Background/Objectives: Immune thrombocytopenia (ITP) is an autoimmune disease characterized by increased platelet destruction and insufficient platelet production. Accurate diagnosis, prognostic assessment, and treatment selection remain challenging. Long non-coding RNAs (lncRNAs) regulate immune responses and may contribute to ITP pathogenesis. This review examines lncRNA expression in ITP and its potential diagnostic, prognostic, and therapeutic relevance. Methods: We reviewed English-language literature published between 1994 and 2026 using PubMed, Scopus, and Google Scholar. We examined studies of specific lncRNAs in ITP, focusing on their expression differences and potential diagnostic and therapeutic implications. Re-sults: The studies examined HCP5, NEAT1, lnc-DC, IFNG-AS1, MEG3, GAS5, MALAT1, and THRIL. Findings suggest these lncRNAs may contribute to ITP pathogenesis and serve as candidate diagnostic and prognostic biomarkers. Some were reported as independent predictors of poor prognosis or were associated with glucocorticoid responsiveness. Potential applications include distinguishing primary from secondary ITP, informing patient selection for splenectomy, and identifying therapeutic targets. These applications remain investigational. Conclusions: Research on lncRNAs provides insight into autoimmune mechanisms underlying ITP and may support improvements in diagnosis, prognostic assessment, and individualized treatment. Although several lncRNAs show promise as biomarkers and therapeutic targets, further research, clinical validation, and methodological standardization are needed before routine clinical implementation.

Essential thrombocythemia (ET) is a Ph(-) myeloproliferative neoplasm characterized by elevated platelet counts. Patients most often have one of the three following driver mutations: JAK2, MPL, or CALR. However, these mutations are not detected in approximately 10–15% of patients, who are thus referred to as “triple-negative” (TN). Background/Objectives: In recent years, there have been breakthroughs in the genetic diagnosis of hematological diseases and progress in understanding their epigenetic basis. Aim: This study aimed to review the available literature and systematize the current knowledge on the molecular abnormalities in essential thrombocythemia. Particular attention was paid to the impacts of genetic mutations and epigenetic changes—such as abnormalities in non-coding RNA expression, DNA methylation, and histone modifications—on disease development and their clinical significance in patients with essential thrombocythemia. The most important publications on genetic and epigenetic mechanisms in essential thrombocythemia were reviewed and summarized. Methods: A review of the available literature was conducted using selected online databases. Publications from 2003 to 2026 were considered, covering the diagnosis and classification criteria for essential thrombocythemia, its genetic and epigenetic basis, and the associated impacts on the disease course. Conclusions: Although understanding the precise roles of genetic and epigenetic abnormalities in essential thrombocythemia remains challenging, they offer many opportunities for use as new diagnostic biomarkers and for the development of novel targeted treatment options. Further research is needed to better understand the genetic and epigenetic changes occurring in ET.

Background/Objectives: Immune thrombocytopenia (ITP) involves immune-mediated platelet destruction and impaired platelet production. Long non-coding RNAs (lncRNAs) regulate immune responses, but their clinical relevance in ITP remains uncertain. This narrative review examines disease-associated expression and mechanistic findings, distinguishing translational potential from established clinical utility. Methods: English-language literature identified through PubMed, Scopus, and Google Scholar was synthesized narratively. Eight named lncRNAs were prioritized because the cited ITP studies provided transcript-specific patient data or functional evidence; exploratory expression profiling and evidence from other diseases were considered separately. Study design, sample size, specimen type, treatment exposure, and validation status informed interpretation. Results: The selected transcripts were HCP5, NEAT1, lnc-DC, IFNG-AS1, MEG3, GAS5, MALAT1, and THRIL. Among the clinical studies with reported sample sizes, ITP groups generally included 20–90 patients, except for a GAS5 polymorphism study involving 302 patients. An independent prognostic association for low HCP5 expression was reported in a single study of 40 patients and has not been externally validated. Other studies described exploratory associations with bleeding, disease duration, or treatment response. Distinguishing primary from secondary ITP and selecting patients for splenectomy are not established applications. Cell experiments and a mouse model support mechanistic hypotheses but do not demonstrate therapeutic efficacy in humans. Conclusions: The evidence supports biological plausibility and translational investigation, rather than routine diagnostic, prognostic, or treatment-guiding use. Prospective validation in clinically representative cohorts and standardized assays are required.