The incidence of copper sulfate poisoning varies across different regions. It is relatively rare in Western countries but more prevalent in South Asian nations, accounting for approximately 40% of all heavy metal poisoning cases. The majority of affected individuals are rural residents, with a mortality rate ranging from 14% to 36%. Copper sulfate poisoning often leads to gastrointestinal corrosion, intravascular hemolysis, hemolytic anemia, methemoglobinemia, and acute multi-organ dysfunction, often resulting in death due to delayed treatment. In June 2024, we successfully managed a case of acute oral copper sulfate poisoning through early interventions, including gastric lavage and sodium dimercaptopropane sulfonate (Na-DMPS) for copper chelation, resulting in the patient's recovery and discharge after 1 week.

Scrub typhus, a re-emerging zoonosis caused by Orientia tsutsugamushi, can present with severe, life-threatening complications, including multi-organ dysfunction and hemolytic anemia. This report details the case of a 40-year-old female with underlying thalassemia who presented with symptoms initially suggestive of pyelonephritis but rapidly progressed to septic shock, multi-organ dysfunction syndrome, and a severe hemolytic crisis. Concurrent Escherichia coli and Enterococcus gallinarum pyelonephritis further complicated the clinical picture. Diagnosis was confirmed by the identification of a characteristic eschar and metagenomic next-generation sequencing. Targeted therapy with doxycycline and broad-spectrum antibiotics, alongside supportive care, led to a favorable outcome. This case underscores the protean manifestations of scrub typhus, highlights its potential to precipitate catastrophic hemolysis in patients with chronic hemolytic disorders, and demonstrates the critical role of advanced diagnostics and a high index of suspicion for dual pathology in guiding effective, life-saving management in endemic regions.

Pernicious anemia (PA) is an autoimmune-mediated vitamin B12 deficiency that classically presents with macrocytic anemia and neurologic dysfunction. The case described highlights a rare variant of PA that paralleled concerns for microangiopathic hemolytic anemia (MAHA) like thrombotic thrombocytopenic purpura (TTP). A 40-year-old African American female with limited past medical history presented with progressive fatigue, lower-extremity weakness, gait instability, and ataxia, accompanied by chronic gastrointestinal symptoms, weight loss, and menorrhagia. Initial evaluation revealed profound macrocytosis, pancytopenia, laboratory evidence of hemolysis, including an elevated lactate dehydrogenase (LDH) and undetectable haptoglobin level without evidence of acute kidney injury (AKI), and neurologic deficits concerning for subacute combined degeneration. This case was complicated by right lower lobe pneumonia, urinary tract infection, and a left Bartholin cyst. Further testing demonstrated elevated methylmalonic acid and homocysteine levels, positive intrinsic factor (IF) antibodies, and only mildly reduced ADAMTS13 activity, which confirmed the diagnosis of PA. The patient was treated with parenteral vitamin B12, folate, and supportive care, resulting in gradual recovery. Although inpatient rehabilitation was recommended, the patient declined and was instead discharged home with arrangements for outpatient follow-up and lifelong intramuscular vitamin B12 replacement therapy. This case underscores the importance of recognizing that, in rare cases, PA can present as a mimicker of thrombotic microangiopathies such as TTP, as early identification can prevent unnecessary therapeutic intervention, reduce morbidity, and facilitate timely, disease-specific therapy.

Hereditary spherocytosis (HS) is a common inherited hemolytic anemia characterized by spherical erythrocytes, splenomegaly, and increased osmotic fragility, with ANK1 mutations being the most frequent cause. We identified a novel ANK1 mutation (c.5096G>A, p.R1699K) in a patient with classic HS phenotypes and a family history of hemolytic anemia. To explore its pathogenicity, we performed a series of hematological and morphological analyses. Compared with wild-type mice, the Ank1 c.5198G>A knock-in mice displayed typical HS features. Hematologically, they showed reduced MCV, MCH, and MCHC. The EMA fluorescence intensity was significantly decreased, and RBCs exhibited increased osmotic fragility. Morphologically, peripheral smears revealed abundant spherocytes, and electron microscopy showed a transformation from normal biconcave discs to spherical erythrocytes. Additionally, the Ank1 c.5198G>A knock-in mice presented with significant splenomegaly. Mechanistically, coimmunoprecipitation analysis indicated a significantly weakened association between ankyrin-1 and β-spectrin in the Ank1 c.5198G>A knock-in mice. This study provides in vivo evidence that the Ank1 R1733K mutation impairs erythrocyte membrane stability and cytoskeletal integrity, recapitulating the HS phenotype in mice. Our findings support the pathogenicity of the ANK1 c.5096G>A mutation and offer a useful model for further investigating the molecular mechanisms of HS.

Patients' compliance with primaquine treatment is low due to the long 14-day duration of primaquine and the toxic side effects, including acute hemolytic anemia. This study aimed to develop a cobalt oxide/nickel cobalt sulfide/poly(1,8-diaminonaphthalene) (Co3O4@NiCo2S4@poly(1,8-DAN))-based electrochemical sensor for monitoring primaquine in urine to combat low adherence. The Co3O4@NiCo2S4@poly(1,8-DAN) nanocomposite was synthesized using hydrothermal and oxidative polymerization and characterized using high-resolution transmission electron microscopy (HRTEM), energy-dispersive X-ray spectroscopy (EDS), scanning electron microscopy (SEM), and Fourier transform infrared spectroscopy (FTIR). Differential pulse voltammetry (DPV) and electrochemical impedance spectroscopy were used to study the electrochemical properties of the nanocomposite. A 5 μL aliquot of Co3O4@NiCo2S4@poly(1,8-DAN) was drop-casted onto the glassy carbon electrode, and DPV was used to evaluate the electrochemical sensor's performance. A linear calibration response was established over primaquine's concentration range of 10-50 µM. The study found a detection limit of 2.51 nM with a linear concentration range of 10-50 µM. Real sample analysis in urine demonstrated recovery ranges of 98.3%-101.1%. This study reports, for the first time, the synthesis of the Co3O4@NiCo2S4@poly(1,8-DAN) ternary nanocomposite and its application for the detection of primaquine.

Anti-glomerular basement membrane (GBM) antibody disease rarely causes thrombotic microangiopathy (TMA). We herein report the case of a 75-year-old Japanese woman who developed refractory TMA during treatment for anti-GBM antibody disease. Although secondary TMA was initially suspected, persistent hemolytic anemia and thrombocytopenia despite plasma exchange, glucocorticoids, and cyclophosphamide led us to suspect complement-mediated TMA. Eculizumab was initiated after genetic testing for complement regulatory factors was performed. The patient became transfusion-independent within one week, and genetic testing identified the c.293C＞T (p.Thr98Ile) variant in CD46. Complement-mediated TMA should thus be considered in refractory cases, and anti-C5 monoclonal antibodies may be an effective therapeutic option.

Autoimmune hemolytic anemia (AIHA) is associated with a significant impairment of quality of life for affected patients and can lead to life-threating hemolytic crises. Complement-mediated destruction of antibody-opsonized erythrocytes is a central pathomechanism in many cases of AIHA. Complement inhibition is therefore a promising and logical therapeutic strategy. Sutimlimab, a monoclonal antibody that targets complement factor C1s was approved in 2022 and can effectively inhibit hemolysis. However, this therapy must be administered as a permanent treatment and is only approved for the specific subtype cold agglutinin disease. In this case series, we report on a novel combination therapy of sutimlimab and rituximab, which led to rapid and durable remission in three patients suffering from severe autoimmune hemolytic anemia (two patients with cold agglutinin syndrome and one patient with primary warm AIHA). In two of these patients, treatment with sutimlimab could be discontinued without any recurrence to date. The other patient is also in remission but with ongoing therapy. This highly informative case series reports on an innovative therapeutic concept and may form the basis for further clinical studies in AIHA.

Thalassemia is one of the most common monogenic disorders in southern China, with the Hakka population exhibiting a distinct genetic profile. This study evaluated whether next-generation sequencing (NGS)-based universal screening offers advantages over traditional cascade screening in this specific population. We enrolled 91,857 reproductive-age individuals in Ganzhou, a high-prevalence Hakka region, comparing 37,500 participants who underwent traditional screening (2019-2021) with 54,357 who received NGS-based screening. NGS-based screening detected thalassemia carriers at a rate 4.74 times higher than traditional screening (15.05% vs. 3.18%), particularly identifying silent α-thalassemia and β[++]-thalassemia variants that were substantially under-detected by the traditional approach. Crucially, while traditional screening identified 98.7% of β‑high‑severity couples, it detected only 71.4% of α‑high‑severity couples and missed 28.6% of those at risk for Hb Bart's hydrops fetalis, as well as 32.7% of couples at risk for severe non‑deletional Hb H disease. Traditional screening cost only USD 3.90 per person (versus USD 21.00 for NGS) and provided faster results (6.40 vs. 13.06 days). NGS-based universal screening provides a more accurate assessment of thalassemia burden and genotype diversity, offering critical advantages for prevention programs. Although traditional cascade screening is more cost-effective, its limited sensitivity for α-thalassemia variants leads to substantial underdetection. These findings underscore the need to tailor screening protocols to local epidemiological and genetic characteristics.

Hemotropic Mycoplasma spp., also known as hemoplasmas, are blood-borne pathogens that infect red blood cells and can cause hemolytic anemia in mammals, including dogs. Mycoplasma haemocanis (Mhc) and 'Candidatus Mycoplasma haematoparvum' (CMhp) are the two most common canine hemoplasma species. However, molecular epidemiological data and information on their genetic diversity remain scarce in Thailand. This study investigated hemoplasma PCR positivity in 472 client-owned dogs from Bangkok and Nakhon Pathom and 199 community dogs from Chiang Mai using a polymerase chain reaction (PCR) assay targeting the 16S rRNA gene. The 23S rRNA and RNase P RNA (rnpB) genes were additionally amplified from positive samples for multilocus characterization. Overall, 48 of 671 dogs were PCR-positive (7.2%; 95% confidence interval: 5.4%-9.3%). PCR positivity was higher in the community-dog/Chiang Mai cohort than in the client-owned cohorts; however, dog type and sampling location were fully confounded, and these comparisons should therefore be interpreted descriptively. Sequence analyses identified Mhc and CMhp. Sequence data suitable for analysis at both the 16S and 23S rRNA genes were obtained from 29 positive samples, and rnpB sequences were obtained from nine of these samples. To the best of our knowledge, this study provides the first 23S rRNA gene sequences of CMhp; no homologous CMhp 23S rRNA gene sequence was available in GenBank for direct comparison.

Chronic automated red blood cell exchange (RCE) is a cornerstone therapy for preventing sickle cell disease (SCD)-related complications, particularly stroke and recurrent vaso-occlusive crises. Current scheduling commonly relies on uniform empirical intervals of 3-6 weeks and does not account for substantial inter-patient variability in hemoglobin S (HbS) rebound kinetics, potentially resulting in undertreatment of rapid rebounders and unnecessary procedures in slower rebounders. We hypothesized that each patient's personalized rate of rise (ROR) of HbS could be used to generate an individualized, risk-adjusted RCE interval. We retrospectively analyzed adult patients with SCD receiving chronic outpatient RCE. The primary cohort comprised 18 patients with HbSS, while a single patient with HbSC was analyzed separately. HbS values from consecutive outpatient procedures were used to calculate an individual ROR (%HbS/day). A personalized scheduling formula was derived: t(interval) = S(risk) × (HbS(threshold) - HbS(post))/ROR(personal), where S(risk) represents an adjustable safety factor for patients at higher clinical risk. Individualized intervals differed markedly from uniform scheduling. Slow rebounders (< 0.5%/day) could potentially extend beyond 5 weeks, whereas rapid rebounders (> 1.0%/day) reached prespecified HbS thresholds within approximately 2-3 weeks. For most patients, the model recommended shorter intervals than those used, suggesting that under current scheduling many patients may exceed their HbS threshold between procedures. Because most patients would require shorter rather than longer intervals to maintain HbS below 30%, strict implementation of the model could increase program-level blood utilization; therefore, its principal value lies in precision and resource reallocation rather than guaranteed net savings. A personalized ROR-based scheduling framework integrates objective HbS kinetics with clinical risk stratification and may be most applicable to patients with stable, reproducible rebound kinetics. Prospective validation and integration into electronic health record systems are warranted to determine whether model-guided scheduling improves clinical outcomes.