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Biomedical subjects

E C Klinkenberg-Knol

Publications and source records attributed to E C Klinkenberg-Knol.

At least 19 recordsLinked to original sources
PubMed1997

The prevalence of gastro-oesophageal reflux disease based on non-specific symptoms in institutionalized, intellectually disabled individuals.

OBJECTIVE: The prevalence of gastro-oesophageal reflux disease (GORD) in randomly selected, institutionalized, intellectually disabled individuals (IQ < 50) in The Netherlands is high. DESIGN: In this study we investigated the prevalence of GORD and reflux oesophagitis (RO) in intellectually disabled individuals specifically selected for symptoms such as: behavioural difficulties such as automutilation, food refusal, fear and restlessness, vomiting, regurgitation and rumination. Predisposing factors were also evaluated. METHODS: One hundred and ten individuals from one institute underwent a 24-h oesophageal pH test and were scored for predisposing factors and non-specific reflux symptoms. A pathological pH test was defined as a pH lower than 4 more than 4.5% of the measured time. Subjects with a pathological pH test (patients) were compared to those with a normal pH test (controls). RESULTS: In seven cases (6.4%) the test failed for technical reasons. In 57 (55.3%) cases a pathological pH test was found. RO was diagnosed in 33 (64.7%) patients. The use of anticonvulsant drugs and cerebral palsy appeared to be predisposing factors, while the non-specific reflux symptoms did not discriminate for GORD. CONCLUSION: The prevalence of GORD was equal in a randomly selected group of intellectually disabled individuals, and in this group, specifically selected on account of possible reflux symptoms. This study confirms that in this particular group, it is nearly impossible to discriminate for the diagnosis of GORD on non-specific reflux symptoms only. However, GORD may be suspected where there are certain predisposing factors, particularly cerebral palsy and use of anticonvulsant drugs.)

Adult↗
PubMed1997

The age-related incidences of oesophageal carcinoma in intellectually disabled individuals in institutes in The Netherlands.

OBJECTIVE: An increased age-related incidence of oesophageal cancer in people with intellectual disability has been suggested by studies in the Netherlands. Gastro-oesophageal reflux disease (GORD), as documented by pH testing, occurs frequently in the intellectually disabled population, being found in nearly 50% of those with an IQ less than 50, while Barrett's oesophagus is found in about 15-26%. DESIGN: We compared the age-related incidence of oesophageal cancer in institutionalized, intellectually disabled individuals in the Netherlands with the age-related incidence in the general Dutch population. METHODS: Data were provided by the Netherlands Cancer Registry. The patient's institute physician was asked to complete a questionnaire about the diagnosis, which was endoscopically and histologically confirmed. RESULTS: The incidence of oesophageal carcinoma was 20 in 168,000 person-years. The expected incidence for oesophageal cancer, based on age-related incidence in the general population, was 7.0, resulting in a standardized morbidity ratio in the population with intellectual disability of 2.9 (confidence limits, 1.8-4.1; P < 0.001). Endoscopic findings were as follows: in 18/20 intellectually disabled carcinoma patients an adenocarcinoma was found; the remaining two patients had a squamous cell carcinoma. Barrett's epithelium was observed in nine patients (45%), eight (42%) of whom showed a peptic stricture as well. In 15 (75%) cancer patients reflux oesophagitis was found, accompanied in 14 cases by a hiatal hernia. CONCLUSION: A standardized morbidity ratio for oesophageal carcinoma of 2.9 was found in the intellectually disabled population as compared to the general population. Early detection and treatment of GORD in the population with intellectual disability is of paramount importance to prevent the development of Barrett's dysplasia and carcinoma.

Adenocarcinoma↗
PubMed1997

The prevalence of Helicobacter pylori infection among inhabitants and healthy employees of institutes for the intellectually disabled.

OBJECTIVES: The prevalence of Helicobacter pylori infection varies in the Netherlands from 5% in children to about 50% in the elderly. In the institutionalized intellectually disabled, a high prevalence of infection has been reported. It is unknown whether there are specific risk factors to obtain H. pylori infection in this population, and whether employees of such institutes are at risk for H. pylori infection. METHODS: Therefore, we analyzed the seroprevalence of H. pylori antibodies by ELISA among 338 intellectually disabled inhabitants and 254 employees of two institutes. H. pylori-positive patients were compared with H. pylori-negative controls. The intellectually disabled and the employees were evaluated for possible risk factors. RESULTS: Of the 338 intellectually disabled, 280 (82.8%, median age 51 yr) were infected with H. pylori. This rate is significantly higher than the prevalence of H. pylori in the Dutch population. The presence of H. pylori was significantly associated with male gender, longer duration of institutionalization, an IQ < 50, rumination, and a history of upper abdominal symptoms. Of the 254 employees, 69 (27.2%) were infected, which is equal to the rate for the total Dutch population. The presence of H. pylori infection among employees was, however, significantly associated with a higher level of physical contact with the intellectually disabled, longer duration of employment, and having upper abdominal symptoms. CONCLUSIONS: Intellectually disabled persons are at high risk of developing H. pylori infection. Employees with close physical contact to the intellectually disabled population for a considerable period of time are also at increased risk. H. pylori infection should be considered a job attributable risk in this profession.

Adolescent↗
PubMed1997

Role of Helicobacter pylori in the pathogenesis of atrophic gastritis.

BACKGROUND: Atrophic gastritis is defined as a loss of the glandular structures and a collapse of the reticulin skeleton of the stomach mucosa. It is often accompanied by intestinal metaplasia. Both conditions result from long-term persistent chronic active gastritis and significantly increase the risk for gastric cancer. METHODS: Review of the role of Helicobacter pylori in the pathogenesis of atrophic gastritis. Specific attention is given to the classifications and histologic features of atrophic gastritis, the frequency with which atrophic gastritis occurs in H. pylori-infected subjects, the factors that influence the process of development of atrophic gastritis in the presence of infection, and the various mechanisms by which this bacterial infection may induce atrophic gastritis. In addition, the possible role of H. pylori in the etiology of auto-immune atrophic gastritis and pernicious anemia is discussed. CONCLUSIONS: H. pylori infection eventually causes atrophic gastritis in a considerable number of infected subjects. In different populations, the prevalence of atrophic gastritis increases by 1 to 3% per annum. Factors that may increase the risk for atrophy are infection at an early age, cytotoxin production by the infecting strain, and lowering of acid output. The association between H. pylori infection and the development of atrophic gastritis significantly supports the role of this infection in gastric carcinogenesis.

Gastritis, Atrophic↗
PubMed1997

Gastroesophageal reflux disease in intellectually disabled individuals: leads for diagnosis and the effect of omeprazole therapy.

OBJECTIVES: The therapeutic approach to gastroesophageal reflux disease (GERD) in intellectually disabled individuals has not been studied extensively. So far, only low response rates to medical and surgical therapy of GERD have been reported. However, the efficacy of proton pump inhibitors, to date the most effective medical therapy for GERD, has never been evaluated in this population. Our purpose, therefore, was to study the effect of omeprazole on healing and symptom relief in the intellectually disabled. METHODS: The treatment scheme was as follows: omeprazole 40 mg was given once daily (o.d.) as a healing dose for 3 months, and omeprazole 20 mg o.d. was given as a maintenance dose for another 3 months, to intellectually disabled subjects with endoscopically proven esophagitis, grades I-IV, according to Savary-Miller classification. After 3 and 6 months, the result of this treatment was evaluated by symptom scoring and/or endoscopy. In case of relapse, the dose was increased. RESULTS: At the first endoscopy, 40 of 107 patients (37%) had grade I, 36 (34%) grade II, 18 (17%) grade III, and 13 (12%) grade IV esophagitis. In 92 of 104 patients (88%), the treatment scheme was effective in healing the esophagitis and keeping patients in remission, independent of the severity of esophagitis. In 11 of 104 (11%) patients, a symptomatic relapse was observed after the dose was decreased to 20 mg o.d. However, all of these patients became symptom free again after the dose was increased to 40 mg o.d., and all were healed endoscopically at the end of the study. One (1%) patient needed omeprazole 60 mg o.d. for healing, but in this patient, no relapse was seen while on a maintenance dose of omeprazole 40 mg o.d. Marked improvement of persistent vomiting, hematemesis, regurgitation, food refusal, iron deficiency anemia, and depressive symptoms was seen at the end of the study. CONCLUSIONS: This study indicates that omeprazole is highly effective for all grades of esophagitis in the intellectually disabled. The dose needed to maintain them in remission can be titrated according to the reflux symptoms.

Adolescent↗
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↗
PubMed1996

Effect of short- and long-term treatment with omeprazole on the absorption and serum levels of cobalamin.

AIMS: To evaluate absorption of protein-bound and unbound cyanocobalamin before and during treatment with omeprazole, and cobalamin levels in patients on long-term treatment with omeprazole. METHODS: In eight former duodenal ulcer patients absorption of unbound and protein-bound cobalamin was determined by measuring 24-h urinary excretion of unbound 58Co-cyancobalamin or protein-bound 57Co-cyanocobalamin during a modified Schilling test. Tests were performed before and during treatment with 20 mg and 40 mg omeprazole daily for 9 days. Serum cobalamin levels were assessed in 25 patients with gastro-oesophageal reflux disease (GERD) before and during long-term maintenance therapy with omeprazole. Mean treatment duration was 56 months (range 36-81 months). RESULTS: Urinary excretion of unbound cobalamin was unchanged with both dosages of omeprazole. Excretion of 57Co-cyanocobalamin, however, decreased significantly during treatment with both 20 mg omeprazole (mean +/- S.E.M.: 1.31 +/- 0.20 vs. 0.54 +/- 0.17%; P < 0.02) and 40 mg omeprazole (1.25 +/- 0.26 vs. 0.29 +/- 0.06%; P < 0.02). Mean serum cobalamin levels (+/- S.E.M.) before and during therapy with omeprazole in GERD patients were 298 +/- 27 and 261 +/- 16 pg/mL (normal range 180-900 pg/mL), respectively (P = N.S.). CONCLUSIONS: Absorption of protein-bound, but not unbound, cyanocobalamin is decreased when measured by a modified Schilling test during treatment with omeprazole. However, no change in serum cobalamin levels was observed in patients with GERD after treatment with omeprazole for up to 7 years.

Adult↗
PubMed1995

Review article: the development of atrophic gastritis--Helicobacter pylori and the effects of acid suppressive therapy.

Helicobacter pylori is uniquely adapted to survival in the strongly acidic gastric lumen. In vitro, both acid and certain acid suppressors affect bacterial growth. In vivo, there is little evidence that acid suppressors have any effect on bacterial survival. In contrast, decrease of acid secretion quickly leads to a spreading of the bacterial infection throughout the body and fundus of the stomach, which is accompanied by an increase of the associated gastritis. Helicobacter pylori gastritis may, in a substantial number of infected subjects, ultimately lead to atrophy and intestinal metaplasia, conditions with an increased risk for gastric cancer. This review summarizes the data on the interrelation between Helicobacter pylori, gastric acid secretion and development of atrophic gastritis.

Animals↗
PubMed1995

Pharmacological management of gastro-oesophageal reflux disease.

Gastro-oesophageal reflux disease (GORD) ranges from episodic symptomatic reflux without oesophagitis to severe oesophageal mucosal damage, such as Barrett's metaplasia or peptic stricture. The multifactorial pathogenesis of GORD prevents medical cure of the disease. GORD is a chronic disease with a high tendency to relapse, requiring a long term treatment strategy in practically all patients. Complete healing of all mucosal lesions is not necessarily the aim of treatment in all patients. In milder forms of reflux disease, symptom relief is the most important goal. Many patients with mild GORD do well on symptomatic self-care with antacids and/or alginate. In addition, lifestyle changes should be advised to all patients: these improve symptoms and enhance the efficacy of therapy. In the acute treatment of GORD the prokinetic drug cisapride has been shown to be effective in relieving symptoms and healing grade I to II oesophagitis. Cisapride decreases symptomatic and endoscopic relapse in patients with mild GORD. Histamine H2-receptor antagonists are effective in relieving reflux symptoms in about 50% of patients, but with regard to healing, H2-antagonists appear to be mainly effective in grades I and II and not in higher grades of oesophagitis. Maintenance treatment with H2-antagonists is mainly symptomatically effective in patients with mild GORD. Proton pump inhibitors (PPIs) provide significantly higher healing rates of reflux oesophagitis than H2-antagonists, even in the more severe cases of oesophagitis and Barrett's ulcers. PPIs are also effective in patients with oesophagitis refractory to treatment with H2-antagonists. PPIs have become the drugs of first choice in healing of all patients with more severe forms of reflux oesophagitis, and increasingly also for patients with milder forms of oesophagitis, certainly those who fail to respond to other drugs. In maintenance treatment of GORD, PPIs are the most effective drugs, offering the possibility of keeping nearly all patients in remission with adjusted doses. Current patient data of up to 5 years indicate the safety of this strategy for this period, but the exact consequences of strong acid inhibition over a longer period still have to be clarified. At present, all but a few patients with GORD can be managed adequately by medical therapy.

Clinical Trials as Topic↗
PubMed1995

Increase of Helicobacter pylori-associated corpus gastritis during acid suppressive therapy: implications for long-term safety.

OBJECTIVES: Helicobacter pylori causes chronic active gastritis with predominant localization in the gastric antrum. This predisposes to development of mucosal atrophy, intestinal metaplasia, and eventually, gastric cancer. The effects of acid suppression on H. pylori infection and associated gastritis are unclear. However rapid development of atrophic gastritis has been consistently observed in a number of studies during low acid output. We therefore studied the histological features of antrum and corpus of the stomach before and during acid suppressive therapy. METHODS: Fifty patients with either reflux esophagitis (n = 21), benign gastric ulcer (six patients), gastric erosions (three patients), or duodenal ulcer (20 patients) were treated for 8 wk with omeprazole 40 mg o.d. Esophagogastroduodenoscopy was performed pre-entry and at 8 wk. Biopsy specimens were sampled from the antrum and corpus for histology and cultures. RESULTS: Seventeen H. pylori-negative patients had no histological signs of active gastritis, before or after therapy. Thirty-three H. pylori-positive patients showed predominant colonization and associated inflammation in the antrum before therapy. After therapy, however, the infection predominantly affected the corpus. The inflammation and bacterial colonization in the antrum significantly decreased, leading to negative antral cultures in 61% (20 of 33 patients). In contrast, the inflammation of the corpus mucosa significantly increased despite stable bacterial counts. CONCLUSIONS: We conclude 1) that H. pylori testing in patients on profound acid suppressive therapy should be performed on combined corpus and antral specimens, and 2) that omeprazole therapy leads to a strong increase in corpus gastritis, which may explain the observed development of corpus atrophy in a substantial number of patients after several years of continuous acid suppressive treatment. Therefore, we suggest that patients in need of long-term acid suppressive therapy should receive bacterial eradication therapy if they are H. pylori positive.

Antacids↗
PubMed1994

Long-term treatment with omeprazole for refractory reflux esophagitis: efficacy and safety.

OBJECTIVE: To evaluate the long-term efficacy and safety of omeprazole in patients with gastroesophageal reflux disease resistant to treatment with histamine-2 (H2)-receptor antagonists. DESIGN: Cohort analytic study with a mean follow-up of 48 months (range, 36 to 64 months). SETTING: Patients receiving ambulatory care from referral centers. PATIENTS: 91 patients with gastroesophageal reflux disease resistant to treatment with an H2-receptor antagonist but subsequently responsive to 40 mg of omeprazole daily. INTERVENTION: Open maintenance therapy consisting of 20 mg of omeprazole daily in 86 patients and 40 mg daily in 5 patients. OUTCOME MEASURES: Endoscopy to assess healing; side effects, laboratory values, fasting serum gastrin level, and gastric corpus biopsies to assess safety. RESULTS: Esophagitis recurred in 47% of the patients receiving 20 mg of omeprazole daily, but all rehealed after the dose was doubled. Seven of 40 patients (18%) had a second relapse after a mean follow-up time of 24 months (range, 9 to 36 months) that was successfully treated with a further 20-mg dose increment for a mean period of 36 months (range, 6 to 39 months). Median gastrin levels increased initially from 60 ng/L before study entry to 162 ng/L (P < 0.01) with treatment and reached a plateau during maintenance treatment. Very high gastrin levels (> 500 ng/L) were observed in a subgroup (11%) of patients. The incidence of micronodular hyperplasia increased from 2.5% of the patients at first biopsy to 20% at the last biopsy (P = 0.001), with a corresponding progression of gastritis to subatrophic or atrophic gastritis from less than 1% to 25% (P < 0.001), which was more pronounced in patients with very high serum gastrin levels. CONCLUSIONS: Maintenance therapy with omeprazole was effective for at least 5 years in patients with gastroesophageal reflux disease resistant to treatment with H2-receptor antagonists. Treatment was accompanied by a persistent increase in serum gastrin levels and an increase of micronodular argyrophil cell hyperplasia and subatrophic or atrophic gastritis.

Barrett Esophagus↗
PubMed1993

Serum pepsinogens after interruption of long-term maintenance therapy with omeprazole in patients with reflux esophagitis.

Administration of omeprazole induces increases in serum concentrations of pepsinogens A and C. In 10 patients with reflux esophagitis who were on continuous maintenance treatment, the effect of cessation of omeprazole administration on serum pepsinogens was studied. Pepsinogens A and C were measured in serum samples on days 0, 1, 2, 4, 7, and 9 after treatment and the results were compared with the values available in eight patients at a time before omeprazole treatment. Serum pepsinogen A levels decreased gradually after cessation of omeprazole administration, and all values fell into the normal range after the seventh day of the study period, but were still higher than before therapy. Seven of 10 patients showed a decrease of pepsinogen C after nine days, but two patients had still increased levels at the end of the study period. The pepsinogen A:C ratio on the ninth day after cessation was significantly lower than on day 0 during omeprazole therapy. We conclude that long-term maintenance therapy with omeprazole induces significant increases in both serum pepsinogens. After cessation of omeprazole treatment, serum pepsinogens rapidly decrease in most patients, but continue to be higher before therapy for at least nine days.

Esophagitis, Peptic↗
PubMed1993

Long-term omeprazole therapy does not affect Helicobacter pylori status in most patients.

Fifty-one patients were treated with 20-60 mg omeprazole for reflux oesophagitis resistant to H2-blocker therapy during a mean of 49 months of follow-up. With use of a standardized enzyme-linked immunosorbent assay technique specific IgG and IgG Helicobacter pylori antibodies were determined in serum obtained at the start of therapy and at the most recent visit. At the start of therapy 26 patients (51%) had evidence of H. pylori infection, as demonstrated by increased IgG and IgA antibody levels. During follow-up, 4 of these 26 patients (15%) became H. pylori seronegative. It is concluded that long-term treatment with omeprazole has no effect on H. pylori status in most patients.

Aged↗
PubMed1992

Medical therapy of patients with reflux oesophagitis poorly responsive to H2-receptor antagonist therapy.

There is substantial clinical experience of omeprazole treatment in patients with reflux oesophagitis, who have an incomplete or failed response to profound and prolonged acid-inhibitory therapy with H2-receptor antagonists. In The Netherlands, most patients with reflux oesophagitis poorly responsive to high-dose H2-receptor antagonists were healed within 3 months of treatment with omeprazole, 40 mg once daily. Only a few patients (less than 10%) with complicated reflux oesophagitis needed a longer duration of treatment or a higher dose of omeprazole to achieve complete endoscopic healing. Follow-up for up to 6 years has shown that most of these patients could be maintained successfully on omeprazole, 20 mg daily. However, about one third of the patients relapsed after healing when the maintenance dose was introduced. Evaluation of these patients who relapsed has shown that they require a higher level of acid-secretory inhibition; a maintenance dose of omeprazole, 40 mg once daily, rehealed the oesophagitis within 3 months. Only a few patients had a second relapse, and these patients were rehealed by an increase of the omeprazole dose to 60 mg daily. Oesophageal pH monitoring in these patients has shown that there is continued pathological oesophageal acid exposure, predominantly during the night, suggesting that the duration of major action of omeprazole was insufficient for production of adequate elevation of intragastric pH during the night. Successful control of reflux disease in these patients was achieved by increasing omeprazole therapy to a regime and dosage that achieved elevation of intragastric pH above 4 throughout the 24-hour period.

Administration, Oral↗
PubMed1992

The role of omeprazole in healing and prevention of reflux disease.

Reflux esophagitis differs from peptic ulcer disease in many respects. Whereas nighttime acid inhibition alone achieves healing in approximately 80 to 90% of patients with peptic ulcer, more profound acid inhibition seems to be necessary in those with GERD. Conventional dosing with H2-receptor antagonists has been successful in only about 50% of the patients with reflux esophagitis. Strong, prolonged 24-hour inhibition of gastric acid secretion is probably the most important factor in the treatment of reflux esophagitis. Omeprazole, a substituted benzimidazole, produces effective 24-hour inhibition on gastric acid secretion. In doses ranging from 20-60 mg once daily, omeprazole has proved to be effective in the short-term treatment of reflux esophagitis, even in patients resistant to treatment with H2-receptor antagonists. Healing of severe, resistant reflux esophagitis therefore is no longer a clinical problem. Reflux esophagitis is a chronic, relapsing condition that cannot be compared to peptic ulcer disease in all aspects. In particular, long-term therapy must be more aggressive than the standard minimum maintenance dose used in peptic ulcer. Not only for healing, but also for prevention of recurrences, strong, prolonged inhibition of acid secretion must be provided. Experience of more than 5 years of continuous treatment with omeprazole, in doses adjusted to prevent recurrences, has demonstrated the high efficacy of this agent in the long-term management of reflux patients. Omeprazole provided the long-standing, strong acid inhibition that is so important in treating this condition. Long-term treatment with omeprazole in patients with resistant reflux disease did induce an initial rise of serum gastrin levels, two to four times the pre-entry value.(ABSTRACT TRUNCATED AT 250 WORDS)

Esophagitis, Peptic↗
PubMed1991

Recent advances in the management of gastro-oesophageal reflux disease.

The basis of treatment of reflux oesophagitis is change in behaviour and lifestyle. In the presence of mild symptoms antacids/alginate may be instituted. In case of Savary grade I and II oesophagitis at endoscopy, H2-receptor antagonists (H2RAs), alone or in combination with a prokinetic or mucosaprotective agent, are the first choice of treatment. Drug treatment should be continued for at least 8-12 weeks. In case of resistance to treatment or in case of severe and/or complicated reflux oesophagitis, omeprazole should be prescribed. Maintenance treatment is necessary in patients with severe reflux oesophagitis and in patients with quick relapses, once therapy has stopped. Full-dose H2RAs are required to prevent recurrences. In case of resistance to H2RAs, omeprazole should be used. Anti-reflux surgery should be considered in patients, especially at young age, who have an insufficient response to medical management, due either to lack of compliance or to therapeutic failure.

Gastroesophageal Reflux↗