• Journal of Chest Surgery
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• v.43 no.3
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• pp.280-284
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• 2010

Background: The postoperative management following lung transplantation has dramatically improved in the recent decade. However, some complications still remain as troublesome problems. We retrospectively reviewed the gastrointestinal complications and their management after lung transplantation. Material and Method: We performed a retrospective review of the medical records of 25 cases in 23 patients who underwent lung and heart-lung transplantations from July 1996 to March 2009. The definition of gastrointestinal complication was the gastrointestinal tract-related disease that occurred after lung transplantation. There were eight postoperative deaths (within postoperative 30 days) that were excluded from the analysis. Result: Twenty three gastrointestinal complications occurred in 11 (64.7%) of the 17 cases. The median follow-up period was 6.9 months (range: 2 months to 111 months), and chronic gastritis (23.5%, 4 of 17 cases) was the most common complication. Severe, prolonged (more than 2 weeks) diarrhea occurred in 3 cases. Three patients had gastric ulcer with one case requiring gastric primary closure for gastric ulcer perforation. This patient had gastric bleeding due to recurrent gastric ulcer 2 months after laparotomy. Cytomegalovirus gastritis and esophagitis occurred in 2 cases and 1 case, respectively, and esophageal ulcer occurred in 2 cases. There were esophageal strictures in 2 patients who underwent esophageal stent insertion. Other complications were one case each of ileus, early gastric cancer requiring endoscopic mucosal resection, gall bladder stone accompanied with jaundice, and pseudomembranous colitis. Conclusion: The incidence of gastrointestinal complication is relatively high in patients after they undergo lung transplantation. Since gastrointestinal complications can induce malnutrition, which might be related to considerable morbidity and mortality, close follow-up is necessary for the early detection and proper management of gastrointestinal complications.

• Journal of Life Science
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• v.28 no.8
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• pp.885-891
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• 2018

Clostridium difficile (C. difficile) toxin A is known to cause acute gut inflammation in humans and animals by triggering cytoskeletal disorganization in gut epithelial cells. In human colonocytes, toxin A blocks microtubule assembly by directly increasing the enzymatic activity of histone deacetylase-6 (HDAC-6), a tubulin-specific deacetylase, thereby markedly decreasing tubulin acetylation, which is essential for microtubule assembly. Microtubule assembly dysfunction-associated alterations (i.e., toxin A-exposed gut epithelial cells) are believed to trigger barrier dysfunction and gut inflammation downstream. We recently showed that potassium acetate blocked toxin A-induced microtubule disassembly by inhibiting HDAC-6. Herein, we tested whether acetic acid (AA), another small acetyl residue-containing agent, could block toxin A-induced tubulin deacetylation and subsequent microtubule assembly. Our results revealed that AA treatment increased tubulin acetylation and enhanced microtubule assembly in an HT29 human colonocyte cell line. AA also clearly increased tubulin acetylation in murine colonic explants. Interestingly, the AA treatment also alleviated toxin A-induced tubulin deacetylation and microtubule disassembly, and MTT assays revealed that AA reduced toxin A-induced cell toxicity. Collectively, these results suggest that AA can block the ability of toxin A to cause microtubule disassembly-triggered cytoskeletal disorganization by blocking toxin A-mediated deacetylation of tubulin.

• Tuberculosis and Respiratory Diseases
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• v.69 no.2
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• pp.115-118
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• 2010

Paclitaxel has been widely used for treating many solid tumors. Although colonic toxicity is an unusual complication of paclitaxel-based chemotherapy, the reported toxicities include pseudomembranous colitis, neutropenic enterocolitis and on rare occasions ischemic colitis. $Genexol-PM^{(R)}$, which is a recently developed cremophor-free, polymeric micelle-formulated paclitaxel, has shown a more potent antitumor effect because it can increase the usual dose of paclitaxel due to that $Genexol-PM^{(R)}$ does not include the toxic cremophor compound. We report here on a case of a 57-year-old man with advanced non-small cell lung cancer and who developed ischemic colitis after chemotherapy with $Genexol-PM^{(R)}$ and cisplatin. He complained of hematochezia with abdominal pain on the left lower quadrant. Colonoscopy revealed diffuse mucosal hemorrhage and edema from the sigmoid colon to the splenic flexure. After bowel rest, he recovered from his symptoms and the follow-up colonoscopic findings showed that the mucosa was healing. Since then, he was treated with pemetrexed monotherapy instead of a paclitaxel compound and platinum.

• Journal of Microbiology and Biotechnology
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• v.26 no.8
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• pp.1446-1451
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• 2016

Clostridium difficile toxin A causes acute gut inflammation in animals and humans. It is known to downregulate the tight junctions between colonic epithelial cells, allowing luminal contents to access body tissues and trigger acute immune responses. However, it is not yet known whether this loss of the barrier function is a critical factor in the progression of toxin A-induced pseudomembranous colitis. We previously showed that NADH:quinone oxidoreductase 1 (NQO1) KO (knockout) mice spontaneously display weak gut inflammation and a marked loss of colonic epithelial tight junctions. Moreover, NQO1 KO mice exhibited highly increased inflammatory responses compared with NQO1 WT (wild-type) control mice when subjected to DSS-induced experimental colitis. Here, we tested whether toxin A could also trigger more severe inflammatory responses in NQO1 KO mice compared with NQO1 WT mice. Indeed, our results show that C. difficile toxin A-mediated enteritis is significantly enhanced in NQO1 KO mice compared with NQO1 WT mice. The levels of fluid secretion, villus disruption, and epithelial cell apoptosis were also higher in toxin A-treated NQO1 KO mice compared with WT mice. The previous and present results collectively show that NQO1 is involved in the formation of tight junctions in the small intestine, and that defects in NQO1 enhance C. difficile toxin A-induced acute inflammatory responses, presumably via the loss of epithelial cell tight junctions.

• Journal of Oral Medicine and Pain
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• v.26 no.1
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• pp.1-10
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• 2001

To investigate the relationship between several intraoral soft tissue lesions(hairy tongue, lichen planus, recurrent aphthous stomatitis, oral candidiasis, glossitis and oral herpetic lesion) and oral mucosal keratinization, exfoliative cytological smear on intraoral mucosal surfaces were performed on each number of patients and 25 controls keratinization cell (yellow-stained cell) ratio was then measured. In hairy tongue, there was no significant difference between patient group and control group in all kind of cells. Only blue cell ratio of women was more than of men in patient group. In lichen planus, there was no difference between patient and control group in yellow cell ratio. Red cell ratio in the control group was more than in the patient group. Blue cell ratio in the patient group was more than that in control group. But there was no sex predilection between both groups in the ratio of all kind of cells. In recurrent aphthous stomatitis, Yellow cell ratio in the control group was more than that in the patient group. Red cell ratio in the control group was more than that in control group. Blue cell ratio in the patient group was more than that in control group. But there was no sex predilection between both groups in the ratio of all kind of cells. In oral candidiasis, Yellow cell ratio in the control group was more than that in the patient group. Red cell ratio in the control group was more than that in control group. Blue cell ratio in the patient group was more than that in control group. There was no sex predilection between both groups in yellow cell ratio. Red cell ratio of women was more than of men in patient group. Blue cell ratio of men was more than of women in patient group. In herpetic lesions, there was no difference between patient and control group in yellow cell ratio. Red cell ratio in the control group was more than in the patient group. Blue cell ratio in the patient group was more than that in control group. Yellow cell ratio of women was more than of men in control group. Red cell ratio of men was more than of women in control group. Blue cell ratio of men was more than of women in patient group. In glossitis, Yellow cell ratio in the control group was more than in the patient group. There was no difference between patient and control group in red cell ratio. Blue cell ratio in the patient group was more than that in control group. Yellow cell ratio of women was more than of men in control group. Red cell ratio and blue cell ratio of men were more than of women in control group. According to above results, the ratio of keratinized cell in atrophic, ulcerated, or pseudomembranous lesions was lowered than in control, but the ratio of keratinized cell in keratotic, vesicular or lesions on keratinized surface lesions had no difference to control group. Thus, keratotic, vesicular or lesions on keratinized surface lesions have not closely relation to mucosal keratinization. And, there was a little sex predilection between men and wemen in mucosal keratinization.

• Journal of Gastric Cancer
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• v.8 no.4
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• pp.237-243
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• 2008

Purpose: Postoperative Infectious complications are recognized as major complications that are associated with surgery. Although many studies have focused on the risk factors of postoperative complications, little is known about the risk factors of infectious complications after gastric cancer surgery, and especially after elective gastrectomy. There is now more and more interest in the risk factors of infectious complications in relation to controlling infection and as indicators of qualitatively assessing infectious complications. The aim of this study was to evaluate the risk factors related with infectious complications after performing elective gastrectomy for treating gastric cancer. Materials and Methods: We retrospectively reviewed a total of 788 patients who had undergone elective gastrectomy for gastric cancer between Jan. 2000 and Dec. 2007. The characteristics of the patients were divided according to the patients' factors and the operations' factors. Results: The patients' mean age was 58.9 (range: 24~91) years; 545 were male and 243 were female. The mean duration of the hospital stay was 20.3 days (range: 5~135 days), the mean operation time was 181.3 minutes (range: 65~440 minutes). The total complication rate was 17.1% (n=135) and the complication rate was 38.5% (n=52) among the 135 patients with infectious complications. The infectious complications were surgical site infection (59.7%), Pneumonia (19.3%), intra-abdominal abscess (11.5%), pseudomembranous colitis (5.7%), bacteremia (1.9%) and hepatic abscess (1.9%). On the univariate analysis, the significant risk factors were male gender, blood transfusion, smoking at the time of diagnosis, alcohol drinking, diabetes mellitus and previous cardiovascular disease (P<0.05 for all). On multivariate analysis that used a logistic regression model, the significant independent risk factors were smoking at the time of diagnosis (OR: 2.877. 95% CI: 1.449~5.713), blood transfusion (OR: 3.440, 95% CI: 1.241~9.534), diabetes mellitus (OR: 3.150, 95% CI: 1.518~6.538), and previous cardiovascular disease (OR: 2.784, 95% CI: 1.4731~5.2539). Conclusion: Pre- or post-operative blood transfusion and the patient's medical history such as previous cardiovascular disease, diabetes mellitus, smoking etc. are the risk factors for infectious complications after undergoing elective gastrectomy for gastric cancer. The patients that have these risk factors need to be treated with great care to prevent infectious disease after elective gastrectomy.