Hughes Jing W, Muegge Brian D, Tobin Garry S, Litvin Marina, Sun Lulu, Saenz Jose B, Gyawali C Prakash, McGill Janet B
Endocr Pract. 2017 Nov;23(11):1297-1303. doi: 10.4158/EP-2017-0056.
Pernicious anemia (PA) develops from atrophic gastritis due to autoimmune destruction of parietal cells and results in achlorhydria, vitamin B12 and iron deficiencies, anemia, neurologic deficits, and premalignant and malignant stomach lesions. We report the presentation, diagnosis and gastric complications of PA in patients from an endocrinology practice.
Thirty-four patients (31 female, 3 male) with PA who underwent esophagogastroduodenoscopy (EGD) or gastrectomy were identified. Pertinent clinical, laboratory, and pathology findings were reviewed and summarized.
The mean age of patients was 58.6 ± 14.2 years; the onset of PA was age 50.2 ± 15.3 years. Anemia reflected vitamin B12 and/or iron deficiencies. Parietal cell antibodies (PCA) were detected in 97% of patients, and intrinsic factor blocking antibody (IFBA) was found in 52%. Fasting gastrin and chromogranin A levels were elevated (1,518.0 ± 1,588.3 pg/mL, and 504.9.1 ± 1,524.9 ng/mL respectively). Autoimmune or immunologic diseases (AIDs) were present in 32/34 patients. Stomach pathology showed premalignant or malignant lesions in 26 patients, including gastric neuroendocrine tumors (GNETs) in 6 and adenocarcinoma in 1. One patient presented with neurologic symptoms and subacute combined degeneration of the posterior column of the spinal cord.
PA should be suspected in patients with unexplained anemia or neurologic symptoms. The diagnosis of PA relies on fasting gastrin and gastric auto-antibody testing, in addition to hematologic evaluation. EGD with measurement of gastric pH and biopsies of the fundus and antrum identifies patients with achlorhydria, atrophic gastritis, and premalignant and malignant stomach lesions. EGD surveillance of patients with high-risk stomach lesions is recommended.
AID = autoimmune or immunologic disease; EGD = esophagogastroduodenoscopy; GNET = gastric neuroendocrine tumor; IFBA = intrinsic factor blocking antibody; PA = pernicious anemia; PCA = parietal cell antibody; T1D = type 1 diabetes.
恶性贫血（PA）由自身免疫性壁细胞破坏导致萎缩性胃炎发展而来，可引起胃酸缺乏、维生素B12和铁缺乏、贫血、神经功能缺损以及胃的癌前病变和恶性病变。我们报告了来自内分泌科的PA患者的临床表现、诊断及胃部并发症。
确定34例接受食管胃十二指肠镜检查（EGD）或胃切除术的PA患者（31例女性，3例男性）。回顾并总结相关临床、实验室及病理检查结果。
患者平均年龄为58.6±14.2岁；PA发病年龄为50.2±15.3岁。贫血反映维生素B12和/或铁缺乏。97%的患者检测到壁细胞抗体（PCA），52%的患者检测到内因子阻断抗体（IFBA）。空腹胃泌素和嗜铬粒蛋白A水平升高（分别为1518.0±1588.3 pg/mL和504.9±1524.9 ng/mL）。32/34例患者存在自身免疫或免疫性疾病（AIDs）。胃部病理显示26例患者有癌前或恶性病变，其中6例为胃神经内分泌肿瘤（GNETs），1例为腺癌。1例患者出现神经症状及脊髓后柱亚急性联合变性。
对于不明原因贫血或神经症状的患者应怀疑PA。PA的诊断除血液学评估外，还依赖于空腹胃泌素及胃自身抗体检测。测量胃pH值并对胃底和胃窦进行活检的EGD可识别胃酸缺乏、萎缩性胃炎以及胃的癌前和恶性病变患者。建议对胃高危病变患者进行EGD监测。
AID = 自身免疫或免疫性疾病；EGD = 食管胃十二指肠镜检查；GNET = 胃神经内分泌肿瘤；IFBA = 内因子阻断抗体；PA = 恶性贫血；PCA = 壁细胞抗体；T1D = 1型糖尿病
