Search In this Thesis
   Search In this Thesis  
العنوان
Role of Clusterin in Androgenetic Alopecia /
المؤلف
Amer, Amira Mohammed.
هيئة الاعداد
باحث / أميرة محمد عامر
مشرف / علا أحمد بكرى
مشرف / شيماء الشافعي سليمان
الموضوع
Dermatology. Skin Diseases. Alopecia. Clusterin.
تاريخ النشر
2019.
عدد الصفحات
150 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الأمراض الجلدية
الناشر
تاريخ الإجازة
4/7/2019
مكان الإجازة
جامعة المنوفية - كلية الطب - الأمراض الجلدية والتناسلية
الفهرس
Only 14 pages are availabe for public view

from 158

from 158

Abstract

Androgenetic alopecia (AGA) is the most common cause of hair
loss. It is a hereditary thinning of the hair induced by androgens in
genetically susceptible men and women. This condition is also known
as male pattern hair loss or common baldness in men.
The etiology of this condition involves the interaction of genetic
and hormonal influences that result in changes in follicular
architecture and alterations of hair growth cycle.
The onset of AGA is extremely variable, and appears to be
determined by the presence of sufficient circulating androgens and the
degree of genetic predisposition. The age of onset is usually the third
and fourth decades, but the hair loss starts immediately after puberty
and continues progressively.
AGA is characterized by progressive, patterned hair loss from
the scalp. It becomes a medical problem when the hair loss is
subjectively viewed as excessive, premature and distressing.
Clinical signs are usually milder in women and associated with
diffuse thinning of the scalp hair.
Metabolic syndrome is a collection of health risks that increase
the chance of developing heart disease, stroke and diabetes. It is also
known as Syndrome X, insulin resistance syndrome and dysmetabolic
syndrome.
Various risk factors have been included in metabolic syndrome.
Factors generally accepted as being characteristic of this syndrome
include abdominal obesity, atherogenic dyslipidemia, raised blood
pressure, insulin resistance with or without glucose intolerance,
prothrombotic state, and proinflammatory state.
AGA may be associated with several diseases as metabolic
syndrome, coronary heart disease, hyperinsulenimia, insulin
resistance, hypertension, prostate cancer and benign prostatic
hyperplasia.
Clusterin (also called apolipoprotein J) is a heterodimeric
secretory glycoprotein, responsible for aiding protein folding of
secreted proteins, and its three isoforms have been differentially
implicated in pro- or antiapoptotic processes. Through this function,
CLU is involved in many diseases related to oxidative stress,
including neurodegenerative diseases, cancers, inflammatory diseases,
and aging.
In humans, clusterin is encoded by the CLU gene on
chromosome8. CLUwas first identified in ram rete testis fluid where it
showed signs of clustering with rat sertoli cells and erythrocytes,
hence its name.
It is expressed in human tissues and body fluids including
epithelial cells, smooth muscle cells and synoviocytes. CLU
expression is detected during the growth phase of the hair cycle, and
the protein is localized to the IRS of the anagen follicle.
The aim of this study was to investigate the possible association
between AGA and serum CLU and to assess the relationship between
CLU level and lipid profile and metabolic syndrome in studied
patients.
This prospective study was carried out on 30 patients presented
with androgenetic alopecia. They were selected from dermatology
outpatient clinic, Menoufia University Hospital during the period from
December 2017 to June 2018. Thirty age and gender matched
apparently healthy volunteers were also included in this study as a control group. All studied cases were subjected to complete history
taking general and dermatological examination including grading of
AGA by Hamilton-Norwood classification, calculation of BMI and
evaluation of metabolic syndrome. Blood samples were taken and sent
to Biochemistry Department, Faculty of Medicine, Menoufia
University. Serum lipids were estimated according to standard
techniques. Detection of CLU was done by ELISA.