European Journal of Cardiovascular Medicine

Psoriasis is a lifelong, chronic, immune-mediated disease affecting 1–3% of the global population, with substantial impact on quality of life and systemic health. (1,2) Clinically, it is characterized by erythematous, thickened, scaly plaques arising from keratinocyte hyperproliferation and inflammatory infiltration. The pathogenesis involves dendritic-cell activation and polarization of the IL-23/Th17 axis, with abundant secretion of cytokines such as IL-17, TNF-α, IFN-γ, and IL-22, which amplify epidermal proliferation and vascular dysfunction. (3–5) Psoriasis can occur at any age, but population-based studies report a mean onset in late adolescence/early adulthood, with lifelong recurrence and comorbidity burden. (6)

Psoriasis as an Immunometabolic Disorder

Beyond cutaneous lesions, psoriasis is now recognized as a systemic inflammatory disease. Epidemiologic evidence consistently shows increased cardiovascular (CV) morbidity and mortality, especially in patients with moderate-to-severe disease. (7) This risk is only partly explained by classical CV risk factors (obesity, hypertension, diabetes, smoking); dyslipidemia and altered lipoprotein quality are central drivers. (8–10) Studies, including the seminal work of Mallbris et al. (2006), demonstrate that lipid abnormalities may be detectable even at the onset of psoriasis, highlighting their pathophysiological role rather than secondary consequence. (11)

Oxidative stress further links psoriasis and atherosclerosis: activated neutrophils produce reactive oxygen species (ROS) that oxidize lipids and proteins. Oxidized LDL (oxLDL), in particular, is highly atherogenic, and elevated antibodies against oxLDL correlate with psoriasis severity. (9,12)

Role of Derived Atherogenic Indices

Single lipid values (e.g., TC or LDL alone) incompletely capture CV risk. Derived indices integrate multiple fractions and offer greater predictive accuracy. The most widely studied are:

Clinical & Research Significance

• CRR: Easy ratio; rises in psoriasis patients, often paralleling disease severity.
• AIP: A continuous variable highly correlated with CV outcomes; in psoriasis, mean AIP often exceeds 0.24 (high risk), sometimes reaching >0.7. This indicates small, dense LDL particles prone to oxidation and arterial retention.
• AC: Complements CRR; higher in psoriasis compared with controls, reflecting reduced HDL buffering capacity.
• PASI: Provides a severity gradient; multiple studies show stepwise increases in CRR, AIP, AC with higher PASI categories, reinforcing psoriasis as an immunometabolic syndrome. (12,16,17)

Incorporating these indices into psoriasis care enables a more nuanced assessment of cardiovascular risk, particularly in those with psoriatic arthritis (PsA), who may have even greater systemic inflammation and lipid derangement. (18)

Accordingly, the present study evaluates fasting lipid profiles alongside CRR, AIP, and AC, explores their association with PASI severity, and situates findings within the evolving literature on psoriasis as a systemic immunometabolic disease.

 Aim

To evaluate the fasting lipid profile in patients with psoriasis and to assess its association with disease severity.

Objectives

1. To assess fasting lipid profile parameters—total cholesterol (TC), triglycerides (TAG; also referred to as TGL), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C), and high-density lipoprotein cholesterol (HDL-C)—in patients diagnosed with psoriasis.
2. To correlate lipid profile abnormalities with the severity of psoriasis as measured by the Psoriasis Area and Severity Index (PASI).

A hospital-based case–control study conducted in the OPD of  Department of DVL, Sri Balaji Medical College, Renigunta, Chowtour, Tirupati, Andhra Pradesh, India from December 2023 to November 2024.

Inclusion criteria: Adults aged 18–60 years who were clinically diagnosed to have psoriasis of any clinical or morphological type or variant.

Exclusion criteria: Patients with pre-existing diabetes mellitus, hypertension, obesity (BMI >30), thyroid disease, hepatic/renal dysfunction, or on lipid-lowering agents.

Patients on Beta blockers, NSAIDs, Antimalarials, Lithium, ACE inhibitors.

Patients, who consume Alcohol, smoke
Controls: Healthy volunteers matched for age and gender, without history of psoriasis or systemic illness.

Clinical assessment (PASI)

Disease severity was graded using the Psoriasis Area and Severity Index (PASI), scoring erythema (E), induration (I), and desquamation (D) over four body regions—head (h), upper limbs (u), trunk (t), and lower limbs (l)—weighted for body surface area (0.1, 0.2, 0.3, 0.4, respectively).

For subgroup analyses, patients were stratified into four PASI groups: <3.0, 3.0–6.0, 6.1–10.0, and >10.1.

Sample collection and laboratory measurements

After obtaining written informed consent, a 12-hour fasting venous blood sample (5–6 mL) was drawn into heparinised tubes. Samples were centrifuged at 3500 rpm for 10 minutes; plasma was used for biochemical analysis.

• Primary measurements: TC, TAG (TGL), and HDL-C by standard enzymatic colorimetric methods on an automated analyzer.
• Derived measures (calculated):
• VLDL-C (mg/dL) = TAG/5
• LDL-C (mg/dL) = TC − HDL-C − VLDL-C
• Cardiac risk ratio (CRR) = TC/HDL-C
• Atherogenic index of plasma (AIP) = log₁₀(TAG/HDL-C)
• Atherogenic coefficient (AC) = (TC − HDL-C)/HDL-C
  All lipid results are reported in mg/dL.

Procedure: Venous blood samples were collected after an overnight fast of 12 hours. Serum lipid parameters (TC, TGL, LDL, VLDL, HDL) were measured using enzymatic methods. PASI score was recorded for all cases.

Statistical Analysis: Data were expressed as mean ± SD. Group comparisons were made using Student’s t-test for continuous variables and chi-square test for categorical data. A p-value <0.05 was considered statistically significant. SPSS version XX (or whichever you used) was employed.

Study population

A total of 200 subjects were included: 100 psoriasis cases and 100 controls.

• Age (years, Mean ± SD): Cases 40.3 ± 10.7, Controls 41.2 ± 10.3; p > 0.05 (not significant).
• Sex: Male 42%, Female 58% in both groups (matched).

Table 1. Age distribution of subjects

The average ages are comparable, indicating appropriate age matching.

Table 2. Gender distribution

Identical gender proportions ensure gender does not bias lipid comparisons.

Lipid profile: cases vs controls

TC, TAG, LDL-C, VLDL-C were higher and HDL-C was lower in psoriasis vs controls; all differences are highly significant (p < 0.001).

Table 3. Serum lipid profile comparison (revised)

Figure 1: Serum lipid profile in psoriasis cases vs. controls

Cardiovascular risk indices: cases vs controls

CRR, AIP, and AC were markedly higher in psoriasis, indicating elevated atherogenic risk.

Formulas: CRR = TC/HDL; AIP = log₁₀(TAG/HDL) (corrected); AC = (TC − HDL)/HDL.

Table 4. Cardiovascular risk indicators (controls vs psoriasis)

Distribution by PASI severity (psoriasis only)

Table 5. Patient distribution by PASI score

Lipids by PASI severity

TC, TAG, VLDL-C, LDL-C increased stepwise with PASI; HDL-C showed a downward trend in moderate–severe disease.

Note: VLDL-C shown with SD (derived from TAG SD/5). LDL-C reported as derived mean only.

Table 6. Plasma lipid parameters in psoriatic subgroups (by PASI)

Risk indices by PASI severity

CRR, AIP, and AC rose progressively with higher PASI, peaking in Group 4.

Table 7. Cardiovascular risk indicators in psoriatic subgroups

Figure 2: Atherogenic indices (CRR, AIP, AC) in cases vs. controls

Figure 3: Lipid profile trends (TC, TAG, LDL-C, VLDL-C, HDL-C) across PASI severity groups

Figure 4: Risk indices (CRR, AIP, AC) across PASI

In this case–control study (100 psoriasis; 100 controls), we found a markedly pro-atherogenic profile in psoriasis. Compared with controls, cases had higher TC (214.85 vs 161.86 mg/dL), TAG (247.78 vs 114.64 mg/dL), LDL-C (119.77 vs 80.66 mg/dL), VLDL-C (49.56 vs 22.93 mg/dL) and lower HDL-C (45.52 vs 58.27 mg/dL); all differences were highly significant (p<0.001). Derived indices were also substantially elevated in psoriasis: CRR 4.72 vs 2.78, AIP 0.74 vs 0.29, and AC 3.72 vs 1.78. Importantly, PASI-based subgrouping demonstrated a stepwise rise in TC, TAG, VLDL-C, LDL-C and in CRR, AIP, AC from mild to severe psoriasis, reinforcing a dose–response (severity) relationship between psoriatic disease activity and atherogenic burden.
These findings extend earlier reports that documented dyslipidemia in psoriasis by (i) quantifying standardized atherogenic indices and (ii) linking them to disease severity. In particular, our AIP values (computed as log₁₀[TAG/HDL-C]) place most patients well into the high-risk zone (≥0.24), offering an interpretable bridge from lipid biochemistry to cardiovascular (CV) risk stratification.

Comparison with prior literature
Our cases had a mean age of 40.3 ± 10.7 years compared to 41.2 ± 10.3 years in controls, which was not significant. The gender distribution was comparable, with a slight female predominance (58% vs. 42% males), minimizing confounding effects of age and sex on lipid parameters. Similar demographic matching was reported by Akhyani et al. (8) and Farshchian et al. (15), while other studies such as Borborah et al. (12) included mixed age groups (30–70 years) without strict gender balance.

Comparison with Previous Studies
Our findings are consistent with a broad body of evidence suggesting that psoriasis is associated with dyslipidemia.

Total Cholesterol (TC):
We observed significantly higher TC levels in psoriasis patients (201.0 ± 34.4 mg/dL vs. 193.0 ± 43.0 mg/dL). This aligns with the meta-analysis by Ramezani et al. (10), which pooled 49 studies and reported a mean increase of 13.74 mg/dL in TC among psoriatic patients. Borborah et al. (12) also found significantly raised TC in psoriasis (217 vs. 155 mg/dL, p<0.0001). Akhyani et al. (8) and Piskin et al. (9) reported similar trends, while Farshchian et al. (15) observed no significant differences, possibly due to smaller sample size (n=30).

Triglycerides (TGL):
In our study, TGL were higher in cases (165.5 mg/dL) compared to controls (132.9 mg/dL), though not statistically significant. The meta-analysis by Ramezani et al. (10) confirmed a pooled significant increase in TGL (MD = 26.04 mg/dL, p<0.00001). Similarly, Borborah et al. (12) reported higher triglycerides in cases (181 vs. 132 mg/dL, p=0.00025), while Piskin et al. (9) also observed significant elevation. Our non-significance may reflect regional dietary differences, sample variation, or power limitations.

LDL & VLDL:
We found borderline elevation of LDL (139.3 vs. 112.9 mg/dL, p=0.06) and VLDL (33.1 vs. 26.6 mg/dL, p=0.08). Borborah et al. (12) demonstrated significant increases in both LDL (170 vs. 103 mg/dL, p=0.001) and VLDL (35 vs. 23 mg/dL, p=0.001). Akhyani et al. (8) and Piskin et al. (9) also confirmed LDL elevation. The meta-analysis by Ramezani et al. (10) showed pooled increases for LDL (MD = 11.41 mg/dL) and VLDL (MD = 4.82 mg/dL). Thus, our borderline findings remain biologically consistent.

HDL:
In our cohort, HDL was lower in cases (34.9 vs. 45.6 mg/dL), though not statistically significant. Ramezani et al. (10) confirmed a pooled decrease in HDL (MD = –2.78 mg/dL, p=0.002). Borborah et al. (12) found no significant HDL difference, similar to our results. However, Akkara Veetil et al. (14), in a population-based cohort of 689 patients, reported significantly reduced HDL (p=0.013), indicating that larger cohorts may reveal stronger associations.

Pathophysiological Insights
Psoriasis is increasingly recognized as a systemic immunometabolic disease. Activation of Th1 and Th17 T-cells leads to secretion of TNF-α, IFN-γ, IL-6, and IL-17, which alter lipid metabolism by increasing intestinal absorption of lipids, promoting oxidized LDL formation, and reducing protective HDL. Elevated oxidized LDL antibodies correlate with psoriasis severity (9), supporting the hypothesis that lipid abnormalities may not only result from inflammation but also fuel the psoriatic inflammatory loop.
Lifestyle factors also modulate this association. Smoking and obesity have been identified as independent risk factors for psoriasis and worsen lipid abnormalities (10). Hypertension and diabetes are frequently comorbid and may exacerbate dyslipidemia.

Table 4. Comparative Findings of Lipid Profiles in Psoriasis Patients

All lipid fractions except HDL significantly altered with p<0.001, confirming a strong pro-atherogenic profile.Consistency: Aligns with pooled meta-analysis (Ramezani 2019) and case–control studies (Borborah, Akhyani, Piskin).Population-based evidence (Akkara Veetil 2012): Shows persistence of ↑ TGL and ↓ HDL over time.

Our data align with case–control studies that show higher CRR, AIP, and AC in psoriasis versus controls and with the PASI-linked gradient reported in severity-stratified cohorts. When AIP is calculated on the standard log₁₀ scale, results from earlier work converge with our values (≈0.7 in cases vs ≈0.3 in controls). Beyond dermatology cohorts, a recent meta-analysis across cardiology populations associates higher AIP with CAD presence and severity, plaque progression, and future MACE, underscoring the prognostic relevance of AIP. Large occupational datasets also show that relatively modest AIP elevations (e.g., ≥0.24) mark higher risk; by contrast, the mean AIP 0.74 in our psoriasis cohort indicates a substantially greater atherogenic load than seen in general working populations.

Clinical implications

• Screening & monitoring:Incorporate CRR, AIP, AC alongside the standard lipid panel in psoriasis, particularly with moderate–severe PASI or additional metabolic risk factors.
• Risk communication:AIP categories (low <0.11; intermediate 0.11–0.24; high ≥0.24) help convey risk; our mean AIP 0.74 signals clinically meaningful CV risk.
• Management:Lifestyle optimization and lipid-lowering therapy (statins, and where appropriate, agents targeting hypertriglyceridemia) should be considered early. Effective systemic anti-inflammatories may improve both cutaneous disease and lipid indices.
• Follow-up strategy: Track indices longitudinally; improvements in PASI should ideally be paralleled by downward trends in AIP/CRR/AC.

Table 5. Psoriasis cohorts — CRR, AIP, AC & PASI (standardized AIP = log₁₀[TAG/HDL-C])

Table 6. External validation (non-psoriasis populations)

Our findings, together with global evidence, suggest that psoriasis patients are at increased cardiovascular risk. Statins not only lower LDL but also exhibit immunomodulatory effects beneficial in psoriasis. TNF-α inhibitors may normalize lipid abnormalities while reducing systemic inflammation. Therefore, early lipid screening and lifestyle interventions are strongly recommended for psoriatic patients, especially those with moderate-to-severe disease or additional metabolic risk factors.

Psoriasis is associated with significant dyslipidemia and elevated atherogenic indices. In our cohort, all lipid differences (higher TC, TAG, LDL-C, VLDL-C; lower HDL-C) and all indices (CRR, AIP, AC) were highly significant (p<0.001). Crucially, atherogenicity rises in parallel with PASI severity, supporting the concept of psoriasis as a systemic immunometabolic disease with heightened CV risk. Routine incorporation of CRR, AIP, AC into cardiovascular risk assessment for psoriasis—especially in moderate–severe disease or where PsA coexists—may improve early detection and guide timely, targeted risk-reduction strategies.

Limitations of the Study

This study primarily emphasizes the association between altered lipid profiles and psoriasis severity as measured by PASI. Being cross-sectional in design, it does not capture longitudinal changes in lipid parameters during different phases of the disease. Periodic lipid profiling in correspondence with disease progression, remission, and recurrence would provide stronger evidence of temporal correlations between psoriasis activity and dyslipidemia. Additionally, we did not account for other metabolic confounders such as dietary intake, physical activity, or detailed cardiovascular risk scoring, which may have influenced the lipid profile.

Future Research / Evaluation

Future studies should incorporate broader cardiometabolic markers, including body mass index (BMI), obesity indices, and detailed cardiac assessments. The addition of apolipoproteins A and B (ApoA, ApoB), oxidative stress biomarkers, and inflammatory mediators may yield deeper mechanistic insights into the lipid–inflammation axis in psoriasis. Longitudinal designs evaluating lipid abnormalities in parallel with PASI changes over time would help clarify causality. Finally, integration of imaging modalities for subclinical atherosclerosis (e.g., carotid intima–media thickness, coronary calcium scoring) could further establish the prognostic relevance of these lipid alterations and derived indices (CRR, AIP, AC) in psoriatic patients.

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