الفهرس 
Aim of the workOnly 14 pages are availabe for public view
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Abstract
Lichen planus (LP) is a chronic inflammatory disorder of the skin, hair, nail, and mucous membrane, affecting 0.2% - 5% of the population in the world. The affected cases are typically middle-aged individuals of both genders. The etiology of the disease remains obscure; however, LP is known to be a T-cell Mediated autoimmune disease, resulting in apoptotic damage of the basal keratinocytes expressing altered self-antigens on their surface.
Clusterin (CLU) was first described as a glycoprotein found nearly ubiquitous in tissues and body fluids. This knowledge is mostly related to the secretory form of CLU (sCLU), which is exported from the cell and released in secretions.
Aim of work:
In the present study, we aimed to investigate the possible relationship between serum clusterin and lichen planus. We aimed also to study the association between clusterin and lipid profile in these cases.
Subjects and methods:
This case-control study was carried out on 40 participants, 20 cases of LP who were selected form Dermatology outpatient clinic, Menoufia University Hospital, and 20 age and gender matched healthy subjects who were selected from healthy hospital staff and blood bank donors.
(kg), height (m), body mass index (BMI) (kg/m2), waist circumference (WC) (cm), blood pressure (BP) (mmHg). Metabolic syndrome was diagnosed according to the NCEP ATP III criteria. Serum CLU was evaluated by ELISA in both patients and controls. In addition to the following: fasting blood sugar (FBS), triglycerides (TG), total cholesterol (Chol), low-density lipoprotein (LDL-C), and high-density lipoprotein (HDL-C).
Results:
In the present study, we found that serum clusterin levels were decreased in patients with LP compared with controls (P= 0.016). The Mean±SD values of clusterin levels were 27.4±17.4 ng/dl and 45.8±31.9 ng/dl among cases and controls respectively.
We reported a statistical significance difference between study groups regarding MS as 25% of cases had MS against 0% of control group (P= 0.017). Moreover, blood pressure was found to be significantly higher in cases than controls (P = 0.008). In addition, there was a significant association between serum clusterin and MS (P= 0.010). We also found that hypertriglyceridemia, one of the hallmarks of MS, was more associated with LP patients than controls (P= 0.001).
Conclusion:
We can conclude that low serum CLU in LP cases could be due to the autoimmune reaction produced by Th-17 response. This decrease in CLU indicates a decrease in cytoprotection at tissue–fluid interfaces, and a decrease in inhibition of complement-mediated cell damage.
MS is more associated with LP patients since chronic inflammation has been suggested as a component of the MS with increased activity of type 1 helper T cells and cytokines such as IL-6 and TNF-α playing a key role.