1. Evaluate serum levels of (MCP-1) in PsA with or without cardiovascular affaction .
2. Detect subclinical cardiovascular affaction in patients with PsA for early diagnosis and management .

Psoriatic arthritis (PSA) is an autoimmune disease arising from the interply between proinflamatory cytokines

[1]and external stimuli in genetically predisposed individuals.[2]

• The disease is chronic and affects the peripheral joints and may include axial skeleton with or without extrarticular manifestations.[3]
• Abnormal activation of the innate and adaptive immune systems contributes to chronic disease processes in both psoriasis and PSA .[4] The skin and the joints exhibit a prominent lymphocytic infiltrate consisting of activated CD4+ and CD8+ T cells as well as an increase in neutrophil infiltration[5].

Patients with PsA have a higher risk of developing a cardiovascular(CV) events than the general population. This could be attributed to the higher prevalence of traditional cardiovascular risk factors and to the disease characteristics such as systemic inflammation. [6] These patients may show asymptomatic cardiomyopathy even in the absence of traditional risk factors [7].Cardiac dysfunction is associated with a poor prognosis, increased mortality, and affact socioecenomic function of patients therefore, the diagnosis of the cardiac dysfunction in the asymptomatic phase of the disease [8] is important for the timely introduction of therapy [9].Monocyte chemotactic protien1(MCP-1) is a member of chemotactic chemokines(CC) which are secreted by immune effector cells and dysfunctional endothelium [10].

• The pivotal function of MCP-1 is to attract monocyte in the arterial wall through increased expression of adhesion molecules on their surface that interacts with endothelium[11].
• MCP-1 induce maturation of monocyte in the arterial wall ,which then become specialized macrophage in early atheroma and produce tissue factors supporting coagulation and proinflammatory cytokines such as IL-1 and IL-6. It affects the functions of the surrounding immune effector cells in locally thickened intima.[12]
• During active disease in psoriatic skin lesions and synovial tissue, activated monocytes represent the major source of proinflammatory mediators, including the chemokine MCP-1 [13]. MCP-1 is thought to be involved in the pathogenesis of oedema and bone erosion in patients with PsA [14].

Inclusion Criteria:

• PsA patients (age ≥ 18years) who fulfilled the CASPAR classification criteria[15]for psoriatic arthritis

Exclusion Criteria:

• PsA patients with

  1. infection.
  2. bone marrow disorders.
  3. other autoimmune diseases.
  4. diabetes.
  5. hypertention .
  6. hyperlipidemia.
  7. liver diseases.
  8. renal diseases.

psoriatic arthritis patients with or without clinically cardiovascular affaction