Motives of contributing personal data for health research: (non-)participation in a Dutch biobank.

BACKGROUND: Large-scale, centralized data repositories are playing a critical and unprecedented role in fostering innovative health research, leading to new opportunities as well as dilemmas for the medical sciences. Uncovering the reasons as to why citizens do or do not contribute to such repositories, for example, to population-based biobanks, is therefore crucial. We investigated and compared the views of existing participants and non-participants on contributing to large-scale, centralized health research data repositories with those of ex-participants regarding the decision to end their participation. This comparison could yield new insights into motives of participation and non-participation, in particular the behavioural change of withdrawal. METHODS: We conducted 36 in-depth interviews with ex-participants, participants, and non-participants of a three-generation, population-based biobank in the Netherlands. The interviews focused on the respondents' decision-making processes relating to their participation in a large-scale, centralized repository for health research data. RESULTS: The decision of participants and non-participants to contribute to the biobank was motivated by a desire to help others. Whereas participants perceived only benefits relating to their participation and were unconcerned about potential risks, non-participants and ex-participants raised concerns about the threat of large-scale, centralized public data repositories and public institutes, such as social exclusion or commercialization. Our analysis of ex-participants' perceptions suggests that intrapersonal characteristics, such as levels of trust in society, participation conceived as a social norm, and basic societal values account for differences between participants and non-participants. CONCLUSIONS: Our findings indicate the fluidity of motives centring on helping others in decisions to participate in large-scale, centralized health research data repositories. Efforts to improve participation should focus on enhancing the trustworthiness of such data repositories and developing layered strategies for communication with participants and with the public. Accordingly, personalized approaches for recruiting participants and transmitting information along with appropriate regulatory frameworks are required, which have important implications for current data management and informed consent procedures.

Predictive accuracy of Edinburgh postnatal depression scale assessment during pregnancy for the risk of developing postpartum depressive symptoms: a prospective cohort study.

OBJECTIVE: To investigate whether the 10-item Edinburgh Postnatal Depression Scale (EPDS) administered antenatally is accurate in predicting postpartum depressive symptoms, and whether a two-item EPDS has similar predictive accuracy. DESIGN: Prospective cohort study. SETTING: Obstetric care in the Netherlands. POPULATION: One thousand six hundred and twenty women from the general population. METHODS: Mean values, area under the receiver operating characteristics curve (AUC), sensitivity, specificity and predictive values of antenatal EPDS for the likelihood of developing postpartum depressive symptoms were calculated. Analyses were repeated for each trimester, several cut-off values and a two-item EPDS (low mood and anhedonia). MAIN OUTCOME MEASURES: Postpartum depressive symptoms, defined as EPDS score≥10. RESULTS: Mean EPDS scores were significantly higher during each trimester in women with postpartum depressive symptoms than in those without the symptoms (P<0.001). Using the prevailing cut-off (≥13), the AUC was reasonable (0.74), sensitivity was 16.8% (95% CI 11.0-24.1), positive predictive value was 41.8% (95% CI 28.7-55.9), specificity was 97.8% (95% CI 97.0-98.5) and negative predictive value was 92.7% (95% CI 91.3-94.0). Using a lower cut-off value (≥5), sensitivity was 70.8% (95% CI 62.4-78.3) and specificity was 65.4% 4 (95% CI 62.9-67.8), but positive predictive value was low (15.9%, 95% CI 13.1-19.0). Negative predictive value was exceedingly high at 96.0% (95% CI 94.6-97.2). Results were similar during the second and third trimester. The predictive accuracy of the two-item EPDS appeared inferior. CONCLUSIONS: The EPDS was not sufficiently accurate in predicting risk of postpartum depressive symptoms. Nevertheless, when using the ≥5 cut-off value, it may be adequate for initial screening, followed by further assessments and possibly antenatal intervention when positive. Furthermore, when negative, women may be reassured that postpartum depressive symptoms are unlikely. A two-item version showed poor predictive accuracy.

Effect of enprostil on serum gastrin and pepsinogen A and C levels in patients on long-term treatment with omeprazole.

BACKGROUND: Treatment of omeprazole induces profound inhibition of gastric acid secretion, resulting in hypergastrinaemia. In rats hypergastrinaemia induced by chronic administration of high doses of omeprazole resulted in ECL-cell hyperplasia and subsequent carcinoid formation. This finding may limit long-term therapy in man. The synthetic prostaglandin E2 analogue enprostil not only inhibits gastric acid secretion but also reduces serum gastrin in normal subjects and in peptic ulcer patients. The present study was undertaken to determine whether enprostil reduces serum gastrin in patients on long-term treatment with omeprazole. METHODS: Eight patients with reflux oesophagitis treated with 40 mg omeprazole once daily for at least 3 months received 35 micrograms enprostil t.d.s. during a 5-day treatment course. Basal and postprandial serum gastrin concentrations and pepsinogen A and C levels were measured on the day before, the first and the final day, and on the day after cessation of treatment. RESULTS: Enprostil significantly (P < 0.05) reduced basal serum gastrin from 65 +/- 15 pmol/L to 51 +/- 13 pmol/L on the first treatment day, and to 41 +/- 9 pmol/L on the final day. Enprostil also significantly (P < 0.05) reduced postprandial integrated serum gastrin from 6173 +/- 849 pmol.h/L to 4516 +/- 906 pmol.h/L and to 3532 +/- 706 pmol.h/L on the first and final treatment days, respectively. On the day after cessation of treatment basal (57 +/- 11 pmol/L) and postprandial integrated serum gastrin concentrations (5766 +/- 864 pmol.h/L) were not significantly different when compared to pretreatment values. Enprostil had no significant influence on serum pepsinogens A and C. CONCLUSION: Short-term co-administration of enprostil lowers the serum gastrin levels in patients on long-term treatment with omeprazole.

Effect of synthetic prostaglandin E2 analog enprostil on omeprazole-induced hypergastrinemia and hyperpepsinogenemia.

This study was undertaken to determine whether the synthetic prostaglandin E2 analog enprostil is able to inhibit basal and postprandial hypergastrinemia induced by omeprazole. We also studied the effect of omeprazole, enprostil, and the combination of both drugs on serum pepsinogen A and C levels. Eight normal subjects received in random order five-day courses of 40 mg omeprazole once a day, 35 micrograms enprostil three times a day, the combination of both drugs, and placebo. Omeprazole induced significant increases in basal and postprandial serum gastrin and in pepsinogen A and C levels. These increments persisted on the day after stopping treatment. Coadministration of enprostil inhibited omeprazole-induced basal hypergastrinemia and postprandial integrated serum gastrin, but not basal serum pepsinogen A and C, while the inhibition on the day after the treatment courses only reached statistical significance for the postprandial integrated serum gastrin concentration. It is concluded that enprostil inhibits omeprazole-induced basal and postprandial hypergastrinemia, with a tendency to protracted inhibition after stopping the drugs, and that enprostil does not significantly influence omeprazole-induced increases in pepsinogen A and C level. Coadministration of enprostil may be helpful in preventing pronounced hypergastrinemia in the few patients who show large serum gastrin increases during treatment with omeprazole.

Inhibition of omeprazole induced hypergastrinaemia by SMS 201-995, a long acting somatostatin analogue in man.

Whether the long acting somatostatin analogue SMS 201-995 (octreotide, Sandostatin) could inhibit the basal and meal stimulated hypergastrinaemia and hyperpepsinogenaemia induced by omeprazole was investigated. Eight healthy subjects were randomised to receive five day courses of SMS 201-995 (25 micrograms subcutaneously three times daily), omeprazole (40 mg once a day), a combination of both drugs, or placebo. Basal and meal stimulated serum gastrin and basal serum pepsinogen A and C values were measured the day before treatment, on day five of treatment, and the day after each course of treatment. Omeprazole caused significant increases in basal and meal stimulated peak and integrated serum gastrin values and pepsinogen A and C levels, which were still significantly raised the day after stopping omeprazole treatment. Giving SMS 201-995 with omeprazole significantly reduced any omeprazole induced increases in basal and meal stimulated peak and integrated serum gastrin levels; serum pepsinogen A and C values were significantly inhibited too. Serum gastrin values during combined therapy were not significantly different from those during placebo treatment, whereas pepsinogen A and C levels were still significantly raised. On the day after stopping combined therapy, basal and meal stimulated peak and integrated serum gastrin and serum pepsinogen C (but not pepsinogen A) levels were not significantly different from values obtained on the day after stopping omeprazole alone. SMS 201-995 without omeprazole significantly inhibited basal and meal stimulated peak and integrated serum gastrin levels. Pepsinogen A was also significantly inhibited by SMS 210-995, but the reduction in pepsinogen C failed to reach statistical significance. In conclusion, SMS 201-995 prevents basal and meal stimulated increases in serum gastrin during omeprazole therapy. This finding may have clinical importance in the few patients who have pronounced hypergastrinaemia because of profound long acting acid inhibition.

Attenuation of the gastric acid and serum gastrin-lowering effects of the prostaglandin E2 analog enprostil.

Enprostil, a synthetic prostaglandin E2 analog, has been shown to decrease gastric acid secretion and plasma gastrin levels during short-term treatment. However, effects of prolonged treatment with enprostil on these parameters in humans are unknown. We have studied the effects of 35 micrograms enprostil twice daily on 24-hour intragastric pH, basal gastrin, and meal-stimulated gastrin release in 10 healthy volunteers. Enprostil, 35 micrograms, was ingested twice daily for 4 weeks. Subjects were studied on day 0 (preentry) and days 1 and 29, when enprostil was taken 30 minutes before the first and third standard test meals at 9 AM and 5 PM. Enprostil significantly increased 24-hour median pH (p < 0.02) on day 1 but not on day 29. Enprostil had no significant effect on basal gastrin levels compared with placebo. However, on day 1, but not on day 29, postprandial gastrin levels were significantly lower compared with preentry (p < 0.05). On day 29 post-prandial gastrin levels after the second standard test meal were significantly higher compared with preentry data (p < 0.05). In conclusion, 35 micrograms enprostil twice daily reduced gastric acidity and serum gastrin levels on the first day of treatment, but this effect attenuated and even transiently reversed during a 4-week treatment period.

Effect of short-term administration of omeprazole on serum gastrin and pepsinogens in antrectomized patients.

Omeprazole, a potent and long-acting inhibitor of gastric acid secretion, is known to increase both serum gastrin and pepsinogen A and C levels in unoperated subjects. It has been suggested that the rise in serum pepsinogens is mediated by the omeprazole-induced increase in serum gastrin. This study was undertaken to determine the role of gastrin in hyper-pepsinogenemia induced by antisecretory therapy. We have studied the effect of a 5-day course of 40 mg of omeprazole daily on fasting serum gastrin and pepsinogen A and C levels in 14 patients with an antrectomy and a Billroth I anastomosis (n = 8) or a Billroth II anastomosis (n = 6). In antrectomized patients omeprazole failed to induce any increase in basal serum gastrin. On the other hand, omeprazole increased significantly serum pepsinogen A levels in both Billroth I and II patients, while the rise in serum pepsinogen C level was significant in Billroth I, but just failed to reach statistical significance in Billroth II patients. We conclude that the stimulation of serum pepsinogens A and C by a short-term treatment with omeprazole is not mediated by increases in serum gastrin. This study further shows that omeprazole stimulates gastrin release only from the antrum and not from extra-antral sources.

IgG subclass response to Helicobacter pylori in patients with chronic active gastritis and duodenal ulcer.

The IgG subclass response is determined by the type of bacteria producing the infection and by genetic factors of the host. Patients with a Helicobacter pylori infection develop a specific immune response that is mainly of the IgA and IgG class. We measured the IgG subclass response in 20 patients with chronic active gastritis without a history of duodenal ulcer and 20 patients with chronic active gastritis and duodenal ulcer diagnosed by endoscopy and histology. A control group included 20 H. pylori-negative patients and 60 H. pylori-positive blood transfusion donors. Systemic IgG subclass response was measured with a modified enzyme-linked immunosorbent assay technique, using as antigen a sonicate of six different H. pylori strains. Mouse monoclonal antibodies against each of the four human IgG subclasses (IgG1, IgG2, IgG3, and IgG4) were used. The total IgG anti-H. pylori antibody titres were equal in all three H. pylori-positive groups and significantly different from that of the negative control group (p less than 0.01). The IgG subclass response in persons infected with H. pylori involved all four subclasses but was predominantly of the IgG1 and IgG2 subclasses. All of the groups with H. pylori infection had significantly higher levels of IgG1 than the negative control group, but no differences were detected among the three groups. However, the duodenal ulcer group had a significantly higher IgG2 response than the gastritis group (mean optical density +/- SEM, 0.382 +/- 0.047 versus 0.200 +/- 0.025, respectively; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Long term serological surveillance after treatment of Helicobacter pylori infection.

Fifteen patients with type B gastritis caused by Helicobacter pylori infection were treated with 'triple' therapy consisting of colloidal bismuth subcitrate, amoxycillin, and metronidazole. All were followed up as outpatients every three months for at least one year. After 'triple' therapy a significant (p less than 0.01) and persistent reduction in IgA and IgG antibody levels against H pylori was detected. In three patients recurrent active infection with H pylori at nine and 12 months was detected by a rise in IgA (three patients) and IgG (two patients) antibody levels against H pylori and worsening of symptoms, and was confirmed by culture and histology. In 11 patients, the absence of infection at 12 months was confirmed by culture and histology. In a control group of 13 patients with type B gastritis who received no antibacterial treatment, specific IgA and IgG antibody levels against H pylori remained unchanged during 12 months of follow up. Although specific IgG against H pylori is the most widely used serological test for screening, our data indicate that specific IgA is also valuable in monitoring treatment. These serological tests are easy to perform, relatively inexpensive, devoid of radioactivity and are very acceptable to patients. It is concluded that serological testing is the preferred method for follow up after treatment for H pylori infection and will probably replace endoscopy or the urea breath test.

Omeprazole in the treatment of Zollinger-Ellison syndrome and histamine H2-antagonist refractory ulcers.

Omeprazole is a very potent and long-acting inhibitor of gastric acid secretion. These characteristics make the drug very suitable for the management of gastric acid hypersecretion and symptom relief in patients with the Zollinger-Ellison syndrome, and in the treatment of patients with ulcers resistant to histamine H2-receptor antagonists. Most patients require only a once-daily dose, whereas in about 30% of patients with Zollinger-Ellison syndrome the dose has to be split. During long-term treatment the required dose of omeprazole is usually rather stable. Up until now neither in patients with Zollinger-Ellison syndrome nor in those with resistant ulcers have convincing reports of resistance to omeprazole been published. However, a relative disadvantage of omeprazole is the observation that symptom-free Zollinger-Ellison syndrome patients are less inclined to undergo the work-up for surgery, which is the only possible curative treatment for these patients. Omeprazole therapy has been well tolerated and no side effects, significant changes in laboratory variables or toxicity have been noted.

Improved specificity of the PABA test with p-aminosalicylic acid (PAS).

Until now use of the PABA test together with [14C] PABA to calculate the PABA excretion index has probably been the best adaptation suggested to enhance the specificity of this non-invasive pancreatic function test. Drawbacks of the method are the application of radioactivity, the fact that children, pregnant women, and patients with renal insufficiency have to be excluded from the test, and the possible interference of drugs and isotopes. We propose simultaneous administration of p-aminosalicylic acid (PAS) in the PABA test and quantification of the urinary PABA and PAS excretion with liquid chromatography. Urinary PABA and PAS excretion in six hours are comparable (69.5 +/- 8.4% and 65.6 +/- 18.4% respectively in five healthy volunteers). Application of the PABA/PAS ratio was compared with the urinary PABA excretion in 21 normal controls, 38 patients with pancreatic disease, and 42 patients without pancreatic pathology. The PABA/PAS ratio and the per cent PABA excretion correlated very well in pancreatic patients: (PABA/PAS ratio) = 0.0149 (% PABA) + 0.052 (r = 0.902). Use of the PABA/PAS ratio enhanced the specificity of the test from 76 to 89%.

Captopril plus hydrochlorothiazide once daily normalizes 24 h blood pressure in patients with essential hypertension.

The hypotensive effect of captopril 50 mg twice daily and of captopril 50 mg + hydrochlorothiazide (HCTZ) 25 mg once daily was studied in 12 patients with mild to moderate essential hypertension, whose blood pressure was not normalized by captopril 25 mg twice daily alone. Both captopril 50 mg twice daily and captopril 50 mg + HCTZ 25 mg once daily caused a significant reduction of outpatient blood pressures as compared with placebo (P less than 0.001). Captopril 50 mg + HCTZ 25 mg once daily also reduced outpatient blood pressures significantly when compared with captopril 25 mg twice daily (P less than 0.01). Both captopril 50 mg twice daily and captopril 50 mg + HCTZ 25 mg once daily significantly reduced 24 h blood pressure (P less than 0.001) without disturbance of its normal circadian rhythm. This effect was more pronounced while on captopril + HCTZ. Captopril 50 mg + HCTZ 25 mg once daily normalizes 24 h blood pressure in most patients with mild to moderate essential hypertension, whose blood pressure is not controlled by captopril 25 mg twice daily alone.

Low dose captopril twice daily lowers blood pressure without disturbance of the normal circadian rhythm.

The effect of captopril 25 to 50 mg twice daily on 24 h blood pressures was compared with placebo in 14 patients with essential hypertension. Captopril was started in a dose of 25 mg b.d. in all patients. This dose was increased to 50 mg b.d. in those patients whose blood pressure was not normalized after 4 weeks (group II, n = 5), while in the others the same dose was continued (group I, n = 9). Blood pressure was measured at the end of the placebo period and after 8 weeks captopril, both in the office with a random zero sphygmomanometer and ambulant at home with a portable automated non-invasive blood pressure measuring device (ICR). In comparing the ICR measurements with those made with a standard mercury sphygmomanometer good agreement between the two methods for both diastolic (r = 0.94, n = 110) and systolic (r = 0.96, n = 110) blood pressure was found. In group I office blood pressures (mean +/- s.e.m.) decreased from 166 +/- 7/100 +/- 3 mm Hg to 144 +/- 4/87 +/- 2 mm Hg (P less than 0.001). In group II these reductions were from 165 +/- 7/104 +/- 2 mm Hg to 152 +/- 5/90 +/- 4 mm Hg (P less than 0.05). During ambulatory monitoring, blood pressure was shown to have a circadian rhythm both on placebo and on captopril. Captopril 25 mg b.d. lowered blood pressure throughout the 24 h observation period, although these reductions were smaller at night than during the day. In group II comparable effects of captopril 50 mg b.d. were demonstrated. Captopril 25 to 50 mg twice daily adequately controls blood pressure in most patients with mild to moderate essential hypertension.

[A comparison of 3 isolation methods for the demonstration of Salmonella bacteria in fryer-chicken feed]. / Een vergelijking van drie isolatie-methoden voor het aantonen van Salmonella-bacteriën in braadkuikenvoeders.

167 Samples of fryer chicken feed were examined for the presence of Salmonella using three different methods of isolation. These methods consisted in the isolation of Salmonella using procedure ISO-3565, this method but supplemented by treatment with hydrogen sulphide (ISO + H2S) and the membrane filter disc immuno-immobilisation method (MFDI). In addition, thirty-three samples were examined by the ISO and ISO + H2S techniques. 200 Grams of feed of each sample were studied. A total number of fifteen samples (7.5 per cent) were found to be positive for Salmonella, thirteen of which were examined by the ISO-3565 method of isolation of Salmonella. When the other methods were employed, only five samples were found to be positive for Salmonella using the ISO + H2S technique and two using the MFDI method. When all three methods were used, they failed to produce positive results in each sample which had been found to be positive for Salmonella. The differences in the number of positive samples were found to be significantly (P less than 0.01) in favour of the ISO method. When a choice has to be made between the method used in the detection of Salmonella, the ISO-3565 method of isolating Salmonella is to be preferred.