European Journal of Cardiovascular Medicine

Psoriasis is a chronic, immune-mediated inflammatory skin disease affecting approximately 0.44-2.8% of the Indian population, with prevalence varying across different geographical regions.¹ Beyond its dermatological manifestations, psoriasis has been increasingly recognized as a systemic inflammatory condition associated with multiple comorbidities, particularly metabolic syndrome and cardiovascular diseases.²

The pathophysiological mechanisms underlying the association between psoriasis and dyslipidemia involve complex interactions between inflammatory cytokines, oxidative stress, and lipid metabolism. Elevated levels of pro-inflammatory cytokines such as IL-6, TNF-α, and IL-17, which are characteristic of psoriasis, have been shown to influence hepatic lipid synthesis, peripheral lipid clearance, and HDL metabolism.³ The concept of "psoriatic march" has emerged as a unifying hypothesis explaining the progression from cutaneous inflammation to systemic manifestations, including dyslipidemia and cardiovascular complications. This paradigm suggests that chronic skin inflammation in psoriasis triggers systemic inflammatory responses that contribute to the development of metabolic dysfunctions, including lipid abnormalities.^4–6

Recent studies from India have demonstrated a significant association between psoriasis severity and lipid abnormalities. A comprehensive case-control study conducted in Gujarat by Gosai et al.⁷ (2024) revealed that psoriasis patients exhibited significantly elevated levels of total cholesterol, triglycerides, LDL-C, and VLDL-C, while HDL-C levels were significantly reduced compared to healthy controls. The study also documented a progressive worsening of lipid parameters with increasing disease severity, as measured by the Psoriasis Area and Severity Index (PASI) score. A study by Praneeth et al.⁸ (2024) from Andhra Pradesh demonstrated that 68.3% of psoriasis patients had dyslipidemia compared to 38.3% in controls, with significant correlations between lipid abnormalities and disease severity. Recent studies highlight that comprehensive lipid indices, such as the Atherogenic Index of Plasma and Comprehensive Lipid Tetrad Index, are elevated in psoriasis, correlate with disease severity, and may better predict cardiovascular risk than individual lipid parameters.⁴

Given the significant burden of psoriasis in India and the growing evidence of its association with metabolic complications, this case-control study aims to investigate the correlation between dyslipidemia and psoriasis disease severity in the Indian population, with particular emphasis on the relationship between lipid profile abnormalities and PASI scores.

Study Design and Setting: This hospital-based case-control study was conducted at the Department of Dermatology, Tertiary care hospital, Gujarat, India, over a period of 18 months from January 2023 to June 2024. The study protocol was approved by the Institutional Ethics Committee and conducted in accordance with the Declaration of Helsinki.

Study Population: A total of 200 participants were enrolled in the study, comprising 100 patients with chronic plaque psoriasis (cases) and 100 age- and sex-matched healthy controls attending the dermatology outpatient department for minor skin conditions other than psoriasis.

Sample Size Calculation: Sample size was calculated based on the expected difference in dyslipidemia prevalence between psoriasis patients (70%) and controls (40%) in study of Gosai et al.⁷ (2024), with 80% power and 5% significance level. The minimum required sample size was 82 participants per group.

Inclusion criteria for cases: The study included adults aged 18–65 years with a clinical diagnosis of chronic plaque psoriasis of at least six months’ duration. Only patients who had not received systemic treatment for psoriasis in the preceding three months and who provided written informed consent were enrolled.

Exclusion criteria for cases: Patients with pustular, erythrodermic, or guttate psoriasis, as well as those with other systemic inflammatory diseases, were excluded. Individuals with a history of cardiovascular disease, diabetes mellitus, thyroid disorders, renal or hepatic dysfunction, pregnancy or lactation, or those currently receiving lipid-lowering medications were also excluded. In addition, patients with a history of alcohol abuse or smoking more than 10 cigarettes per day were not eligible for participation.

Control Group Selection: Healthy volunteers with no history of psoriasis or other chronic inflammatory conditions, matched for age (±5 years) and sex, were selected as controls. All controls underwent the same clinical and laboratory evaluations as cases.

Clinical Assessment: Dermatological examination was performed by a qualified dermatologist. Disease severity was assessed using the Psoriasis Area and Severity Index (PASI) score, calculated based on erythema, infiltration, desquamation, and affected body surface area.⁹ Patients were categorized based on the Psoriasis Area and Severity Index (PASI). Those with a PASI score of less than 5 were classified as having mild psoriasis, scores between 5 and 10 were considered moderate, and scores greater than 10 were categorized as severe psoriasis.¹⁰

Laboratory Investigations: After overnight fasting of 12 hours, venous blood samples (5 mL) were collected from all participants between 8:00-10:00 AM. Serum was separated by centrifugation at 3000 rpm for 10 minutes and analyzed within 2 hours of collection.

Lipid Profile Analysis: Serum lipid parameters were estimated using an automated clinical chemistry analyzer (Cobas 6000, Roche Diagnostics) with enzymatic colorimetric methods. Total cholesterol (TC) was measured using the CHOD-PAP method, and triglycerides (TG) were analyzed by the GPO-PAP method. High-density lipoprotein cholesterol (HDL-C) was determined using a direct homogeneous assay. Low-density lipoprotein cholesterol (LDL-C) was calculated using the Friedewald formula (LDL-C = TC – HDL-C – TG/5) for samples with triglyceride levels <400 mg/dL, while very-low-density lipoprotein cholesterol (VLDL-C) was calculated as TG/5.

Definition of Dyslipidemia: Dyslipidemia was defined according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines as the presence of any one of the following abnormalities: total cholesterol (TC) ≥200 mg/dL, triglycerides (TG) ≥150 mg/dL, low-density lipoprotein cholesterol (LDL-C) ≥130 mg/dL, or high-density lipoprotein cholesterol (HDL-C) <40 mg/dL in men and <50 mg/dL in women.⁷

Additional Parameters: Other metabolic parameters assessed included fasting blood glucose, estimated using the hexokinase method, and blood pressure, which was measured in the sitting position after five minutes of rest. Anthropometric indices were also recorded, including body mass index (BMI), calculated as weight in kilograms divided by the square of height in meters (kg/m²), and waist circumference, measured at the midpoint between the lower rib margin and the iliac crest.

Quality Control Laboratory equipment was calibrated regularly using standard reference materials. Inter-observer variability for PASI scoring was minimized by training two dermatologists and using mean values. All samples were analyzed within 2 hours of collection to prevent degradation.

Statistical Analysis: Data analysis was performed using SPSS version 26.0 (IBM Corp., Armonk, NY). Continuous variables were expressed as mean ± standard deviation (SD) or median with interquartile range (IQR) based on normality distribution. Categorical variables were presented as frequencies and percentages. Comparison between groups was performed using Student's t-test for normally distributed data and Mann-Whitney U test for non-normally distributed data. Chi-square test was used for categorical variables. Correlation between lipid parameters and PASI scores was assessed using Pearson's correlation coefficient. Logistic regression analysis was employed to identify predictors of dyslipidemia in psoriasis patients. Odds ratios (OR) with 95% confidence intervals (CI) were calculated. A p-value <0.05 was considered statistically significant.

Table 1: Baseline Characteristics of Study Population

The mean age of psoriasis patients (42.8 ± 11.6 years) was comparable to that of the controls (43.5 ± 12.2 years; p = 0.72). The male-to-female ratio was similar in both groups (64:36 vs. 62:38; p = 0.84). Body mass index (BMI) and waist circumference did not differ significantly between the two groups. A slightly higher proportion of cases were smokers (22% vs. 18%) and alcohol users (15% vs. 13%), although these differences were not statistically significant [Table 1]. Among psoriasis patients, 50% had disease duration of more than 5 years. Based on PASI scores, 55% of patients had mild disease, 28% moderate, and 17% severe psoriasis [Figure 1].

Table 2: Comparison of Lipid Profile Between Cases and Controls

Psoriasis patients exhibited a significantly more atherogenic lipid profile compared to controls. The mean total cholesterol (209.6 ± 38.5 mg/dL vs. 178.4 ± 32.1 mg/dL; p < 0.001), triglycerides (189.7 ± 64.3 mg/dL vs. 142.2 ± 48.5 mg/dL; p < 0.001), LDL-C (128.4 ± 34.2 mg/dL vs. 102.7 ± 28.3 mg/dL; p < 0.001), and VLDL-C (37.9 ± 11.2 mg/dL vs. 28.4 ± 9.5 mg/dL; p < 0.001) levels were all significantly higher in cases than controls. In contrast, mean HDL-C levels were significantly lower in psoriasis patients compared to controls (41.8 ± 8.6 mg/dL vs. 50.7 ± 9.1 mg/dL; p < 0.001) [Table 2].

The prevalence of dyslipidemia was markedly higher in the psoriasis group. Hypercholesterolemia was present in 44% of cases versus 24% of controls (OR = 2.5, 95% CI: 1.3–4.7; p = 0.004). Hypertriglyceridemia was observed in 52% of cases compared to 28% of controls (OR = 2.8; p = 0.001). Low HDL-C was significantly more common among cases (48%) compared to controls (22%) (OR = 3.2; p < 0.001). High LDL-C was also more prevalent in cases (39% vs. 21%; OR = 2.4; p = 0.007). Overall, 74% of psoriasis patients had at least one lipid abnormality, compared to 45% of controls (p < 0.001) [Figure 3].

Figure 3: Prevalence of Dyslipidemia in Psoriasis Cases vs Controls

Table 3: Lipid Profile According to Psoriasis Severity (by PASI Score)

A progressive worsening of lipid parameters was observed with increasing disease severity. Patients with severe psoriasis had significantly higher total cholesterol (232.6 ± 40.1 mg/dL), triglycerides (228.3 ± 58.9 mg/dL), LDL-C (149.6 ± 35.8 mg/dL), and VLDL-C (45.6 ± 12.4 mg/dL) compared to those with mild disease (196.2 ± 32.4, 171.5 ± 48.2, 118.3 ± 30.4, and 34.3 ± 10.5 mg/dL respectively). HDL-C levels declined with increasing severity (44.6 ± 7.9 mg/dL in mild vs. 37.1 ± 6.5 mg/dL in severe psoriasis; p = 0.001). The ANOVA analysis confirmed a statistically significant trend across PASI categories (p < 0.05 for all lipid fractions) [Table 3].

Table 4: Derived Atherogenic Indices in Psoriasis Cases vs Controls

Psoriasis patients demonstrated significantly elevated atherogenic indices compared to controls. The mean Cardiac Risk Ratio (TC/HDL-C) was 5.12 ± 1.4 in cases versus 3.65 ± 1.1 in controls (p < 0.001). The Atherogenic Index of Plasma (AIP) was also significantly higher in cases (0.62 ± 0.21) than controls (0.28 ± 0.15; p < 0.001). Similarly, the Atherogenic Coefficient (4.12 ± 1.6 vs. 2.65 ± 1.2; p < 0.001) and Comprehensive Lipid Tetrad Index (1832 ± 740 vs. 1098 ± 510; p < 0.001) were markedly elevated in psoriasis patients. These findings highlight the enhanced cardiovascular risk burden associated with psoriasis [Table 4].

Table 5: Correlation Between PASI Scores and Lipid Parameters (Pearson’s Correlation Analysis)

Pearson’s correlation analysis demonstrated a strong positive correlation between psoriasis severity (PASI score) and lipid abnormalities. Higher PASI scores were significantly associated with elevated total cholesterol (r = 0.68, p <0.001), triglycerides (r = 0.72, p <0.001), LDL-C (r = 0.64, p <0.001), and VLDL-C (r = 0.69, p <0.001). In contrast, HDL-C showed a significant negative correlation with PASI scores (r = –0.58, p <0.001), indicating that greater disease severity was associated with lower HDL-C levels [Table 5].

Table 6: Multivariate Logistic Regression Analysis for Predictors of Dyslipidemia in Psoriasis Patients

Multivariate logistic regression analysis identified independent predictors of dyslipidemia among psoriasis patients. A disease duration of more than five years was associated with a twofold higher risk of dyslipidemia (OR = 2.3, 95% CI: 1.2–4.5; p = 0.01). Patients with severe psoriasis (PASI >10) had nearly a fourfold increased risk (OR = 3.8, 95% CI: 1.9–7.6; p <0.001). Overweight status (BMI ≥25 kg/m²) was also a significant predictor (OR = 1.9, 95% CI: 1.1–3.4; p = 0.03). Male gender was not significantly associated with dyslipidemia (OR = 1.6, 95% CI: 0.7–2.4; p = 0.12) [Table 6].

This comprehensive case-control study provides robust evidence for the significant association between dyslipidemia and psoriasis disease severity in Indian population. Our findings demonstrate that psoriasis patients exhibit a characteristic atherogenic lipid profile with elevated levels of total cholesterol, triglycerides, LDL-C, and VLDL-C, coupled with reduced HDL-C levels compared to healthy controls.

Prevalence and Pattern of Dyslipidemia: The prevalence of dyslipidemia in our study population (74% in psoriasis patients vs 45% in controls) is consistent with recent Indian studies. Gosai et al.⁷ (2024) reported similar findings with 74% dyslipidemia prevalence in Gujarat, while Praneeth et al.⁸ (2024) from Andhra Pradesh documented 68.3% prevalence. Study by Girisha et al.¹ (2017) from South India reported similar patterns of dyslipidemia, with significantly higher prevalence of hypertriglyceridemia (34% vs 20.5%) and reduced HDL levels (27.6% vs 13.5%) in psoriasis patients compared to controls.¹ While our study and most international studies have reported elevated LDL-C levels in psoriasis patients, the study by Nakhwa et al.² (2014) from Pondicherry found comparable LDL levels between cases and controls. This discrepancy may be attributed to differences in study populations, dietary habits, genetic factors, or disease characteristics.

The pattern of lipid abnormalities observed in our study follows the characteristic "atherogenic dyslipidemia" profile commonly associated with metabolic syndrome. This includes elevated triglycerides, reduced HDL-C, and increased small dense LDL particles, which collectively contribute to enhanced cardiovascular risk.⁴ The significant elevation of all atherogenic lipid fractions (TC, TG, LDL-C, VLDL-C) coupled with reduced anti-atherogenic HDL-C supports the concept of psoriasis as a systemic inflammatory condition with metabolic implications.

Correlation with Disease Severity: Our study demonstrated a strong correlation between lipid abnormalities and psoriasis severity, with progressive worsening of lipid parameters across higher PASI categories, indicating a dose–response relationship between cutaneous inflammation and systemic metabolic dysfunction. Similar trends have been reported in recent Indian studies, including Gosai et al.⁷ (2024). In the present study, the strong correlations observed (r = 0.64–0.72) between PASI scores and lipid parameters suggest that psoriasis activity directly influences lipid metabolism, likely mediated by systemic inflammation and elevated cytokines such as IL-6, TNF-α, and IL-17.³ A comprehensive meta-analysis by Alajroush et al.¹¹ (2024) involving over one million adults worldwide demonstrated significant associations between psoriasis severity and metabolic disorders, including dyslipidemia.

Atherogenic Indices and Cardiovascular Risk: In the present study, elevated atherogenic indices in psoriasis patients confirm their higher cardiovascular risk burden. The Comprehensive Lipid Tetrad Index, nearly 1.7-fold higher in cases than controls, underscores that traditional lipid profiles may underestimate risk, highlighting the need for advanced cardiovascular risk assessment tools in psoriasis, especially in severe disease.⁴

Pathophysiological Mechanisms: Dyslipidemia in psoriasis is driven by chronic systemic inflammation, which alters hepatic lipid metabolism through increased synthesis of acute-phase reactants such as C-reactive protein and fibrinogen. Pro-inflammatory cytokines, notably TNF-α and IL-6, further suppress lipoprotein lipase activity, impairing triglyceride clearance and elevating circulating lipid levels.² Oxidative stress also contributes to dyslipidemia in psoriasis, with elevated malondialdehyde levels correlating with disease severity. Lipid peroxidation promotes the formation of oxidized LDL, which is highly atherogenic and augments cardiovascular risk.⁴ The ‘lipid paradox’ in psoriasis, where elevated HDL levels coexist with increased cardiovascular risk, may be explained by qualitative changes in HDL. Emerging evidence indicates that HDL in psoriasis is often dysfunctional, with reduced reverse cholesterol transport capacity despite normal or elevated levels. ²

Cardiovascular Risk Assessment: The elevated atherogenic indices in our study underscore the need for comprehensive cardiovascular risk assessment in psoriasis patients, extending beyond traditional lipid profiles. Incorporating novel biomarkers such as lipoprotein(a), high-sensitivity C-reactive protein, and advanced lipid testing may improve risk stratification. Recent guidelines, including the EULAR recommendations, advocate cardiovascular risk assessment in psoriasis comparable to that in rheumatoid arthritis, reflecting the shared inflammatory basis of heightened cardiovascular risk.¹¹

Treatment Considerations: Management of dyslipidemia in psoriasis should follow standard lipid-lowering guidelines, with emphasis on aggressive control of multiple risk factors. Statins remain first-line agents and may offer additional anti-inflammatory benefits, though evidence regarding their impact on psoriasis outcomes is mixed, as highlighted in a systematic review by Mehta et al.¹² (2024). Lifestyle interventions—including dietary modification, exercise, and weight management—should be integrated into care, as they may improve both psoriasis severity and cardiovascular risk

LIMITATIONS

This hospital-based study may be subject to selection bias, as patients attending tertiary care are more likely to have severe disease or comorbidities, limiting generalizability to the broader psoriasis population. Although patients with known cardiovascular, diabetic, or thyroid disease were excluded, undetected subclinical conditions may have influenced lipid profiles. The short study duration precluded assessment of treatment effects or long-term cardiovascular outcomes, and lifestyle factors such as diet and physical activity, which strongly affect lipid metabolism, were not systematically evaluated. Finally, while standard enzymatic methods were used for lipid estimation, advanced lipid testing was not performed, which could have provided additional insights into lipoprotein particle characteristics.

This comprehensive case-control study provides compelling evidence for the significant association between dyslipidemia and psoriasis disease severity in Indian population. The findings demonstrate that psoriasis patients exhibit a characteristic atherogenic lipid profile with elevated levels of total cholesterol, triglycerides, LDL-C, and VLDL-C, coupled with reduced HDL-C levels compared to healthy controls. The strong correlation between lipid parameter abnormalities and PASI scores suggests that disease activity directly influences lipid metabolism, with progressive worsening of lipid parameters observed with increasing disease severity. The identification of independent predictors for dyslipidemia, including disease duration >5 years, PASI score >10, BMI ≥25 kg/m², and male gender, provides valuable tools for risk stratification and targeted screening strategies. The significantly elevated atherogenic indices observed in psoriasis patients highlight the enhanced cardiovascular risk burden and emphasize the need for comprehensive risk assessment beyond traditional lipid profiles.

RECOMMENDATIONS

Based on our findings and current evidence, we recommend routine lipid screening for all psoriasis patients, with particular emphasis on those with PASI >10 or disease duration >5 years. Risk stratification using predictors such as male gender, BMI ≥25 kg/m², longer disease duration, and higher PASI scores can help identify patients requiring closer monitoring. Advanced lipid testing and atherogenic indices may further refine cardiovascular risk assessment, especially in severe cases. Comprehensive management should involve multidisciplinary collaboration between dermatologists, cardiologists, and primary care physicians, alongside aggressive lifestyle interventions including dietary counseling, exercise, and weight management. Finally, systemic therapy choices should consider their metabolic effects, with preference for agents that improve or do not adversely affect lipid profiles.

1. Girisha, B. S., N. Thomas, and G. S. Rao. "Metabolic Syndrome in Psoriasis among Urban South Indians: A Case Control Study Using SAM-NCEP Criteria." Journal of Clinical and Diagnostic Research, vol. 11, no. 2, 2017, pp. WC01–WC04.
2. Nakhwa, Y. C., R. Rashmi, and K. H. Basavaraj. "Dyslipidemia in Psoriasis: A Case Controlled Study." ISRN Dermatology, 2014, Article ID 729157.
3. Sahoo, S. R., K. Das, B. Panda, et al. "Serum Interleukin (IL)-6, Lipid Profile, and Association With Disease Severity in Patients With Psoriasis: A Cross-sectional Study." Cureus, vol. 16, no. 10, 2024, e69547.
4. Sunitha, S., M. Rajappa, D. M. Thappa, et al. "Comprehensive Lipid Tetrad Index, Atherogenic Index and Lipid Peroxidation: Surrogate Markers for Increased Cardiovascular Risk in Psoriasis." Indian Journal of Dermatology, vol. 60, no. 3, 2015, pp. 268–273.
5. Salihbegovic, E. M., N. Hadzigrahic, E. Suljagic, et al. "Psoriasis and Dyslipidemia." Materia Socio-Medica, vol. 27, no. 1, 2015, pp. 15–17.
6. Rajendran, A., M. V. Harikumar, and A. Swaminathan. "Lipid Abnormalities and Electrocardiographic Changes in Patients With Psoriasis in a Tertiary Care Hospital." Cureus, vol. 17, no. 4, 2025, e82164.
7. Gosai, A., R. Sao, and B. K. Mahaseth. "A Study of Dyslipidemia in Psoriasis Patients: A Case-Control Study." Journal of Cardiovascular Disease Research, vol. 15, no. 5, 2024, pp. 1234–1242.
8. Praneeth, N. G., H. P. Bandi, S. Koduru, and R. S. R. "Altered Lipid Profile in Psoriasis Patients and Its Association with Disease Severity." European Journal of Cardiovascular Medicine, vol. 14, no. 6, 2024, pp. 123–132.
9. Fredriksson, T., and U. Pettersson. "Severe Psoriasis–Oral Therapy with a New Retinoid." Dermatology, vol. 157, no. 4, 1978, pp. 238–244.
10. Kiran, A., Z. Babar, A. Naheed, and U. Mirza. "Frequency of Dyslipidemia in Patients with Psoriasis and Association with Disease Severity." Pakistan Journal of Medical and Health Sciences, vol. 15, no. 12, 2021, pp. 3430–3432.
11. Alajroush, W. A., A. I. Alrshid, A. H. Alajlan, et al. "Psoriasis and Metabolic Disorders: A Comprehensive Meta-Analysis of Million Adults Worldwide." Cureus, vol. 16, no. 1, 2024, e66632.
12. Mehta, H., T. Narang, S. Dogra, S. Handa, J. Hatwal, and A. Batta. "Cardiovascular Considerations and Implications for Treatment in Psoriasis: An Updated Review." Vascular Health and Risk Management, 31 Dec. 2024, pp. 215–229.