lect.
(6) Dr/ Fuad Aldubai
This system is composed of 20 proteins synthesized in the liver. These
proteins are present in serum and tissue fluids except urine and CSF.
They are present in inactive form and become activated only in response
to any of the following three pathways.
Pathways of complement activation
1. Classical pathway.
2. Alternative pathway.
3. Lectin pathway.
1- Classical pathway
a) Initiated by antigen antibody complexes (IgG & IgM)
b) The reaction starts by binding of C1to Fc portion of antibody.
c) Then C4 is activated and cleaved into two fragments which are <a>
which diffuses to blood and <b> fragment that joins the preceding
complex.
d) Then C2 will be activated and cleaved also into two fragments. C2b
will join C4b to form C4b2b complex which will act as C3 convertase.
1
Dr/ Fuad Al-Dubai
e) C3 convertase cleaves C3 into C3a and C3b. C3b joins C4b2b to
form C4b2b3b complex which will act as C5 convertase.
f) C5 convertase cleaves C5 into C5a and C5b. C5b will be inserted in
the cell membrane of the microbe. C5b will then bind C6, 7, 8, 9 to
form membrane attack complex which results in disruption of the
cell and the entry of water and electrolytes into the cell leading to
its lysis.
2- Alternative pathway
1) This pathway is activated in the absence of antibodies.
2) It is initiated by binding of C3b to the surface of the microbe as
(bacterial polysaccharides). So it bypasses C1& C4 & C2
3) Factor B will then attach to C3b on the microbial surface.
4) Factor D will cleave factor B into two fragments Ba that diffuses to
the blood and Bb that remains bound to C3b to form C3bBb
complex.
5) Then properdin will attach to the above complex to form C3bBbP
complex which will act as C3 convertase.
6) C3 convertase will cleave C3 into C3a and C3b. C3b will be attached
to C3bBbP to form C3bBbP3b which will act as C5 convertase.
7) Subsequent steps are the same as classical pathway.
2
Dr/ Fuad Al-Dubai
3- Lectin pathway
A. This pathway is activated in absence of antibodies.
B. However, it is activated by binding of lectin to mannose residues on
the surface of the microbe.
C. Then this pathway proceeds through C4 and C2 in a manner
identical with the classical pathway, and the subsequent steps are
essentially the same.
3
Dr/ Fuad Al-Dubai
pathways of complement
Differences between classical and alternative pathways
1- The classical pathway is specific immunity, while alternative pathway is
innate immunity.
2- The classical pathway is initiated by antigen antibody complexes but
alternative pathway is initiated by microbial surface structures.
3- The classical pathway requires the interaction of all components but
alternative pathway does not require C1, C4, C2.
4
Dr/ Fuad Al-Dubai
4- The alternative pathway involves properdin system.
Regulation of complement system
Complement activation if left unchecked would exhaust complement
system. So regulation is achieved by:
1) The natural instability and short active life of activated components.
2) Serum inhibitors such as C1inhibitor and C3b inactivator.
Biological activities of the complement
1- Cytolysis:
Cell lysis occurs due to insertion of membrane attack complex in
the cell membrane of the microbes.
2- Opsonization:
Means microbes are phagocytosed better when coated with C3b.
This is due to presence of C3b receptors on the surface of
phagocytes.
5
Dr/ Fuad Al-Dubai
Opsonization
3- Inflammatory reaction:
C5a is chemotactic to phagocytes.
C3a, C4a, C5a are anaphylatoxins. They cause degranulation of
mast cells with release of histamine that cause vasodilatation and
promote inflammatory reactions.
4- Immune complex clearance:
6
Dr/ Fuad Al-Dubai
Immune complexes with C3b on their surfaces become bound to
C3b receptors on RBCs and are carried to liver and spleen where
they are removed.
5- Enhancement of antibody response:
Binding of C3d (C3b breakdown product) to B cells increases
antibody production. Patients with C3 deficiency are susceptible to
infections.
7
Dr/ Fuad Al-Dubai
major histocompatibility (MHC) antigens
Dr/ Fuad Aldubai
Transplantation
is grafting tissues from one individual to another or from one place to
another in the same individual.
The main problem in organ transplantation is the occurrence of graft
rejection.
Graft rejection is due the presence of tissue antigens that differ from
one to another, thus stimulating immune response that causes rejection.
These tissue antigens are known as human leukocyte antigens (HLA) or
major histocompatibility (MHC) antigens.
These antigens are genetically determined by MHC genes which are
present on chromosome 6.
There are 3 classes of MHC genes (Class I, II, III).
MHC antigens class I
1- Class I antigens are 3 types (HLA-A, HLA-B, HLA-C).
2- There are about 20 different antigenic types of HLA-A, 50 for HLA-B, 8
for HLA-C.
3- They are present on all nucleated cells.
In virally infected cells, viral antigens are expressed on cell surface in
association with class I MHC antigens. This association activates CD8 T
cells that will kill virus infected cells. This is known as MHC restriction.
Class I antigens are typed by microcytotoxicity assay using host leucocytes,
specific antibodies and complement.
MHC antigens class II
1- Class II antigens are called HLA-D antigens.
2- HLA-D includes HLA-DR, HLA-DQ and HLA-DP.
3- There are about 6 antigenic types for HLA-DP, 9 for HLA-DQ and 20 for
HLA-DR.
4- Class II antigens are present only on the surface of antigen presenting
cells and activated T cells.
5- CD4 T helper cells recognize antigens on the surface of APCs only if
they are associated with class II antigens (MHC restriction).
Class II antigens can be typed by mixed lymphocyte reaction (MLR).
MHC antigens class III
1- Class III MHC genes are involved in production of complement
proteins (C2, C4)
2- They have no relation with graft rejection.
3- Significance of MHC antigens
4- Transplantation and graft rejection
5- CD4 T cells + MHC class II
6- CD8 T cells + MHC class I
7- Paternity testing
8- Association with diseases:
- SLE is associated with HLA-DR3
- Rheumatoid arthritis + HLA-DR4
أ .ﻣﺮض اﻟﺬﺋﺒﺔ اﻟﺤﻤﺮاء Systemic lupus Erythematosis
ﻳﻌﺪ ﻣﺮض اﻟﺬﺋﺒﺔ اﻟﺤﻤﺮاء ،ﻣﻦ أﺷﻬﺮ أﻣﺮاض اﻟﻤﻨﺎﻋﺔ اﻟﺬاﺗﻴﺔ ،وﻳﺼﻴﺐ ﻫﺬا اﻟﻤﺮض اﻟﺠﻠﺪ
وﻳﺤﺪث ﺧﻠﻼ ً ﻓﻲ ﻣﻌﻈﻢ أﻋﻀﺎء اﻟﺠﺴﻢ .وﻧﺴﺒﺔ اﻹﺻﺎﺑﺔ ﺑﻪ ﻓﻲ اﻹﻧﺎث ،أرﺑﻌﺔ أﺿﻌﺎف ﻧﺴﺒﺘﻬﺎ
ﻓﻲ اﻟﺬﻛﻮر .وﻫﻮ ﻳﺘﻤﻴﺰ ﺑﻔﺘﺮات ﻧﺸﺎط ،ﺗﻌﻘﺒﻬﺎ ﻓﺘﺮات ﻗﺪ ﻳﺘﺤﺴﻦ ﻓﻴﻬﺎ اﻟﻤﺮﻳﺾ ،وﺗﻘﻞ ﺣﺪة
اﻟﻤﺮض.
) (1اﻟﺘﻔﺴﻴﺮ اﻟﻤﻨﺎﻋﻲ ﻟﻠﺬﺋﺒﺔ اﻟﺤﻤﺮاء
ُﻳﻌﺰى ﺣﺪوث ﻫﺬا اﻟﻤﺮض إﻟﻰ وﺟﻮد أﺟﺴﺎم ﻣﻀﺎدة ﻟﻠﺤﺎﻣﺾ اﻟﻨﻮوي .DNAﻓﻲ ﺟﺴﻢ
اﻟﻤﺮﻳﺾ ،وﻛﺬﻟﻚ وﺟﻮد ﺧﻼﻳﺎ ذات ﺷﻜﻞ ﺧﺎص ﺗﺤﺖ اﻟﻤﺠﻬﺮ ،ﺳﻤﻴﺖ :ﺧﻼﻳﺎ اﻟﺬﺋﺒﺔ اﻟﺤﻤﺮاء
،Lupus Erythematosis cellsوﺗﺨﺘﺼﺮ .L.E. cellsوﺗﻮﺟﺪ ﻫﺬه اﻷﺟﺴﺎم اﻟﻤﻀﺎدة ﻓﻲ
اﻟﺪم ،واﻷﻧﺴﺠﺔ اﻟﻤﺼﺎﺑﺔ ،ﻣﺜﻞ اﻟﺠﻠﺪ ،واﻟﻜﻠﻰ .وﻟﻢ ُﻳﻌﺮف ،ﺣﺘﻰ اﻵن ،ﺳﺒﺐ وﺟﻮد ﻫﺬا اﻟﺠﺴﻢ
اﻟﻤﻀﺎد ﻟﻠﺤﺎﻣﺾ اﻟﻨﻮوي ،اﻟﺬي ﻳﺴﻤﻰ .Anti- DNAﻛﻤﺎ اﻛﺘﺸﻔﺖ أﺟﺴﺎم ﻣﻀﺎدة أﺧﺮى ،ﺿﺪ
ﻛﺮات اﻟﺪم اﻟﺤﻤﺮاء ،واﻟﺒﻴﻀﺎء واﻟﺼﻔﺎﺋﺢ اﻟﺪﻣﻮﻳﺔ .وﻳﺆدي ذﻟﻚ إﻟﻰ ﺣﺪوث ﻧﺰﻳﻒ وأﻧﻴﻤﻴﺎ.
ﺗﻌﺪ زﻳﺎدة اﻹﺻﺎﺑﺔ ﻓﻲ ﺑﻌﺾ اﻷﻓﺮاد ،واﻟﻌﺎﺋﻼت ،دﻟﻴﻞ ﻋﻠﻰ اﻻﺳﺘﻌﺪاد اﻟﻮراﺛﻲ ﻟﻠﻤﺮض ،وذﻟﻚ
ﻓﻲ ﺑﻌﺾ اﻟﺤﺎﻻت ،اﻟﺘﻲ ﺗﺤﺘﻮي ﻋﻠﻰ ﻧﻮع ﻣﻌﻴﻦ ﻣﻦ اﻟﺒﺼﻤﺔ ،أو اﻟﺸﻔﺮة اﻟﺠﻴﻨﻴﺔ.
أﺛﺒﺘﺖ اﻷﺑﺤﺎث أن ﻫﺮﻣﻮن اﻷﻧﻮﺛﺔ ،Estrogen Hormoneﻳﺴﺎﻋﺪ ﻋﻠﻰ ﺗﻜﻮﻳﻦ اﻷﺟﺴﺎم
اﻟﻤﻀﺎدة ﻟﻠﺤﻤﺾ اﻟﻨﻮوي ،ﻛﻤﺎ ﻳﺴﺎﻋﺪ ،ﻛﺬﻟﻚ ،ﻋﻠﻰ زﻳﺎدة ﺣﺪة اﻷﻋﺮاض .وﻋﻠﻰ اﻟﻌﻜﺲ ﻣﻦ ذﻟﻚ،
ن ﻫﺮﻣﻮﻧﺎت اﻟﺬﻛﻮرة ،Androgensﺗﻘﻠﻞ ﻣﻦ ﺗﻜّﻮن اﻷﺟﺴﺎم اﻟﻤﻀﺎدة ﻟﻠﺤﺎﻣﺾ اﻟﻨﻮوي .وﻫﺬا
ﻓﺈ ّ
ﻳﻔﺴﺮ ﺣﺪوث اﻟﻤﺮض ﻓﻲ اﻹﻧﺎث ،ﺑﺪرﺟﺔ أﻛﺒﺮ ﻣﻦ ﺣﺪوﺛﻪ ﻓﻲ اﻟﺬﻛﻮر.
) (2اﻷﻋﺮاض
)أ( اﻟﺠﻠﺪ
ُﺗﻌﺪ إﺻﺎﺑﺔ اﻟﺠﻠﺪ ﻫﻲ اﻷﻛﺜﺮ ﺷﻴﻮﻋًﺎ ﻋﻦ ﺑﺎﻗﻲ اﻷﻋﻀﺎء ،وﺗﻈﻬﺮ ﻋﻠﻰ ﻫﻴﺌﺔ ﺑﻘﻊ ﺣﻤﺮاء ﻣﻐﻄﺎة ﺑﻘﺸﺮ
رﻗﻴﻘﺔ ﻋﻠﻰ اﻟﺨﺪﻳﻦ ،واﻷﻧﻒ .وﺗﺰداد ﻫﺬه اﻟﺒﻘﻊ ﻋﻨﺪ اﻟﺘﻌﺮض ﻟﻠﺸﻤﺲ ،وﺗﺄﺧﺬ أﺣﻴﺎﻧﺎ ﺷﻜﻞ
اﻟﻔﺮاﺷﺔ ،Butterfly Shapeأي ﻳﻌﺪ اﻷﻧﻒ ﻫﻮ ﺟﺴﻢ اﻟﻔﺮاﺷﺔ ،واﻟﺒﻘﻊ ﻋﻠﻰ اﻟﺨﺪﻳﻦ ﺗﻤﺜﻞ
أﺟﻨﺤﺘﻬﺎ .وﻗﺪ ﺗﺨﺘﻔﻲ ﻫﺬه اﻟﺒﻘﻊ ﺑﻼ أﺛﺮ ،وﻗﺪ ﺗﺴﺒﺐ ﻧﺪﺑﺔ ﺑﺴﻴﻄﺔ ﺑﺎﻟﺠﻠﺪ.
)ب( اﻟﻤﻔﺎﺻﻞ واﻟﻌﻀﻼت
ُﺗﻌﺪ إﺻﺎﺑﺔ اﻟﻤﻔﺎﺻﻞ واﻟﻌﻀﻼت ،وﺣﺪوث آﻻم ﺑﻬﺎ ،ﻣﻦ أﻛﺜﺮ أﻋﺮاض ﻣﺮض اﻟﺬﺋﺒﺔ اﻟﺤﻤﺮاء
ﺣﺪوﺛًﺎ .وﻫﻲ ﺗﺼﻴﺐ ﻛﺎﻓﺔ ﻣﻔﺎﺻﻞ اﻟﺠﺴﻢ.
)ج( اﻷﻏﺸﻴﺔ اﻟﺒﻠﻮرﻳﺔ واﻟﺒﺮوﺗﻴﻨﻴﺔ
ُﻳﺤﺪث ﻣﺮض اﻟﺬﺋﺒﺔ اﻟﺤﻤﺮاء ،اﻟﺘﻬﺎﺑًﺎ ﺑﺎﻟﻐﺸﺎء اﻟﺒﻠﻮري اﻟﻤﺤﻴﻂ ﺑﺎﻟﺮﺋﺔ ،وﻳﺼﺎﺣﺒﻪ أﻟﻢ وﺻﻌﻮﺑﺔ ﻓﻲ
اﻟﺘﻨﻔﺲ؛ ﻛﺬﻟﻚ ﻳﺤﺪث اﻟﺘﻬﺎب ﻓﻲ اﻟﻐﺸﺎء اﻟﻤﺒﻄﻦ ﻟﻠﻘﻠﺐ ،ﻳﺴﺒﺐ ﻫﺒﻮﻃًﺎ ﺣﺎدًا ﺑﺎﻟﻘﻠﺐ .ﻛﻤﺎ ﻳﻤﻜﻦ
أن ﻳﺼﻞ اﻻﻟﺘﻬﺎب إﻟﻰ اﻟﻐﺸﺎء اﻟﺒﺮﻳﺘﻮﻧﻲ اﻟﻤﺤﻴﻂ ﺑﺎﻷﻣﻌﺎء ،وﻳﺼﺎﺣﺐ ذﻟﻚ أﻟﻢ ﺑﺎﻟﺒﻄﻦ ،وﻗﻲء
ﻣﺴﺘﻤﺮ ،ﻗﺪ ﻳﺆدي إﻟﻰ اﻟﻮﻓﺎة ،ﻣﺎ ﻟﻢ ﻳﻌﺎﻟﺞ ﻓﻮرًا.
)د( اﻟﻜﻠﻰ واﻟﺠﻬﺎز اﻟﻌﺼﺒﻲ
ﺤِﺪث ﺗﺮﺳﻴﺐ ﻟﻠﻤﺮﻛﺒﺎت اﻟﻤﻨﺎﻋﻴﺔ ﺑﺄﻧﺴﺠﺔ اﻟﻜﻠﻰ ،ﻣﻤﺎ ﻳﺴﺒﺐ ﻓﺸﻼ ً ﻛﻠﻮﻳًﺎ وارﺗﻔﺎﻋًﺎ ﻓﻲ ُﻳ ْ
اﻟﻀﻐﻂ .وﻛﺬﻟﻚ ﻗﺪ ُﻳﺤﺪث ﺗﺮﺳﻴﺐ ﻟﻬﺬه اﻟﻤﺮﻛﺒﺎت اﻟﻤﻨﺎﻋﻴﺔ ﻓﻲ اﻟﻤﺦ ،ﻣﺴﺒﺒﺔ ،اﻛﺘﺌﺎﺑًﺎ ،وﺻﺪاﻋًﺎ
ﻧﺼﻔﻴًﺎ أو ﺷﻠﻼ ً.
)هـ( اﻹﺟﻬﺎض اﻟﻤﺘﻜﺮر
ُﻳﻌﺪ ﺣﺪوث إﺟﻬﺎض ﻣﺘﻜﺮر ،دون ﺳﺒﺐ واﺿﺢ ،أﺣﺪ أﻋﺮاض ﻫﺬا اﻟﻤﺮض .وُﻳﻨﺼﺢ ﺑﻌﺪم إﻗﺪام
اﻟﻤﺼﺎﺑﺎت ﺑﻬﺬا اﻟﻤﺮض ،ﻋﻠﻰ اﻟﺤﻤﻞ ،ﻟﺨﻄﻮرﺗﻪ ﻋﻠﻰ ﻗﻠﺐ وﺻﺤﺔ اﻟﺠﻨﻴﻦ واﻷم.
) (3اﻟﺘﺸﺨﻴﺺ اﻟﻤﻌﻤﻠﻲ
)أ( ﺳﺮﻋﺔ اﻟﺘﺮﺳﻴﺐ Erythrocyte Sedimentation Rate: ESRﺗﻜﻮن ﻋﺎﻟﻴﺔ ﻓﻲ ﻣﻌﻈﻢ
اﻟﺤﺎﻻت ،وﺗﺪل ﻋﻠﻰ وﺟﻮد ﻧﺸﺎط زاﺋﺪ ﻓﻲ اﻟﺠﻬﺎز اﻟﻤﻨﺎﻋﻲ.
)ب( أﻧﻴﻤﻴﺎ ﻟﻜﻞ ﻣﻜﻮﻧﺎت اﻟﺪم :Pancytopeniaﺗﺘﻤﻴﺰ ﺑﺤﺪوث ﻧﻘﺺ ﻓﻲ ﻋﺪد ﻛﺮات اﻟﺪم
اﻟﺤﻤﺮاء ،وﻧﻘﺺ ﻓﻲ ﻋﺪد ﻛﺮات اﻟﺪم اﻟﺒﻴﻀﺎء ،وﻧﻘﺺ ﻓﻲ ﻋﺪد اﻟﺼﻔﺎﺋﺢ اﻟﺪﻣﻮﻳﺔ.
)ج( إﺟﺮاء اﺧﺘﺒﺎرات ﺧﺎﺻﺔُ :ﻳﺮاد ﺑﻬﺎ اﻟﻜﺸﻒ ﻋﻦ اﻷﺟﺴﺎم اﻟﻤﻀﺎدة ﻟﻠﺤﺎﻣﺾ اﻟﻨﻮوي ،DNA
وﻛﺬﻟﻚ اﻷﺟﺴﺎم اﻟﻤﻀﺎدة ﻟﻌﻮاﻣﻞ اﻟﺘﺠﻠﻂ وﻛﺮات اﻟﺪم اﻟﺤﻤﺮاء.
)د( ﻗﻴﺎس ﻣﻌﺎﻣﻞ اﻟﺮوﻣﺎﺗﻮﻳﺪ :Rheumatoid factorﻳﻮﺟﺪ ﻫﺬا اﻟﻤﻌﺎﻣﻞ ،ﻓﻲ ﺑﻌﺾ أﻧﻮاع
اﻟﺮوﻣﺎﺗﻮﻳﺪ ،وﺗﺴﻤﻰ "ﻣﻌﺎﻣﻞ اﻟﺮوﻣﺎﺗﻮﻳﺪ اﻟﻤﻮﺟﺒﺔ" ،وﻓﻲ ﺣﺎﻟﺔ ﻋﺪم وﺟﻮده ،ﺗﺴﻤﻰ "ﻣﻌﺎﻣﻞ
اﻟﺮوﻣﺎﺗﻮﻳﺪ اﻟﺴﺎﻟﺒﺔ" .وﻳﺴﺘﺨﺪم ﻫﺬا اﻟﻤﻌﺎﻣﻞ ﻟﺘﻘﺴﻴﻢ أﻧﻮاع اﻟﺮوﻣﺎﺗﻮﻳﺪ .وﻗﺪ ﺛﺒﺖ أن %30ﻣﻦ
ﺣﺎﻻت اﻟﺬﺋﺒﺔ اﻟﺤﻤﺮاء ،ﺗﻜﻮن إﻳﺠﺎﺑﻴﺔ ﻟﻬﺬا اﻟﻤﻌﺎﻣﻞ.
) (4اﻟﻌﻼج
)أ( ﻋﻼج ﻋﺎم
وﻳﺸﻤﻞ إﻋﻄﺎء اﻟﻔﻴﺘﺎﻣﻴﻨﺎت ،وﻋﻼج ارﺗﻔﺎع اﻟﺤﺮارة ،وﺗﻨﺎول ﻣﻬﺪﺋﺎت ﻵﻻم اﻟﻤﻔﺎﺻﻞ ،وﻋﻼج
اﻟﻤﻀﺎﻋﻔﺎت ،ﻣﺜﻞ أﻣﺮاض اﻟﻘﻠﺐ واﻟﺮﺋﺔ ،ﺣﺴﺐ درﺟﺔ اﻹﺻﺎﺑﺔ اﻟﻨﺎﺗﺠﺔ.
)ب( ﻋﻼج ﻣﺘﺨﺼﺺ
وﻳﺸﻤﻞ اﺳﺘﺨﺪام اﻷﺳﺒﺮﻳﻦ ،وﺑﻌﺾ اﻷدوﻳﺔ اﻟﻤﺴﺘﺨﺪﻣﺔ ﻓﻲ ﻋﻼج اﻟﻤﻼ رﻳﺎ ،اﻟﺘﻲ ﺛﺒﺘﺖ ﻓﺎﺋﺪﺗﻬﺎ
ﻓﻲ ﻋﻼج ﺑﻌﺾ ﺣﺎﻻت اﻟﺬﺋﺒﺔ اﻟﺤﻤﺮاء .وﻛﺬﻟﻚ اﺳﺘﺨﺪام ﻣﺮﻛﺒﺎت ﻏﻴﺮ ﻛﻮرﺗﻴﺰوﻧﻴﺔ .ﺛﻢ ﻳﺄﺗﻲ
اﻟﻌﻼج اﻟﺤﺎﺳﻢ ﻟﻤﻌﻈﻢ ﻫﺬه اﻟﺤﺎﻻت ﺑﺎﺳﺘﺨﺪام ﻣﺮﻛﺒﺎت اﻟﻜﻮرﺗﻴﺰون ،إﻣﺎ ﻣﻮﺿﻌﻴًﺎ ﻋﻠﻰ اﻟﺠﻠﺪ
اﻟﻤﺼﺎب ،أو ﻋﻦ ﻃﺮﻳﻖ ﺟﺮﻋﺎت ﺑﺎﻟﻔﻢ ،أو اﻟﺤﻘﻦ ،ﻣﻊ اﻟﺘﻘﻠﻴﻞ اﻟﺘﺪرﻳﺠﻲ ﻟﻬﺬه اﻟﺠﺮﻋﺎت ﻋﻨﺪ
ﺗﺤﺴﻦ اﻟﺤﺎﻟﺔ.
ﻣﻼﺣﻈﺔ :اﺳﺘﺨﺪام ﻣﺮﻛﺒﺎت اﻟﻜﻮرﺗﻴﺰون ﻳﺆدى إﻟﻰ إﺿﻌﺎف اﻟﺠﻬﺎز اﻟﻤﻨﺎﻋﻲ.
ب .ﻣﺮض اﻟﺮوﻣﺎﺗﻮﻳﺪ Rheumatoid Arthritis
ُﻳﻌﺪ اﻟﺮوﻣﺎﺗﻮﻳﺪ ﻣﻦ اﻷﻣﺮاض اﻟﻤﺰﻣﻨﺔ ،وﻫﻮ ﻳﺼﻴﺐ ﻣﻔﺎﺻﻞ اﻟﺠﺴﻢ اﻟﻤﺨﺘﻠﻔﺔ ﺑﺼﻮرة أﺳﺎﺳﻴﺔ،
وﻟﻜﻨﻪ ﻳﺼﻴﺐ ،ﻛﺬﻟﻚ ،أﺟﻬﺰة أﺧﺮى ،ﻣﺜﻞ :اﻟﺠﻬﺎز اﻟﻌﺼﺒﻲ ،واﻟﺠﻬﺎز اﻟﺒﻮﻟﻲ ،واﻟﺠﻬﺎز اﻟﺪوري .وﻣﺜﻞ
ﻣﻌﻈﻢ أﻣﺮاض اﻟﻤﻨﺎﻋﺔ اﻟﺬاﺗﻴﺔ.
وُﺗﻌﺪ اﻟﻤﻔﺎﺻﻞ اﻟﺼﻐﺮى ﺑﺎﻟﻜﻔﻴﻦ واﻟﻘﺪﻣﻴﻦ ،ﻣﻦ أﻛﺜﺮ اﻟﻤﻔﺎﺻﻞ ﺗﻌﺮﺿًﺎ ﻟﻺﺻﺎﺑﺔ ﺑﻬﺬا اﻟﻤﺮض،
اﻟﺬي ﻳﻤﺘﺪ ﻟﻴﺸﻤﻞ ﺑﺎﻗﻲ اﻟﻤﻔﺎﺻﻞ .وﻗﺪ ﻳﺆدي أﺣﻴﺎﻧًﺎ إﻟﻰ ﺣﺪوث اﻟﺘﻬﺎﺑﺎت ﺑﺎﻷوﻋﻴﺔ اﻟﺪﻣﻮﻳﺔ ،أو
اﻷوﻋﻴﺔ واﻟﻐﺪد اﻟﻠﻴﻤﻔﺎوﻳﺔ .وﻛﺬﻟﻚ ﻳﺤﺪث ﻧﻘﺼًﺎ ﻓﻲ ﻛﺮات اﻟﺪم اﻟﺒﻴﻀﺎء ،وﺗﻀﺨﻤًﺎ ﻓﻲ اﻟﻄﺤﺎل.
يﻋﺰى ﺣﺪوث ﻣﺮض اﻟﺮوﻣﺎﺗﻮﻳﺪ إﻟﻰ اﻻﺳﺘﻌﺪاد اﻟﻮراﺛﻲ ،واﻟﺒﺼﻤﺔ اﻟﺠﻴﻨﻴﺔ ،أو إﻟﻰ وﺟﻮد ﻧﻮع و ُ
ﻣﻌﻴﻦ ﻣﻦ ﻓﺼﺎﺋﻞ اﻟﺨﻼﻳﺎ اﻟﺒﻴﻀﺎء ،ﺣﻴﺚ ﻟﻮﺣﻆ ذﻟﻚ ﻓﻲ ﻛﺜﻴﺮ ﻣﻦ اﻟﻤﺮﺿﻰ .ﻛﻤﺎ أﺛﺒﺖ ﺑﻌﺾ
اﻟﻌﻠﻤﺎء وﺟﻮد ﻋﻼﻗﺔ ﺑﻴﻦ ﻣﺮض اﻟﺮوﻣﺎﺗﻮﻳﺪ ،وﺑﻴﻦ اﻹﺻﺎﺑﺔ ﺑﻨﻮع ﻣﻌﻴﻦ ﻣﻦ اﻟﻔﻴﺮوﺳﺎت أو
اﻟﺒﻜﺘﺮﻳﺎ.
) (1اﻟﺘﻐﻴﺮات اﻟﻤﻨﺎﻋﻴﺔ ،اﻟﻤﺆدﻳﺔ إﻟﻰ ﺣﺪوث اﻷﻋﺮاض
ُﺗﻔﺮز اﻟﺨﻼﻳﺎ اﻟﻠﻴﻤﻔﺎوﻳﺔ اﻟﻤﻮﺟﻮدة ﺑﺎﻟﻤﻔﺼﻞ ،أﺟﺴﺎﻣًﺎ ﻣﻀﺎدةُ ،ﺗﺴﻤﻰ "ﻋﺎﻣﻞ اﻟﺮوﻣﺎﺗﻮﻳﺪ"
،Rheumatoid Factorﻳﻌﺪه اﻟﺠﺴﻢ ﻏﺮﻳﺒًﺎ ﻋﻨﻪ ،ﻓﻴﻔﺮز اﻟﺠﻬﺎز اﻟﻤﻨﺎﻋﻲ أﺟﺴﺎﻣًﺎ ﻣﻀﺎدة ﻣﻦ
اﻟﻨﻮع .IgG ,IgMوﺗﺘﺤﺪ اﻷﺟﺴﺎم اﻟﻤﻀﺎدة ﻣﻊ ﻋﺎﻣﻞ اﻟﺮوﻣﺎﺗﻮﻳﺪ ،ﻣﻜﻮﻧﺔ ﻋﻘﺪًا ﻣﻨﺎﻋﻴﺔ ﺑﺮوﺗﻴﻨﻴﺔ،
ﺗﺘﺮﺳﺐ ﻓﻲ ﺧﻼﻳﺎ اﻟﻐﺸﺎء أﻟﺰﻻﻟﻲ ﻟﻠﻤﻔﺼﻞ .Synovial Membrane
وﻳﻌﻤﻞ ﻫﺬا اﻟﺘﺮﺳﻴﺐ ،ﻋﻠﻰ ﺗﻨﺸﻴﻂ اﻟﻤﺮﻛﺐ أﻟﺒﺮوﺗﻴﻨﻲ اﻟﻤﻜﻤﻞ ،The complementوﺗﻔﺮز
ﻣﻮاد وﻧﻮاﺗﺞ ﻟﻬﺬا اﻟﺘﻔﺎﻋﻞ ،ﺗﺠﺬب ﻛﺮات اﻟﺪم اﻟﺒﻴﻀﺎء ،وﻳﺰداد اﻻﻟﺘﻬﺎب ،وﻳﺰداد إﻓﺮاز اﻟﻤﻮاد،
واﻷﻧﺰﻳﻤﺎت واﻟﺘﻔﺎﻋﻞ ،ﻣﻊ ﻋﺎﻣﻞ اﻟﺮوﻣﺎﺗﻮﻳﺪ ،ﻓﺘﺘﻜﻮن ﻋﻘﺪ ﻣﻨﺎﻋﻴﺔ ﺟﺪﻳﺪة ،ﺗﺘﺮﺳﺐ ﻓﻲ اﻟﻤﻔﺼﻞ،
ﻣﺎ ﻳﺴﺒﺐ أﻟﻤًﺎ ﺷﺪﻳﺪًا ﻓﻴﻪ ،ﺧﺼﻮﺻًﺎ ﻋﻨﺪ اﻟﺤﺮﻛﺔ .وﻣﻊ اﺳﺘﻤﺮار ﻋﻤﻠﻴﺔ اﻟﺘﺮﺳﻴﺐ ﻫﺬه ،ﻳﺼﺒﺢ
ﺳﻄﺢ اﻟﻌﻈﺎم ﻋﺎرﻳًﺎ ﻣﻦ اﻟﻐﻀﺎرﻳﻒ ،اﻟﺘﻲ ﺗﺤﻤﻰ ﻧﻬﺎﻳﺎت اﻟﻌﻈﺎم ﻣﻦ اﻻﺣﺘﻜﺎك ،ﺑﻌﻀﻬﺎ ﺑﺒﻌﺾ،
وﻳﺤﺪث ﺗﻀﺨﻢ ﻓﻲ ﺣﺠﻢ اﻟﻤﻔﺼﻞ ،وارﺗﺨﺎء ﻓﻲ اﻷرﺑﻄﺔ اﻟﻤﺤﻴﻄﺔ ﺑﻪ ،وﻳﻨﺘﻬﻲ اﻟﻤﺮض ﺑﺤﺪوث
ﺗﺸﻮﻫﺎت ﻓﻲ اﻟﻤﻔﺎﺻﻞ.
) (2اﻷﻋﺮاض
ﻏﺎﻟﺒﻴﺔ اﻟﻤﺼﺎﺑﻴﻦ ﺑﻤﺮض اﻟﺮوﻣﺎﺗﻮﻳﺪ ،ﻣﻦ ﻣﺘﻮﺳﻄﻲ اﻟﻌﻤﺮ ﺑﻴﻦ 40-20ﻋﺎﻣًﺎ .وﺗﺒﺪأ اﻟﺸﻜﻮى
ﺑﺄﻋﺮاض ﻋﺎﻣﺔ ،ﻣﺜﻞ اﻟﺸﻌﻮر ﺑﺎﻹرﻫﺎق ،وﻓﻘﺪ اﻟﺸﻬﻴﺔ ،واﻟﻮزن ،ﻣﻊ ارﺗﻔﺎع ﻃﻔﻴﻒ ﻓﻲ اﻟﺤﺮارة.
وﻳﺒﺪأ اﻟﺸﻌﻮر ﺑﺘﻴﺒﺲ ﻓﻲ اﻟﻤﻔﺼﻞ ،أو ﺣﺪوث أﻟﻢ ﻋﻨﺪ اﻟﺤﺮﻛﺔ ،ﺧﺼﻮﺻًﺎ ﻓﻲ اﻟﺼﺒﺎح .ﺛﻢ ﻳﺒﺪأ
اﻟﺘﻴﺒﺲ ،واﻷﻟﻢ ﻓﻲ اﻟﺘﺤﺴﻦ ﻣﻊ اﻟﺤﺮﻛﺔ أﺛﻨﺎء اﻟﻨﻬﺎر .وأﻫﻢ ﻣﺎ ﻳﻤﻴﺰ أﻋﺮاض آﻻم اﻟﻤﻔﺎﺻﻞ ﻟﻤﺮﺿﻰ
اﻟﺮوﻣﺎﺗﻮﻳﺪ ،ﻋﻦ ﻏﻴﺮه ﻣﻦ آﻻم اﻟﻤﻔﺎﺻﻞ وأﻣﺮاﺿﻬﺎ ،ﻫﻮ ﺣﺪوث اﻷﻟﻢ ﻓﻲ اﻟﺼﺒﺎح ،وﺗﺤﺴﻨﻪ ،ﺑﻌﺪ
ذﻟﻚ.وﻛﺬﻟﻚ ﺣﺪوث ﺗﻮرم ،واﺣﻤﺮار ،وﺳﺨﻮﻧﺔ ،ﻓﻲ اﻟﻤﻔﺼﻞ .ﻛﻤﺎ أن اﻹﺻﺎﺑﺔ ﺗﺒﺪأ ﻓﻲ ﻣﻌﻈﻢ
اﻟﺤﺎﻻت باﻟﻤﻔﺎﺻﻞ اﻟﺼﻐﺮى ،ﻣﺜﻞ أﺻﺎﺑﻊ اﻟﻴﺪ ،واﻟﺮﺳﻐﻴﻦ ،وﺗﺤﺪث ﻓﻲ اﻟﻨﺎﺣﻴﺔ اﻟﻴﻤﻨﻰ ،واﻟﻴﺴﺮى
ﻣﻌًﺎ وﺑﺎﻟﺪرﺟﺔ ﻧﻔﺴﻬﺎ .وﺗﺴﺘﻤﺮ إﺻﺎﺑﺔ اﻟﻤﻔﺎﺻﻞ ﻟﻤﺮﻳﺾ اﻟﺮوﻣﺎﺗﻮﻳﺪ ،ﻓﺘﺼﻞ إﻟﻰ ﻣﻔﺎﺻﻞ اﻟﻔﺨﺬ
واﻟﺮﻛﺒﺘﻴﻦ واﻟﻘﺪﻣﻴﻦ واﻟﻜﺘﻔﻴﻦ واﻟﻜﻮع ،ﺑﻞ ﻗﺪ ﺗﺼﻞ إﻟﻰ اﻟﻔﻘﺮات اﻟﻌﻨﻘﻴﺔ ،أﻣﺎ ﺑﺎﻗﻲ اﻟﻔﻘﺮات ﻓﻼ
ﺗﺘﻌﺮض ﻟﻺﺻﺎﺑﺔ .وﻗﺪ ﻳﻤﺘﺪ ﺗﺄﺛﻴﺮ اﻟﻤﺮض إﻟﻰ أﺟﻬﺰة أﺧﺮى ﻓﻲ اﻟﺠﺴﻢ ،ﻣﺜﻞ:
ا ﻟ ﻘﻠ ﺐ )(1
ﻳﺼﺎﺣﺐ ﻣﺮض اﻟﺮوﻣﺎﺗﻮﻳﺪ ،اﻟﺘﻬﺎب ﻓﻲ اﻟﺠﺰء اﻟﺨﺎرﺟﻲ ﻟﻌﻀﻠﺔ اﻟﻘﻠﺐ ،Pericardiumوﻧﺘﻴﺠﺔ
ﻟﺬﻟﻚ ﻗﺪ ﻳﺤﺪث ارﺗﺸﺎح Effusionﻓﻲ اﻟﻐﺸﺎء اﻟﻤﺤﻴﻂ ﺑﺘﻠﻚ اﻟﻌﻀﻠﺔ Pericardial
،Membraneﻣﺎ ﻳﺆدي إﻟﻰ أﻟﻢ ﻓﻲ اﻟﺼﺪر ،وارﺗﻔﺎع ﻓﻲ اﻟﺤﺮارة ،وﺳﺮﻋﺔ ﻓﻲ اﻟﺘﻨﻔﺲ.
) (2اﻟﺠﻬﺎز اﻟﺘﻨﻔﺴﻲ
ﻳﺤﺪث اﻟﺘﻬﺎب ﻓﻲ اﻟﻐﺸﺎء اﻟﺒﻠﻮري اﻟﻤﺒﻄﻦ ﻟﻠﺮﺋﺔ ،واﻧﺴﻜﺎب ﺑﻠﻮري ،ﻣﺎ ﻳﺆدي إﻟﻰ ﺿﻴﻖ ﻓﻲ
اﻟﺘﻨﻔﺲ.
)ج( اﻷوﻋﻴﺔ اﻟﺪﻣﻮﻳﺔ
ﺗﺘﺮﺳﺐ اﻟﻌﻘﺪ اﻟﻤﻨﺎﻋﻴﺔ اﻟﺒﺮوﺗﻴﻨﻴﺔ ﻓﻲ ﺟﺪر اﻷوﻋﻴﺔ اﻟﺪﻣﻮﻳﺔ ،أو داﺧﻠﻬﺎ ،ﻣﺤﺪﺛﺔ ﻗﺼﻮرًا ﻓﻲ
وﺻﻮل اﻟﺪم إﻟﻰ ﺑﻌﺾ اﻷﺟﻬﺰة اﻟﺤﻴﻮﻳﺔ ،ﻣﺜﻞ اﻟﻘﻠﺐ ،ﻓﺘﺴﺒﺐ ذﺑﺤﺔ ﺻﺪرﻳﺔ ،أو اﻟﻜﻠﻰ ،ﻓﺘﺆدي
إﻟﻰ ﻓﺸﻞ ﻛﻠﻮي ﺣﺎد ،أو اﻟﺠﻬﺎز اﻟﻬﻀﻤﻲ ،ﻣﺤﺪﺛﺔ اﻧﺴﺪادًا ﻣﻌﻮﻳًﺎ.
)د( اﻟﺠﻠﺪ
وﺗﺘﺮﺳﺐ اﻟﻌﻘﺪ اﻟﺒﺮوﺗﻴﻨﻴﺔ اﻟﻤﻨﺎﻋﻴﺔ ﺗﺤﺖ اﻟﺠﻠﺪ ،ﻓﻲ اﻟﻤﻨﺎﻃﻖ اﻟﻤﻌﺮﺿﺔ ﻟﻠﻀﻐﻂ واﻻﺣﺘﻜﺎك ،ﻣﺜﻞ
أﺳﻔﻞ اﻟﻜﻮع ،وﻣﺆﺧﺮة اﻟﺮأس ،واﻟﻔﻘﺮات اﻟﻌﺠﺰﻳﺔ .وﻫﻲ ﻏﻴﺮ ﻣﺆﻟﻤﺔ ،وﺗﻜﻮن ﻣﺴﺘﺪﻳﺮة ،أو
ﺑﻴﻀﺎوﻳﺔ ،ﺛﺎﺑﺘﺔ ،أو ﻣﺘﺤﺮﻛﺔ.
)هـ( اﻟﻌﻴﻦ
ﻳﺤﺪث ﺟﻔﺎف ﻓﻲ اﻟﻌﻴﻦ ﻓﻲ ﺣﻮاﻟﻲ %10ﻣﻦ اﻟﺤﺎﻻت ،ﻧﺘﻴﺠﺔ ﻟﻘﻠﺔ إﻓﺮاز اﻟﺪﻣﻮع ﺑﺴﺒﺐ ﺗﺮﺳﺐ
اﻟﻌﻘﺪ اﻟﺒﺮوﺗﻴﻨﻴﺔ اﻟﻤﻨﺎﻋﻴﺔ ﻓﻲ اﻟﻐﺪد اﻟﺪﻣﻌﻴﺔ .وﻳﺼﺎﺣﺐ ذﻟﻚ ﺟﻔﺎف ﻓﻲ اﻟّﻠﻌﺎب ،ﻧﺘﻴﺠﺔ ﺣﺪوث
ﺗﺮﺳﻴﺐ ﻟﻠﻌﻘﺪ الﺑﺮوﺗﻴﻨﻴﺔ اﻟﻤﻨﺎﻋﻴﺔ ،ﻓﻲ اﻟﻐﺪد اﻟﻠﻌﺎﺑﻴﺔ.