Ulcer Formation (ulcer + formation)

Distribution by Scientific Domains

Selected Abstracts

Primary lung cancer associated with Werner syndrome

Shunichiro Ohnishi
A 52-year-old man with Werner Syndrome (WS) was admitted to our hospital for the treatment of skin ulcers on his thighs. Routine chest radiography revealed an abnormal shadow in the left upper lung field. Computed tomography (CT) revealed a poorly demarcated homogeneous mass (diameter, 4 cm) in the S1 + 2 lung area; no pleural effusion was observed. CT-guided percutaneous needle biopsy revealed the presence of an adenocarcinoma. Other imaging studies did not reveal any lymph-node involvement or presence of metastatic lesions. The patient was diagnosed with stage IB adenocarcinoma (T2N0M0), and a left upper lobectomy was successfully carried out; postoperative wound healing was steady and uneventful, with no obvious ulcer formation. Primary lung cancers very rarely develop in patients with WS; non-epithelial tumors are usually observed in such patients. Patients with WS usually develop severe skin problems, such as refractory skin ulcers in the extremities; however, our patient did not develop any skin-related complications after surgery. As the expected lifespan of patients with WS is increasing, we need to pay attention not only to the rare non-epithelial malignancy, but also cancer. Further, the expected short lifespan of patients with WS, as well as the possibility of skin-related problems after surgery, should not be considered while deciding whether to take the option of surgery in the case of malignancy. Geriatr Gerontol Int 2010; 10: 319,323. [source]

Influence of gender difference and gastritis on gastric ulcer formation in rats

Edgar SL Liu
Abstract Background: Male patients with gastritis are found to have a high risk of developing peptic ulcer diseases. However, how gastritis or gender difference affects gastric ulcer formation is unclear. The present study aimed to investigate the relationship between ethanol-induced acute gastritis and gastric ulcer formation in rats. Methods: Acute gastritis or gastric ulcer was induced in the rat stomach by 80% ethanol or 60% acetic acid, respectively. Rats were killed either with gastritis alone or thereafter at day 1, 3 or 6 after ulcer induction. The number of proliferating and apoptotic cells, the mucosal mucus and prostaglandin E2 (PGE2) level were also determined. Results: Male rats with acute gastritis potentiated gastric ulcer formation, while gastritis in female rats prevented ulceration. Female rats with gastritis had a significantly faster ulcer-healing rate. More apoptotic cells were found in the gastritis groups, but only the female gastritis group produced more proliferating cells and had a decrease in the apoptosis-over-proliferation ratio. The mucus level was higher in female rats after ulcer induction. Mucosal PGE2 level was higher in female rats with acute gastritis. Both mucus and PGE2 were increased during ulcer healing in both genders. Conclusions: This study shows that gender difference plays a role in the pathogenesis of ulcer formation. The number of cells with apoptosis or proliferation determines, in part, the gender difference on gastric ulcer formation in rats. Gastric PGE2 not only contributes to this process, but also together with gastric mucus participates in the ulcer-healing process in the stomach. [source]

Effect of the oral absorption of benzenesulfonanilide-type cyclooxygenase-1 inhibitors on analgesic action and gastric ulcer formation

Xiaoxia Zheng
Abstract A benzensulfonanilide-type cyclooxygenase-1 (COX-1)-selective inhibitor, ZXX2-77: 4-amino-4,-chloro- N -methylbenzenesulfonanilide (4a), has been reported as a novel analgesic that does not cause gastric damage. This compound has a weak analgesic effect but has potent in vitro COX-1 inhibitory activity. Since the reason for the weak analgesic effect in vivo was thought to be the low rate of oral absorption, the blood concentration of ZXX2-77 (4a) was measured in rats. It was found that the Cmax value (1.2 然) of ZXX2-77 (4a) at a dose of 30 mg/kg did not reach the COX-1 IC50 value (3.2 然). On the other hand, ZXX2-79 (4b) (SO2NH derivative of ZXX2-77 (4a); 4-amino-4,-chlorobenzenesulfonanilide), which shows less potent COX inhibitory activities (COX-1 IC50,=,12 然, COX-2 IC50,=,150 然) than those of ZXX2-77 (4a) in vitro, was found to be more absorbable (Cmax,=,16 然 at a dose of 30 mg/kg in rats) than ZXX2-77 (4a). Furthermore, ZXX2-79 (4b) not only showed a potent analgesic effect in a formalin test but also caused little gastric damage. These findings indicate that demethylated sulfonamide compounds are more easily absorbed than are N -methylated sulfonamide compounds and suggest that COX-1-selective inhibitors will be useful as analgesics that do not cause gastric damage. 2008 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci [source]

Effect of thyroid hormones on stress ulcer formation

Ayhan Koyuncu
Background: Stress ulcers are gastric mucosal lesions that may cause life-threatening upper gastrointestinal bleeding. Although it is known that hyperthyroid status prevents stress ulcer formation, the effect of thyroid hormones given just as the stress is beginning has not been studied. The aim of this study was to assess the effect of thyroid hormone supplementation on gastric stress ulcers at the beginning of the restraint stress. Methods: Thyroid hormones were administered to rats 2 days before or at the beginning of the restraint stress. The linear length of the gastric mucosal lesions, mucosal pH and thyroid hormone levels were measured and histopathological examinations were carried out. Results: It was found that both triiodothyronin and thyroxin reduce the length and depth of the stress ulcers (P < 0.001). Conclusion: Although the mechanisms by which the thyroid hormones act on stress ulcers are uncertain, current experimental studies suggest that thyroid hormones reduce the formation of stress ulcers in rats when given before or at the beginning of the stress. [source]

Procollagen type I gene expression and cell proliferation are increased in lipodermatosclerosis

A.M. DeGiorgio-Miller
Summary Background, Lipodermatosclerosis (LDS) is characterized by a hardening and hyperpigmentation of lower leg skin as a consequence of chronic venous insufficiency. The degree of skin hardening or fibrosis associated with LDS is proposed to relate directly to skin breakdown and venous ulcer formation as well as to a subsequent delay in ulcer healing. Objectives, To determine whether elevated procollagen type I gene expression and increased cell proliferation are responsible for the fibrotic changes associated with LDS. Methods, Skin biopsies were obtained from the legs of patients with varying degrees of chronic venous disease and were assessed for procollagen gene expression by in-situ hybridization and for cell proliferation by immunolocalization of proliferating cell nuclear antigen. Results, The number of cells expressing procollagen type I mRNA (COL1A1) was significantly higher in the dermis of LDS-affected skin compared with samples from the other patient groups. In addition, there was a significant increase in the number of dermal fibroblasts undergoing proliferation in both LDS samples and skin samples prior to LDS changes compared with control samples. However, there was no significant difference in level of inflammation in biopsy samples between patient classes. Conclusions, These results suggest that enhanced cell proliferation and procollagen gene expression are both involved in LDS development. Furthermore, fibrotic changes may occur in the absence of, or subsequent to, any significant inflammatory response, indicating that additional profibrotic factors produced in the skin as a consequence of chronic venous insufficiency may play a role in LDS formation. [source]