Genome-wide DNA methylation profiles analysis in primary warm autoimmune hemolytic anemia patients

Zhao, Manjun; Zhang, Yang; Yang, Jin; Chen, Lei; Zhang, Ziying; Wang, Huaquan; Shao, Zhang; Xing, Limin

doi:10.1080/16078454.2023.2240138

Cited by 2 publications

(1 citation statement)

References 43 publications

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“…As a crucial regulator in the development and differentiation of immune cells, impaired DNA methylation profiles may substantially induce autoreactivity in the immune cells. This predisposes a person to immune irregularities and increases the possibility of progression in autoimmune anomalies ( 44 – 46 ). Epigenetic modification via DNA methylation recently gained consideration as a potential biomarker ( 47 , 48 ).…”

Section: Dna Methylation In Autoimmune Diseasementioning

confidence: 99%

Functional significance of DNA methylation: epigenetic insights into Sjögren’s syndrome

Wang,

Riaz,

Wang

et al. 2024

Front. Immunol.

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Sjögren’s syndrome (SjS) is a systemic, highly diverse, and chronic autoimmune disease with a significant global prevalence. It is a complex condition that requires careful management and monitoring. Recent research indicates that epigenetic mechanisms contribute to the pathophysiology of SjS by modulating gene expression and genome stability. DNA methylation, a form of epigenetic modification, is the fundamental mechanism that modifies the expression of various genes by modifying the transcriptional availability of regulatory regions within the genome. In general, adding a methyl group to DNA is linked with the inhibition of genes because it changes the chromatin structure. DNA methylation changes the fate of multiple immune cells, such as it leads to the transition of naïve lymphocytes to effector lymphocytes. A lack of central epigenetic enzymes frequently results in abnormal immune activation. Alterations in epigenetic modifications within immune cells or salivary gland epithelial cells are frequently detected during the pathogenesis of SjS, representing a robust association with autoimmune responses. The analysis of genome methylation is a beneficial tool for establishing connections between epigenetic changes within different cell types and their association with SjS. In various studies related to SjS, most differentially methylated regions are in the human leukocyte antigen (HLA) locus. Notably, the demethylation of various sites in the genome is often observed in SjS patients. The most strongly linked differentially methylated regions in SjS patients are found within genes regulated by type I interferon. This demethylation process is partly related to B-cell infiltration and disease progression. In addition, DNA demethylation of the runt-related transcription factor (RUNX1) gene, lymphotoxin-α (LTA), and myxovirus resistance protein A (MxA) is associated with SjS. It may assist the early diagnosis of SjS by serving as a potential biomarker. Therefore, this review offers a detailed insight into the function of DNA methylation in SjS and helps researchers to identify potential biomarkers in diagnosis, prognosis, and therapeutic targets.

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Section: Dna Methylation In Autoimmune Diseasementioning

confidence: 99%

Functional significance of DNA methylation: epigenetic insights into Sjögren’s syndrome

Wang,

Riaz,

Wang

et al. 2024

Front. Immunol.

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A rare case report of severe aplastic anaemia caused by long-term use of zidovudine

Zhou,

Wang,

et al. 2024

BMC Infect Dis

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Background Zidovudine is an antiviral drug used to treat acquired immune deficiency syndrome (AIDS). Anaemia is a common adverse effect of zidovudine that usually occurs in the first 2 to 4 weeks of initial treatment. Here, we describe a patient with HIV infection who developed severe aplastic anaemia 11 years after taking zidovudine. To our knowledge, this is the first case of severe aplastic anaemia caused by the long-term use of zidovudine. Case presentation A 28-year-old male patient with AIDS developed severe aplastic anaemia after taking zidovudine for 11 years. The patient went to the emergency department due to weakness and falls. He was diagnosed with severe anaemia because his haemoglobin (Hb) level was 31 g/L and his red blood cell (RBC) count was 0.89 × 10 12 /L. Gastrointestinal bleeding, haematological diseases and autoimmune haemolytic anaemia were ruled out by gastroenteroscopy, stool routine examination and bone marrow puncture biopsy after admission. When the causality of adverse drug reactions was assessed, the Naranjo score of zidovudine was 8, indicating that severe aplastic anaemia was likely related to zidovudine. Given that bone marrow suppression is a side effect of zidovudine, this drug was discontinued. Lamivudine and dolutegravir sodium tablets were subsequently used as antiviral therapies. The patient’s symptoms of anaemia improved with the transfusion of suspended RBCs, oral polysaccharide iron complex capsules and folic acid tablets. After 2 weeks of treatment, the patient’s symptoms of fatigue improved, with a Hb level of 70 g/L and a RBC count of 2.13 × 10 12 /L, which were significantly better than before, and he was discharged. At the follow-up 6 weeks after discharge, the patient’s Hb level was 156 g/L, his RBC count was 4.67 × 10 12 /L, and the anaemia was resolved. Conclusions Zidovudine has bone marrow suppression toxicity, which manifests as anaemia and can occur at any stage of use. Thus, we should not only pay attention to the initial stage of medication but also regularly monitor the patient via routine blood tests in the later stage. If anaemia occurs during the use of zidovudine, physicians should consider the possibility that anaemia is related to the administration of zidovudine and prescribe medication cessation and symptomatic treatment.

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Genome-wide DNA methylation profiles analysis in primary warm autoimmune hemolytic anemia patients

Cited by 2 publications

References 43 publications

Functional significance of DNA methylation: epigenetic insights into Sjögren’s syndrome

Functional significance of DNA methylation: epigenetic insights into Sjögren’s syndrome

A rare case report of severe aplastic anaemia caused by long-term use of zidovudine

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