Hemoplasmas are Gram-negative bacteria that can cause hemolytic anemia in a variety of mammalian species, including non-human primates. This study investigated the molecular prevalence and genetic characteristics of hemoplasmas in free-ranging long-tailed macaques in three previously unreported provinces in southern Thailand. In total, 210 blood samples were collected from long-tailed macaques in Phang Nga, Phetchaburi, and Satun provinces. DNA was extracted from the blood samples and screened for hemoplasmas using a broad-range nested polymerase chain reaction (PCR) assay targeting the 16S rRNA gene. Positive samples were sequenced for species identification, and phylogenetic analysis was performed to determine their genetic relationships. Overall, 35.7% (75/210; 95% CI = 29.2-42.6%) of the samples tested positive for hemoplasmas. Sequence analysis showed 99.3-100.0% identity with Candidatus Mycoplasma haematomacacae. Phylogenetic analysis confirmed that all sequences clustered within the Ca. M. haematomacacae clade, together with other reported isolates from macaques in several countries, including Thailand. In conclusion, this study has provided molecular evidence of Ca. M. haematomacacae infection in long-tailed macaques in areas where such infections had not been previously reported. Based on the results of this study, long-tailed macaques in various regions of Thailand might be infected with and act as reservoirs for this pathogen.

Massive splenomegaly refers to a marked and clinically significant enlargement of the spleen beyond normal limits. Although uncommon, it is clinically significant because it may be associated with hematologic, infectious, infiltrative, malignant, or portal hypertensive disorders. Chronic hemolytic anemias are a recognized cause of marked splenic enlargement due to persistent erythrocyte destruction and reticuloendothelial hyperplasia. Ongoing hemolysis also increases bilirubin production, predisposing patients to pigment gallstone formation and biliary tract disease. We report the case of a 29-year-old male who presented with jaundice and imaging findings consistent with choledocholithiasis. His medical history was notable for chronic hemolytic anemia and recurrent episodes of jaundice. Magnetic resonance cholangiopancreatography confirmed common bile duct stones and marked splenomegaly. The patient underwent exploratory laparotomy with splenectomy and common bile duct exploration followed by choledochoduodenal anastomosis. Intraoperatively, a massively enlarged spleen and hepatomegaly were identified. Significant bleeding from the splenic pedicle required vascular control and a blood transfusion. The postoperative course was favorable, with progressive reduction in bilirubin levels and no evidence of further complications. Histopathological examination demonstrated a congestive spleen with extensive hemorrhagic areas. This case highlights the importance of a multidisciplinary approach in the evaluation and management of massive splenomegaly and illustrates that timely surgical treatment can achieve satisfactory outcomes in selected patients.

Thrombotic microangiopathy (TMA) is an acute syndrome characterized by microangiopathic hemolytic anemia, thrombocytopenia, and ischemic end-organ damage resulting from platelet-rich microthrombi obstructing the microvasculature. The kidney is particularly vulnerable to TMA-mediated injury due to its numerous microvessels, often leading to acute kidney injury (AKI). AKI induced by TMA can manifest in oncological conditions, although infrequently. Rectal cancer presenting with TMA-related AKI as the initial manifestation is even rarer, posing a diagnostic challenge for nephrologists. We describe a 62-year-old man admitted with AKI followed by severe thrombocytopenia and anemia. During the diagnostic workup to exclude thrombotic thrombocytopenic purpura, the patient achieved complete hematological recovery after hemodialysis and plasma exchange (PEX), which enabled the performance of a renal biopsy. The underlying etiology was TMA on renal biopsy. However, persistent elevation of lactate dehydrogenase and new‑onset of bone pain prompted further evaluation. The magnetic resonance imaging scan and positron emission tomography-computed tomography subsequently confirmed rectal cancer with bone and liver metastases. This case illustrates that AKI secondary to cancer-related TMA may present as the initial clinical manifestation of an underlying malignancy. Renal biopsy plays a crucial role in establishing a definitive diagnosis and guiding subsequent management. Furthermore, PEX was associated with hematological improvement in this patient, but its overall clinical benefit remains to be determined as the patient remained dialysis‑dependent.

Autoimmune hemolytic anemia (AIHA) is an uncommon but recognized complication of intravenous immunoglobulin (IVIG) therapy in Kawasaki disease (KD). The mechanism is thought to involve passive transfer of donor isohemagglutinins that bind to recipient red blood cell (RBC) antigens, causing immune-mediated hemolysis. We describe four pediatric cases of IVIG-induced AIHA following treatment for KD. We retrospectively reviewed four KD patients who developed hemolytic anemia temporally associated with IVIG administration. Clinical data included age, blood type, transfusion requirement, and outcomes. All four patients were non-O blood types. Hemolysis developed within days of IVIG infusion, confirmed by a positive direct antiglobulin test. Two patients required red blood cell transfusions for symptomatic anemia. The lowest recorded hemoglobin levels ranged from 6.6 to 7.9 g/dL. None required corticosteroids or additional immunosuppression. All patients achieved full recovery with iron and folate supplementation. No coronary aneurysms or long-term complications were observed. IVIG-induced AIHA is a rare but clinically significant complication of KD therapy, particularly in non-O blood group patients. Routine post-infusion hemoglobin monitoring and early recognition of anemia are essential. Supportive management alone is typically sufficient, and prognosis remains excellent when the condition is promptly identified and managed.

Prior surveys of chronic automated red blood cell exchange (RCE) for patients with sickle cell disease (SCD) have identified considerable procedural variability, especially with the use of isovolemic hemodilution red blood cell exchange (IHD-RCE). We conducted a survey of chronic RCE practices among American Society for Apheresis (ASFA) members to identify opportunities for practice harmonization and future studies. The ASFA SCD Research Subcommittee developed a 72-item survey of chronic RCE practices, with a focus on IHD-RCE. The survey was validated internally and distributed by email to all ASFA members from September 2024 to February 2025. One survey response from each institution was retained for data analysis. Descriptive statistics were performed. Sixty-two survey responses, including three from international institutions, were retained for analysis. Sixty-one percent of respondents (38/62) reported using at least one fixed RCE target, with end hematocrit being the most common fixed parameter (40%, 25/62), followed by fraction of cells remaining (31%, 19/62) and hemoglobin S% (27%, 17/62). Most respondents (60%, 37/61) performed IHD-RCE at their institution, though other details such as the minimum hematocrit, exclusion criteria, and response to adverse effects were variable. Consistent pre- and post-RCE laboratory monitoring practices were reported. Consistent with earlier surveys, procedural variability in chronic RCE practices for patients with SCD is observed. This highlights opportunities to compare outcomes where practice variability exists. Consensus guidelines based on institutional practices with optimal outcomes should be developed.

Objective: To summarize current evidence on the use of buprenorphine for chronic pain management in individuals with sickle cell disease (SCD) and identify gaps for future research.

Autoimmune hemolytic anemia (AIHA) is an immune-mediated disorder in which red blood cells are destroyed by autoantibodies. It is classified as warm, cold, or mixed depending on the type of antibody involved. The clinical presentation can range from mild anemia to severe hemolysis, and it may occur as a primary condition or secondary to infections, autoimmune disorders, or hematological malignancies. Diagnosis relies on clinical findings combined with immunohematological tests, specifically the direct antiglobulin test (DAT). We describe the cases of three patients with different types of AIHA. The first patient was a 58-year-old woman who presented with severe anemia, low blood counts, and hepatosplenomegaly. Her blood tests revealed cold agglutinins and a positive DAT, and further evaluation identified B-cell acute lymphoblastic leukemia (B-ALL), confirming secondary cold AIHA. The second patient was a 55-year-old woman who presented with anemia, jaundice, and evidence of hemolysis, leading to a diagnosis of warm AIHA. The third patient was an 18-year-old woman who presented with severe anemia and splenomegaly. Her blood tests demonstrated both warm and cold antibody activity, and she was diagnosed with mixed AIHA. All three patients were treated with appropriate therapies and supportive care, resulting in clinical and hematological improvement. This case series illustrates the different ways AIHA can present and highlights the need for detailed immunohematological testing to identify the exact type, as well as the differences in treatment and management across AIHA subtypes. It also emphasizes the importance of searching for an underlying cause, as this guides treatment and improves outcomes.

This study investigated the polyphenolic composition, antioxidant capacity, and antianemic effects of aqueous leaf (JPEL) and berry (JPEB) extracts of Juniperus phoenicea ssp. turbinata L. (J. phoenicea ssp. turbinata). The plant is traditionally used to treat various ailments. HPLC-DAD analysis identified quercetin as the major compound (JPEB 49.09%; JPEL 31.34%), followed by p-coumaric acid (27.07% in JPEB), catechin (14.69% in JPEL), and gallic acid (JPEB 13.69%; JPEL 12.08%). Antioxidant activity was assessed using DPPH and reducing power assays, with the most active extract showing IC50 = 23.95 ± 0.64 µg/mL and EC50 = 300 ± 1.41 µg/mL. In vivo, 25 rats were assigned to 5 groups: negative control, PHZ-induced anemic control (40 mg/kg), JPEL-treated, JPEB-treated (300 mg/kg/day for 21 days), and a positive control (ascorbic acid, 10 mg/kg/day). Both extracts significantly ameliorated PHZ-induced hematological disturbances, restoring values toward normal. Molecular docking revealed favorable binding affinities of key phytochemicals with deoxy-hemoglobin and the TRPV4 ankyrin domains, suggesting potential interactions at these targets. However, these in silico findings are predictive and do not confirm functional protection or protein stabilization. The experimental results demonstrated antioxidant activity and improvement of hematological parameters in the animal model. These findings suggest that J. phoenicea ssp. turbinata extracts may warrant further investigation as natural sources of bioactive compounds. Nevertheless, additional pharmacological, toxicological, and clinical studies are required to validate these effects and assess their relevance for therapeutic applications.

Fludarabine treatment in patients with chronic lymphocytic leukemia (CLL) has been associated with immune dysregulation and the development of autoimmune hemolytic anemia (AIHA). Prior research indicates a potential correlation between the expression of the SLC28A3 gene, which encodes human concentrative nucleoside transporter 3 (responsible for fludarabine uptake), and treatment response. This retrospective study investigated the relationship between baseline SLC28A3 expression levels, quantified via reverse-transcriptase polymerase chain reaction (qRT-PCR), and the incidence of AIHA in a cohort of CLL patients receiving fludarabine and cyclophosphamide (FC) therapy. Patients were categorized into two groups: "FC-emergent AIHA," encompassing patients who developed AIHA during or following FC therapy, and "no FC-emergent AIHA," which included patients with pre-existing AIHA prior to any treatment and those who remained AIHA-free throughout follow-up. A comparative analysis of these groups revealed no significant differences in most clinical and biological variables. However, a statistically significant difference was observed in median baseline SLC28A3 expression, which was sevenfold lower in the "FC-emergent AIHA" group compared to the "no FC-emergent AIHA" group. Furthermore, SLC28A3 expression did not significantly correlate with most of the other clinical or biological parameters, including time to first treatment or overall survival. These findings suggest that diminished baseline SLC28A3 expression may correlate with an elevated risk of fludarabine-emergent AIHA in CLL patients. Further validation through larger, prospective cohorts is essential to confirm the predictive utility of SLC28A3 expression for optimizing fludarabine-based therapeutic strategies.

Although autoimmune hemolytic anemia (AIHA) is a well-known paraneoplastic syndrome in hematologic malignancies, it has rarely been reported in solid tumors. Documented cases of secondary warm AIHA (wAIHA) linked to solid tumors, particularly cervical cancer, are exceedingly rare. The present study reports 1 case of wAIHA occurring in a 73-year-old patient following radical chemoradiotherapy for cervical cancer. To the best of our knowledge, this association between wAIHA and cervical cancer has not been previously reported. The present case report highlights cervical cancer as a novel etiology of secondary AIHA and emphasizes the need for clinical vigilance to avoid diagnostic delays in post-treatment anemia.