Mucosal healing after high dose pantoprazole in acute corrosive injury of esophagus

R. Nanda, A. Mohammed
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Abstract

INTRODUCTION : The ingestion of corrosive agents is still an important public health issue in our country. The GIT injuries caused by caustic agents can range from minor to fatal, or can lead to chronic disease with poor quality of life. Corrosive agents with a pH level less than two or more than twelve can rapidly penetrate the layers of the oesophagus and result in necrosis and scar formation in the mucosa. Acidic agents produce coagulation necrosis and eschar formation that may limit tissue penetration and may even spare the oesophagus when the transit is rapid. On the other hand, Alkaline agents when ingested produce liquefaction necrosis and can cause serious oesophageal injury by penetrating to deep muscle layers. The basic histopathologic reaction of tissue subjected to caustic burn is the synthesis, deposition and remodelling of collagen. Following full-thickness injuries to the oesophageal wall, the normal oesophagus is replaced by dense connective tissue. Collagen overproduction has been estimated to cause stenosis in half of the patients suffering severe burns. Consequently, when treating caustic burn injuries, it is necessary to prevent stenosis by inhibiting collagen synthesis or changing the properties of the deposited collagen. The optimal management protocol in the treatment of severe caustic injury remains controversial. The main goal of medical treatment is to inhibit inflammatory reaction or stricture formation secondary to oesophageal burning. Stricture formation is thought to be overcome by suppressing fibroplasia and scarring. Many agents directed at wound healing and stricture prevention have been used in several experimental studies in past. Results of such treatment protocols including steroids, antibiotics, heparin, indomethacin, sucralfate, vitamin E, as well as total parenteral nutrition are all controversial in treatment of corrosive burns. Randomised control trials on the role of proton pump inhibitors in caustic injuries of GIT are lacking. A few experimental studies have investigated the relationship between proton pump inhibitors and corrosive burns and has shown that proton pump inhibitors can reduce inflammation in early phase of caustic injury. Proton pump inhibitors, by decreasing gastric acid secretion and thereby GER can prevent worsening of corrosive injury. In addition proton pump inhibitors has also been shown to have anti-inflammatory and antioxidant properties. A prospective study from turkey on 13 patients have showed that omeprazole can be used effectively in treatment of acute corrosive injury of esophagus. There are no studies from India which have attempted to assess the usefulness of proton pump inhibitors in treatment of acute corrosive injury of esophagus. This prompted us to study the usefulness of pantoprazole in the treatment of patients presenting with acute corrosive injury of the oesophagus. AIM OF THE STUDY : To study the efficacy of high dose pantoprazole in causing mucosal healing after acute corrosive injury of esophagus. CONCLUSION : Treatment of corrosive injury is controversial and there are no definitive protocols. Intravenous proton pump inhibitors are widely used in treatment of corrosive injuries despite lack of evidence. Our study has demonstrated that effective mucosal healing can be achieved by intravenous proton pump inhibitor infusion. Though majority of patients in our study had minor grade of injury, 27% of the patients included in the study had 2b and 3a injury. When analysis is confined to these patients, 53% showed improvement by 1 grade, 33.3% showed improvement by 2 grades and 13.3% did not show improvement. Therefore it is evident from above that high dose pantoprazole is also beneficial in patients with higher grade of injury and may prevent late complications in these patients. A larger randomised placebo controlled trial in patients with higher grade of oesophageal injury is needed to determine if high dose pantoprazole should form standard of care in treatment of patients with acute corrosive injury of oesophagus.
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大剂量泮托拉唑治疗食管急性腐蚀性损伤后粘膜愈合
导读:腐蚀性物质的摄入在我国仍然是一个重要的公共卫生问题。由腐蚀剂引起的胃肠道损伤从轻微到致命不等,或可导致慢性疾病,生活质量差。pH值小于2或大于12的腐蚀性物质可以迅速穿透食道层,导致粘膜坏死和瘢痕形成。酸性药剂会产生凝固性坏死和瘢痕形成,这可能会限制组织的渗透,甚至在快速通过时可能会避免食道。另一方面,摄入碱性物质会产生液化性坏死,并可穿透深层肌肉层,造成严重的食管损伤。烧灼组织的基本组织病理反应是胶原蛋白的合成、沉积和重塑。食管壁全层损伤后,正常食管被致密结缔组织所取代。据估计,半数严重烧伤患者的血管狭窄是由胶原蛋白过量引起的。因此,在治疗烧灼伤时,有必要通过抑制胶原合成或改变沉积胶原的性质来防止狭窄。严重烧灼伤的最佳治疗方案仍存在争议。医学治疗的主要目的是抑制炎症反应或继发于食管烧伤的狭窄形成。狭窄的形成被认为是通过抑制纤维增生和瘢痕形成来克服的。许多针对伤口愈合和预防狭窄的药物已经在过去的一些实验研究中使用。包括类固醇、抗生素、肝素、吲哚美辛、硫糖铝、维生素E以及全肠外营养在内的治疗方案对腐蚀性烧伤的治疗结果都存在争议。缺乏质子泵抑制剂在胃肠道腐蚀性损伤中的作用的随机对照试验。一些实验研究探讨了质子泵抑制剂与腐蚀性烧伤之间的关系,并表明质子泵抑制剂可以减轻腐蚀性损伤早期的炎症。质子泵抑制剂通过减少胃酸分泌,从而抑制胃液的腐蚀损伤。此外,质子泵抑制剂也被证明具有抗炎和抗氧化的特性。土耳其13例患者的前瞻性研究表明,奥美拉唑可有效治疗急性食管腐蚀性损伤。没有来自印度的研究试图评估质子泵抑制剂在治疗食管急性腐蚀性损伤中的有效性。这促使我们研究泮托拉唑治疗急性食道腐蚀性损伤的有效性。研究目的:探讨大剂量泮托拉唑对食管急性腐蚀性损伤后粘膜愈合的影响。结论:腐蚀性损伤的治疗存在争议,目前尚无明确的治疗方案。静脉注射质子泵抑制剂广泛用于治疗腐蚀性损伤,尽管缺乏证据。我们的研究表明,通过静脉注射质子泵抑制剂可以实现有效的粘膜愈合。虽然我们的研究中大多数患者为轻度损伤,但有27%的患者为2b和3a级损伤。当分析仅限于这些患者时,53%的患者表现出1级的改善,33.3%的患者表现出2级的改善,13.3%的患者没有表现出改善。由此可见,大剂量泮托拉唑对损伤程度较高的患者也有益,并可预防这些患者的晚期并发症。需要在较高程度食管损伤患者中进行更大规模的随机安慰剂对照试验,以确定大剂量泮托拉唑是否应成为急性食管腐蚀性损伤患者治疗的标准护理。
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