Efficacy of keratinocyte growth factor (palifermin) for the treatment of caustic esophageal burns

Abstract

Current treatment strategies against the development of corrosive esophageal strictures remain unsatisfactory. Thus, the aim of the present study was to investigate the efficacy of keratinocyte growth factor, in the form of palifermin, for the prevention of stricture development following esophageal caustic injuries in a rat model. A total of 32 female Wistar albino rats were divided into four groups, which included the control (C), burn (B), steroid (S) and steroid plus palifermin (S/P) groups. An experimental corrosive esophageal burn model was established in the B, S and S/P groups. Weight gain was recorded and histopathological evaluation was performed for each group. Weight gain in the S and B groups was compared with the control group and statistically significant differences were observed. In addition, statistically significant differences in weight gain were observed between the S/P group and the B group. Histopathologically, statistically significant differences were identified with regard to submucosal collagen deposition, muscularis mucosa and tunica muscularis damage when comparing the B group with the C group. In addition, statistically significant differences were observed when comparing the S and S/P groups with the B group. Furthermore, significant submucosal collagen deposition and tunica muscularis damage were observed in the S group when compared with the S/P group. The stenosis indexes in the C and S groups were significantly lower compared with the B group. In addition, the stenosis index in the S/P group was significantly lower compared with the S group. To the best of our knowledge, the present study is the first to investigate the effect of palifermin on corrosive esophageal burns. The addition of palifermin to the corrosive esophageal burn standard treatment regimen was found to reduce the degree of fibrosis and ameliorate histopathological damage in an experimental model of corrosive esophagitis in rats.

Beneficial effects of garlic (Allium Sativum) oil inexperimental corrosive esophageal burns

“…[4] While ingestion of alkaline substances causes liquefaction necrosis in esophageal mucosa and submucosa, in severe cases, acidic substances cause coagulation necrosis in the muscularis mucosae layer. [20] Acute necrotic phase is seen over the first 1-4 days and is characterized by decreased tissue perfusion, increased lipid peroxidation, hydrolysis, reactive oxygen radicals, and beginning of inflammation. Following the subacute phase and long-term period, the scar formation begins with fibroblast proliferation.…”

“…[9] To reduce inflammation and collagen synthesis and to prevent fibroplasia and stricture formation, many clinical and experimental studies have evaluated the medical efficiency of antioxidant and anti-inflammatory agents, such as sucralfate, palifermin, dimethyl sulfoxide, prednisolon, retinoic acid, zinc, trapidil, trimetazidine, and pentoxifylline. [9][10][11][12][13]20,21] Despite decreased stricture formations in these studies, the rate of stricture formation remained at 70%-100% in highgrade corrosive esophagitis. [9] Garlic oil, a diallyl trisulfide, is the main active constituent of garlic and is one of the oldest medicine.…”

“…The stricture formation occurs via collagen accumulation. [12,20] The main goal of any medical treatment is to reduce any inflammation because the severity of the acute inflammatory reaction plays the most significant role in stricture formation. [21] The current treatment protocols in corrosive esophagitis remain limited to antibiotics and steroids administration and neutralizations during the acute phase.…”

The protective and anti-inflammatory effect of methylene blue in corrosive esophageal burns: An experimental study

“…[4] Alkaline substances cause liquefaction necrosis, while acidic substances cause coagulation necrosis that is mostly limited to the mucosa. [22] The acute necrotic phase occurs during the first 1-4 days following the injury and is characterized by decreased perfusion of the tissue, increased lipid peroxidation, hydrolysis, and reactive oxygen radicals and the beginning of the inflammatory reaction. Following the subacute phase, scar formation related to fibroblast proliferation and stricture formation related to collagen accumulation may occur.…”

“…Following the subacute phase, scar formation related to fibroblast proliferation and stricture formation related to collagen accumulation may occur. [12,22] The medical treatment needs to reduce the inflammation because the degree of the acute inflammatory reaction plays the most important role in stricture formation. [23] The current management protocol for corrosive esophagitis is still limited to antibiotics, steroids, and neutralization in the acute phase, although there are many other treatment methods that vary according to the phase and the severity of the damage.…”