Promising way to address massive intragastric clotting in patients with acute upper gastrointestinal bleeding: A case report.

BACKGROUND: Massive intragastric clotting (MIC) makes endoscopic therapy difficult in patients with acute upper gastrointestinal bleeding. Literature data on how to address this problem are limited. Here, we report on a case of massive stomach bleeding with MIC that was successfully treated endoscopically using an overtube of single-balloon enteroscopy. CASE SUMMARY: A 62-year-old gentleman with metastatic lung cancer was admitted to the intensive care unit due to tarry stools and hematemesis of 1500 mL of blood during hospitalization. Emergent esophagogastroduodenoscopy revealed massive blood clots and fresh blood in the stomach with evidence of active bleeding. Bleeding sites could not be observed even by changing the patient's position and aggressive endoscope suction. The MIC was successfully removed using an overtube connected with a suction pipe, which was inserted into the stomach with an overtube of a single-balloon enteroscope. An ultrathin gastroscope was also introduced through the nose into the stomach to guide the suction. A massive blood clot was successfully removed, and an ulcer with oozing bleeding at the inferior lesser curvature of the upper gastric body was revealed, facilitating endoscopic hemostatic therapy. CONCLUSION: This technique appears to be a previously unreported method to suction MIC out of the stomach in patients with acute upper gastrointestinal bleeding. This technique could be considered when other methods are not available or if they fail to remove massive blood clots in the stomach.

Mitochondrial damage mediates genotoxicity of arsenic in mammalian cells.

Arsenic is an important environmental carcinogen that affects millions of people worldwide through contaminated water supplies. For decades, arsenic was considered a nongenotoxic carcinogen. Using the highly sensitive A(L) mutation assay, we previously showed that arsenic is, indeed, a potent gene and chromosomal mutagen and that its effects are mediated through the induction of reactive oxygen species. However, the origin of these radicals and the pathways involved are not known. Here we show that mitochondrial damage plays a crucial role in arsenic mutagenicity. Treatment of enucleated cells with arsenic followed by rescue fusion with karyoplasts from controls resulted in significant mutant induction. In contrast, treatment of mitochondrial DNA-depleted (rho(0)) cells produced few or no mutations. Mitochondrial damage can lead to the release of superoxide anions, which then react with nitric oxide to produce the highly reactive peroxynitrites. The mutagenic damage was dampened by the nitric oxide synthase inhibitor, N(G)-methyl-L-arginine. These data illustrate that mitochondria are a primary target in arsenic-induced genotoxic response and that a better understanding of the mutagenic/carcinogenic mechanism of arsenic should provide a basis for better interventional approach in both treatment and prevention of arsenic-induced cancer.

Arsenic induces oxidative DNA damage in mammalian cells.

Although arsenic is a well-established human carcinogen, the underlying carcinogenic mechanism(s) is not known. Using the human-hamster hybrid (A(L)) cell mutagenic assay that is sensitive in detecting mutagens that induce predominately multilocus deletions, we showed previously that arsenite is indeed a potent gene and chromosomal mutagen and that oxyradicals may be involved in the mutagenic process. In the present study, the effects of free radical scavenging enzymes on the cytotoxic and mutagenic potential of arsenic were examined using the AL cells. Concurrent treatment of cells with either superoxide dismutase or catalase reduced both the cytotoxicity and mutagenicity of arsenite by an average of 2-3 fold, respectively. Using immunoperoxidase staining with a monoclonal antibody specific for 8-hydroxy-2'-deoxyguanosine (8-OHdG), we demonstrated that arsenic induced oxidative DNA damage in A(L) cells. This induction was significantly reduced in the presence of the antioxidant enzymes. Furthermore, reducing the intracellular levels of non-protein sulfhydryls (mainly glutathione) using buthionine S-R-Sulfoximine increased the total mutant yield by more than 3-fold as well as the proportion of mutants with multilocus deletions. Taken together, our data provide clear evidence that reactive oxygen species play an important causal role in the genotoxicity of arsenic in mammalian cells.