Schwannoma is a benign, encapsulated, slow-growing tumor that arises from Schwann cells. Approximately 25%-45% of extracranial schwannomas occur in the head and neck region, accounting for 1%-8% of all neoplasms. However, involvement of the infraorbital nerve is exceptionally rare. This report describes the surgical management of an infraorbital nerve schwannoma using a transconjunctival approach with lateral canthotomy, and documents the clinical, functional and aesthetic outcomes at 12 months. A 32-year-old woman with a history of hypochromic microcytic anemia presented with a progressively enlarging mass in the right infraorbital region that had been present for four years, associated with mild paresthesia in the nasolabial region. The main reason for consultation was aesthetic concern due to facial protrusion. Physical examination revealed a firm, painless subcutaneous mass without local inflammatory signs. Contrast-enhanced computed tomography revealed a solid, lobulated lesion measuring approximately 60 mm in maximum diameter in the right infraorbital region. Imaging features suggested an origin from the infraorbital foramen and involvement of the corresponding nerve; there was no evidence of osteolysis. Fine-needle aspiration cytology (FNAC) suggested a mesenchymal neoplasm. Surgical excision was performed under general anesthesia via a transconjunctival approach with lateral canthotomy. The infraorbital nerve was identified and preserved intraoperatively. Histopathological examination confirmed a schwannoma, showing spindle-shaped cells with Verocay bodies. The patient had a favorable clinical course. At the 12-month follow-up, facial symmetry and preserved sensory function were confirmed, as was the absence of recurrence.

Congenital dyserythropoietic anemia type IV (CDA IV) is a rare inherited erythroid disorder within the broad phenotypic spectrum associated with pathogenic variants in Krüppel-like factor 1 (KLF1), a master transcriptional regulator of erythropoiesis. This study aimed to describe the clinical picture, genetic causes, global distribution, and treatment of CDA IV. We retrospectively reviewed three pediatric patients diagnosed and treated at the Department of Pediatrics, The First Affiliated Hospital of Guangxi Medical University, since December 2014. Demographic, clinical, genetic, laboratory, treatment, transplantation, and follow-up data were collected, including conditioning regimens, graft-versus-host disease (GVHD) prophylaxis, engraftment, complications, and donor chimerism. We also conducted a literature review of CDA IV cases reported worldwide between January 1991 and December 2024. All three children developed symptoms within the first month of life. They had neonatal jaundice and anemia. One of them needed intrauterine transfusion. Gene testing found four KLF1 variants: c.525_526insCGGCGCC, c.1012C > T, c.1012C > A, and c.973G > A. Before hematopoietic stem cell transplantation (HSCT), all three patients needed regular red blood cell transfusions and had iron overload. All three then received HSCT from a parent or sibling. Neutrophils and platelets engrafted in every case. Donor chimerism stayed above 95% during follow-up, and no graft failure happened. No patient had acute or chronic GVHD. Viral reactivation after HSCT was mainly cytomegalovirus (CMV) and Epstein-Barr virus (EBV) infection, and no severe infection was seen. At the last follow-up, all three patients were free of transfusion. Serum ferritin levels went down after HSCT, but liver or heart iron overload did not fully go away in some patients. For carefully chosen children with severe transfusion-dependent KLF1-related red cell disease, allogeneic HSCT may be a feasible curative option. Stable donor chimerism and lasting freedom from transfusion can be achieved. CDA IV has many clinical forms and can be mistaken for thalassemia or Evans syndrome, so early gene testing is very important for correct diagnosis. In areas where thalassemia is common, KLF1 mutation screening should be considered when the cause of microcytic anemia is unclear. Bigger studies with longer follow-up are still needed to better judge the long-term results of HSCT.

Brunner's gland hyperplasia (BGH) is an uncommon benign proliferative condition of the Brunner's glands. It is often asymptomatic and typically discovered incidentally during endoscopic procedures. We report a case of a patient with BGH diagnosed with endoscopic ultrasound biopsy after an initial negative endoscopic mucosal biopsy. A 52-year-old male presented with palpitations and exertional dyspnea as well as melenic stools of a 3-week duration. Laboratory testing was remarkable for a hemoglobin level of 5.9 g/dl and a mean corpuscular volume of 62 fl. Esophagogastroduodenoscopy and mucosal biopsy were inconclusive, necessitating endoscopic ultrasound with fine-needle biopsies. Due to bleeding, the mass was resected, and histological examination revealed the diagnosis of BGH. This case underscores the importance of considering BGH in the differential diagnosis of gastrointestinal bleeding.

Background/Objectives: Omentin-1 (intelectin-1) is an adipocytokine with anti-inflammatory, insulin-sensitizing, and iron-regulatory properties. This study aimed to compare circulating omentin-1 levels in patients with (IDA) and β-thalassemia trait and to evaluate their associations with haematological, iron-related, and metabolic parameters. Methods: A total of 90 adults (n = 90), including 29 patients with IDA, 31 individuals with β-thalassemia trait, and 30 healthy controls. Haematological indices, iron parameters, biochemical markers, and plasma omentin-1 levels were measured. Group comparisons, correlation analyses, multivariable linear regression, and receiver operating characteristic (ROC) curve analyses were performed. Results: Plasma omentin-1 concentrations were significantly lower in patients with hypochromic microcytic anaemia than in healthy controls (36.4 vs. 147.7 ng/mL, p < 0.001). Among subgroups, the lowest levels were observed in IDA patients, followed by β-thalassemia trait and controls (p < 0.001). Omentin-1 showed positive correlations with haemoglobin, MCV, MCH, ferritin, serum iron, total cholesterol, HDL-C, and LDL-C, whereas negative correlations were observed with age, HbA1c, glucose, RDW, and total iron-binding capacity (all p < 0.05). In multivariable analysis, age (β = -0.215, p = 0.046), female sex (β = 0.305, p = 0.028), and MCV (β = 0.334, p = 0.015) were independent predictors of omentin-1 levels. ROC analysis demonstrated excellent discrimination between IDA and controls (AUC = 0.93) and good discrimination between β-thalassemia trait and controls (AUC = 0.79). Conclusions: Omentin-1 levels are reduced in IDA and β-thalassemia trait and are closely associated with iron status, erythroid indices, and metabolic parameters. Omentin-1 may serve as an adjunct biomarker for hypochromic microcytic anaemia, particularly in distinguishing affected individuals from healthy subjects. However, its limited utility in distinguishing iron-deficiency anaemia from β-thalassemia trait indicates that it should be used alongside established haematological and iron-related parameters.

Hookworm infection, while often asymptomatic, may rarely cause Löffler syndrome. We report the case of a 45-year-old female farmer who presented with a 10-year history of recurrent chest pain. Laboratory tests revealed marked eosinophilia (33.4%) and microcytic anemia. Cardiac and abdominal imaging findings were normal. Stool microscopy confirmed hookworm infection. Treatment of oral mebendazole (400 mg twice daily) for three days resulted in complete resolution of symptoms, normalization of eosinophil count, and clearance of parasites on follow-up. This case highlights hookworm infection as a potential cause of eosinophilia and chest pain in endemic regions.

Crohn's colitis may rarely present with severe bleeding and tumor-mimicking colonic lesions, creating concern for malignancy. A 20-year-old bedridden man with cerebral palsy had recurrent hematochezia and transfusion-dependent microcytic anemia, with hemoglobin 2.8 g/dL. Colonoscopy showed diffuse raised island-like plaques with vascular-pattern loss, rectal sparing, edematous ileocecal valve, and an oozing transverse-colon lesion requiring clipping. Multisite biopsies showed chronic active colitis with crypt distortion, cryptitis, and crypt abscesses, without granulomas, dysplasia, or malignancy. Tissue tuberculosis polymerase chain reaction was negative; interferon-gamma release assay was unavailable. Crohn's colitis was favored by clinicopathologic correlation. Bleeding resolved after corticosteroids, infliximab, and azathioprine; hemoglobin improved to 9.9 g/dL.

Background Anemia is a common and often underrecognized comorbidity in patients with hypothyroidism. Its etiology is multifactorial and is influenced by thyroid hormone deficiency, nutritional status, and concomitant chronic conditions. Understanding the prevalence, hematological patterns, and predictors of anemia in patients with hypothyroidism is necessary to improve clinical outcomes. This study aimed to assess the prevalence of anemia, describe its types and features, examine its association with thyroid hormone status, and identify the independent predictors of anemia in patients with hypothyroidism. Materials and methods A retrospective study was conducted in 444 patients diagnosed with hypothyroidism. Demographic, clinical, and laboratory data were extracted from the electronic medical records. Hematological indices were compared between the anemic and non‑anemic groups using independent t-tests and chi-square tests. Multivariate logistic regression was performed to identify the independent predictors of anemia after adjusting for age, sex, diabetes, and hypertension. Results Anemia was present in 112 (25.2%) patients. In anemic patients, the most common type was normocytic anemia, occurring in 64 (57.1%), followed by microcytic anemia in 46 (41.1%) and macrocytic anemia in two (1.8%). Patients with anemia had significantly higher platelet counts than those without anemia (p < 0.001). Markers of thyroid function (TSH, T3, and T4) did not differ significantly between the groups (p > 0.05). Multivariate analysis revealed that female sex (adjusted odds ratio (AOR) = 3.210, 95% confidence interval (CI): 1.323-7.789, p = 0.010) and the presence of chronic diseases (AOR = 3.458, 95% CI: 1.829-6.536, p < 0.001) were independent predictors of anemia. Conclusions One in four patients with hypothyroidism had anemia, and the most common type was normocytic anemia. No significant differences in thyroid hormone levels were observed between anemic and non-anemic patients. Female sex and chronic diseases were significant risk factors for anemia, emphasizing the importance of targeted screening and comprehensive evaluation of these subgroups. Early diagnosis and treatment of anemia may improve overall clinical outcomes in patients with hypothyroidism.

Hemoglobin variants and α-thalassemia deletions are uncommon causes of unexplained hypoxemia in children. This study reports a Chinese family affected by compound heterozygous HBA2 mutations that decrease hemoglobin-oxygen affinity. Clinical data, oxygen saturation (SpO2) trends, chest imaging, capillary hemoglobin electrophoresis, and genetic testing were conducted on the proband and his family members. The proband had persistently low SpO2 after pneumonia resolution, without respiratory distress; his 4-year-old brother experienced similar hypoxemia with normal cardiopulmonary evaluations. Capillary electrophoresis showed increased variant hemoglobin fractions in both siblings and their mother. Genetic analysis revealed compound heterozygosity: a maternally inherited HBA2: c.275T > C (p.L92P, Hb Port Phillip) and a paternally inherited -α[3.7] deletion. The proband's mother is heterozygous for the point mutation and asymptomatic, while the father carries the -α[3.7] deletion. This is the first report of a compound heterozygote for Hb Port Phillip and -α[3.7] deletion with hypoxemia in a Chinese family, thus broadening the phenotype-genotype spectrum of hemoglobinopathies. The unexpected low oxygen saturation may result from a hemoglobin variant in the setting of mild microcytic anemia; hemoglobin electrophoresis and genetic testing are crucial for accurate diagnosis and can prevent unnecessary interventions.

Atraumatic splenic rupture is a rare but potentially life-threatening condition, most commonly associated with infectious, hematological, neoplastic, inflammatory, or iatrogenic disorders. Cytomegalovirus (CMV)-associated splenic rupture is an exceptionally uncommon complication in immunocompetent individuals. We report the case of a 46-year-old immunocompetent man who presented to the emergency department with acute abdominal pain and a low-grade fever. Laboratory investigations revealed mild microcytic anemia, thrombocytopenia, elevated inflammatory markers, and mild transaminase elevation. Contrast-enhanced abdominal computed tomography demonstrated splenomegaly, a large perisplenic collection consistent with a subcapsular hematoma, and moderate hemoperitoneum, raising suspicion of atraumatic splenic rupture. During clinical observation, the patient developed hemodynamic instability, prompting emergency exploratory laparotomy. Intraoperative findings included massive hemoperitoneum, capsular laceration involving the upper pole, and an extensive subcapsular hematoma. Splenectomy was performed. Postoperative serological investigations revealed markedly elevated anti-CMV IgM levels associated with low anti-CMV IgG levels and low IgG avidity, consistent with acute CMV infection. The pathological examination supported the diagnosis of CMV-associated atraumatic splenic rupture. No antiviral therapy was deemed necessary following infectious disease consultation, and the patient recovered uneventfully with planned post-splenectomy vaccination. CMV infection has increasingly been linked to thrombotic and vascular complications, even in immunocompetent individuals. Proposed mechanisms of splenic rupture include endothelial dysfunction, transient prothrombotic states, lymphocytic infiltration of splenic tissue, ischemic injury, and reduced capsular elasticity. Since clinical manifestations are often nonspecific and may mimic other causes of acute abdomen, diagnosis can be challenging. Contrast-enhanced computed tomography remains the gold standard for diagnosis and therapeutic planning. Management depends on the severity of splenic injury and the patient's hemodynamic status; however, splenectomy remains the preferred treatment in cases of severe injury or hemodynamic deterioration. This case highlights the importance of considering CMV infection in the differential diagnosis of atraumatic splenic rupture and underscores the value of early imaging and prompt intervention in optimizing patient outcomes.

Hemosuccus pancreaticus is an uncommon but potentially life-threatening cause of upper gastrointestinal bleeding. We report the case of a 47-year-old man with a history of alcohol use disorder and alcohol use disorder and a previous episode of alcohol-induced acute pancreatitis who presented with melena, severe microcytic anemia, and recurrent epigastric pain. Upper endoscopy demonstrated blood emerging from the major papilla alternating with bile, raising suspicion for hemosuccus pancreaticus. Contrast-enhanced computed tomography revealed a large pseudoaneurysm of the pancreatoduodenal artery within the pancreatic head, likely secondary to chronic inflammatory changes. The patient underwent successful endovascular coil embolization, resulting in complete cessation of bleeding and an uneventful recovery. This case highlights the role of upper endoscopy in early recognition of hemosuccus pancreaticus and underscores the effectiveness of endovascular therapy in managing pseudoaneurysm-related hemorrhage.