Laboratory findings and pathology of psoriatic arthritis

Abstract

Over recent years there has been a great deal of interest in the immunology, molecular biology and pathology of psoriasis and PsA. The pathogenetic mechanisms in PsA are less well understood than those described for psoriasis. There are almost certainly genetic and immune components. What is not clear is whether there is a primary immune defect or whether unknown stimuli lead to the recruitment of the immune system and establishment of the disease; nor is it absolutely clear whether PsA is an extension of psoriasis in certain prone individuals. Vascular abnormalities are the earliest histopathological changes to occur in the psoriatic plaque and are also prominent in the psoriatic synovium. Espinoza et al (1982) have suggested there may be a primary vascular defect in PsA. The fact that vascular changes occur before infiltration of immunocompetent cells and are the first changes to resolve with treatment of psoriasis is likely to be significant. Abnormalities in the cellular kinetics and growth factor sensitivity of keratinocytes, fibroblasts and synoviocytes have been highlighted previously. The ability of these cells to produce growth factors and express HLA class II antigens demonstrates the potential for them to initiate and maintain inflammation. The development and possible increased incidence of PsA in patients with such profound immunodeficiency as acquired immune deficiency syndrome suggests that T helper cells do not play a significant role in the establishment of the disease (Arnett et al, 1991). Previously, many immune changes were described. Unfortunately they are non-specific and do not indicate a fundamental defect or marker of PsA. Vasey (1985) has suggested that insidious exposure to Gram-positive bacteria from the gut, tonsils and psoriatic plaques results in chronically stimulated monocytes, macrophages and dendritic cells. These cells are able to migrate throughout the body. Repeated microtrauma may result in the homing of these cells to sites of injury in the skin, synovium and tendons. Interaction with genetically hyperactive synoviocytes and keratinocytes with concomitant release of growth factors may precipitate early lesions of psoriasis and PsA. This hypothesis needs to be substantiated, but it ties together some of the varying observations seen. Many abnormal laboratory findings have been described. Unfortunately, none of the serological changes is sufficiently specific to be of great help in diagnosis. CRP levels and the ESR remain the best promise as markers of the inflammatory component of the arthritis, while other indicators correlate with certain facets of the disease pathology, but as yet have not found a true niche in the management of PsA.(ABSTRACT TRUNCATED AT 400 WORDS)