الفهرس 
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Abstract
Immune thrombocytopenic purpura (ITP) is an acquired autoimmune
disorder and the most common cause of isolated thrombocytopenia in children.
It is diagnosed clinically, based upon onset of thrombocytopenia in the absence
of other hematologic abnormalities, or other causes of low platelets. It is caused
by the production of anti-platelet antibodies. These auto antibodies opsonize
platelets for splenic clearance, resulting in low levels of circulating platelets.
It causes a characteristic purpuric rash and an increased tendency to bleed .Two distinct clinical types manifest as an acute condition and a chronic condition. The acute form often follows an infection and has a spontaneous resolution within 2 months. chronic idiopathic thrombocytopenic purpura persists longer than one year without a specific cause.
In mild cases, only careful observation may be required but very low counts or significant bleeding may prompt treatment with corticosteroids, intravenous immunoglobulin, anti-D immunoglobulin, or immunosuppressive drugs. Splenectomy and platelet transfusions may be +required in severe bleeding together with a very low count. Sometimes the body may compensate by making abnormally large platelets.
Cannabinoid receptors play an important role in immune modulation they are represented in many cells, including immune cells where the immune T cells. It was found that ,there is a mutation in the gene responsible for cannabinoid receptors in cases of chronic immune thrombocytopenic purpura . where adenosine in the second and third codon No. 63 turns to Guanisen which would lead to change printing of glutamine to arginine altering the immuomodulating properties of CB2.
The aim of our study is detection of polymorphism in this gene in ITP cases
and its correlation with the course and the outcome of the disease .
The current study was carried out on 40 diagnosed ITP(Immune thrombocytopenic purpura) patients and 10 normal controls the same age group. All patients were children, 22patients were acute and 18 patients were chronic. All our cases and controls were subjected to detailed history taking, complete clinical examination, and laboratory investigations including complete blood count, bone marrow aspiration, and CNR2 gene expression by REFLEP –PCR.
Among the 22 patients with acute ITP, 10 were males and 12 were females. Their ages ranged from 0.9 – 13years with a mean of 6.6 ± 3.4 years and Mean platelet count was 40.1 ± 22.5× 103 / µL with a range of 1.0 – 80 × 103 / µL, mean TLC4.9±2.8×103/ µL, mean HB11.6±1.1gm/dl.
And Among 18 patient with chronic ITP group, 9 were males and 9 were females. Their ages ranged from 0.8 – 11 years with a mean of 5.7 ± 2.9 years and Mean platelet count was 110.3 ± 31.1 × 103 / µL with a range of 22.0 – 137 × 103 / µL, Mean TLC 8.9±2.9×103/ µL, mean HB 12.1±1.2gm/dl.
Among 10 normal volunteers, 6 were males and 4 were females. Their ages ranged from 0.4 – 11 years with a mean of 4.8± 3.5 years and Mean platelet count was 320.1 ± 89.2 × 103 / µL with a range of 220.0– 479 × 103 / µL, mean TLC 8.5±3.3×103 / µL and mean HB12.6±1.2gm/dl.
Among the 22 acute ITP patients 2(11.1%) were found to be QQ ,16(72.2%) were found to be QR genotype and 4(16.7%) RR genotype .Among the 18 chronic ITP patients, 0(0.0%)QQ, 4(22.7%)QR and 14(77.3%)RR for the gene.Among the 10 normal volunteers,1(10%)QQ, 7(70%)QR ,and 2(20%) RR genotype.
CNR2 genotyping in ITP patients revealed that 45% of patients had the QR(AA/GG) heterotype and 50% had the RR(AA/AA) homotype.
The allelic frequencies and genotype distribution in ITP patients showed significant differences with respect to control samples (p=0.002and p=0.001, respectively). In addition, the relative odds ratio (OR) suggested a double risk for developing ITP in RR homozygous children with respect to QR heterozygous and QQ homozygous children.
when acute and chronic ITP patients were separately analyzed in comparison with controls, a significant overrepresentation of the RR genotype and of the R allele was observed only for the chronic form(p=0.002 and p=0.003, respectively). Furthermore, the associated risk to develop chronic ITP increased more than two-fold for RR homozygous children.
Conclusion and recommendations:
Finally, Data presented in this study confirm the role of CB2 in autoimmunity susceptibility and reveal a significant association between CB2 and childhood ITP.
The CNR2 Q63R polymorphism represents a genetic risk factor in the patho- physiology of chronicity development of ITP in children. This may help in prediction of disease progression and help in choosing appropriate treatment protocols thus improving the outcome of the disease.
Further studies to support these findings are highly recommended.