Estimation of tissue and serum lipocalin-2 in psoriasis vulgaris and its relation to metabolic syndrome.

Adipose tissue is now considered an endocrine organ secreting different cytokines known as adipocytokines. Lipocalin-2 has been recently identified as an adipokine present in the circulation, it is related to insulin resistance, obesity, atherosclerotic diseases and type 2 diabetes. Lipocalin-2 and psoriasis are assumed to be closely associated with the metabolic syndrome. The aim of the present study is to estimate the level of lipocalin-2 in the serum and tissue of psoriatic patients and to correlate these levels with markers of metabolic syndrome, CRP and disease severity. This study was done on 30 patients of psoriasis and 30 healthy controls. All patients and controls were subjected to clinical examination. Serum, tissue levels of lipocalin-2 and C-reactive protein (CRP) were measured by enzyme linked immunosorbent assay technique. Metabolic syndrome parameters including anthropometric measures, lipid profiles, blood sugar and blood pressure were studied. Patients with psoriasis showed significant association with metabolic syndrome parameters than controls. Tissue lipocalin-2 was significantly higher than serum levels in psoriasis patients. A significant difference was detected in tissue levels of lipocalin-2 and not in the serum between patients and controls. Both tissue and serum lipocalin-2 correlated with CRP. Although there was a correlation between tissue and serum levels of lipocalin-2 in patients, there was no correlation between both of them with metabolic syndrome and related disorders. Our results revealed that patients with psoriasis are at increased risk of metabolic and cardiovascular complications, tissue lipocalin-2 is more specific to psoriasis than serum lipocalin-2. Lipocalin-2 has no role in determining severity of the disease. Neither tissue nor serum lipocalin-2 conveys cardiovascular risk in psoriasis patients.

Detection of myxovirus resistance protein A in lichen planus lesions and its relationship to hepatitis C virus.

BACKGROUND: Lichen planus (LP) is an inflammatory disease of the skin and oral mucosa. Studies suggested that type I interferons (IFNs) could play an important role in the cytotoxic inflammation in LP. Type I IFNs stimulate the production of several IFN-induced proteins including myxovirus resistance protein A (MxA protein). The association of LP and chronic hepatitis C is well established, with variable prevalence rates among different populations. Many authors have considered hepatitis C virus (HCV) as a possible antigen for inducing cytotoxic immune response in LP. OBJECTIVES: To investigate the role of type I IFNs in LP through the detection of MxA protein, and to compare the expression of MxA protein between HCV-positive and HCV-negative patients with LP in an attempt to clarify the role of HCV in the pathogenesis of LP. METHODS: The study included 33 skin biopsies from patients with LP and 10 control biopsies. MxA mRNA was detected by reverse transcription-polymerase chain reaction. HCV-specific antibodies were detected in patient sera by enzyme-linked immunosorbent assay. RESULTS: Our analysis revealed a significantly higher level of MxA protein in all the LP skin biopsies compared with controls. The expression was significantly higher in HCV-positive patients than in HCV-negative patients. CONCLUSIONS: Type I IFNs play a role in the pathogenesis of LP, and HCV could induce LP through increasing the production of type I IFNs.

The role of heat shock protein 60, vascular endothelial growth factor and antiphospholipid antibodies in Behçet disease.

BACKGROUND: Behçet disease is a systemic inflammatory disease of unknown aetiology. T cells in this disease proliferate vigorously in response to a specific peptide of heat shock protein (HSP) 60 in an antigen-specific fashion. Vascular endothelial cell growth factor (VEGF) is a cytokine participating in the inflammatory process. One of the prominent features of Behçet disease is vasculitis as a result of endothelial dysfunction. Antiphospholipid antibodies (APA) may play a role in the development of thrombosis by inhibiting production of prostacyclin by endothelial cells. OBJECTIVES: To investigate the role of HSP60, VEGF and APA in Behçet disease and their relation to clinical manifestations and disease activity. METHODS: Thirty patients with Behçet disease were included; 17 were in the active stage and 13 were in the inactive. Fifteen age- and sex-matched healthy subjects served as controls. Complete clinical examination and Doppler examination were done. Serum levels of HSP60, VEGF and APA were performed. RESULTS: Serum levels of HSP60, VEGF and APA were significantly higher in patients than in controls; however, their level did not correlate with disease activity. The serum level of VEGF correlated significantly with the presence of vascular manifestations and ocular involvement. The serum level of APA was greater in patients with thrombosis. HSP60 has an important role in aetiopathogenesis of Behçet disease, which sheds new light on its autoimmune nature. CONCLUSIONS: An elevated serum level of VEGF may be a risk factor for the development of ocular disease contributing to poor visual outcome.