Background: Megaloblastic anemia is a hyperchromic macrocytic anemia caused by impaired DNA synthesis and delayed cell division, most commonly resulting from deficiencies of cobalamin and folic acid. Vitamin B12 is obtained from animal-derived foods such as meat, fish, eggs, and dairy products. In the stomach, it is released from dietary proteins by gastric acid and subsequently binds to an intrinsic factor, after which it is absorbed in the distal ileum. Therefore, vitamin B12 deficiency may occur following gastric or intestinal resection surgery. Another common cause of vitamin B12 deficiency is pernicious anemia, which results from autoimmune atrophic gastritis leading to decreased secretion of intrinsic factor. Vitamin B12 deficiency is most frequently observed in individuals over 60 years of age, and its clinical manifestations vary depending on the severity of deficiency. Patients with mild to moderate deficiency commonly present with fatigue, general symptoms of anemia, glossitis, and neurological disturbances. In cases of severe deficiency, profound hematological abnormalities, severe neurological manifestations, and cardiac involvement such as cardiomyopathy may be observed. In this report, we present a clinical case of a 46-year-old male who developed severe vitamin B12 deficiency anemia following total gastrectomy, complicated by anemia-induced mild hypokinesia of the anterior and inferior walls of the heart. Conclusion If vitamin B12 deficiency–related anemia is accurately diagnosed, appropriately treated, prevented, and monitored starting from the primary health care level, it can have a positive impact on patients’ quality of life. Given that this condition may present with diverse clinical manifestations, a multidisciplinary team approach involving specialists in hematology, neurology, psychiatry, gastroenterology, cardiology, and nutrition enables early identification and prevention of potential complications, thereby improving overall clinical outcomes.

Background: Sjögren’s syndrome is a chronic autoimmune disease characterized by lymphocytic infiltration of the exocrine glands, particularly the lacrimal and salivary glands, as a result of genetic and environmental factors, and it is mainly manifested by mucosal dryness. Sjögren’s syndrome is a rare disorder with a prevalence of approximately 6 cases per 1,000 population and shows a marked female predominance. It is most commonly diagnosed between the ages of 40 and 60 years. Anemia is observed in about 70% of patients diagnosed with Sjögren’s syndrome; however, autoimmune hemolytic anemia occurs in only approximately 3% of cases. In this report, we present a rare case of Sjögren’s syndrome that manifested with warm autoimmune hemolytic anemia. Conclusion In cases of autoimmune hemolytic anemia of unknown etiology, it is crucial to investigate the underlying causes leading to hemolysis in order to establish the differential diagnosis and to confirm or exclude the condition. Sjögren’s syndrome typically presents initially with sicca symptoms, with chronic anemia developing during the course of the disease and its treatment. In contrast, in our case, persistent manifestations of autoimmune hemolytic anemia over a prolonged period represented the initial clinical presentation that led to the diagnosis of Sjögren’s syndrome. Immunological markers play a key role in the diagnosis of this syndrome, as they are essential for early detection of Sjögren’s syndrome, timely diagnostic confirmation, monitoring of disease progression, and adjustment of therapeutic dosing.

Objectives: Waldenstrom Macroglobulinemia (WM) is a malignant disease of the B lymphocytes. We report on a patient in Mongolia having WM complicated with hyperviscosity syndrome. Methods: A 28 year-old Mongolian woman had symptoms due to hyperviscosity syndrome such as vision loss, headache, dizziness and, epistaxis. Upon examination, her morphology, biochemistry, histology, flow cytometry and serum protein electrophoresis indicated WM complicated with hyperviscosity syndrome. Results: The patient was was successfully treated with a combination chemotherapy and plasmapheresis. Conclusion: Hyperviscosity syndrome manifestations should be treated with plasmapheresis.