[Clinicopathological study of acute esophageal mucosal lesion].

Acute esophageal mucosal lesion (AEML) is a comprehensive disease that includes necrotizing esophagitis and acute erosive esophagitis, which result in upper gastrointestinal bleeding. However, little is known about AEML. We examined the clinicopathological features of 57 AEML cases. AEML presented as acute diffuse esophagitis showing an endoscopically erosive mucosa. The disease did not include corrosive injury, radiation-induced damage, infectious esophagitis, or acute exacerbation of chronic gastroesophageal reflux disease. AEML predominantly affected elderly men, and upper gastrointestinal bleeding was the frequent presenting symptom. Severe underlying diseases such as cranial nerve disease or pneumonia were observed in 98% of the patients. Esophageal sliding hernia and gastroduodenal ulcers were endoscopically observed in 67% and 63% of the patients, respectively. Deaths due to exacerbation of the underlying diseases accounted for 16%. Most cases rapidly improved with conservative management using a proton pump inhibitor or an H2 blocker. Therefore, AEML should be considered a disease having characteristics different from those of common gastroesophageal reflux disease.

The inducible prostaglandin E synthase mPGES-1 regulates growth of endometrial tissues and angiogenesis in a mouse implantation model.

Endometriosis is one of the most common gynecological diseases in women of reproductive age. Although cyclooxygenase (COX)-2 inhibitors are effective in the treatment of endometriosis, the adverse cardiovascular effects associated with these inhibitors have limited their use. Microsomal prostaglandin E synthase-1 (mPGES-1) is an inducible enzyme downstream of COX-2 in prostaglandin E(2) biosynthesis. Previously, we developed mPGES-1 knockout mice (mPGES-1(-/-)) and have identified for the first time the roles of ectopic lesion- and host-associated mPGES-1 in angiogenesis and the growth of endometrial tissues. When mPGES-1(-/-) endometrial fragments were implanted into wild type (WT) mice (mPGES-1(-/-)→WT), or WT fragments implanted into mPGES-1(-/-) mice (WT→mPGES-1(-/-)), the growth of the implants was suppressed at days 14 and 28 after implantation, compared toWT→WT transplantation. An even greater degree of suppression was observed in mPGES-1(-/-) endometrial fragments implanted into mPGES-1(-/-) mice (mPGES-1(-/-)→mPGES-1(-/-)). After WT-WT implantation, mPGES-1 expression was localized at the border of the implanted endometrial tissues. Microvessel density, determined by CD31 immunostaining, was markedly suppressed in the mPGES-1(-/-) endometrial fragments implanted into mPGES-1(-/-) mice, with some suppression also observed in the mPGES-1(-/-)→WT and WT→mPGES-1(-/-) groups. The expression of vascular endothelial growth factor (VEGF-A) was significantly reduced in mPGES-1(-/-) endometrial tissues implanted into mPGES-1(-/-) mice at days 14 and 28, in comparison to the WT→WT group. These results suggested that mPGES-1 enhanced angiogenesis and growth of the endometrial implant, and indicate that mPGES-1 may be a good therapeutic target for endometriosis.