Association of growth differentiation factor 15 (GDF15) polymorphisms with serum GDF15 and ferritin levels in β-thalassemia

Athiyarath, Rekha; George, Biju; Srivastava, Alok; Edison, Eunice Sindhuvi

doi:10.1007/s00277-014-2113-1

Cited by 11 publications

(11 citation statements)

References 13 publications

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“…And this is similar to Athiyarath et al. [ 27 ] who showed increased GDF‐15 in thalassemic patients with median of 6059.87 pg/ml. Cardiac involvement is an important complication of thalassemia major.…”

Section: Discussionsupporting

confidence: 89%

“…TGF super family, was elevated in beta-thalassemia and contributes to hepcidin suppression this is consistent with our study, as it was higher in cases by median of 1839.89 pg/ml than in controls (median of 256.14 pg/ml) of highly statistically significant value (p < 0.001). And this is similar to Athiyarath et al[27] who showed increased GDF-15 in thalassemic patients with median of 6059.87 pg/ml. Cardiac involvement TA B L E 6…”

supporting

confidence: 89%

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GDF‐15 is associated with atherosclerosis in adults with transfusion‐dependent beta‐thalassemia

Efat

Wahb

Shoeib

et al. 2022

eJHaem

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Objectives: To study serum growth differentiation factor‐15 (GDF‐15) serum level in β‐thalassemia patients and its relation to carotid intima‐media thickness. Background: Thalassemia is a common genetic disease resulting in decreased beta‐chains, leading to manifested anemia. It may be subsequently complicated by iron overload, which induces numerous morbidities and even death. Growth differentiation factor‐15 (GDF‐15) is a strong and independent predictor of mortality and disease progression in patients with atherosclerosis alongside with carotid‐intimal media thickness (CIMT). Patients and methods: This monocentric case‐control study was done on 90 subjects in the period from January 2020 to March 2021. Sixty transfusion‐dependent beta‐thalassemia (TDβT) cases (≥18 years) were selected from the thalassemia clinic of Hematology division at Menoufia University hospitals. We included also 30 sex and age matched healthy as the controls. Routine investigations were done beside. Serum GDF‐15 was measured by ELISA. CIMT was measured by Doppler Ultrasonography. Results: CIMT on both sides was statistically significant higher in cases (median of 0.08 cm) than in the controls (median of 0.04). GDF‐15 was also significantly higher in cases (median of 1839.89 pg/dl) than in controls (median of 256.14 pg/dl). So, we found that GDF‐15 is a predictor of and associated with atherosclerosis in thalassemic adults (OR = 39.198, p value 0.008, 95% CI: 2.576–596.5). Conclusion: GDF‐ 15 is increased in TDβT. CIMT (as a marker of subclinical atherosclerosis) is increased in these patients alongside with GDF‐15, is a predictor, and associated with atherosclerosis in thalassemic adults.

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Section: Discussionsupporting

confidence: 89%

supporting

confidence: 89%

GDF‐15 is associated with atherosclerosis in adults with transfusion‐dependent beta‐thalassemia

Efat

Wahb

Shoeib

et al. 2022

eJHaem

View full text Add to dashboard Cite

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“…It overlapped enhancer histone marks in three tissues, including placenta, and DNAse hypersensitivity sites in nine tissues, including ovary. A summary of the variants in LD with the lead SNP and associated with altered GDF15 expression is shown in Supplementary Data 2 17 – 20 , 39 – 42 , 44 , with the full list of variants in LD with the lead SNP identified using HaploReg listed in Supplementary Data 1 . One of the variants associated with HG in SCAN1, rs17725099 ( p = 1.03 × 10 −13 ) and in LD with rs16982345 ( r 2 = 0.77), was the top association signal ( β = 0.16, p = 1.47 × 10 –107 ) in a conference abstract which identified variants influencing GDF15 levels in patients with cardiovascular disease 18 .…”

Section: Resultsmentioning

confidence: 99%

Placenta and appetite genes GDF15 and IGFBP7 are associated with hyperemesis gravidarum

et al. 2018

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Hyperemesis gravidarum (HG), severe nausea and vomiting of pregnancy, occurs in 0.3–2% of pregnancies and is associated with maternal and fetal morbidity. The cause of HG remains unknown, but familial aggregation and results of twin studies suggest that understanding the genetic contribution is essential for comprehending the disease etiology. Here, we conduct a genome-wide association study (GWAS) for binary (HG) and ordinal (severity of nausea and vomiting) phenotypes of pregnancy complications. Two loci, chr19p13.11 and chr4q12, are genome-wide significant (p < 5 × 10−8) in both association scans and are replicated in an independent cohort. The genes implicated at these two loci are GDF15 and IGFBP7 respectively, both known to be involved in placentation, appetite, and cachexia. While proving the casual roles of GDF15 and IGFBP7 in nausea and vomiting of pregnancy requires further study, this GWAS provides insights into the genetic risk factors contributing to the disease.

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“…Controversially, iron levels might not increase hepcidin expression in β-thalassemia with ineffective erythropoiesis according to high levels of hepcidin suppressors (e.g. growth differentiation factor 15, twisted gastrulation factor 1, bone morphogenetic protein-binding endothelial cell precursor-derived regulator or erythroferrone), which do have a greater influence on decreasing hepcidin levels [27,42,43]. However, the increased hepcidin levels in the GTE + DFP treatment could not result from the iron-loading effect with regard to the reduction of the plasma NTBI levels and iron accumulation in the tissues when compared with the non-treatment group.…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Combined treatment of 3-hydroxypyridine-4-one derivatives and green tea extract to induce hepcidin expression in iron-overloaded β-thalassemic mice

Upanan

Pangjit

Uthaipibull

et al. 2015

Asian Pacific Journal of Tropical Biomedicine

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A B S T R A C T Objective:To evaluate the efficacy of deferiprone (DFP), 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) or green tea extract (GTE) in enhancing expression of hepatic hepcidin1 (Hamp1) mRNA and relieving iron overload in β-globin knockout thalassemic mice. Methods:The β-globin knockout thalassemic mice were fed with a ferrocene-supplemented diet for 2 months and oral administration of deionized water, DFP (50 mg/kg), CM1 (50 mg/kg), GTE (50 mg epigallocatechin 3-gallate equivalent/kg), GTE along with DFP (50 mg/kg), and GTE along with CM1 (50 mg/kg) every day for 3 months. Levels of hepatic Hamp1 mRNA, plasma non-transferrin bound iron, plasma alanine aminotransferase activity and tissue iron content were determined.Results: All chelation treatments could reduce plasma non-transferrin bound iron concentrations. Additionally, hepatic Hamp1 mRNA expression was significantly up-regulated in the mice in a GTE + DFP combined treatment, correlating with a decrease in the plasma alanine aminotransferase activity and tissue iron deposition. Conclusions:The GTE + DFP treatment could ameliorate iron overload and liver oxidative damage in non-transfusion dependent β-thalassemic mice, by chelating toxic iron in plasma and tissues, and increasing hepcidin expression to inhibit duodenal iron absorption and iron release from hepatocytes and macrophages in the spleen. There is probably an advantage in giving GTE with DFP when treating patients with iron overload.

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Association of growth differentiation factor 15 (GDF15) polymorphisms with serum GDF15 and ferritin levels in β-thalassemia

Cited by 11 publications

References 13 publications

GDF‐15 is associated with atherosclerosis in adults with transfusion‐dependent beta‐thalassemia

GDF‐15 is associated with atherosclerosis in adults with transfusion‐dependent beta‐thalassemia

Placenta and appetite genes GDF15 and IGFBP7 are associated with hyperemesis gravidarum

Combined treatment of 3-hydroxypyridine-4-one derivatives and green tea extract to induce hepcidin expression in iron-overloaded β-thalassemic mice

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