• The Journal of Korean Medicine
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• v.23 no.3
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• pp.188-199
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• 2002

Objectives : Banhasasim-tang has been clinically used to treat upper gastric intestinal discomfort. The object of this study is to examine the defense effect of Banhasasim-tang for acute duodenal injury of the mouse. Methods and Materials : Twenty-one rats were divided into 3 groups and treated as follows: the control group was untreated mice. The ADE group was acute duodenal-damage-elicited mice. The BST group was Banhasasim-tang treated mice before acute duodenal damage elicitation. The groups were examined with common morphology, paneth cells in intestinal crypt, absorptive cells and goblet cells in epithelium, cell division in mucose, COX-l as mucosal protector, COX-2 (which appears to play an important role in inflammation), IL-2R-inducing cellular immuno-chainreaction, and the distribution of apoptotic cells. Results : 1. Common morphology: the ADE group was observed with duodenal injury - loss of villi, infiltration of cells concerned to inflammation (lymphocytes, granular leukocytes) to submucosal layer - by hemorrhagic erosions, while the BST group was seen the same as normal in proportion to increasing treatment time before injury. 2. Histochemical change: the ADE group was observed with noticeable decreased distribution of absorptive cells with microvilli, acid mucin secreted goblet cell, neutral mucin secreted goblet cell, paneth cells compared to the normal group. The BST group was seen to have distribution of epithelium cells resembling normal in proportion to increasing treatment time before injury. 3. Imnunohistochemical change: the ADE group showed a change of factors leading to duodenal injury as reduce of cytokinesis, COX-1, increase of COX-2, IL-2R-. In contrast, the BST group tended to reduction of cytokinesis, COX-1, increase of COX-2, IL-2R- in proportion to increasing taking time before injury. 4. Apoptosis change: the ADE group showed increasing apoptosis cells, in contrast to the BST group which was the same as normal in proportion to increasing treatment time before injury. Conclusions : According to the above results, by increasing the defense system of mucosal epithelium, Banhasasim-tang is thought to effectively protect tissue against ulcers resulting from acute duodenal injury.

• Journal of Trauma and Injury
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• v.18 no.2
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• pp.112-118
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• 2005

Background: N-Butyl Cyanoacrylate (NBCA) is a liquid embolic material that can be useful for transcatheter arterial embolization (TAE) of acute bleeding especially in patients with coagulopathy, because it does not depend on coagulation for its therapeutic effect. The aims of this study were to evaluate the clinical efficacy and safety of TAE with NBCA in acute bleeding patients. Methods: Between August 2003 and September 2004, TAE using NBCA for acute bleeding was performed in 23 patients (16 men, 7 women; mean age, 56.5years). The causes of bleeding were gastric ulcer (n=5), postoperative bleeding (n=4), post-biopsy bleeding (n=3), postpartum bleeding (n=3), duodenal ulcer (n=2), angiodysplasia (n=2), gastric lymphoma (n=1), iatrogenic injury (n=1), CMV gastritis (n=1), stab injury of the liver (n=1). TAE was performed using 1:3 mixtures of NBCA and iodized oil. The angiographic and clinical success rate, recurrent bleeding rate, procedure-related complication and clinical outcomes were evaluated. Results: The angiographic and clinical success rate was 100% and 91.3% (21/23), respectively. There was no serious ischemic complication. Recurrent bleeding occurred in 2 patients (8.7%) and they were managed with successful second TAE (n=1) and endoscopic treatment (n=1). Nine patients (39.1%) had coagulopathy at the time of TAE and clinical success rate in this group of patients was 88.9% (8/9). Conclusions: TAE with NBCA is highly effective and safe treatment modality for acute bleeding patients, especially when the patient has a coagulopathy.

• Journal of The Korean Society of Clinical Toxicology
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• v.16 no.2
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• pp.157-160
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• 2018

Chronic silica nephropathy has been associated with tubulointerstitial disease, immune-mediated multisystem disease, chronic kidney disease, and end-stage renal disease. On the other hand, acute intentional exposure is extremely rare. The authors' experienced a 44-year-old man who took rapid cement hardener (sodium silicate) in a suicide attempt whilst in a drunken state. He visited the emergency department approximately 1 hour after ingestion. Information on the material was obtained after 3 L gastric lavage. The patient complained of a sore throat, epigastric pain, and swollen to blood tinged vomitus. Proton pump inhibitors, hemostats, steroid, and fluids were administered. Nine hours after ingestion, he was administered 200 mL hematochezia. Immediately after, a gas-troenterologist performed an endoscopic procedure that revealed diffuse hyperemic mucosa with a color change and variable sized ulceration in the esophagus, whole stomach, and duodenal $2^{nd}$ portion. Approximately 35 hours later, persistent oligouria and progressive worsening of the renal function parameters (BUN/Cr from 12.2/1.2 to 67.5/6.6 mg/dL) occurred requiring hemodialysis. The patient underwent 8 sessions of hemodialysis for 1 month and the BUN/Cr level increased to 143.2/11.2 mg/dL and decreased to 7.6/1.5 mg/dL. He was discharged safely from the hospital. Follow up endoscopy revealed a severe esophageal stricture and he underwent endoscopic bougie dilatation. Acute cement hardener (sodium silicate) intoxication can cause renal failure and strong caustic mucosal injury. Therefore, it is important to consider early hemodialysis and treatment to prevent gastrointestinal injury and remote esophageal stricture.