الفهرس 
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Abstract
SUMMARY, CONCLUSIONS AND RECOMMENDATIONS-W 161 3(
SUMMARY, CONCLUSIONS AND RECOMMENDATIONS
Familial Mediterranean Fever (FMF) remains an under recognized cause of transient symptoms; usually localized to serosal surface including peritoneum; pleura; pericardium and synovia; associated with febrile episodes; the pathogensis of FMF still unclear.
Our study included 25 FMF patients (14 during attacks and 11 in between the attacks), the diagnosis of FMF was based on typical history of repeated attacks of fever; peritonitis, pleuritis and arthritis, with dramatic response to colchicine therapy, also the study included 10 normal subjects as control group.
To each of them, the followings were done:
(i) Routine investigations:
■Full medical history including age, sex and duration of the disease.
■Full clinical examination.
■Complete blood picture.
■Erythrocyte Sedimentation Rate (ESR).
■Urine analysis.
(ii) Investigations reflecting immune processes:
■Rheumatoid factor (RF).
■Anti Nuclear Antibodies (ANA).
■Anti double strandedlds DNA).
•Immunoglobulin
(iii) Investigations reflecting inflammatory processes: *CvtokineA:
■Interleukin 1 B (IL-1B).
■Tumour Necrosis Factor (TNFa).
(iv) Acute phase reactants:
■Serum Glycoprotein (SGP).
SUMMARY, CONCLUSIONS AND RECOMMENDATIONS= .w162 W.
•C-Reactive protein (CRP).
•Complement 3 (C3).
The results of our study showed that :
■ Erythrocyte Sedimentation Rate (ESR) was moderately elevated in FMF patients.
•Rheumatoid factor (RF), antinuclear antibodies (ANA)
and Anti double stranded (ds DNA) were negative in all FMF patients.
•Cytokines (1L1(3 and TNFa) were significantly higher in
FMF patients in comparison to control group specially during attack.
•Acute phase reactants CRP, SGP and C3 were significantly higher in FMF cases compared to control group and more noticeable during attack.
•There were significant positive correlation between
cytokines and acute phase reactants in all patients a part from those in remission.
•IgD increased in FMF cases in comparison to control but had no correlation with cytokines or acute phase reactants neither during attack nor in remission.
•Colchicine therapy did not alter the level of cytokines and acute phase reactants in all FMF patients.
from our work we can concluded that :
•FMF is an inflammatory disease rather than an autoimmune disease.
•Cytokines (IL1( and TNFa) and acute phase reactants (CRP, SGP and C3) may contribute in FMF pathogenesis.
•Colchicine control the FMF attack through mechanisms other than the change of cytokines or acute phase proteins.
•IgD may increase in FMF patients but has no role in
initiation of FMF attack or in alternation of cytokines and acute phase protein cascade.
SUMMARY, CONCLUSIONS AND RECOMMENDATIONS= W163W
Finally, further studies might be recommended :
I- Estimation of local cytokines and acute phase reactants in serosal surface (peritoneum; pericardium and pleura) and synovia of FMF patients in correlation with their serum level.
2-Genetic counscilling might pave the way for solving this enigma. Therefore we recommended further studies including the relationship between genetic markers, cytokines and acute phase reactants in a trial to find the initial trigger (s) in FMF patients.
3-Gene therapy in future might be the clue for treatment of FMF patients, the rate of success of this mode of therapy should be accompanied by return of cytokines and acute phase reactants to their normal level with subsequent avoidence of the deleterious effects.