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العنوان
Immunologicalaspect of atrophic rhinitis /
المؤلف
Abou Saif, Mohamed Nabil Hussain.
هيئة الاعداد
باحث / محمد نبيل حسين ابوسيف
مشرف / هاشم فؤاد
مشرف / نوال عفيفى
مشرف / احمد فتحى
الموضوع
E.N.T.
تاريخ النشر
1978.
عدد الصفحات
94 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الحنجرة
تاريخ الإجازة
1/1/1978
مكان الإجازة
جامعة بنها - كلية طب بشري - انف واذن
الفهرس
Only 14 pages are availabe for public view

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Abstract

This study included 20 patients with atrophic rhinitis
and 10 normal adults as a control group.
Besides the ordinary routine laboratory tests, both the
pathologic and control groups were subjected to the following
immunologic tests :
1. In vitro leucocyte migration test: A crude extract of
healthy adult nasal mucosa was used against the patient’s
lymphocytes in a concentration of 200 ug/ml.
2. The spontaneous rosette test: to determine the absolute
number of peripheral blood T-lymphocytes.
In the first test, eighteen out of the 20 patients (90%)
showed inhibition of leucocyte migration. One case showed
stimulation of migration and one case showed normal migration.
None of the controls showed evidence of inhibition of leucocytes
migration.
Our findings in rosette test showed a significant decrease
in the relative proportion of T-cells (percentage of
rosette forming cells) as well as in the absolute number
of T-lymphocytes in patients with atrophic rhinitis as
compared to normal control.
The absolute number of lymphocytes bears no relation
to the expression of leucocyte migration test. The test
depends on presence of functioning sensitized lymphocytes
irrespective of the total number.
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The results suggests the presence of an auto-immune mechanism
involved in the pathogenesis of atrophic rhinitis. This
altered cellular reactiVity or loss of tolerance to nasal
tissues and cells may be precipitated primarily by virus
infection, malnutrition and iron deficiency,which triggers
off a destructive auto-immune process, with the release of
antigen of nasal mucosa in the circulation. The lymphocytes
fail to recognize the liberated antigen as being self and
mount a destructive attack against them.
It has been suggested that incorporation of host antigens
into the outer coat of the viral particle may pl~ a part in
provking auto-antibodies to the altered antigens (Kleim, 1967
and Mellors et al., 1969).
Further study is needed to recognise which component of
the nasal mucosa acts as antigen towards the lymphocyte population
in patients with atrophic rhinitis as well as the
type of immunodeficiency underlying this disease. This may
serve for a better understanding of the pathogenesis of the
disease, hoping for early recognition, more effective lines
of management as well as the promise of possible prevention.
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