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Last update 08 May 2025

Transient Erythroblastopenia of Childhood

Last update 08 May 2025

Basic Info

Synonyms

ERYTHROBLASTOPENIA, TRANSIENT, Erythroblastopenia, transient, Familial transient erythroblastopenia of childhood

+ [10]

Introduction

An acquired pure red cell aplasia that is self-limited. It is the most common cause of decreased red blood cell production in the pediatric population, and typically presents as a normocytic anemia with reticulocytopenia in an otherwise asymptomatic and normal child with no evidence of other causes for anemia, including blood loss, hemolysis, nutritional deficiency, or malignancy.

Clinical Trials associated with Transient Erythroblastopenia of Childhood

JPRN-jRCTs031230310

/ RecruitingPhase 2IIT

A pilot study of the long-term safety and efficacy of oral sirolimus in patients with relapsed or refractory acquired chronic pure red cell aplasia - A pilot study of sirolimus for aPRCA

Start Date28 Aug 2023

Sponsor / Collaborator-

NCT04423367

/ CompletedPhase 2IIT

Safety and Efficacy of Bortezomib Plus Dexamethasone for Acquired Pure Red Cell Aplasia Failure or Relapse After First-line Treatment: A Prospective Phase II Trial

This is an open-label, single-arm study to evaluate the safety and efficacy of bortezomib plus dexamethasone for acquired pure red cell aplasia failure or relapse after first-line treatment.

Start Date13 Sep 2020

Sponsor / Collaborator

Hematology Hospital of Chinese Academy of Medical Sciences

JPRN-UMIN000033866

/ RecruitingNot ApplicableIIT

Next generation sequencing diagnostics of relapsing/refractory acquired pure red cell aplasia in adults (PRCA-NGS2017 study) - NGS diagnostics in PRCA

Start Date01 Sep 2018

Sponsor / Collaborator

Akita University

100 Clinical Results associated with Transient Erythroblastopenia of Childhood

100 Translational Medicine associated with Transient Erythroblastopenia of Childhood

0 Patents (Medical) associated with Transient Erythroblastopenia of Childhood

402

Literatures (Medical) associated with Transient Erythroblastopenia of Childhood

01 Jul 2025·Annals of Vascular Surgery

Efficacy and Safety of Tranexamic Acid in Noncardiac Arterial Procedures: A Systematic Review and Meta-Analysis

Review

Author: Yeung, Kak Khee ; Wiersema, Arno M ; Bakker, Nathalie C ; Steunenberg, Thomas A H ; Jongkind, Vincent ; Tournoij, Erik

BACKGROUNDNoncardiac arterial procedures (NCAPs) are associated with a high risk of bleeding. Tranexamic acid (TXA) is used among surgical disciplines to reduce blood loss; however, its effectiveness and safety in NCAP remain unclear. This review evaluates the efficacy and safety of TXA during NCAP.METHODSSystematic review and meta-analysis was performed in accordance with Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines. Literature searches in PubMed, Embase, and Cochrane databases (October 2023 and October 2024) identified studies investigating TXA in open and endovascular NCAP. Meta-analyses were conducted using Cochrane's Review Manager.RESULTSFive studies (n = 4304) were identified. One randomized controlled trial of TXA in noncardiac surgery (n = 9535), including a vascular cohort (14.8%; n = 699 TXA, n = 700 placebo), showed lower composite bleeding outcomes in the overall cohort receiving TXA (9.5% vs 11.7%; P < 0.001), but not in the vascular cohort (hazard ratio 0.85; 95% confidence interval [CI] 0.64-1.13). Another trial found no difference in blood loss or transfusion rates in 100 patients undergoing open abdominal aortic aneurysm surgery. Both trials reported no increased cardiovascular or thromboembolic complications (TECs) or 30-day mortality. A prospective study showed similar thrombosis-related technical failure rates in traumatic vascular injury patients (TXA 6.3% vs 3.8%, P = 0.14) and no significant differences in bleeding or hematoma (TXA 11.4% vs 4.3%, P = 0.13). In 297 carotid endarterectomy (CEA) patients, TXA significantly reduced postoperative hematoma (7.9% vs 1.3%; P = 0.01) without increasing TEC or stroke. TXA during an intraoperative hemostasis protocol during CEA (TXA n = 8) reported similar results. Meta-analysis showed no significant differences in TEC (risk ratio [RR] 1.10; 95% CI 0.71-1.70) or reoperation rates (RR 0.55; 95% CI 0.19-1.63).CONCLUSIONTXA does not increase the risk of TEC in NCAP. However, there is currently insufficient evidence that TXA reduces bleeding complications.

01 Apr 2025·The American Journal of Dermatopathology

Thiotepa-Induced Toxicity: A Clinical Mimic of Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis Featuring Severe Mucositis, Diffuse Dusky Discoloration, and Skin Sloughing

Article

Author: Shaker, Nada ; Ben Musa, Ruwaida ; Bhowmik, Rituja ; Sangueza, Omar P. ; Phelps, Robert ; Pradhan, Dinesh ; Niedt, George

Background:Thiotepa, an alkylating agent commonly used in chemotherapy, is increasingly recognized to induce cutaneous reactions resembling toxic erythema of chemotherapy (TEC). This condition is characterized by erythema, hyperpigmentation, and mucositis, often affecting intertriginous areas, and can mimic the early stages of Stevens–Johnson syndrome (SJS) or toxic epidermal necrolysis (TEN).Case description:A 31-year-old woman with a history of systemic lupus erythematosus, antiphospholipid antibody syndrome, seizures, and chronic kidney disease was admitted for the management of central nervous system (CNS) lymphoma. Seven days after receiving thiotepa during an autologous stem cell transplant, she developed severe mucositis, requiring intubation for airway protection, followed by a dusky, gray, full-body rash with sloughing in the groin, axillae, and buttocks. A skin biopsy from the back revealed vacuolar interface changes, eccrine gland necrosis, and occasional necrotic keratinocytes at the dermal-epidermal junction, with no evidence of full-thickness necrosis or significant eosinophilic infiltration. The differential diagnosis included thiotepa-induced toxicity, SJS/TEN, and drug eruption. Based on the patient's clinical presentation and the biopsy findings, thiotepa-induced TEC was favored over SJS/TEN.Discussion:Thiotepa is a potent lipophilic alkylating agent widely used in chemotherapy for pediatric and adult patients with various solid tumors and hematologic malignancies. Its anticancer mechanism involves DNA alkylation, leading to DNA strand cross-linking that disrupts replication and transcription, ultimately inhibiting cancer cell proliferation and survival. While thiotepa is primarily utilized in high-dose preparative regimens for stem cell transplantation in pediatric patients, its use in the adult population remains comparatively limited.This case emphasizes the importance of differentiating thiotepa-induced TEC from severe cutaneous adverse reactions such as SJS/TEN. While these conditions share clinical and histologic features, the absence of extensive epidermal necrosis, satellite cell necrosis, and systemic involvement, along with recent thiotepa exposure, supported a diagnosis of TEC.Conclusions:This case highlights the diagnostic challenge of distinguishing thiotepa-induced TEC from SJS/TEN in post-transplant patients. Recognizing the characteristic involvement of intertriginous areas and eccrine gland necrosis in TEC is critical for accurate diagnosis and management. Awareness of this potential complication in patients receiving thiotepa is essential to avoid misdiagnosis and inappropriate treatment.

17 Mar 2025·Journal of Clinical Investigation

Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury

Review

Author: Baker, Megan L. ; Cantley, Lloyd G.

Acute kidney injury (AKI) encompasses pathophysiology ranging from glomerular hypofiltration to tubular cell injury and outflow obstruction. This Review will focus on the tubulointerstitial processes that underlie most cases of AKI. Tubular epithelial cell (TEC) injury can occur via distinct insults, including ischemia, nephrotoxins, sepsis, and primary immune-mediated processes. Following these initial insults, tubular cells can activate survival and repair responses or they can develop mitochondrial dysfunction and metabolic reprogramming, cell-cycle arrest, and programmed cell death. Developing evidence suggests that the fate of individual tubular cells to survive and proliferate or undergo cell death or senescence is frequently determined by a biphasic immune response with initial proinflammatory macrophage, neutrophil, and lymphocyte infiltration exacerbating injury and activating programmed cell death, while alternatively activated macrophages and specific lymphocyte subsets subsequently modulate inflammation and promote repair. Functional recovery requires that this reparative phase supports proteolytic degradation of tubular casts, proliferation of surviving TECs, and restoration of TEC differentiation. Incomplete resolution or persistence of inflammation can lead to failed tubular repair, fibrosis, and chronic kidney disease. Despite extensive research in animal models, translating preclinical findings to therapies remains challenging, emphasizing the need for integrated multiomic approaches to advance AKI understanding and treatment.

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Transient Erythroblastopenia of Childhood

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