Heckert J, Thomas R M, Parkman H P
GI Section, Department of Pathology, Temple University School of Medicine, Philadelphia, PA, USA.
Neurogastroenterol Motil. 2017 Aug;29(8). doi: 10.1111/nmo.13068. Epub 2017 Apr 4.
The aims of this study were to describe the histology in gastroparesis, specifically to relate histopathology to etiology of gastroparesis (idiopathic and diabetic gastroparesis), gastric emptying, and clinical response to gastric electric stimulation.
Full thickness gastric body sections obtained during insertion of gastric stimulator in gastroparetics were stained with Hematoxylin & Eosin, Masson Trichrome and immunohistochemical stains for Neuron-Specific Enolase and c-Kit.
In all, 145 gastroparetics (71 diabetics, 71 idiopathic, 2 post-surgical, and 1 chronic intestinal pseudo-obstruction) had full thickness gastric body biopsies. A lymphocytic infiltrate was seen in the intermyenteric plexus in 22 diabetic and 23 idiopathic gastroparesis patients. Fibrosis was present in the inner circular layer in 13 diabetic and 15 idiopathics and in the outer longitudinal layer in 46 diabetic and 51 idiopathics. Diabetic gastroparesis had less ganglion cells (3.27±1.82 vs 4.81±2.81/hpf; P<.01) and less ganglia (0.90±0.44 vs 1.10±0.50/hpf; P=.01) than idiopathic gastroparesis. Interstitial cells of Cajal (ICC) count was slightly lower in the inner circular layer in diabetic than idiopathics (2.77±1.47 vs 3.18±1.34/hpf; P=.08). Delayed gastric emptying was associated with reduced ICCs in the myenteric plexus. Global therapeutic response to gastric electric stimulation was inversely related to ganglia/hpf (R=-.22; P=.008). In diabetics, improvements in nausea, vomiting, and abdominal pain were inversely related to fibrosis.
Histologic assessment of full thickness gastric biopsy specimens allows correlation of histopathology to the gastroparesis disease process, its etiology, gastric emptying, and response to gastric electric stimulation treatment.
本研究旨在描述胃轻瘫的组织学特征，特别是将组织病理学与胃轻瘫的病因（特发性和糖尿病性胃轻瘫）、胃排空以及胃电刺激的临床反应相关联。
在胃轻瘫患者插入胃刺激器期间获取的胃体全层切片，用苏木精和伊红、马松三色染色以及神经元特异性烯醇化酶和c-Kit的免疫组织化学染色。
总共145例胃轻瘫患者（71例糖尿病患者、71例特发性患者、2例手术后患者和1例慢性肠道假性梗阻患者）进行了胃体全层活检。在22例糖尿病性和23例特发性胃轻瘫患者的肌间神经丛中可见淋巴细胞浸润。13例糖尿病患者和15例特发性患者的内环层存在纤维化，46例糖尿病患者和51例特发性患者的外纵层存在纤维化。糖尿病性胃轻瘫的神经节细胞（3.27±1.82对4.81±2.81/高倍视野；P< .01）和神经节（0.90±0.44对1.10±0.50/高倍视野；P = .01）比特发性胃轻瘫少。糖尿病患者内环层的 Cajal 间质细胞（ICC）计数略低于特发性患者（2.77±1.47对3.18±1.34/高倍视野；P = .08）。胃排空延迟与肌间神经丛中 ICC 减少有关。对胃电刺激的总体治疗反应与神经节/高倍视野呈负相关（R = -.22；P = .008）。在糖尿病患者中，恶心、呕吐和腹痛的改善与纤维化呈负相关。
胃活检标本全层的组织学评估可使组织病理学与胃轻瘫疾病过程、其病因、胃排空以及胃电刺激治疗反应相关联。
