ABSTRACT
We present an atypical and rare case of a previously healthy 27-year-old male who presented with acute onset of abdominal pain, bloody diarrhea, and syncope. At the Emergency Department, vital signs were stable with no signs of shock. Physical examination revealed diffuse tenderness of the abdomen and cherry red blood was noted upon rectal examination. Blood tests showed marked leukocytosis without anemia. Sigmoidoscopy was performed which revealed hematochezia with no obvious site of bleeding. The patient was admitted to the hospital with a working diagnosis of dysentery and received supportive care. During the following days, blood tests revealed an ongoing decline of hemoglobin levels which necessitated a new workup of gastrointestinal bleeding. Investigation modalities including upper and lower endoscopies as well as angiography failed to demonstrate a bleeding site. Scintigraphy, which was performed next, demonstrated an increased radiotracer activity in the right abdomen consistent with small bowel bleeding. Following these results, the patient underwent urgent laparotomy and surgical resection was performed. The histopathological findings were consistent with a Dieulafoy lesion. This case illustrates the importance of the complementary role of various modalities in locating the bleeding site along the gastrointestinal tract.
ABSTRACT
This data article contains analysis of data observed in E0 mice placed on high fat diet, and treated by intraperitoneal injections of either normal saline (control) or the heparanase inhibitor PG545, in two different doses. Mice body weights and food intake were measured weekly and analyzed data are presented in graphs. Data will be of value for further understanding the role of the enzyme heparanase in controlling food intake and body weight. For further interpretations, see please "Heparanase inhibition attenuates atherosclerosis progression and liver steatosis in E0 mice" (Muhammad et al. 2018).
ABSTRACT
BACKGROUND AND AIMS: Increased oxidative stress is associated with accelerated atherosclerosis. Emerging evidence highlights the role of heparanase in atherogenesis, where heparanase inhibitor PG545 reduces oxidative stress in apolipoprotein E deficient mice (E0 mice). Herein, we studied the effects of PG545 on atherosclerosis progression in E0 mice. METHODS: Male E0 mice fed a high-fat diet (nâ¯=â¯20) were divided into 3 groups treated with weekly intraperitoneal injections of either low (0.2 mg/mouse) or high dose (0.4 mg/mouse)PG545 or normal saline (controls) for twelve weeks. Body weight and food intake were measured weekly. At the end of the treatment period, blood pressure was measured, animals were sacrificed and serum samples were collected and assessed for biochemical parameters and oxidative stress. Aortic vessels and livers were collected for atherosclerotic plaques and histopathological analysis, respectively. RESULTS: Blood pressure decreased in mice treated with low, but not high dose of PG545. In addition, heparanase inhibition caused a dose-dependent reduction in serum oxidative stress, total cholesterol, low-density lipoproteins, triglycerides, high-density lipoproteins, and aryl esterase activity. Although food intake was not reduced by PG545, body weight gain was significantly attenuated in PG545 treated groups. Both doses of PG545 caused a marked reduction in aortic wall thickness and atherosclerosis development, and liver steatosis. Liver enzymes and serum creatinine were not affected by PG545. CONCLUSIONS: Heparanase inhibition by PG545 caused a significant reduction in lipid profile and serum oxidative stress along with attenuation of atherosclerosis, aortic wall thickness, and liver steatosis. Moreover, PG545 attenuated weight gain without reducing food intake. Collectively, these findings suggest that heparanase blockade is highly effective in slowing atherosclerosis formation and progression, and decreasing liver steatosis.
