Zinc is an essential trace element, but excessive exposure can disrupt copper metabolism and lead to clinically significant hematologic abnormalities. This systematic review aimed to synthesize published evidence on zinc-induced hematologic toxicities. Literature search was performed in PubMed and Scopus to identify descriptive studies reporting zinc-induced hematologic toxicity in humans. Eligible studies described anemia, neutropenia, leukopenia, thrombocytopenia, pancytopenia, or bone marrow suppression attributed to zinc exposure. Data on patient demographics, zinc source and dose, duration of exposure, laboratory and bone marrow findings, treatment strategies, and outcomes were extracted. Study quality was assessed using Joanna Briggs Institute critical appraisal tools. Thirty-four publications describing 37 individual cases were included, spanning from 1972 to 2025. Zinc exposure most commonly resulted from oral supplements, denture adhesive creams, and coin ingestion, with reported daily elemental zinc doses ranging from approximately 50 mg to more than 1500 mg and exposure durations ranging from weeks to years. Anemia was present in nearly all cases, most often accompanied by neutropenia and leukopenia, with pancytopenia occurring in cases of severe or prolonged exposure. Serum copper levels were reduced in all patients. Bone marrow examination frequently revealed vacuolated hematopoietic precursors and ring sideroblasts, leading to frequent initial misdiagnosis as myelodysplastic syndrome. Discontinuation of zinc exposure with copper supplementation resulted in hematologic recovery in the majority of cases, typically within weeks to months, while neurological manifestations improved more slowly and were sometimes incomplete. Zinc-induced hematologic toxicity is an uncommon but underrecognized and largely reversible condition. Excessive zinc exposure should be considered in patients presenting with unexplained anemia and cytopenias. Routine assessment of zinc exposure and copper status can prevent misdiagnosis, support timely treatment, and decrease the risk of persistent neurological complications.

Backgroundand Objectives: Reliable prognostic biomarkers in sepsis that are inexpensive and universally available remain limited. Eosinophil counts decrease in systemic illness, but the prognostic value of static versus dynamic eosinophil measures in sepsis is uncertain. We investigated the association between eosinophil measurements, including early trajectories, and in-hospital mortality in a large sepsis cohort. Materials and Methods: We conducted a retrospective observational study of adult patients hospitalized with sepsis between 2021 and 2024 at a tertiary referral center. Absolute eosinophil counts were assessed at admission, at eosinophil nadir, and dynamically at approximately 48 and 72 h. Eosinophil trajectories were categorized as persistently undetectable, decrease, non-decrease, or rise from undetectable. Multivariable logistic regression models adjusted for demographic factors, comorbidities, and markers of disease severity were used to evaluate associations with in-hospital mortality. Results: Among 3932 patients, in-hospital mortality was 48.5%. Static eosinophil measures at admission and at eosinophil nadir were lower in non-survivors but were not independently associated with mortality after adjustment. Pancytopenia at eosinophil nadir was independently associated with increased mortality (OR 1.65, 95% CI 1.37-1.99). In contrast, eosinophil dynamics provided additional prognostic information. A decrease in eosinophil counts at 72 h was independently associated with higher mortality (OR 1.43, 95% CI 1.08-1.91), while 48 h changes were not. Persistently undetectable eosinophil trajectories were associated with the highest mortality, whereas recovery from undetectable levels was associated with lower risk. Conclusions: In sepsis, static eosinophil counts lack independent prognostic value, whereas delayed eosinophil decline and persistently suppressed trajectories are associated with increased in-hospital mortality. Eosinophil dynamics were associated with in-hospital mortality and may provide additional information on the host response during sepsis.

Dengue fever poses a significant diagnostic and therapeutic challenge in immunocompromised hosts, particularly in solid organ transplant recipients. We report a severe case in a patient during the early post-operative period following liver transplantation for hepatocellular carcinoma, who was concurrently receiving adjuvant chemotherapy with oxaliplatin and fluorouracil. This unique confluence of iatrogenic immunosuppression and chemotherapy-induced myelosuppression resulted in a life-threatening presentation characterized by grade 3 bone marrow suppression, severe anemia, overt gastrointestinal hemorrhage from gastric ulcers and colonic erosions, and acute kidney injury, necessitating intensive care management. Diagnosis was confirmed via dengue virus RNA testing, which was critical in differentiating the etiology from other potential causes of fever and pancytopenia in this complex setting. Management required a delicate balance of aggressive multidisciplinary supportive care, including endoscopic hemostasis and judicious blood product support, alongside cautious adjustment of immunosuppressive therapy to control the viral infection without precipitating graft rejection. This case underscores the severe, multifaceted complications dengue can precipitate in patients with dual vulnerabilities from transplantation and oncological therapy, highlighting the imperative for high clinical suspicion, rapid molecular diagnostics, and a coordinated, multidisciplinary approach to navigate competing clinical priorities and achieve a successful outcome.

Methotrexate (MTX) has long been a first-line anti-rheumatic agent due to its efficacy and cost-effectiveness. While generally safe at the recommended weekly dosage of 5-25 mg for rheumatoid arthritis, medication errors can lead to acute toxicity, severe adverse effects, and potentially fatal outcomes. We report a case of a 51-year-old male who experienced fatal pancytopenia following an MTX medication error during treatment for rheumatoid arthritis. His blood MTX concentration measured 0.04 μmol/L 11 days after discontinuation. Postmortem examination revealed MTX-related toxicity in multiple organs, including the liver and intestines. The spleen showed a prominent increase in plasma cells, including numerous Mott cells. Forensic analysis established the cause of death as acute MTX intoxication, directly stemming from a chain of medical negligence involving prescribing, verification, and administration failures. This case underscores the necessity of rigorous therapeutic drug monitoring, individualized dosing, and robust systemic safeguards to prevent iatrogenic fatalities, highlighting its critical medicolegal and educational implications for forensic and clinical practice.

Hemophagocytic lymphohistiocytosis (HLH) secondary to Pneumocystis jirovecii pneumonia (PJP) is extremely rare in children. We present the case of a 10-year-old girl with a history of idiopathic thrombocytopenic purpura (ITP) on long-term oral prednisone, who was admitted for progressive fever, cough, and dyspnea. Metagenomic next-generation sequencing of blood and bronchoalveolar lavage fluid confirmed PJP. Despite targeted antifungal therapy and respiratory support, she developed persistent high-grade fever, pancytopenia, hyperferritinemia, hypofibrinogenemia, and hemophagocytosis on bone marrow aspirate by day 10, meeting diagnostic criteria for HLH. Genetic testing was declined by the parents. Management included dexamethasone, continuous renal replacement therapy, and plasmapheresis. Unfortunately, her condition deteriorated, and she was discharged upon parental request on day 22, succumbing on the same day. To our knowledge, this is the first reported pediatric case of HLH secondary to PJP in China. This case highlights that in children with PJP-especially those on immunosuppressive therapy-the development of persistent fever and cytopenia should prompt immediate evaluation for secondary HLH to enable timely intervention.

Azathioprine is a thiopurine immunosuppressive medication widely used in the treatment of autoimmune diseases and organ transplantation. Although hematologic toxicity is well recognized, hepatotoxicity and hypersensitivity reactions are less commonly encountered but clinically significant adverse effects. We present the case of a 20-year-old female with systemic lupus erythematosus and class III lupus nephritis who developed progressive nausea, fatigue, eosinophilia, pancytopenia, and marked transaminase elevation shortly after initiation of azathioprine therapy. Imaging excluded biliary obstruction, while endoscopic and histologic evaluation demonstrated inflammatory changes with eosinophilic infiltration. Liver biopsy confirmed acute intrahepatocellular cholestatic hepatitis. Discontinuation of azathioprine led to rapid biochemical improvement and resolution of eosinophilia. This case highlights an early hypersensitivity-mediated presentation of azathioprine-induced liver injury and underscores the importance of early recognition and prompt drug withdrawal.

Severe aplastic anemia (SAA) is a rare pediatric bone marrow failure disorder marked by profound pancytopenia and high risk of infection, bleeding, and organ dysfunction. Despite advances in definitive therapy, children with SAA remain vulnerable to rapid deterioration during neutropenic sepsis. The role of extracorporeal membrane oxygenation (ECMO) in this population is poorly defined due to substantial hemorrhagic, thrombotic, and infection risks, thus necessitating careful risk-benefit assessment. A four-year-old child presented with febrile neutropenia and profound pancytopenia and was diagnosed with idiopathic severe aplastic anemia based on bone marrow biopsy demonstrating marked hypocellularity. Her course was complicated by persistent marrow failure and recurrent infections despite supportive care. Four months later, she developed refractory septic shock requiring ECMO, which was complicated by severe bleeding, disseminated intravascular coagulation, venous thrombosis, and progressive multi-organ failure, resulting in death. This case highlights the narrow therapeutic window of ECMO in pediatric SAA, in which profound cytopenias and immunosuppression markedly increase morbidity. While ECMO may provide temporary cardiopulmonary stabilization, its benefit depends on the likelihood of hematologic recovery and a clear pathway to definitive therapy. The use of ECMO in pediatric severe aplastic anemia, therefore, requires cautious patient selection, early multidisciplinary collaboration, and proactive goals-of-care discussions to ensure alignment with prognosis and family-centered values.

Deficiency of adenosine deaminase 2 (DADA2) is a rare autosomal recessive autoinflammatory disorder manifesting with variable clinical features, including systemic inflammation, vasculopathy, and recurrent ischemic or hemorrhagic strokes. Recurrent strokes have been well-established as part of the spectrum of DADA2 in keeping with the presentation of our patient. However, movement disorders in DADA2 have not been well-described. We report a case presenting with childhood-onset recurrent febrile illness, recurrent ischemic strokes, progressive generalized dystonia, intellectual disability and vasculitic rash. Neuroimaging revealed old pontine and bilateral thalamic infarcts while blood investigations revealed elevated inflammatory markers, pancytopenia and immunodeficiency. This case highlights the importance of recognizing DADA2 as a potentially treatable cause of early-onset stroke and movement disorder, emphasizing the need for timely diagnosis and targeted therapy.

Idiopathic dyskeratosis congenita (DC) is a disorder characterized by mucocutaneous alterations, bone-marrow failure, immune deficiency, liver cirrhosis, and other morbidities, due to alterations in telomere maintenance, which, in most cases, lead to short telomeres and poor tissue regeneration and function. The main cause of mortality is bone-marrow failure. A non-local diffusion-advection model with zero-flux boundary conditions is used to simulate the generational and temporal evolution of a hematopoietic stem cell (HSC) population in order to investigate the progression of DC. Blood-cell production from progenitor cells that had exited the HSC compartment was quantified. The influence of variations in initial proliferation potential ([Formula: see text]) and telomerase activity (s) on the onset of pancytopenia was examined. Age-and weight-dependent blood cell demands are modeled for both sexes, establishing a physiological baseline against which DC-related deficiencies are compared. Simulations revealed that lower [Formula: see text] values and reduced telomerase activity accelerate stem cell exhaustion, resulting in early pancytopenia, sometimes before age of 2 years. In contrast, patients with moderately higher [Formula: see text] values developed pancytopenia later in life, with onset delayed until the third or fourth decade. Treatment simulations demonstrated that a two-year course of danazol, a synthetic androgen, can slow telomere attrition. These findings suggest that pharmacological intervention may delay hematopoietic failure and possibly improve the production of oocytes with better-preserved telomeres in female DC patients. Our model provides a valuable framework for assessing (or understanding, or both) disease progression and evaluating therapeutic strategies in telomeropathy-associated bone marrow failure.