scholarly journals Association of gene polymorphism with menorrhagia combined with thyroid pathology

2020 ◽  
Vol 0 (56) ◽  
pp. 73-77
Author(s):  
O. A. Andriets ◽  
O. M. Yuzko ◽  
Y. V. Tsysar
2021 ◽  
Vol 14 (4) ◽  
pp. 549-556
Author(s):  
Iryna Ivanivna Kamyshna ◽  
◽  
◽  
Larysa Borysivna Pavlovych ◽  
Igor Volodymyrovych Malyk ◽  
...  

Vitamin D is known to alter immune regulation. It binds to the vitamin D receptors (VDR) expressed on T lymphocytes and macrophages. In individuals with Hashimoto’s thyroiditis, serum vitamin D levels were found to be lower compared to healthy controls. The study’s objective was to investigate the association between VDR gene polymorphism (rs2228570) with blood serum levels of 25-OH vitamin D in patients with thyroid pathology from western Ukraine. The study involved a total of 153 patients with various forms of thyroid pathology. 25-OH vitamin D levels in the serum of the patients and healthy individuals were quantified with ELISA using the 25-OH vitamin D Total (Vit D-Direct) Test System ELISA Kit (Monobind Inc.®, United States, Product Code: 9425-300) on the EIA Reader Sirio S (Seac, Italy). Genotyping of the VDR (rs2228570) gene polymorphism was performed using TaqMan probes and TaqMan Genotyping Master Mix (4371355) on CFX96™Real-Time PCR Detection System (Bio-Rad Laboratories, Inc., USA). Polymerase chain reaction (PCR) for TaqMan genotyping was carried out according to the kit instructions (Applied Biosystems, USA). Our research identified that that genotype variants of VDR rs2228570 are not risk factors for reduced serum 25-OH vitamin D or vitamin D deficiency in patients with various forms of thyroid pathology patients in the West-Ukrainian population. Vitamin D levels were significantly lower in the carriers of AA and AG genotypes with hypothyroidism caused by autoimmune thyroiditis. In AA genotype carriers with postoperative hypothyroidism, 25-OH vitamin D levels were significantly lower compared to AA genotype carriers with autoimmune thyroiditis.


2021 ◽  
Vol 55 (4) ◽  
pp. 193-203
Author(s):  
Iryna I. Kamyshna ◽  
Larysa B. Pavlovych ◽  
Larysa P. Sydorchuk ◽  
Igor V. Malyk ◽  
Aleksandr M. Kamyshnyi

Abstract Objective. Brain-derived neurotrophic factor (BDNF) is identified as an important growth factor involved in learning and memory. Patients with Hashimoto’s thyroiditis can suffer from cognitive dysfunction, whereas BDNF is directly regulated by thyroid hormones. It seems reasonable to propose that changes in BDNF expression underlie some of the persistent neurological impairments associated with hypothyroidism. Methods. The study involved a total of 153 patients with various forms of thyroid pathology. BDNF levels in the sera of the patients and healthy individuals were quantified using enzyme-linked immunosorbent assay with highly sensitive Human BDNF ELISA Kit. Genotyping of the BDNF (rs6265) gene polymorphism using TaqMan probes and TaqMan Genotyping Master Mix (4371355) on CFX96™Real-Time PCR Detection System. Polymerase chain reaction (PCR) for TaqMan genotyping was carried out according to the kit instructions. Results. Distribution rs6265 variants in the patients depending on the different types of thyroid pathology showed no significant difference in the relative frequency of BDNF polymorphic variants. Presence of hypothyroidism, regardless of its cause (autoimmune or postoperative), there was a decrease in the serum BDNF levels in all genotypes carriers compared with the control group. The analysis of the correlation between BDNF levels and the levels of thyroid-stimulating hormone (TSH), thyroxine (T4), anti-thyroglobulin (anti-Tg), and anti-thyroid peroxidase (anti-TPO) antibodies showed a significant inverse relationship between BDNF and TSH levels (p<0.001), a direct correlation between BDNF and T4 levels in the blood (p<0.001), and a weak direct relationship between anti-Tg and BDNF levels (p=0.0157). Conclusion. The C allele presence is protective and associates with the lowest chances for reduced serum BDNF levels in thyroid pathology patients in the West-Ukrainian population. However, the T-allele increases the risk of low BDNF levels almost 10 times in observed subjects.


2001 ◽  
Vol 120 (5) ◽  
pp. A709-A709
Author(s):  
A TAKAGI ◽  
J XUAN ◽  
R DEGUCHI ◽  
J NAGATA ◽  
H KIJIMA ◽  
...  

2007 ◽  
Author(s):  
Scott H. Fraundorf ◽  
Brad E. Sheese ◽  
Lauren K. White ◽  
Mary K. Rothbart ◽  
Michael I. Posner

2012 ◽  
Vol 50 (05) ◽  
Author(s):  
A Schöller ◽  
A Kalmár ◽  
VÁ Patai ◽  
Z Nagy ◽  
B Barták ◽  
...  

1995 ◽  
Vol 73 (05) ◽  
pp. 746-749 ◽  
Author(s):  
E Sacchi ◽  
M Pinotti ◽  
G Marchetti ◽  
G Merati ◽  
L Tagliabue ◽  
...  

SummaryA protein S gene polymorphism, detectable by restriction analysis (BstXI) of amplified exonic sequences (exon 15), was studied in seven Italian families with protein S deficiency. In the 17 individuals heterozygous for the polymorphism the study was extended to platelet mRNA through reverse transcription, amplification and densitometric analysis. mRNA produced by the putative defective protein S genes was absent in three families and reduced to a different extent (as expressed by altered allelic ratios) in four families. The allelic ratios helped to distinguish total protein S deficiency (type I) from free protein S deficiency (type IIa) in families with equivocal phenotypes. This study indicates that the study of platelet mRNA, in association with phenotypic analysis based upon protein S assays in plasma, helps to classify patients with protein S deficiency.


Sign in / Sign up

Export Citation Format

Share Document