Bilirubin concentrations in thalassemia heterozygotes in university students

Huang, Yeen; Huang, May-Jen; Wang, Hai-Lung; Chan, Chung-Chuan; Huang, Ching‐Shan

doi:10.1111/j.1600-0609.2011.01578.x

Cited by 7 publications

(6 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, as more SNPs in the UGT1A1 gene were found, we determined that our method of classifying study subjects was inaccurate. For example, UGT1A1 activities may differ considerably among subjects who carry compound heterozygous variations because some carry two while others can carry three or four SNPs …”

Section: Discussionmentioning

confidence: 99%

“…Since 2000, we have published 14 studies on the relationship between variants in the UGT1A1 gene and Gilbert's syndrome (or neonatal hyperbilirubinemia). 9,11,[17][18][19][20][21][22][23][24][25][26][27][28] In our previous reports, the study subjects were usually divided into several groups, such as those carrying the wild type UGT1A1 gene, those carrying heterozygous variations, subjects with compound heterozygous variations, and those carrying homozygous and compound homozygous variations in the UGT1A1 gene, because we assumed that UGT1A1 activity gradually decreased as the number of variant alleles increased. However, as more SNPs in the UGT1A1 gene were found, we determined that our method of classifying study subjects was inaccurate.…”

Section: Discussionmentioning

confidence: 99%

“…For example, UGT1A1 activities may differ considerably among subjects who carry compound heterozygous variations because some carry two while others can carry three or four SNPs. 9,11,[17][18][19][20][21][22][23][24][25][26][27][28] Classifying subjects based on genotype is a more suitable method because genotypes represent variation of all SNPs in the UGT1A1 gene. 11 However, in this study, we realized that we would encounter it would be a laborious process to precisely analyze the OR for each genotype since the number (n = 24) of genotypes is too much.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Effect of UDP‐glucuronosyltransferase 1A1 activity on risk for developing Gilbert's syndrome

Huang

Chen

Huang

et al. 2019

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

Variations at the six nucleotides −3279 (T > G), −53 (A[TA]6TAA > A[TA]7TAA), 211 (G > A), 686 (C > A), 1091 (C > T), and 1456 (T > G) in the UDP‐glucuronosyltransferase 1A1 (UGT1A1) gene were determined in 178 Taiwanese patients with Gilbert's syndrome and in 200 healthy adults. Every subject was classified as a genotype depending on variation status of the six nucleotides in the UGT1A1 gene. The UGT1A1 activity for each genotype was calculated and then those genotypes were divided into 10 subgroups (Q1~Q10) according to their UGT1A1 activities, by using 10% as an interval. There were 24 genotypes observed, with UGT1A1 activity ranged 9%~100% of normal. There were two and six subjects with Gilbert's syndrome and none of healthy controls carrying genotypes in the Q1 and Q2 subgroups, respectively. The odds of developing Gilbert's syndrome were significantly higher for subjects carrying genotypes in the Q3, Q4, and Q5 subgroups than for those with genotype in the Q10 subgroup (odds ratios: 240.22, 59.80, and 14.67, respectively, P < .001 for each). Among the 178 patients of Gilbert's syndrome, serum bilirubin value was inversely correlated with UGT1A1 activity (r = −.306, P < .001). The sensitivity was 72.0% and the specificity was 90.5% by using UGT1A1 activity ≦40% of normal as the cut‐off point to distinguish between healthy subjects and patients of Gilbert's syndrome. Our results demonstrate that UGT1A1 activity is certainly a determinate for serum bilirubin value and UGT1A1 activity ≦40% of normal is a proper risk factor for the development of Gilbert's syndrome.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of UDP‐glucuronosyltransferase 1A1 activity on risk for developing Gilbert's syndrome

Huang

Chen

Huang

et al. 2019

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

show abstract

“…ALT serum level is considered an indicator of the necroinflammatory process of the liver (46) . To assess the extension of liver cell damage a sensitive indicator of liver function is used namely serum bilirubin; hyperbilirubinemia in β-TM could be pre-hepatic (hemolytic), hepatic or post-hepatic (obstructive) (47) . The incidence of gallbladder stones (cholelithiasis) and hepatic duct stones (choledocholithiasis) is 30-80% in patients with β-TM.…”

Section: Liver Diseasementioning

confidence: 99%

Clinical Complications of Beta-Thalassemia Major

Shawkat¹,

Jwaid²

2019

IJPS

View full text Add to dashboard Cite

Beta thalassemia syndrome (β-TM) syndrome is a group of hereditary blood disorders that are mainly characterized by reduction or absence of β-globin chain synthesis. Without iron chelation therapy (ICT) the regular blood transfusion would increase the iron stores to several times. Endocrine glands are vulnerable to iron overload causing endocrine dysfunction. Iron deposition within the parathyroid gland causes hypoparathyroidism particularly after ten years of age. Pancreatic islets are very susceptible to oxidative damage due to iron overload; their high divalent metal expression makes them highly susceptible to iron-catalyzing oxidative stress. The pathogenicity of osteopathy in β-TM is multifactorial comprising environmental (diet and lifestyle), iatrogenic (medicines), genetic and acquired factors (expansion of bone marrow, hemochromatosis, deficiency of growth hormone, hepatitis and hypogonadism). The increase in blood transfusion and RBCs break down in addition to iron accumulation and deposition are the main factors causing splenomegaly. Liver disease is one of the major complications affecting patients with β-TM.Liver damage is multifactorial with iron overload is considered the main causative factor, as well as hepatitis C (HCV) and hepatitis B (HBV) infections which are acquired on recurrent blood transfusions. The free radicals of deposited iron overcome the cellular antioxidant mechanisms resulting in peroxidative cellular injury. As a result, iron overload is the leading cause of left ventricular cardiomyopathy development.

show abstract

“…The wavelet threshold denoising algorithm can obtain a better signal-to-noise ratio when the appropriate wavelet basis function and threshold rule are selected, and the algorithm calculation complexity is simpler than that of EMD-CIIT [4] and EMD. Huang et al [5] analyzed and modeled the signal noise of CCD spectrometer, and used wavelet denoising method and empirical mode decomposition-clear iterative interval threshold (EMD-CIIT) method to denoise different types of spectral signal noise spectrum, and analyzed the optimal denoising algorithm under different noise conditions. This system adopts wavelet threshold denoising as the denoising, and the number of layers and wavelet basis function of wavelet denoising can be flexibly selected according to noise conditions.…”

Section: Introductionmentioning

confidence: 99%

A signal denoising system for CCD spectrometer based on FPGA

Zeng,

Li,

Xiong

2023

Fourth International Conference on Signal Processing and Computer Science (SPCS 2023)

View full text Add to dashboard Cite

Bilirubin concentrations in thalassemia heterozygotes in university students

Cited by 7 publications

References 21 publications

Effect of UDP‐glucuronosyltransferase 1A1 activity on risk for developing Gilbert's syndrome

Effect of UDP‐glucuronosyltransferase 1A1 activity on risk for developing Gilbert's syndrome

Clinical Complications of Beta-Thalassemia Major

A signal denoising system for CCD spectrometer based on FPGA

Contact Info

Product

Resources

About