis of MGD. These findings support the use of serum total cholesterol as a useful biomarker in evaluating patients with lid margin disease. [Figure 1]

A significant inverse correlation was identified between HDL cholesterol levels and MGD. The Pearson correlation coefficient was –0.626, with a p-value of < 0.001, indicating that lower HDL levels were associated with a higher probability of MGD. This relationship is clinically relevant, as HDL is known to have anti-inflammatory and lipid-clearing roles that may protect meibomian gland function. These results suggest that reduced HDL levels could be a contributing factor in glandular obstruction or dysfunction. HDL may serve as a protective marker, and its deficiency could signal ocular surface compromise. [Figure 2]

Low-density lipoprotein (LDL) levels showed a strong positive correlation with MGD status. The Pearson correlation coefficient was 0.627, and the p-value was < 0.001, indicating a robust and statistically significant relationship. These findings imply that higher LDL levels may predispose individuals to meibomian gland blockages, possibly due to increased meibum viscosity or pro-inflammatory effects. Elevated LDL could thus serve as a reliable indicator of MGD risk in dyslipidaemic patients. This reinforces the importance of assessing LDL in patients presenting with chronic ocular surface complaints. [Table 2]

Triglyceride (TG) levels demonstrated a statistically significant positive correlation with MGD. The correlation coefficient (r) was 0.601, and the p-value was < 0.001, denoting a moderately strong association. This suggests that elevated TG levels may be linked with increased meibomian gland dysfunction, potentially by altering the lipid composition of glandular secretions. Elevated TG, like other dyslipidemic markers, may thus contribute to obstructive gland pathology. These findings highlight TG as another lipid fraction of interest in the systemic assessment of MGD. [Figure 3]

Receiver operating characteristic (ROC) analysis was performed to assess the diagnostic utility of lipid parameters in predicting MGD. Total cholesterol showed the highest area under the curve (AUC = 0.882), indicating excellent discriminative power. LDL and triglycerides also demonstrated good AUC values (0.856 and 0.845, respectively), while HDL showed an inverse association with an AUC of 0.827. The high AUC values indicate that lipid profile indices, particularly total cholesterol and LDL, may serve as effective screening tools for MGD. These results support the integration of lipid profiling in ophthalmic evaluation protocols. [Table 3]

Table 1: Mean lipid profile indices among cases and controls

Table 2: Correlation analysis between LDL and MGD

Table 3: Receiver Operating Characteristic curve and Area Under Curve for various lipid indices

Figure 1: Correlation of total cholesterol with MGD

Figure 2: Correlation of HDL levels with MGD

Figure 3: Correlation of Triglycerides levels with MGD

This study confirms a significant association between Meibomian Gland Dysfunction (MGD) and dyslipidemia, aligning with a growing body of evidence that systemic lipid derangements may contribute to ocular surface pathologies. Elevated levels of total cholesterol, LDL, and triglycerides, coupled with reduced HDL, were significantly associated with the presence and severity of MGD in our study population. These findings mirror those of Bukhari et al., who reported that serum lipid abnormalities, particularly elevated total cholesterol and triglycerides, are common in patients with moderate to severe MGD [1,11,12].

Mechanistically, the meibum secreted by Meibomian glands contains cholesterol esters and lipids essential for tear-film stability. Dyslipidemia may alter the viscosity and melting point of these secretions, promoting ductal blockage and inflammation. Dao et al. observed that higher serum cholesterol levels correlated with gland dropout and poor expressibility, further substantiating the pathological role of systemic lipids in MGD [2]. In our study, total cholesterol and LDL demonstrated the highest predictive utility for MGD, with AUC values exceeding 0.82, reinforcing their diagnostic relevance.

A recent meta-analysis by Zhang et al. emphasized the pooled strength of association between dyslipidemia and MGD across multiple cohorts, showing that individuals with MGD had significantly higher pooled cholesterol and triglyceride levels [3]. Our data reflect this pattern, as the mean cholesterol difference between MGD cases and controls exceeded 50 mg/dL. Moreover, HDL, known for its anti-inflammatory and lipid-clearing roles, was inversely associated with MGD in our cohort, consistent with earlier observations from the International Workshop on Meibomian Gland Dysfunction [4].

In the Indian context, Kumar et al. reported similar findings in a cross-sectional cohort, with a notable prevalence of lipid abnormalities in MGD patients lacking prior metabolic diagnoses [5]. This underlines the value of lipid screening in ophthalmic clinics, particularly in resource-limited settings where systemic disorders may go undiagnosed. Moreover, Tulsyan et al. demonstrated that MGD severity increased progressively across serum cholesterol quartiles, suggesting a dose-response relationship between lipid levels and gland dysfunction [11].

Other regional studies such as those by Nithisha et al. and Padwal & Pawar have also emphasized the clinical importance of evaluating serum lipid profiles in patients with MGD, showing significant statistical associations with LDL and triglycerides [13,14]. These studies further reinforce the hypothesis that dyslipidemia is not just a comorbid condition but may be a contributing factor in the pathophysiology of obstructive MGD.

Kaur et al. explored the relationship of various systemic risk factors with MGD severity and concluded that lipid abnormalities had a stronger correlation with gland dropout than age or screen exposure alone [15]. Our findings also suggest that systemic lipid derangement is a more robust predictor of MGD presence than traditional ocular surface symptoms alone, given the moderate-to-strong correlation coefficients observed in this analysis.

Several studies, including those by Ranjan & Jha and Dhawan, have advocated for the incorporation of lipid profiling into MGD assessment protocols [16,17]. They argue that lipid management, alongside warm compress and lid hygiene, may improve meibomian gland function and reduce recurrence rates. This integrated approach, involving ophthalmologists and primary care physicians, may yield better long-term outcomes for patients.

Furthermore, recent insights from Irfan et al. and Rajashree Reddy et al. support the clinical implementation of ROC-based thresholds for lipid markers in MGD diagnosis, with total cholesterol and LDL emerging as reliable screening indices [18,19]. These parameters are cost-effective and widely available, supporting their use in primary and secondary care. Finally, Hiremath’s observational study highlighted that lipid abnormalities were present in over 60% of patients with symptomatic MGD, echoing the findings of our case–control design [20].

Taken together, these results underscore the bidirectional relationship between ocular surface disorders and systemic metabolic health. The presence of dyslipidemia in MGD patients suggests the need for early metabolic evaluation and lifestyle modification, particularly in those with refractory lid-margin disease. Routine screening of lipid profiles in MGD cases could facilitate timely intervention, potentially improving not just ocular comfort but also reducing cardiovascular risk in the long term.

This hospital-based case–control study demonstrates a significant association between Meibomian Gland Dysfunction (MGD) and dyslipidemia, particularly elevated total cholesterol, LDL, and triglycerides, along with reduced HDL levels. The strong correlations observed between lipid parameters and MGD status suggest that systemic lipid imbalance may contribute to glandular obstruction, inflammation, and tear film instability. The diagnostic performance of total cholesterol and LDL, as evidenced by high ROC AUC values, indicates their potential utility as screening biomarkers for MGD severity. These findings support a more integrated approach in ophthalmic care, where patients with chronic lid margin disease or refractory dry eye symptoms should undergo basic lipid profile testing. Early identification of dyslipidemia in such individuals can facilitate timely systemic intervention, potentially improving both ocular and cardiovascular outcomes. In view of this, interdisciplinary collaboration between ophthalmologists and primary care physicians is crucial for comprehensive management of patients with MGD and underlying metabolic risk factors.

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