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Biomedical subjects

G F Nelis

Publications and source records attributed to G F Nelis.

At least 19 recordsLinked to original sources
PubMed1996

Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication.

BACKGROUND: Helicobacter pylori infection plays an important part in the development of atrophic gastritis and intestinal metaplasia, conditions that predispose patients gastric cancer. Profound suppression of gastric acid is associated with increased severity of gastritis caused by H. pylori, but it is not known whether acid suppression increases the risk of atrophic gastritis. METHODS: We studied patients from two separate cohorts who were being treated for reflux esophagitis: 72 patients treated with fundoplication in Sweden and 105 treated with omeprazole (20 to 40 mg once daily) in the Netherlands. In both cohorts, the patients were followed for an average of five years (range, three to eight). After fundoplication, the patients did not receive acid-suppressive therapy. The presence of H. pylori was assessed at the first visit by histologic evaluation in the fundoplication group and by histologic and serologic evaluation in the omeprazole group. The patients were not treated for H. pylori infection. Before treatment and during follow-up, the patients underwent repeated gastroscopy, with biopsy sampling for histologic evaluation. RESULTS: Among the patients treated with fundoplication, atrophic gastritis did not develop in any of the 31 who were infected with H. pylori at base line or the 41 who were not infected; 1 patient infected with H. pylori had atrophic gastritis before treatment that persisted after treatment. Among the patients treated with omeprazole, none of whom had atrophic gastritis at base line, atrophic gastritis developed in 18 of the 59 infected with H. pylori(P<0.001) and 2 of the 46 who were not infected (P=0.62). CONCLUSIONS: Patients with reflux esophagitis and H. pylori infection who are treated with omeprazole are at increased risk of atrophic gastritis.

Adolescent↗
PubMed1995

Long-term sequelae of Helicobacter pylori gastritis.

Chronic Helicobacter pylori gastritis has been put forward as a risk factor for development of gastric mucosal atrophy and gastric cancer. The purpose of our study was to investigate the long-term effects of H pylori gastritis on the gastric mucosa. We prospectively studied 49 subjects negative for H pylori and 58 positive subjects for a mean follow-up of 11.5 years (range 10-13 years). Serum samples were obtained at the initial and follow-up visits for determination of H pylori IgG antibodies. Gastroscopies with biopsy sampling were done in all patients at both visits. Biopsy specimens were used for assessment of H pylori infection and histology. Development of atrophic gastritis and intestinal metaplasia occurred in 2 (4%) uninfected and 16 (28%) infected subjects. Regression of atrophy was noted in 4 (7%) infected subjects. Development of atrophic gastritis and intestinal metaplasia was significantly associated with H pylori infection (p = 0.0014; odds ratio 9.0, 95% CI 1.9-41.3). The proportion of atrophic gastritis in the study population showed an annual increase of 1.15% (0.5-1.8%). We conclude that H pylori infection is a significant risk factor for development of atrophic gastritis and intestinal metaplasia. Our findings support strongly the causative role of this infection in gastric carcinogenesis.

Adolescent↗
PubMed1994

Anti-neutrophil cytoplasmic antibodies (ANCA) in sera from patients with inflammatory bowel disease (IBD). Relation to disease pattern and disease activity.

Anti-neutrophil cytoplasmic antibodies producing a perinuclear fluorescence pattern on ethanol-fixed granulocytes (p-ANCA) were found in 33 of 67 patients (49%) with ulcerative colitis (UC) but also in 14 of 35 patients (40%) with Crohn's disease (CD). In the latter condition p-ANCA were equally present in subgroups with colonic, ileocolonic, or ileal involvement only. Titers of p-ANCA were higher in patients with UC compared to CD patients, in particular when comparing patients with active disease. In contrast to findings in CD, patients with active UC had higher titers of p-ANCA than patients with inactive UC. Although p-ANCA were incidentally directed to lactoferrin, both in UC and CD, and to proteinase-3 and myeloperoxidase in UC only, the antigenic nature of p-ANCA could not be identified in most of the cases. We conclude that, within the spectrum of inflammatory bowel disease, the presence of p-ANCA is not specific for UC. When titers of p-ANCA are taken into account, the presence of high-titered p-ANCA, however, suggests active UC.

Adolescent↗
PubMed1994

Anti-neutrophil cytoplasmic antibodies (ANCA) in inflammatory bowel disease: characterization and clinical correlates.

ANCA were detected by indirect immunofluorescence in 34 out of 67 patients with ulcerative colitis (UC, 51%) and in 14 out of 35 patients with Crohn's disease (CD, 40%). All but one ANCA-positive sera produced a perinuclear pattern of fluorescence (P-ANCA) on ethanol-fixed neutrophils. On paraformaldehyde-fixed neutrophils 76% of P-ANCA-positive sera in UC and 50% of P-ANCA-positive sera in CD produced cytoplasmic fluorescence, indicating that, indeed, cytoplasmic antigens are recognized by a considerable number of these sera. By Western blot analysis using whole neutrophil extract as a substrate 46% of sera from patients with UC and 32% of sera from patients with CD showed reactivity with either lactoferrin, polypeptides occurring as a doublet of 66/67 kD mol. wt, or polypeptides occurring as a doublet of 63/54 kD mol. wt, respectively. Identical patterns of reactivity have been observed among P-ANCA-positive sera from patients with autoimmune liver disease and rheumatoid arthritis. These data suggest that ANCA of restricted specificities are not specific for inflammatory bowel disease (IBD), but are present in diverse conditions characterized by chronic idiopathic inflammation.

Adolescent↗
PubMed1994

Does long-term inhibition of gastric acid secretion with omeprazole lead to small intestinal bacterial overgrowth?

OBJECTIVE: Gastric acid secretion and small intestinal motility are the main mechanisms of defense against bacterial overgrowth of the proximal digestive tract. Bacterial colonization of the stomach during gastric acid inhibition has been documented, but is probably without clinical consequence. However, small intestinal bacterial overgrowth can have serious clinical implications with malabsorption and diarrhoea. METHODS: We prospectively investigated small intestinal bacterial overgrowth in 40 patients receiving long-term omeprazole treatment using the [14C]glycocholic breath test. Tests were performed before omeprazole treatment, after 6 weeks treatment with 40 mg o.m. and after 26 weeks treatment with 20 mg; in the test each patient served as his own control. RESULTS: Breath tests, using individual curves, peak values, time at which the peak appeared and the area under the curve, did not differ significantly during treatment from those before treatment. CONCLUSIONS: We conclude that long-term strong inhibition of gastric acid secretion does not lead to small intestinal bacterial overgrowth.

Adult↗
PubMed1993

Antineutrophil antibodies in inflammatory bowel disease recognize different antigens.

Anti-neutrophil cytoplasmic antibodies (ANCA) were observed in 31 out of 68 sera (45%) from Ulcerative Colitis (UC) patients and in 13 out of 38 Crohn's Disease (CD) sera (34%). The presence of ANCA was not related to disease activity, nor to the localization of the disease manifestations. By Western Blotting ANCA showed reactivity with either lactoferrin, polypeptides occurring as a doublet of 66/67 kD MW, or polypeptides occurring as a doublet of 63/54 kD MW.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1992

[2 patients with a non-Hodgkin lymphoma located in the pancreas].

A small percentage (around 1.5%) of pancreatic malignancies are well treatable non-Hodgkin's lymphomas. Two patients with this disease are described. One patient was treated with both surgery and chemotherapy, the other with chemotherapy only. The results in both patients were excellent with complete responses being achieved. The literature on pancreatic non-Hodgkin's lymphomas is reviewed.

Aged↗
PubMed1990

Role of fructose-sorbitol malabsorption in the irritable bowel syndrome.

Because even after low doses of fructose and sorbitol, fructose-sorbitol malabsorption has been found in a high number of patients with the irritable bowel syndrome, an etiological role of fructose-sorbitol malabsorption in the irritable bowel syndrome has been suggested. However, these studies have been uncontrolled. Therefore, a controlled study of fructose-sorbitol malabsorption in the irritable bowel syndrome compared with healthy controls was performed. Seventy-three patients, 23 men and 50 women with a mean age 43.1 +/- 1.7 years (range, 18-66 years) with the irritable bowel syndrome were compared with 87 age- and sex-matched control subjects. Fructose-sorbitol malabsorption was determined by a breath-hydrogen test (Lactoscreen, Hoek Loos, Schiedam, The Netherlands) following an oral load of 25 g fructose and 5 g sorbitol after a 10-hour fast. Fructose-sorbitol malabsorption, as shown by an H2 peak of 20 ppm over basal values, was found in 22 (30.1%) of the patients and 35 (40.2%) of the control subjects. With a lower peak level of 10 ppm over basal values, these percentages were 45.2% and 57.5%, respectively. Also, the highest H2 peak values (15.2 +/- 2.3 ppm vs. 21.5 +/- 2.6 ppm), time to reach peak levels (110.7 +/- 5.4 min vs. 107.1 +/- 5.9 min), and area under the H2 curve (1310 +/- 219 ppm.min vs. 1812 +/- 255 ppm.min) did not discriminate between patients and controls. During the test, symptoms developed in 31 of 70 patients and in 3 of 85 control subjects (P less than 0.0001). Symptomatic patients did not differ from asymptomatic patients regarding the presence or absence of fructose-sorbitol malabsorption, H2 peak values, and area under the curve. No differences could be identified between male and female patients or controls. In conclusion, fructose-sorbitol malabsorption is frequently seen in patients with irritable bowel syndrome, but this is not different from observations in healthy volunteers. Therefore, fructose-sorbitol malabsorption does not seem to play an important role in the etiology of irritable bowel syndrome.

Adult↗
PubMed1989

Anorexia, weight loss, and diarrhea as presenting symptoms of angiokeratoma corporis diffusum (Fabry-Anderson's disease).

Fabry-Anderson's disease or angiokeratoma corporis diffusum (ACD) is an X-linked sphingolipidosis with a systemic character and occurs in 2-5 per million births (1-3). The basic defect is the absence of a lysosomal enzyme x-galactosidase A. This enzyme is necessary for the metabolization of ceramide trihexoside (globotriglycosyl ceramide), a breakdown product of cell membranes (4, 5). Clinically the disease is characterized by cutaneous angiokeratoma's and severe pain in the limbs from the second decade, followed by progressive renal insufficiency and cardiovascular and cerebrovascular damage in the third or fourth decade (6-8). In patients with established ACD, gastrointestinal symptoms have been described incidentally, mainly mild diarrhea (9, 10). We describe a kindred with ACD showing two extraordinary clinical features: (1) Anorexia, weight loss, and diarrhea were the presenting symptoms and antedated limb pain by many years, which has not been described before. (2) The disease was associated with another rare X-linked disorder: hypoplastic amelogenesis imperfecta.

Adult↗
PubMed1989

Safety profile of omeprazole. Adverse events with short-term treatment.

Omeprazole is a very potent inhibitor of gastric acid secretion and has proven to be efficacious in the healing of peptic ulcer and reflux oesophagitis. A search for adverse events during short-term treatment with omeprazole has been made, based on data from published comparative trials, data on file at the manufactor's (Hässle Research Laboratories, Mölndal, Sweden) and personal series. Omeprazole does not show more adverse events than drugs currently widely in use for the treatment of acid-related disorders. A change in a wide range of laboratory parameters has not been observed, except for a rise in basal and meal-stimulated serum gastrin which can be ascribed directly to the inhibition of acid secretion. For short-term treatment omeprazole can be considered as a safe drug.

Clinical Trials as Topic↗
PubMed1985

Influence of RP 40749 on basal and meal-stimulated serum-gastrin, serum-pepsinogen I, and gastrin-content of the antral mucosa in duodenal ulcer patients.

Eighteen patients with active duodenal ulcer were treated with a novel antisecretory drug, RP 40749, either 100 mg or 150 mg as a daily nocturnal dose for 28 days. In these patients we evaluated the clinical course, endoscopic healing rates after 28 days, routine laboratory parameters, basal serum gastrin and pepsinogen I levels, meal-stimulated serum gastrin concentration, and the gastrin content of the antral mucosa. All nine patients receiving 150 mg RP 40749 and eight of nine patients receiving 100 mg RP 40749 healed their ulcers completely within 28 days, becoming rapidly symptom-free after an average of three days. The basal (53.8 +/- 5.2 vs 99.8 +/- 11.4 pg/ml) and meal-stimulated serum gastrin levels (109.2 +/- 12.1 vs 189.2 +/- 16.7 pg/ml) rose significantly after treatment with RP 40749, as did the gastrin content of the antral mucosa (11.3 +/- 2.1 vs 26.0 +/- 5.1 micrograms/g), suggesting increased synthesis and secretion of gastrin. Between the 100 mg and 150 mg groups, no significant differences in response were observed. Serum pepsinogen I levels (64.9 +/- 7.3 vs 147.9 +/- 17.9 ng/ml) increased after treatment; the increase after 150 mg RP 40749 was significantly greater than that after 100 mg RP 40749. The increase of serum pepsinogen levels are probably due to a spillover effect resulting from a blockade in exocrine secretion into the lumen. There were no relevant changes in routine laboratory parameters.

Adult↗
PubMed1983

Nitrofurantoin-induced pancreatitis: report of a case.

A patient with nitrofurantoin-induced pancreatitis is described, representing the first patient with this condition to be reported in the literature. The diagnosis of nitrofurantoin-induced pancreatitis was confirmed by rechallenge. The clinical and biochemical picture cleared rapidly after discontinuation of the drug. The conclusion is proffered that nitrofurantoin-induced jaundice is not always due to cholestatic hepatitis, but can result from obstruction of the common bile duct due to edema of the pancreatic head secondary to nitrofurantoin pancreatitis.

Aged↗