Clinical significance of serum soluble intercellular adhesion molecule 1 in gastric cancer. (73/2511)

We studied the correlation between serum soluble intercellular molecule 1 (sICAM-1) and clinicopathological features in patients with gastric cancer. The impact of sICAM-1 on prognosis was also evaluated. The sera from 224 patients with gastric cancer, 44 healthy individuals, and 35 patients with benign gastrointestinal diseases (4 patients with submucosal stomach tumors, 6 patients with gastric ulcers, 1 patient with Crohn disease, 2 patients with ulcerative colitis, 7 patients with gall stones, 5 patients with chronic pancreatitis, and 10 patients with liver cirrhosis) were measured for sICAM-1 titer using a sandwich enzyme immunoassay method. There was no correlation between the serum titer of sICAM-1 and the age or gender of healthy controls. Among patients with benign gastrointestinal diseases, the patients with liver cirrhosis had a significantly higher mean serum sICAM-1 titer than that of healthy controls (P < 0.0001). The mean serum sICAM-1 titer of all patients with gastric cancer was not significantly different from that of healthy controls. However, among the patients with stage IV and recurrent disease, the serum sICAM-1 titer of those with hematogenous metastasis was significantly higher than that of patients without hematogenous metastasis (P = 0.001). The patients with a high serum sICAM-1 titer of more than 304 ng/ml (mean of healthy controls plus SD) showed a significantly worse prognosis than patients with a low serum sICAM-1 titer (P = 0.010). Nevertheless, serum sICAM-1 titer was not an independent predictor of prognosis by multivariate analysis. In conclusion, serum sICAM-1 cannot be used as a tumor marker for early diagnosis. However, sICAM-1 in sera may still be worthwhile to measure for monitoring hematogenous metastasis.  (+info)

Gastrointestinal health care resource use and costs associated with nonsteroidal antiinflammatory drugs versus acetaminophen: retrospective cohort study of an elderly population. (74/2511)

OBJECTIVE: To estimate gastrointestinal (GI) health care resource use and direct costs associated with prescription nonsteroidal antiinflammatory drugs (NSAIDs) in an elderly population. METHODS: Using the Government of Quebec's health insurance database, we obtained the medical, pharmaceutical, and demographic records of 73,850 senior citizens who, between 1993 and 1997, had either an NSAID or an acetaminophen prescription dispensed. The date of their first dispensed prescription for an NSAID or acetaminophen was termed their index date. Patients who were not taking oral corticosteroids or anticoagulants at their index date, were not diagnosed with cancer at their index date, and were not hospitalized and did not have any GI events during the year prior to their index date were included in the study. Patients who had a dispensed NSAID prescription at their index date formed the NSAID cohort; the others formed the acetaminophen cohort. All patients were followed up for 2 years. The daily direct costs of GI events incurred during NSAID therapy by the NSAID cohort were compared with those incurred during a similar followup period by the acetaminophen cohort. The difference in these average daily costs was attributed to NSAID use. RESULTS: The NSAID cohort included 5,268 senior citizens and the acetaminophen cohort 2,245. More GI adverse events were observed in the NSAID cohort (odds ratio 2.48, 95% confidence interval 2.06, 3.00). The average daily direct cost of GI events for a day of NSAID therapy attributed to the NSAIDs was $0.84 (Canadian). On average, for each Canadian dollar spent on NSAIDs, an additional $0.66 was spent on their side effects. CONCLUSION: Safer alternatives to NSAIDs would significantly reduce medical care costs for patients in need of NSAID therapy.  (+info)

Nasogastric hyperalimentation through a polyethylene catheter: an alternative to central venous hyperalimentation. (75/2511)

We performed nasogastric hyperalimentation with polyethylene catheters and appropriate feeding solutions in 12 cachectic patients who had been referred as candidates for central venous hyperalimentation. Most patients had primary gastrointestinal disease. The duration of hyperalimentation averaged 31 days. Seven patients obtained rapid weight gain (average 0.3 kg/day) with the nasogastric hyperalimentation alone. An additional two were successfully repleted with the addition of parenteral fluids via peripheral veins. In the nine repleted patients, serum albumin rose by average 19%, 24-hr urine creatinine by average 21%, and triceps skinfold by average 46%. The nature of the weight gain in the nine successful cases was analyzed by the metabolic balance study technique. Average composition of the increment in weight was: 50% protoplasm, 48% extracellular fluid, 19% adipose tissue, and less than 1% bone. We conclude that nasogastric hyperalimentation can replace central venous hyperalimentation in a substantial proportion of patients now receiving the latter type of treatment.  (+info)

The primacy of the gastrointestinal tract as a target organ of acute graft-versus-host disease: rationale for the use of cytokine shields in allogeneic bone marrow transplantation. (76/2511)

Acute graft-versus-host disease (GVHD), the major complication of allogeneic bone marrow transplantation (BMT), limits the application of this curative but toxic therapy. Studies of inflammatory pathways involved in GVHD in animals have shown that the gastrointestinal (GI) tract plays a major role in the amplification of systemic disease. Damage to the GI tract increases the translocation of inflammatory stimuli such as endotoxin, which promotes further inflammation and additional GI tract damage. The GI tract is therefore critical to the propagation of the "cytokine storm" characteristic of acute GVHD. Experimental approaches to the prevention of GVHD include reducing the damage to the GI tract by fortification of the GI mucosal barrier through novel "cytokine shields" such as IL-11 or keratinocyte growth factor. Such strategies have reduced GVHD while preserving a graft-versus-leukemia effect in animal models, and they now deserve formal testing in carefully designed clinical trials. (Blood. 2000;95:2754-2759)  (+info)

Clinical epidemiology and natural history of gastroesophageal reflux disease. (77/2511)

In the MUSE classification of gastroesophageal reflux disease (GERD), esophagitis is assessed by the presence of metaplasia, ulcer, stricture, or erosion, each being graded as absent, mild or severe. Daily reflux symptoms affect about 4 to 7 percent of the population; erosive esophagitis occurs in about 2 percent; the prevalence rate of Barrett's metaplasia is 0.4 percent; and esophageal adenocarcinoma leads to two deaths per million living population. In persons with GERD symptoms, about 20 percent are found to have erosive esophagitis, while ulcers or strictures are found in less than 5 percent of all patients with erosive esophagitis. No clear-cut temporal progression exists between successive grades of disease severity, as the most severe grade of GERD is reached at the onset of the disease. Mild forms of GERD tend to be more common in women than men, while severe GERD characterized by erosive esophagitis, esophageal ulcer, stricture or Barrett's metaplasia are far more common in men than women. All forms of GERD affect Caucasians more often than African Americans or Native Americans. The prevalence of GERD is high among developed countries in North America and Europe and relatively low in developing countries in Africa and Asia. During the past three decades, hospital discharges and mortality rates of gastric cancer, gastric ulcer and duodenal ulcer have declined, while those of esophageal adenocarcinoma and GERD have markedly risen. These opposing time trends suggest that corpus gastritis secondary to Helicobacter pylori infection protects against GERD. This hypothesis is consistent with the geographic and ethnic distributions of GERD. Case-control studies also indicate that cases with erosive esophagitis are less likely to harbor active or chronic corpus gastritis than controls without esophagitis.  (+info)

Helicobacter pylori and dyspepsia. (78/2511)

It is clear that non-ulcer (or functional) dyspepsia is a heterogeneous syndrome that includes a subset of patients with unrecognized gastroesophageal reflux. Patient heterogeneity combined with inadequate study methodology has led to enormous confusion in interpreting the relationship between Helicobacter pylori and non-ulcer dyspepsia. The possibility that H. pylori is associated with gastroesophageal reflux disease may explain, in part, the difficulty in establishing a link between non-ulcer dyspepsia and H. pylori infection. It is unclear whether the prevalence of H. pylori is increased in non-ulcer dyspepsia over and above the background population. H. pylori does not appear to be linked to heartburn or other specific upper gastrointestinal tract symptoms. The results of eradication trials in H. pylori-infected patients with non-ulcer dyspepsia have been equivocal and generally flawed. There is no doubt that H. pylori is not a sufficient cause of non-ulcer dyspepsia, because it is well documented in the literature that dyspepsia can occur in the absence of infection and infection can occur in the absence of symptoms. At this stage, there is insufficient evidence to support the hypothesis that H. pylori is etiologically linked to non-ulcer dyspepsia, but data from well designed large randomized controlled trials of eradication therapy, are awaited with great interest.  (+info)

Helicobacter pylori modulation of gastric acid. (79/2511)

Helicobacter pylori plays major causative roles in peptic ulcer disease and gastric cancer. Elevated acid secretion in patients with duodenal ulcers (DUs) contributes to duodenal injury, and diminished acid secretion in patients with gastric cancer allows carcinogen-producing bacteria to colonize the stomach. Eradication of H. pylori normalizes acid secretion both in hyper-secreting DU patients and hypo-secreting relatives of gastric cancer patients. Therefore, we and others have asked how H. pylori causes these disparate changes in acid secretion. H. pylori gastritis more or less restricted to the gastric antrum in DU patients is associated with increased acid secretion. This is probably because gastritis increases release of the antral acid-stimulating hormone gastrin and diminished mucosal expression of the inhibitory peptide somatostatin. Bacterial products and inflammatory cytokines including TNFalpha may cause these changes in endocrine function. Gastritis involving the gastric corpus tends to diminish acid secretion, probably because bacterial products and cytokines including IL-1 inhibit parietal cells. Pharmacological inhibition of acid secretion increases corpus gastritis in H. pylori-infected subjects, so it is envisaged that gastric hypo-secretion of any cause might become self-perpetuating. H. pylori-associated mucosal atrophy will also contribute to acid hypo-secretion and is more likely in when the diet is high in salt or lacking in antioxidant vitamins. Data on gastric acid secretion in patients with esophagitis are limited but suggest that acid secretion is normal or slightly diminished. Nevertheless, H. pylori infection may be relevant to the management of esophagitis because: (i) H. pylori infection increases the pH-elevating effect of acid inhibiting drugs; (ii) proton pump inhibitors may increase the tendency of H. pylori to cause atrophic gastritis; and (iii) successful eradication of H. pylori is reported to increase the likelihood of esophagitis developing in patients who had DU disease. Points (ii) and (iii) remain controversial and more work is clearly required to elucidate the relationship between H. pylori, acid secretion, gastric mucosa atrophy and esophagitis.  (+info)

Helicobacter pylori, proton pump inhibitors and gastroesophageal reflux disease. (80/2511)

Proton pump inhibitors have become of pivotal importance for the treatment of GERD. The purpose of this paper is to review the interaction between Helicobacter pylori and PPIs in the treatment of GERD. H. pylori exaggerates the acid suppressive effects of PPIs. During treatment with these drugs, H. pylori-positive subjects thus have a higher intragastric pH than H. pylori-negative subjects. The mechanism for this phenomenon remains to be elucidated. We hypothesize that it is related to H. pylori-induced corpus gastritis, which impairs parietal cell function. The available evidence suggests that this phenomenon has no clinical relevance for the treatment of GERD. The 24-hr esophageal pH during PPI treatment does not depend on the H. pylori status, nor does the medication dose needed for maintenance therapy or the number of clinical relapses during such therapy depend on the H. pylori status. PPIs, on the other hand, also affect H. pylori. During treatment with these drugs, the pattern of bacterial colonization and associated gastritis shifts proximally. The increased gastritis of the body mucosa is associated with a more rapid development of atrophic gastritis, a condition characterized by a loss of gastric glands and associated with an increased cancer risk. For these reasons, one has to consider H. pylori eradication in infected GERD patients in need of PPI maintenance therapy.  (+info)