Contributions
Type: Publication Only
Background
Iron deficiency anemia (IDA) is the most common in infancy and childhood hematologic diseases. It is seen in all age groups. Nutrition plays an important role in the development of IDA which is the most common cause of nutritional anemia. In our country, IDA has been determined in 12.7% of children between 4-months and 18-years old. One of the clinical features of IDA is loss of appetite and nutrition plays a major rol in IDA. Ghrelin stimulates appetite and food intake. It is considered that appetite and eating behavior are controlled with complex mechanisms by certain areas located at hypothalamus in central nervous system (CNS). The neurons containing ghrelin involved in appetite were found at arcuate nucleus of hypothalamus. Ghrelin at this localization controlles food intake. In addition to becoming hunger hormone, ghrelin regulates eating behavior and weight balance. Also ghrelin, before and after fasting, controlles behavioral, metabolic and gastrointestinal adaptations. The significant positive correlation was found between body iron and ghrelin levels. Ghrelin levels progresively decrease from iron decrease to development of IDA.
Aims
The frequency of ghrelin gene polymorphism was aimed to be investigated in children diagnosed as IDA and healthy control group. In this way, we aimed to determine ghrelin gene polymorphism in healthy children of our society. It was aimed which determined polymorphisms are seen more frequently. Thus, we aimed to determine difference between the ratios of healthy children and children with IDA. Among children with the same nutrition manner, common living conditions, we aimed to answer question that the real reason of IDA development may be occurance of a polymorphism at ghrelin gene.
Methods
In our study, total 57 children with IDA, 27 female (47.4%) and 30 male (52.6%), and 57 healthy control group were assessed. -501 promoter, arg51Gln, Leu72Met, and Gln90Leu polymorphisms at ghrelin gene were studied in patients and contol group.
Results
In terms of -501 A/C polymorphism at ghrelin gene, A allele was found statistically significant in patients group (p<0.05). For promoter -501 A/C polymorphism, the frequencies of genotype was not different from the control group (p<0.05). When genotype and allele frequencies were compared with control group for Arg51Gln, Leu72Met and Gln90Leu polymorphisms, there is no statistically significant difference (p<0.05).
Summary
We suggest that ghrelin gene may play an important role in IDA immunogeneticy. Also we think that studies are needed to be done in both Turkish population and other populations for the determiation of other polymorphisms in this gene which may contribute to this disease. To verify our data, the same polymorphisms should be futher investigated in patients with IDA in different populations by more futher studies. We suggest that increased promoter -501 variant frequency in ghrelin gene may be one of he mechanisms involved in etiopathogenesis of IDA.
Keyword(s): Genetic polymorphism
Session topic: Publication Only
Type: Publication Only
Background
Iron deficiency anemia (IDA) is the most common in infancy and childhood hematologic diseases. It is seen in all age groups. Nutrition plays an important role in the development of IDA which is the most common cause of nutritional anemia. In our country, IDA has been determined in 12.7% of children between 4-months and 18-years old. One of the clinical features of IDA is loss of appetite and nutrition plays a major rol in IDA. Ghrelin stimulates appetite and food intake. It is considered that appetite and eating behavior are controlled with complex mechanisms by certain areas located at hypothalamus in central nervous system (CNS). The neurons containing ghrelin involved in appetite were found at arcuate nucleus of hypothalamus. Ghrelin at this localization controlles food intake. In addition to becoming hunger hormone, ghrelin regulates eating behavior and weight balance. Also ghrelin, before and after fasting, controlles behavioral, metabolic and gastrointestinal adaptations. The significant positive correlation was found between body iron and ghrelin levels. Ghrelin levels progresively decrease from iron decrease to development of IDA.
Aims
The frequency of ghrelin gene polymorphism was aimed to be investigated in children diagnosed as IDA and healthy control group. In this way, we aimed to determine ghrelin gene polymorphism in healthy children of our society. It was aimed which determined polymorphisms are seen more frequently. Thus, we aimed to determine difference between the ratios of healthy children and children with IDA. Among children with the same nutrition manner, common living conditions, we aimed to answer question that the real reason of IDA development may be occurance of a polymorphism at ghrelin gene.
Methods
In our study, total 57 children with IDA, 27 female (47.4%) and 30 male (52.6%), and 57 healthy control group were assessed. -501 promoter, arg51Gln, Leu72Met, and Gln90Leu polymorphisms at ghrelin gene were studied in patients and contol group.
Results
In terms of -501 A/C polymorphism at ghrelin gene, A allele was found statistically significant in patients group (p<0.05). For promoter -501 A/C polymorphism, the frequencies of genotype was not different from the control group (p<0.05). When genotype and allele frequencies were compared with control group for Arg51Gln, Leu72Met and Gln90Leu polymorphisms, there is no statistically significant difference (p<0.05).
Summary
We suggest that ghrelin gene may play an important role in IDA immunogeneticy. Also we think that studies are needed to be done in both Turkish population and other populations for the determiation of other polymorphisms in this gene which may contribute to this disease. To verify our data, the same polymorphisms should be futher investigated in patients with IDA in different populations by more futher studies. We suggest that increased promoter -501 variant frequency in ghrelin gene may be one of he mechanisms involved in etiopathogenesis of IDA.
Keyword(s): Genetic polymorphism
Session topic: Publication Only