Psoriasis is a chronic autoimmune condition primarily affecting the skin, although it can also impact joints in the form of psoriatic arthritis. The disease is characterized by the rapid proliferation of keratinocytes, which are the predominant T cell type in the outermost layer of the skin. This accelerated skin cell turnover leads to the formation of the thick, scaly patches often seen in psoriasis.¹

A representative area of psoriasis is selected for each body region. The intensity of redness, thickness, and scaling of the psoriasis is assessed as mild, moderate and severe.²

The pathogenesis of psoriasis is multifactorial, meaning that it arises due to a combination of genetic predisposition and environmental triggers. Key factors include: Genetic Factors: Certain gene variations, particularly those related to immune system regulation, are linked to a higher risk of developing psoriasis.^3,4

The HLA-Cw6 gene is one of the most strongly associated with psoriasis. In psoriasis, there is an abnormal activation of T-cells (a type of white blood cell) that play a central role in the inflammatory process. These T-cells release cytokines that promote inflammation and keratinocyte proliferation. Environmental Triggers include infections (such as streptococcal throat infections), physical trauma (Koebner phenomenon), stress, medications (like beta-blockers), and weather changes (extreme cold or dry conditions). Inflammatory Cascade include Cytokines like TNF-alpha, IL-17, and IL-23, which play critical roles in driving the inflammatory process that leads to the skin changes observed in psoriasis.^5,6

Adenosine Deaminase (ADA): ADA plays a role in purine metabolism and it has involvement in keratinocyte hyperproliferation in psoriasis. Increased ADA levels are associated with elevated DNA synthesis in psoriatic keratinocytes.²

C - reactive protein (CRP): CRP, specifically high-sensitive CRP (hsCRP), is highlighted as an inflammatory marker, with elevated levels indicating ongoing inflammation. Elevated hsCRP levels are also correlated with increased psoriasis severity, psoriatic arthritis, and cardiovascular risks.

Elevated serum uric acid levels are linked with psoriasis severity and an increased risk of cardiovascular mortality, emphasizing the systemic impact of the disease⁷.

Serum ferritin, which is a protein that stores iron in the body, has been studied in relation to psoriasis, as inflammation in conditions like psoriasis can affect iron metabolism. While ferritin is primarily a marker of iron stores, it also acts as an acute-phase reactant, meaning its levels can rise in response to inflammation, infections, or other stressors in the body⁸.

75 Psoriatic Patients: The participants with psoriasis were equally divided into three groups based on their PASI (Psoriasis Area and Severity Index) scores: Mild psoriasis: PASI score <10, Moderate psoriasis: PASI score between 10 and 20, Severe psoriasis: PASI score > 20.

25 Healthy Controls: Healthy subjects of matching age and sex to the psoriasis patients were included as the control group to compare the results. All study population belonged from the department of dermatology B.J Govt. Medical College and Sassoon Hospital Pune.

All participants signed an informed consent form, indicating that they agreed to take part in the study after being informed of the study's aims and procedures. Exclusion Criteria:

Psoraitic patients with no prior use of specific treatments systemic or topical steroids, Methotrexate, Biologics, Phototherapy used within 4 months before inclusion in the study. Psoriasis types: Erythrodermic psoriasis, Pustular psoriasis was excluded from the study.

A total of 5 ml of venous blood was withdrawn from each participant.  Blood was allowed to clot for 15 minutes. After clotting, the blood sample was centrifuged to separate the serum. The serum was separated into two aliquots: One aliquot was used for determining Serum ferritin levels. The second aliquot was used for assays of Adenosine Deaminase (ADA), Uric acid, high-sensitivity C - reactive protein (hsCRP)

The ADA concentration was measured using the Non Giusti and Galanti Method on transasia XL640 instrument. The serum uric acid was assayed by an enzymatic colorimetric uricase method. The hsCRP was assayed using an immunoturbidimetry method. Serum ferritin was measured by Electrochemiluminescence by Roche e411.

 Statistical Analysis:

The analysis was performed using SPSS for Windows, release 20 (SPSS Inc., Chicago, Illinois, USA). Quantitative Data: Presented as Mean ± standard deviation (SD): Used for normally distributed data. Median and range: Used for skewed or non-normally distributed data. Chi-square and Fisher’s exact tests: These tests were used to determine the relationship between qualitative variables One-way ANOVA: Used to compare quantitative data between more than two independent groups, assuming normal distribution. Independent t-test: Used to compare the PASI scores and laboratory results between two groups p-value < 0.001 was considered statistically significant, p<0.05 is statistically highly significant p >0.05 is insignificant.

This study included 75 psoriatic patients classified according to PASI score into mild, moderate, and severe psoriatic group. Each group included 25 patients. Twenty-five healthy subjects were included as a control group. There were no statistically significant differences of age and sex between different psoriatic groups and the control group. Table 1 shows the demographic data of psoriatic patients and of the control group.

Table 1: Demographic data of the studied groups

Table 2:  PASI Score of psoriatic patients

Table 3: Comparison of adenosine deaminase, high-sensitive C-reactive protein, Serum uric acid, and serum ferritin between psoriasis and control (*Chi-square test)

Table 4: Comparison of adenosine deaminase, High-sensitive C-reactive protein, Serum uric acid, and serum ferritin between psoriasis and controls. (Kruskal–Wallis test)

p₁ = Comparison of mild group with the control group

p₂ = Comparison of moderate group with the control group

p₃ = Comparison of severe group with the control group

Table 5: Correlations of psoriasis area severity index score with laboratory results in psoriatic patients (Spearman correlation coefficient)

The results suggest that inflammatory biomarkers ADA, hsCRP, uric acid and serum ferritin are elevated in the psoriatic patient group compared to the control group, and the difference is statistically significant. Table 3 

ADA, hsCRP, serum uric acid, and serum ferritin are significantly elevated in all psoriatic groups (mild, moderate, and severe) compared to the control group. This indicates that these biomarkers are associated with psoriasis in general, regardless of disease severity.

There were significant differences found in ADA between moderate and severe psoriasis and control. There were no significant differences found in ADA mild psoriasis and control. There were significant differences found in hsCRP between mild, moderate and severe psoriasis and control. There were significant differences found in uric acid between moderate and severe psoriasis and control. There were no significant differences found in uric acid between mild psoriasis and control. There was no significant difference found in serum ferritin between mild and moderate psoriasis and control. (Table 4). Furthermore, a significant correlation between PASI score and ADA, hsCRP, serum uric acid was found. Furthermore, no significant correlation between PASI score and serum ferritin was found (Table 5)

Psoriasis is not just a skin condition, but a chronic and systemic disease, that affects the entire body, potentially involving other organs and systems, such as joints (psoriatic arthritis) ⁹.

The disease has an immune-inflammatory origin, meaning it is driven by an overactive immune system. The body mistakenly attacks its own tissues, particularly the skin, leading to T cell-mediated inflammation-: T-cells (a type of white blood cell) play a central role in triggering inflammation and the abnormal skin cell production in psoriasis. The immune system's response leads to hyperproliferation of keratinocytes (the primary skin cells), causing them to multiply too quickly and form the characteristic scaly patches of psoriasis¹⁰.

Studies on ADA levels in psoriatic patients show mixed results. Some studies, agreed with us in, found that ADA levels were higher in the sera of psoriatic patients compared to healthy controls, indicating an association between increased ADA activity and psoriasis⁴.

The study by Tikhonov et al.⁵ found double the activities of ADA and purine nucleoside phosphorylase (PNP) in the skin of psoriatic patients. This suggests that the increase in ADA activity is not just a serum phenomenon but could also be localized in the skin, which is the primary site of the disease manifestation in psoriasis.

Many studies have reported a decrease in serum ADA levels following psoriasis treatment with different therapies, including Cyclosporine, Etanercept PUVA (psoralen + ultraviolet A therapy), PTU (propylthiouracil). These treatments have been shown to reduce ADA levels, suggesting that they might suppress the immune response or reduce T-cell activation, both of which could be involved in the pathogenesis of psoriasis^3,11.

Matched with our study, Bukulmez et al^[4]. and Yildirum et al^[12]. found correlation between serum ADA and PASI score. In spite of the fact that PASI score is the most widely used measure for assessment of psoriasis¹³.

The hsCRP showed a significant increase in psoriatic patients as one group and in each psoriatic group (mild, moderate, and severe) compared with the controls. This result is in agreement with many studies reporting higher CRP and hsCRP levels in psoriatic patients. They also found a decrease in their levels after treatment with different modalities indicating that hsCRP is a well-established biomarker for inflammation in psoriatic patients. There is correlation with hsCRP with PASI score.^14-18

Many studies, including^18,19, have reported that serum uric acid levels are elevated in psoriasis patients compared to healthy controls. This supports the idea that hyperuricemia is common in psoriasis. A history of psoriasis has been associated with an increased risk of gout, which is often linked to elevated serum uric acid levels²⁰. The elevated ADA activity in psoriatic patients may contribute to the increased serum uric acid levels. ADA breaks down adenosine to inosine, which is further metabolized into uric acid. Elevated ADA activity in psoriasis could be a cause of the increased serum uric acid, linking the two biomarkers (ADA and serum uric acid) in the pathogenesis of psoriasis. Increased serum uric acid was observed in psoriatic patients and was found to significantly decrease after treatment of psoriasis¹⁸. Patients with psoriasis and hyperuricemia showed marked improvement in their psoriasis when treated for hyperuricemia. Kwon et al.²¹ matched with our study found significant correlation between serum uric acid levels and PASI scores.

Elevated serum ferritin has been increased in many studies of psoriatic patients. This increase is often thought to reflect the ongoing systemic inflammation associated with psoriasis. Ferritin is an acute-phase reactant, meaning its levels can rise during periods of inflammation, which is a hallmark of psoriasis due to the immune response and cytokine release (such as TNF-α, IL-6, and IL-1). Since psoriasis is an inflammatory disease, the elevation of ferritin might be interpreted as a marker of disease activity.²²

ADA (Adenosine Deaminase), hsCRP (high-sensitivity C-reactive protein), serum uric acid (Serum uric acid), and serum ferritin were found to be higher in psoriatic patients compared to healthy controls. ADA is elevated, supporting the role of T-cell activation in the pathogenesis of psoriasis. This is consistent with psoriasis being an immune-mediated inflammatory disease. hsCRP is a marker of inflammation, and its increased levels align with the chronic inflammatory nature of psoriasis.

Serum uric acid is often elevated in psoriasis and may be linked to purine metabolism disruptions, potentially playing a role in disease progression.

Serum Ferritin, another inflammatory marker, is also higher, reflecting the general inflammatory state in psoriasis.

Despite the increase in these biomarkers, only ADA  and hsCRP showed significant correlations with the PASI (Psoriasis Area and Severity Index) score  and uric acid showed positive correlation with severe psoriasis and  PASI (Psoriasis Area and Severity Index) score. However there were no significant correlations between the levels of, Serum Ferritin, and the PASI (Psoriasis Area and Severity Index) score.

This suggests that while these biomarkers are elevated in psoriatic patients, only ADA and hs CRP levels directly correlate with disease severity as measured by PASI. However serum ferritin and uric acid levels may not directly correlate with disease severity as measured by PASI.

1. Deng Y, Chang C, Lu Q. The inflammatory response in psoriasis: A comprehensive review. Clin Rev Allergy Immunol 2016;50:377-89.
2. Das RP, Jain AK, Ramesh V. Current concepts in the pathogenesis of psoriasis. Indian J Dermatol 2009;54:7-12.
3. Köse K, Utaş S, Yazici C, Akdaş A, Keleştimur F. Effect of propylthiouracil on adenosine deaminase activity and thyroid function in patients with psoriasis. Br J Dermatol 2001;144:1121-
4. Bukulmez G, Akan T, Ciliv G. Serum adenosine deaminase levels in patients with psoriasis: A prospective case-control study. Eur J Dermatol 2000;10:274-6
5. Tikhonov IV, Markusheva LI, Toguzov RT. Metabolism of purine compounds in psoriasis. Klin Lab Diagn 1998;3:3-6.
6. Koizumi H, Iizuka H, Aoyagi T, Miura Y. Adenosine deaminase in human epidermis from healthy and psoriatic subjects. Arch Dermatol Res 1983;275:310-4.
7. Gerkowicz A, Pietrzak A, Szepietowski JC, Radej S, Chodorowska G. Biochemical markers of psoriasis as a metabolic disease. Folia Histochem Cytobiol 2012;50:155-70.
8. Zinkevičienė A, Kainov D, Lastauskienė E, Kvedarienė V, Bychkov D, Byrne M, et al. Serum biomarkers of allergic contact dermatitis: A pilot study. Int Arch Allergy Immunol 2015;168:161-4.
9. Das RP, Jain AK, Ramesh V. Current concepts in the pathogenesis of psoriasis. Indian J Dermatol 2009;54:7-12.
10. Hashemi M, Mehrabifar H, Daliri M, Ghavami S. Adenosine deaminase activity, trypsin inhibitory capacity and total antioxidant capacity in psoriasis. J Eur Acad Dermatol Venereol 2010;24:329-34.
11. Chaudhry SD, Mittal RA, Gupta V, Saini AS, Ghalaut VS. Adenosine-deaminase (ADA) activity in psoriasis (A preliminary study). Indian J Dermatol Venereol Leprol 1988;54:293-4.
12. Yıldırım FE, Karaduman A, Pinar A, Aksoy Y. CD26/dipeptidyl-peptidase IV and adenosine deaminase serum levels in psoriatic patients treated with cyclosporine, etanercept, and psoralen plus ultraviolet A phototherapy. Int J Dermatol 2011;50:948-55
13. Feldman SR, Krueger GG. Psoriasis assessment tools in clinical trials. Ann Rheum Dis 2005;64 Suppl 2:ii65-8.
14. Beygi S, Lajevardi V, Abedini R. C-reactive protein in psoriasis: A review of the literature. J Eur Acad Dermatol Venereol 2014;28:700-11.
15. Coimbra S, Oliveira H, Reis F, Belo L, Rocha S, Quintanilha A, et al. C-reactive protein and leucocyte activation in psoriasis vulgaris according to severity and therapy. J Eur Acad Dermatol Venereol 2010;24:789-96.
16. Rajappa M, Shanmugam R, Munisamy M, Chandrashekar L, Rajendiran KS, Thappa DM, et al. Effect of antipsoriatic therapy on oxidative stress index and sialic acid levels in patients with psoriasis. Int J Dermatol 2016;55:e422-30.