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PubMedDate not supplied

Helicobacter pylori infection delays ulcer healing in patients operated on for perforated duodenal ulcer.

BACKGROUND: A majority of duodenal ulcers are associated with Helicobacter pylori infection; eradication of the infection improves ulcer healing and reduces the ulcer recurrence rate. However, the frequency of H. pylori infection in patients with perforated duodenal ulcer is not clearly established. We studied the frequency of H. pylori infection in patients with perforated duodenal ulcer and its impact on their clinical presentation. METHODS: All patients presenting with perforated duodenal ulcer underwent emergency laparotomy and simple omental patch repair. Postoperatively they received standard antibiotics for 1-2 weeks along with ranitidine; ranitidine alone was continued thereafter till an endoscopy 4-6 weeks later. Positive rapid urease test along with identification of H. pylori on histology was taken as evidence of H. pylori infection. Patients who received anti-H. pylori therapy or nonsteroidal anti-inflammatory drugs (NSAIDs) postoperatively and/or proton pump inhibitors or antibiotics, during 4 weeks preceding the endoscopy, were excluded. RESULTS: 30 patients (27 men; mean [SD] age 32.9 [9.7 years]) presenting during the period June 1999 to October 2000 were studied. Upper gastrointestinal endoscopy was done 10.9 (6.3) weeks after surgery. Seventeen (56.6%) patients were infected with H. pylori; this group had significantly more men (17/17 versus 10/13 among uninfected) and fewer NSAID users (2/17 vs. 7/13). Median duration of epigastric pain before presentation was 18 weeks in the H. pylori-infected group as compared to one week in the non-infected group (p<0.001). Significantly more patients continued to have epigastric pain after surgery in the infected group (7/17 vs. 0/13). At endoscopy, active duodenal ulcer was present in 13 of 17 patients with evidence of H. pylori infection and none of the noninfected patients (p<0.001). Age, sex, duration between surgery and endoscopy, NSAID use, smoking and maintenance ranitidine use had no impact on ulcer healing after the surgery. CONCLUSIONS: In patients operated on for perforated duodenal ulcer, H. pylori infection was the only significant factor responsible for persistence of ulcer after surgery. We advocate H. pylori eradication therapy in patients operated on for perforated duodenal ulcer.

Adult↗
PubMed1982

[Studies on defensive factors of experimental ulcers (2). Increasing action of aceglutamide aluminum on defensive factors in acetic acid ulcers of rats (author's transl)].

Severe ulcers were produced in rats by injections of 20% acetic acid in a volume of 0.05 ml into the subserosal layer of two portions in the corpus, and the effects of aceglutamide aluminum on hexosamine, sialic acid, uronic acid and hydroxyproline contents of the mucosa and stroma in the ulcerated regions were compared with the effects of L-glutamine. When aceglutamide aluminum (1,000 mg/kg x 2/day) was orally administered for 4 consecutive days beginning the day of the operation, this drug inhibited the ulcer index and the perforations in ulcerated regions by 18 and 66%, respectively. In addition, the drug remarkably increased the total amounts (microgram/ulcer areas/rat) of hexosamine, sialic acid, and uronic acid in the mucosa of ulcerated regions. It was notable than with the sialic acid contents, an increase in the concentration (microgram/100 mg dry tissue) was also observed. On the other hand, in the stroma of ulcerated regions, the contents of those components containing hydroxyproline were little affected by this drug. Following daily oral administration for 14 consecutive days, aceglutamide aluminum (1,000 mg/kg x 2/day) brought about more potent effects than those following the 4 days administrations, and this drug showed a 37% inhibition of the ulcer index and a complete inhibition of the perforations. Moreover, the drug pronouncedly increased both total amounts and concentrations of hexosamine, sialic acid, and uronic acid in the mucosa in the ulcerated portions. Of these components, the increment of the sialic acid content was the greatest. In the stroma of ulcerated portions, total amounts and concentrations of those components containing hydroxyproline were significantly increased by this drug, although the increase in the stroma were less than those in the mucosa. These effects of aceglutamide aluminum were far more potent than those of L-glutamine at the same dose. From the above results, aceglutamide aluminum may accelerate ulcer repair by potentiating defensive factors through the increases of components forming the mucus and granuloma in ulcerated tissues.

Acetates↗
PubMed1996

Use of air enema radiography to assess depth of ulceration during acute attacks of ulcerative colitis.

BACKGROUND Acute colitis is usually assessed by means of plain abdominal radiographs, the diagnostic utility of which can be enhanced by barium enema. Colonoscopy can also be useful. The latter methods may be laborious and carry risk. We describe a radiographic technique using air as the contrast medium to show mucosal or deeper ulceration. METHODS Of 60 patients undergoing colectomy for acute ulcerative colitis, 35 had air enema radiography and 14 had plain films with sufficient amount of spontaneously occurring gas to allow visualisation of the mucosa, during the 10 days before surgery. The degree of inflammation on air enema films and the extent of histopathological ulceration in colectomy specimens were independently graded and compared with each other. Depth of ulceration was compared with clinical data including a preoperative risk stratification, the APACHE II score. FINDINGS The degree of inflammation on air enema radiography correlated significantly with depth of ulceration at histopathological examination (rs 0.61, p<0.001). Presence of mucosal changes had a close association with deep ulceration extending into the muscularis propria layer or beyond (p<0.001). Air enema radiography had a high sensitivity (0.91) for presence of and specificity (0.75) in the exclusion of deep ulceration, with positive and negative predictive values of 0.88 and 0.80. 42 of 49 patients were correctly classified as regards deep ulcers. The correlation between higher preoperative APACHE II scores and severity of histopathological colitis was weak (rs 0.30, p<0.05). INTERPRETATION Air enema radiography reliably assesses the presence of colonic ulceration in patients with an acute attack of ulcerative colitis. It is a first-line investigation to assess the presence of deeper ulceration in acute colitis.

APACHE↗
PubMed2000

Elevation of TFF1 gene expression during healing of gastric ulcer at non-ulcerated sites in the stomach: semiquantification using the single tube method of polymerase chain reaction.

BACKGROUND: The Trefoil factor family 1 (TFF1), one of the trefoil peptides, has been considered to play protective and reparative roles of experimentally induced ulcers in the stomach. However, the alteration of the TFF1 mRNA in the non-ulcerated areas of living human gastric mucosa in gastric ulcer is not well known. We examined TFF1 gene expression at non-ulcerated sites during the healing of a gastric ulcer by semiquantitative determination of the TFF1 mRNA. METHODS: Gastric mucosal biopsy specimens were taken before and after the healing of the gastric ulcer from seven consecutive patients and from seven patients diagnosed with non-ulcer dyspepsia (NUD). The relative value of TFF1 mRNA (RTFF1) was calculated by the single tube method of polymerase chain reaction (ST-PCR) and Southern hybridization. Immunohistochemistry using monoclonal antibodies was performed to confirm the presence of the TFF1 peptide. The status of Helicobacter pylori and the severity of gastritis were investigated simultaneously. RESULTS: The mean relative values of TFF1 mRNA at both the gastric angle (RTFF1AS) and the gastric body (RTFF1BS) of patients with gastric ulcers at the healed stage were significantly higher than those at the open stage (P< 0.05). The mean RTFF1AS at both the open and healed stages were lower than those of RTFF1BS at the open and healed stages, respectively, The mean RTFF1B at the open stage was lower than that in NUD (not significant), but the mean of RTFF1B at the healed stage was significantly higher than that in NUD. The RTFF1AS and RTFF1BS of all patients did not correlate with H. pylori status nor with the severity of gastritis. The induction of TFF1 mRNA at the non-ulcerated background sites seemed not to be related to the status of H. pylori or to the severity of gastritis. CONCLUSIONS: These results suggest that the increased levels TFF1 mRNA during the healing of gastric ulcers might be closely related to the protection and the cell differentiation at the non-ulcerated areas of living human gastric mucosa.

Actins↗
PubMed2000

Pressure ulcer risk in spinal cord injury: predictors of ulcer status over 3 years.

OBJECTIVE: To identify predictors of pressure ulcers in men with spinal cord injury over a 3-year period. DESIGN: Longitudinal, two-panel, cohort. SETTING: Community. PARTICIPANTS: One hundred eighteen men with spinal cord injury. MEASURES: Interviews, questionnaires, and physical examinations were completed in two phases, 3 years apart. Information obtained included demographic and spinal cord injury characteristics; ulcer history; health beliefs and practices; measures of impairment, disability, and handicap; and skin integrity. RESULTS: Thirty-one percent of the participants reported having a pressure ulcer in the 12 months before Phase 2. Some Phase 1 predictors of self-reported ulcers in the year before Phase 2 were a younger age at onset of spinal cord injury, previous pressure ulcer surgery, and the presence of a pressure ulcer in the year before Phase 1. On examination at Phase 2, 59% presented with an ulcer. Phase 1 predictors of ulcer presence at Phase 2 examination were similar to predictors for self-reported ulcers. CONCLUSION: Individuals with the identified predictive characteristics are at greater risk for developing pressure ulcers. These individuals should receive additional interventions to reduce that risk. Potential interventions include more systematic and frequent follow-up, frequent review of pressure ulcer prevention and management strategies, and provision of needed personal assistance and relevant equipment.

Activities of Daily Living↗
PubMed2005

Tapping into the influence of keratinocyte allografts and biocenosis on healing of chronic leg ulcers: split-ulcer controlled pilot study.

BACKGROUND: Cultured keratinocytes may represent an alternative therapy aiming at boosting leg ulcer healing. There is no evidence-based study comparing objectively the healing rate of split-ulcer portions covered or not covered by cultured keratinocytes. OBJECTIVE: To assess the effect of cultured keratinocytes on the healing rate of leg ulcers. METHOD: Five applications of fresh (cela, XCELLentis, Ghent, Belgium) or frozen (CryoCeal, XCELLentis) cultured allogeneic keratinocytes were performed at weekly intervals to treat large leg ulcers (mean diameter > 5 cm) in four patients. A split-ulcer study was designed to secure a control area covered only by petrolatum gauze. Clinical, planimetric, bacteriologic, and immunohistologic assessments of the keratinocyte-treated and control parts of the ulcers were performed. RESULTS: Compared with controls, planimetry revealed a beneficial effect afforded by cryopreserved cultured keratinocytes on the ulcer healing rate of two of four ulcers (+12 and 81%). The healing effect was obtained on the ulcers associated with the lowest bacterial load. Cultured keratinocytes did not qualitatively and quantitatively modify the ulcer biocenosis. They did not affect the number of any type of inflammatory cells present in the granulation tissue (type I dermal dendrocytes, macrophages, T lymphocytes, granulocytes). No specific side effect of cultured keratinocytes was evidenced. CONCLUSION: In this small case series, it appears that cultured allogeneic keratinocytes may be helpful in the healing process of venous leg ulcers. However, a clean wound with reduced bacterial load seems to be the prerequisite condition for obtaining a beneficial effect.

Aged↗
PubMed1978

[Studies on predilection area of gastric ulcer viewed from healing process of experimental gastric ulcers (author's transl)].

Clinically, it is true that gastric ulcer is more common along the lesser curvature and less common along the greater curvature. To elucidate this difference in ulcerognesis, two experimental ulcers were prepared in dogs at the sites, one at the angular incisure and the other at the corresponding greater curvature after the method by Hatafuku & Thal. The fates of these ulcers studied endoscopically, macroscopically, histologically and with the use of microangiography. The results obtained are summarized as follows. 1) When two ulcers only were prepared, better healing was consistent for the greater curve ulcer. 2) Experimental ulcers with simultaneous ligation of gastric vessels resulted in poor healing of both ulcers, though the greater curve ulcer showed better healing than the lesser curve ulcer. 3) Endoscopically, dogs with vessel ligation showed antral congestion and edema. These findings, however, disappeared in 3 to 4 weeks. 4) Histamine injection accelerated the rate of early perforation and both experimental ulcers showed no tendency of healing. In conclusion, delayed healing was almost consistent for the lesser curve ulcer under various conditions. The cause for this may be explained by the increased motility with repeated ischemic condition at the lesser curvature.

Animals↗
PubMed2003

Characterization of "unhealed gastric ulcers" produced with chronic exposure of acetic acid ulcers to indomethacin in rats.

We previously discovered that a 4-wk course of indomethacin delivered to rats with acetic acid ulcers resulted in production of "unhealed gastric ulcers" that persisted for up to 12 wks after treatment cessation. The present study examined the mechanism underlying such "unhealed gastric ulcers" with biochemical and histological procedures. "Unhealed gastric ulcers" were induced with a 4-wk indomethacin treatment (1 mg/kg, twice daily) in rats with acetic acid ulcers. Two and 4 wks after treatment cessation, ulcer size was significantly larger in rats receiving indomethacin compared with control animals. Ulcerated tissue prostaglandin E2 levels were significantly lower during indomethacin treatment, but the levels tended to increase after treatment cessation compared with levels measure in the group receiving vehicle. Myeloperoxidase activity levels were significantly higher during indomethacin treatment; such levels persisted after treatment cessation. Histologically, greater degrees of fibrosis and neutrophil accumulation, as well as a lesser degree of angiogenesis were observed in the "unhealed gastric ulcers" compared to ulcers that healed in a normal fashion. It was concluded that severe fibrosis, persistent neutrophil infiltration, and poor angiogenesis in the ulcer base might represent factors involved in the mechanism underlying production of "unhealed gastric ulcers".

Acetic Acid↗
PubMed1991

Gastric secretory investigation of recurrent ulcer after surgery for duodenal ulcer.

The results of gastric secretory studies in 192 cases of recurrent ulcer after surgery for duodenal ulcer were analyzed and compared with the secretory data collected in a control group of 74 duodenal ulcer patients who had undergone various forms of gastric surgery, but who did not develop a recurrent ulcer (controls). The patients studied comprised 46 cases of recurrent ulcer after partial gastrectomy, 10 cases of recurrent ulcer after partial gastrectomy and bilateral truncal vagotomy, 56 cases of recurrent ulcer after truncal vagotomy and drainage, 52 cases of recurrent ulcer after highly selective vagotomy, and finally 28 cases in which the recurrent ulcer led to the diagnosis of the Zollinger-Ellison syndrome. The entire study was based upon an analysis of the basal acid output, the response to maximal stimulation by pentagastrin or by histalog and by insulin in the case of previous vagotomy, and finally on an assessment of basal serum gastrin. The analysis has suggested minimal secretory levels with discriminative values useful for the postoperative diagnosis of recurrent ulcer and for an assessment of the completeness of vagotomy (ratio PAO Insulin/PAO pentagastrin or histalog). Moreover, an analysis of various elements of the sequential basal pentagastrin-insulin test permitted us to approach the pathophysiological mechanism responsible for ulcer recurrence, and to identify suitable criteria for selection of the best treatment.

Adult↗
PubMed1997

Do ulcers burn out or burn on? Managing duodenal ulcer diathesis in the Helicobacter pylori era. Ad Hoc Committee on FDA-Related Matters.

Now that the Food and Drug Administration is examining various treatment regimens for eradication of Helicobacter pylori (H. pylori) infection, the question of whom to treat has come to the forefront. Widespread attempts to eradicate the bacterium are not without risk, including the possibility of accelerating the emergence of resistant strains of the organism, in addition to possible adverse events of agents used to cure the infection. These risks are of concern to the Agency in the process of granting marketing approvals for various therapies. The association of H. pylori and duodenal ulcer (DU) is no longer disputed; however, data to date have been generated in studies of patients with active (acute) DU. In these patients, the benefits of eradication therapy are clear. Patients with a documented history of DU who do not have an ulcer crater at the time of presentation have not been well studied in controlled trials. If they are at similar risk for recurrence and complications, it follows that they, too, should be candidates for H. pylori testing and treatment. However, if, as some believe, duodenal ulcer disease becomes "inactive" or "burns out" with time, an argument could be made for expectant treatment for this subgroup of patients. The present review examines the available literature on the natural history of DU disease and explores the validity of the hypothesis of duodenal ulcer "burn out." Analysis of the data shows that there is little support for the phenomenon of duodenal ulcer disease "burn out," and that, in fact, DU disease resulting from H. pylori infection is a chronic, relapsing condition, lasting for decades, if not a lifetime. The literature is compatible with the view that, in the majority of patients, DU occurs on a background of an "ulcer diathesis" that is fueled by H. pylori infection, and "burns on, not out", until and unless the infection is extinguished. The true incidence of ulcer relapse is difficult to predict due to the common occurrence of asymptomatic ulcers and the poor correlation of symptoms with the presence of ulcer. Therefore, treatment of patients with a history of duodenal ulcer disease should be advocated, even if their ulcer disease is not "active," because the risk of recurrence and complications does not diminish unless the H. pylori bacterium is eradicated.

Acute Disease↗
PubMed1999

Helicobacter pylori infection is a protective factor for bleeding gastric ulcers but not for bleeding duodenal ulcers in NSAID users.

BACKGROUND: The effect of Helicobacter pylori infection on NSAID-induced gastroduodenal damage is unclear. AIM: To determine the role of H. pylori and NSAID use in complicated peptic ulcers. METHODS: A total of 185 consecutive patients with bleeding peptic ulcers and 185 hospitalized matched controls were studied prospectively. Additionally, 75 consecutive uncomplicated peptic ulcers and 75 community controls were also studied. Active H. pylori infection was determined by urea breath test and/or both urease test and histology. Serum CagA and VacA status were determined at random in 135 infected patients and 82 controls. NSAID use was determined by structured data collection. RESULTS: H. pylori (odds ratio [OR]=5. 98; 2.9-12.3) and NSAID use (OR=5.74; 3.4-9.7) were independent risk factors for duodenal ulcer bleeding, whereas NSAID use was the main risk factor for bleeding gastric ulcers (OR=12.4; 5.5-27.9). Interaction of both factors was associated with reduced risk for bleeding gastric ulcers (OR=0.19; 0.04-0.88) but not for bleeding duodenal ulcers, which showed a similar risk to any one factor alone. This was observed for all types of NSAID use, including low-dose aspirin, and infection by CagA positive strains. H. pylori was the only factor involved in common uncomplicated duodenal ulcers. CONCLUSION: Interaction of both H. pylori infection and NSAID use decreases the risk of bleeding due to gastric ulcers, but not that due to duodenal ulcers.

Duodenal Ulcer↗
PubMed1998

Analysis of the expression of CagA and VacA and the vacuolating activity in 167 isolates from patients with either peptic ulcers or non-ulcer dyspepsia.

OBJECTIVES: The goals of this study were: 1) to examine the prevalence of cytotoxin-associated protein (CagA), vacuolating cytotoxin (VacA), and the vacuolating cytotoxin activity (VCA) in vitro of infecting Helicobacter pylori isolates and 2) to clarify the relation between the expression of these virulence factors and the occurrence of peptic ulceration. METHODS: One hundred sixty-seven clinical isolates of H. pylori from patients with peptic ulcer disease (gastric ulcer, 62 cases; duodenal ulcer, 48 cases) and nonulcer dyspepsia (57 cases) were studied regarding their genetic and phenotypic properties. RESULTS: Type 1 bacteria, which had both CagA and VCA, and type 2 bacteria, which did not express either CagA or VCA, represented 62.9% and 7.8%, respectively; the remaining 29.4% had an intermediate phenotype, expressing either CagA independent of the presence of VCA (CagA+VCA-) or vice versa (CagA-VCA+). CagA+VCA- and CagA-VCA+ bacteria represented 17.4 % and 12.0%, respectively, both of which were more numerous than the type 2 category. The proportion of the CagA-positive isolates was significantly higher in both the duodenal ulcer (97.9%) and gastric ulcer (83.9%) patients than in the non-ulcer dyspepsia patients (61.4%) (p < 0.01). On the other hand, the proportion of VacA/VCA-positive isolates was not significantly different between peptic ulcer disease and non-ulcer dyspepsia. CONCLUSIONS: The currently used classification of this bacterium based on the concomitant expression of CagA and VacA/VCA into the two major types is not adequate. The CagA-positive phenotype thus may be important as a virulence marker for peptic ulcer disease independent of the presence of VacA/VCA.

Adult↗
PubMed2006

Omeprazole maintenance therapy prevents recurrent ulcer bleeding after surgery for duodenal ulcer.

AIM: To evaluate the omeprazole maintenance therapy in patients with recurrent ulcer bleeding after surgery for duodenal ulcer. METHODS: We studied 15 consecutive patients with recurrent ulcer bleeding after surgery for duodenal ulcer. Omeprazole (20 mg/d) maintenance therapy was given after ulcer healing. In addition to clinical follow-up, ambulatory 24-h gastric pH assay was performed before and during omeprazole therapy in those patients and controls with previous duodenal ulcer surgery but no ulcer recurrence. RESULTS: All the 15 ulcers were healed after being treated with omeprazole (40 mg/d) for 2 mo. Eleven patients with two (1-9) episodes of recurrent ulcer bleeding completed the follow-up (43, 12-72 mo). None of them had a bleeding episode while on omeprazole. One patient discontinued the therapy and had recurrent bleeding. The median 24-h fraction time of gastric pH<4 in patients was 80, 46-95%, and was reduced to 32, 13-70% by omeprazole (P=0.002). CONCLUSION: Long-term maintenance therapy with omeprazole (20 mg/day) is effective in preventing recurrent ulcer bleeding.

Aged↗
PubMed2004

The effects of ulcer size on the wound radius reductions and healing times in neuropathic diabetic foot ulcers.

The main problems in the treatment of diabetic foot ulcers are prolonged wound healing and not necessary amputations, which may sometimes be caused by the impression that the results of conservative treatment are somewhat unpredictable. The aim of this study was to determine the effects of ulcer size on the wound radius reduction and healing times using a previously established equation for wound healing in neuropathic diabetic foot ulcers. This prospective study evaluates wound healing in 120 diabetic patients with neuropathic foot ulcers who were grouped according to four different ulcer areas (A 100 150 200 mm (2)). Ulcer healing was assessed by planimetric measurement of the wound area every second week until wound healing. The time course of wound healing in the different groups was compared by the weekly wound radius reduction using the equation R = sqrt A/pi. The average healing time in group A was 70 (95 %-CI 64 - 77) days with a wound radius reduction of 0.42 mm/week (95 %-CI 0.28 - 0.56). In group B the average healing time was 79 (95 %-CI 75 - 82) days and the weekly wound radius reduction was 0.47 mm (95 %-CI 0.45 - 0.49). The average healing time in group C was 85 (95 %-CI 80 - 89) days with a wound radius reduction of 0.53 mm/week (95 %-CI 0.42 - 0.56). In group D the average healing time was 97 (95 %-CI 91 - 103) days. The weekly wound radius reduction was 0.57 mm (95 %-CI 0.49 - 0.81). Wound radius reductions and the time needed for healing are affected by the ulcer area, a measure of ulcer size, in neuropathic diabetic foot ulcers. The calculation of the weekly wound radius reduction for different ulcer areas may be a useful tool in daily clinical practice to identify ulcers who do not respond adequately to the treatment.

Aged↗
PubMed2006

Assessing the outcome of the management of diabetic foot ulcers using ulcer-related and person-related measures.

OBJECTIVE: The purpose of this study was to compare different outcome measures in the audit of management of diabetic foot ulcers RESEARCH DESIGN AND METHODS: Data collected prospectively in a consecutive cohort of patients referred to a specialist multidisciplinary foot care clinic between 1 January 2000 and 31 December 2003 were analyzed. A single index ulcer was selected for each patient and classified according to both the Size (Area and Depth), Sepsis, Arteriopathy, and Denervation [S(AD)SAD] and University of Texas (UT) systems. Ulcer-related outcomes (healing, resolution by ipsilateral amputation or by death, and persisting unhealed) were determined at 6 and 12 months and compared with patient-related outcomes (survival, any amputation, and being free from any ulcer) at 12 months. RESULTS: In 449 patients (63.7% male, mean age 66.7 +/- 13.2 years), 352 (78.4%) ulcers were superficial [S(AD)SAD/UT grade 1] and 134 of these (38.1% of 352) were neither ischemic nor infected. A total of 183 (40.8% of 449) ulcers were clinically infected, and peripheral arterial disease was present in 216 patients (48.1%). Seventeen patients (3.8%) were lost to follow-up and were excluded from analysis. Of the ulcers, 247 (55.0% of 449) and 295 (65.7%) healed without amputation by 6 and 12 months, respectively. Median (range) time to healing was 78 (7-364) days. Of all index ulcers, 5.8 and 8.0% were resolved by amputation, and 6.2 and 10.9% by death by the same time points; 27.8 and 11.6% persisted unhealed. In contrast, patient-related outcomes revealed that of 449 patients only 202 (45.0%) were alive, without amputation, and ulcer free at 12 months. This group had had 272 (1-358) days without any ulcer. A total of 48 (10.7%) patients had undergone some form of amputation, and 75 (16.7%) had died. CONCLUSIONS: These data illustrate the extent to which ulcer-related outcomes may underestimate the true morbidity and mortality associated with diabetic foot disease. It is suggested that when attempts are made to compare the effectiveness of management in different centers, greater emphasis should be placed on patient-related outcome measures.

Aged↗
PubMed1989

Refractory duodenal ulcers (nonhealing duodenal ulcers with standard doses of antisecretory medication).

To evaluate possible differences between patients with refractory duodenal ulcers and those with duodenal ulcers that respond to standard doses of antisecretory medications, we determined basal acid outputs by nasogastric suction and daily smoking histories in 75 patients with endoscopically documented active duodenal ulcers. Patients were treated for at least eight weeks with standard doses of antisecretory medications and endoscopic healing or nonhealing was documented. Fifty-five patients that had complete healing of their duodenal ulcers had a mean basal acid output of 6.6 +/- 5.3 meq/hr, and 18/55 had daily cigarette smoking histories, whereas 20 patients that had nonhealing duodenal ulcers had a mean basal acid output of 20.0 +/- 9.6 meq/hr, and 8/20 had daily cigarette smoking histories. There were no significant differences between the two groups with regard to age, duodenal ulcer size, or cigarette smoking history. However, there were significant differences in male-female ratio (P less than 0.02) and in mean basal acid output (P less than 0.001), and all patients with nonhealing duodenal ulcers had basal acid outputs of greater than 10.0 meq/hr. Patients with nonhealing duodenal ulcers were treated with increased doses of ranitidine, mean 675 mg/day (range 600-1200 mg/day), and all had complete healing endoscopically documented. These results indicate that patients treated with standard doses of antisecretory medications with nonhealing duodenal ulcers have increased basal acid outputs of greater than 10.0 meq/hr, and the duodenal ulcers heal with increased doses of antisecretory medication.

Adult↗
PubMed2005

Antiulcerogenic and ulcer healing effects of Solanum nigrum (L.) on experimental ulcer models: possible mechanism for the inhibition of acid formation.

Solanum nigrum, an herbal plant which is recommended in ayurveda for the management of gastric ulcers. Therefore, the purpose of the study was to investigate the antiulcer effect of Solanum nigrum fruits extract (SNE) on cold restraint stress (CRU), indomethacin (IND), pyloric ligation (PL) and ethanol (EtOH) induced gastric ulcer models and ulcer healing activity on acetic acid induced ulcer model in rats. The treatment with SNE at higher dose significantly inhibited the gastric lesions induced by CRU (76.6%), IND (73.8%), PL (80.1%) and EtOH (70.6%), respectively, with equal or higher potency than omeprazole. SNE showed concomitant attenuation of gastric secretory volume, acidity and pepsin secretion in ulcerated rats. In addition, SNE (200 and 400mg/kgb.w.) accelerated the healing of acetic acid induced ulcers after the treatment for 7 days. Further, to ascertain the antisecretory action, the effects of SNE on H(+)K(+)ATPase activity and plasma concentration of gastrin hormone in ulcerated rats were determined. SNE significantly inhibits H(+)K(+)ATPase activity and decreases the gastrin secretion in EtOH-induced ulcer model. The severity of the reaction of ulcerogen and the reduction of ulcer size by SNE was evident by histological findings. Toxicity studies of SNE have also been carried out for its safety evaluation. SNE, thus, offers antiulcer activity by blocking acid secretion through inhibition of H(+)K(+)ATPase and decrease of gastrin secretion. These results further suggest that SNE was found to possess antiulcerogenic as well as ulcer healing properties, which might also be due to its antisecretory activity.

Animals↗
PubMed2002

Esophageal ulceration triggers expression of hypoxia-inducible factor-1 alpha and activates vascular endothelial growth factor gene: implications for angiogenesis and ulcer healing.

Our previous studies demonstrated that enhanced epithelial cell proliferation is important for healing of experimental esophageal ulcers. However, the roles of angiogenesis, its major mediator, vascular endothelial growth factor (VEGF), and the mechanism(s) regulating VEGF expression during esophageal ulcer healing remain unknown. Esophageal ulcers were induced in rats by focal application of acetic acid. We studied expressions of hypoxia-inducible transcription factor-1 alpha (HIF-1 alpha), an activator of the VEGF gene, and VEGF by reverse transcriptase-polymerase chain reaction, Western blotting, and immunostaining. To determine the efficacy of VEGF gene therapy in esophageal ulcer healing, we studied whether a single local injection of plasmid cDNA encoding recombinant human VEGF(165) affects ulcer healing and angiogenesis. Esophageal ulceration induced HIF-1 alpha protein expression and VEGF gene activation reflected by increased VEGF mRNA (240%) and VEGF protein (310%) levels. HIF-1 alpha protein was expressed in microvessels bordering necrosis where it co-localized with VEGF. Injection of cDNA encoding VEGF(165) significantly enhanced angiogenesis and accelerated esophageal ulcer healing. These results: 1) suggest that HIF-1 alpha may mediate esophageal ulceration-triggered VEGF gene activation, 2) indicate an essential role of VEGF and angiogenesis in esophageal ulcer healing, and 3) demonstrate the feasibility of gene therapy for the treatment of esophageal ulcers.

Animals↗