			Home About us Contact

Ulcer Margin (ulcer + margin)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Influences of Helicobacter pylori on gastric angiogenesis and ulcer healing in mice

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2002
Edhi Gunawan
Abstract Background and Aims:Helicobacter pylori infection is associated with peptic ulcers; however, it is unclear whether the bacterium delays ulcer healing. We investigated the influence of H. pylori on ulcer healing in mice. We also examined the influence of H. pylori infection on angiogenesis. Methods: An acetic acid ulcer was made in male BALB/c mice. Three days later (day 0), the animals were inoculated with H. pylori SS1 strain. The healing process of the ulcer was examined macroscopically and microscopically on days 0, 6 and 9. The index of angiogenesis was also determined using carmine dye injection. Results: On day 0, angiogenesis began at the ulcer margin while the mucosal epithelia had not yet regenerated. On days 6 and 9, angiogenesis and epithelial regeneration developed and ulcer size reduced. These phenomena were significantly suppressed in mice infected with H. pylori. Conclusion:Helicobacter pylori infection significantly suppressed angiogenesis and delayed ulcer healing. These results indicate that H. pylori plays an important role in ulcer healing. © 2002 Blackwell Publishing Asia Pty Ltd [source]

Influence of Helicobacter pylori infection and cetraxate on gastric mucosal blood flow during healing of endoscopic mucosal resection-induced ulcers

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2001
Kyoichi Adachi
Abstract Background and Aim: Helicobacter pylori (H. pylori) infection is known to affect the gastric microcirculation, and cetraxate is reported to accelerate gastric ulcer healing, possibly by augmenting gastric mucosal blood flow (MBF). The aim of this study is to clarify the effect of H. pylori infection and cetraxate on MBF during gastric ulcer healing. Methods: Forty-two patients who had undergone endoscopic mucosal resection (EMR) were studied. Mucosal blood flow was measured by the use of a laser Doppler flowmeter in the surrounding mucosa and at the ulcer margin, before, 1 day, 1 week and 4 weeks after EMR. Helicobacter pylori infection was confirmed by the use of bacterial culture and histology. After EMR, patients were randomly assigned to receive 30 mg lansoprazole (u.i.d; L-regimen) or 30 mg lansoprazole (u.i.d.) with 200 mg cetraxate (q.i.d; LC-regimen) for 4 weeks. Results: The MBF ratio (MBF at ulcer margin/MBF in surrounding mucosa) 1 week after EMR was significantly lower than that before or 4 weeks after EMR only in H. pylori -positive patients treated with the L-regimen. No such decrease in MBF was observed after 1 week in H. pylori -positive patients treated with the LC-regimen or in H. pylori -negative patients. Conclusion: A transient decrease in MBF was detected at the ulcer margin during healing of EMR-induced ulcers in H. pylori -infected patients. Cetraxate seemed to prevent this decrease in MBF. [source]

Amoebiasis cutis: Clinical suspicion is the key to early diagnosis

AUSTRALASIAN JOURNAL OF DERMATOLOGY, Issue 1 2010
Ghanshyam K Verma
ABSTRACT Amoebiasis cutis is a rare manifestation of Entamoeba histolytica, primarily an intestinal pathogen, which occurs as a complication of amoebic dysentery. Primary cutaneous amoebiasis occurs from contamination of pre-existing wounds. A high degree of clinical suspicion and demonstration of trophozoites from lesions are important for making an early diagnosis lest these patients should suffer significant morbidity. A HIV-negative and otherwise healthy 40-year-old man presented with a well-defined, indurated, painful, progressively enlarging plaque with overlying ulcers and pus discharging sinuses involving buttocks, perianal/perineal area and part of the left thigh of 3 years' duration. A wide array of investigations was unhelpful but demonstration of Entamoeba histolytica trophozoites in wet-drop preparation from the ulcer margin was diagnostic. The trophozoites were also visualized both in H&E and periodic acid Schiff-stained histological sections. Resolution of lesion was observed 2 weeks after treatment with oral metronidazole 800 mg three times a day and wound care. [source]

Granulocyte/macrophage colony-stimulating factor treatment of human chronic ulcers promotes angiogenesis associated with de novo vascular endothelial growth factor transcription in the ulcer bed

BRITISH JOURNAL OF DERMATOLOGY, Issue 1 2006
F. Cianfarani
Summary Background, Granulocyte/macrophage colony-stimulating factor (GM-CSF), a cytokine with pleiotropic functions, has been successfully employed in the treatment of chronic skin ulcers. The biological effects underlying GM-CSF action in impaired wound healing have been only partly clarified. Objectives, To investigate the effects of GM-CSF treatment of chronic venous ulcers on lesion vascularization and on the local synthesis of the angiogenic factors vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF). Methods, Patients with nonhealing venous leg ulcers were treated with intradermal injection of recombinant human GM-CSF, and biopsies were taken at the ulcer margin before and 5 days after administration. Wound vascularization was analysed by immunohistochemistry using antiplatelet endothelial cell adhesion molecule-1/CD31 and anti-,-smooth muscle actin antibodies. VEGF and PlGF transcription was assessed by in situ hybridization. To identify the cell populations transcribing VEGF within the ulcer bed, the VEGF hybridization signal was correlated with the immunostaining for different cell type markers on serial sections. Direct induction of VEGF transcription by GM-CSF was investigated in GM-CSF-treated cultured macrophages and keratinocytes. Results, Blood vessel density was significantly increased in the ulcer bed following GM-CSF treatment. VEGF transcripts were localized in keratinocytes at the ulcer margin both before and after GM-CSF treatment, whereas a VEGF hybridization signal was evident within the ulcer bed only following administration. PlGF mRNA was barely detectable in keratinocytes at the ulcer margin and was not visibly increased after treatment. Unlike VEGF, a specific PlGF hybridization signal could not be detected in cells within the ulcer following GM-CSF administration. Monocytes/macrophages were the main cell population transcribing VEGF after GM-CSF treatment. In vitro analysis demonstrated that VEGF transcription can be directly stimulated by GM-CSF in a differentiated monocytic cell line, but not in keratinocytes. Conclusions, Our data show that increased vascularization is associated with GM-CSF treatment of chronic venous ulcers and indicate that inflammatory cell-derived VEGF may act as an angiogenic mediator of the healing effect of GM-CSF in chronic ulcers. [source]