Khaliq Laiba, Kabir Kaiser F, Pyai Khin, Hadid Tarik, Collins-Hamel Benjamin
Internal Medicine, Ascension Macomb Oakland, Warren, USA.
Internal Medicine, Michigan State University College of Osteopathic Medicine, Warren, USA.
Cureus. 2023 Aug 3;15(8):e42908. doi: 10.7759/cureus.42908. eCollection 2023 Aug.
While macrocytic anemia is common in vitamin B12 deficiency, rarely, pancytopenia and hemolytic anemia can occur. Homocysteine levels are elevated in severe B12 deficiency, and this is linked to thrombus formation with potentially life-threatening complications. We present a patient with severe vitamin B12 deficiency complicated by hyperhomocysteinemia and obstructive shock from pulmonary embolism. A 56-year-old male with no medical history presented to the hospital with altered mentation. The patient's family stated he was experiencing bilateral paresthesias of his lower extremities, progressive depression, anxiety, and insomnia. Initial vitals were blood pressure of 76/36, heart rate of 70 beats per minute, respiratory rate of 14, and temperature of 36.3 degrees Celsius. He was intubated due to severe encephalopathy. Relevant labs indicated severe macrocytic anemia, thrombocytopenia, decreased B12 levels, elevated methylmalonic acid, and elevated homocysteine. Imaging demonstrated a right common femoral vein thrombosis and subsegmental pulmonary emboli. Peripheral blood smear revealed schistocytes, anisopoikilocytosis, and decreased platelet count. The patient required fluid resuscitation, antibiotics, and multiple blood products. Vitamin B12 was administered intramuscularly, which improved the anemia. Esophagogastroduodenoscopy (EGD) demonstrated gastritis. Gastric and duodenal biopsies were negative for and celiac disease. He was negative for intrinsic factor (IF) antibodies but had elevated gastrin levels. An intravenous unfractionated heparin infusion was started when the platelet count was above 50000. The patient was extubated after seven days. Heparin was transitioned to apixaban and an inferior vena cava (IVC) filter was placed. Hyperhomocysteinemia is a known pro-thrombotic factor that can lead to the development of venous thromboembolism. B12 malabsorption can stem from inflammatory bowel disease, celiac disease, gastritis, pancreatic insufficiency, gastrectomy, gastric bypass surgery, or antibodies to IF. While this case showed gastritis and negative IF antibodies, gastrin levels were elevated, indicating a mixed picture. This highlights the challenge of definitively diagnosing pernicious anemia as the cause of vitamin B12 deficiency. Vitamin B12 deficiency may lead to critical illness in which thromboembolism develops secondary to hyperhomocysteinemia.
虽然巨幼细胞贫血在维生素B12缺乏症中很常见，但全血细胞减少症和溶血性贫血很少发生。严重的B12缺乏症会导致同型半胱氨酸水平升高，这与血栓形成及潜在的危及生命的并发症有关。我们报告了一名患有严重维生素B12缺乏症并伴有高同型半胱氨酸血症和肺栓塞导致的梗阻性休克的患者。一名无病史的56岁男性因精神状态改变入院。患者家属称他双下肢有感觉异常，伴有进行性抑郁、焦虑和失眠。初始生命体征为血压76/36，心率每分钟70次，呼吸频率14次，体温36.3摄氏度。由于严重脑病，他被插管。相关实验室检查显示严重巨幼细胞贫血、血小板减少、B12水平降低、甲基丙二酸升高和同型半胱氨酸升高。影像学检查显示右股总静脉血栓形成和亚段肺栓塞。外周血涂片显示破碎红细胞、异形红细胞增多和血小板计数减少。患者需要液体复苏、抗生素和多种血液制品。肌肉注射维生素B12后贫血有所改善。食管胃十二指肠镜检查（EGD）显示胃炎。胃和十二指肠活检对 和乳糜泻呈阴性。他的内因子（IF）抗体呈阴性，但胃泌素水平升高。当血小板计数高于50000时开始静脉输注普通肝素。患者7天后拔管。肝素改为阿哌沙班，并放置了下腔静脉（IVC）滤器。高同型半胱氨酸血症是一种已知的促血栓形成因素，可导致静脉血栓栓塞的发生。B12吸收不良可能源于炎症性肠病、乳糜泻、胃炎、胰腺功能不全、胃切除术、胃旁路手术或IF抗体。虽然该病例显示胃炎且IF抗体阴性，但胃泌素水平升高，表明情况复杂。这凸显了明确诊断恶性贫血作为维生素B12缺乏症病因的挑战。维生素B12缺乏症可能导致危重病，其中血栓栓塞继发于高同型半胱氨酸血症。
