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Biomedical subjects

H G Dammann

Publications and source records attributed to H G Dammann.

At least 19 recordsLinked to original sources
PubMed2004

Effects of acetylsalicylic acid on ascorbic acid concentrations in plasma, gastric mucosa, gastric juice and urine--a double-blind study in healthy subjects.

OBJECTIVE: This study investigated concentrations of ascorbic acid (ASC) in gastric mucosa, gastric juice, urine and plasma in healthy subjects under steady state and fasted conditions with and without concomitant administration of acetylsalicylic acid (ASA). MATERIAL AND METHODS: This was a prospective, randomized, double-blind, parallel-group study in healthy subjects. It has assessed the effects of a 6-day administration of 0.8 g ASA or 0.48 g ASC, 3 times daily and the combination of both on concentrations of ASC in gastric mucosa, gastric juice, urine and plasma. Treatments were switched after 6 days without any washout for assessment of compartment sensitivity to changes in study medication resulting in an overall 14-day study period. Each of the 3 treatment groups consisted of 15 subjects. RESULTS: ASC concentrations were highest in the gastric mucosa (251+/-11 microg/g), followed by gastric juice (29+/-6 microg/ml), plasma (10+/-0.2 microg/ml), and urine (5+/-1 microg/ml). On day 7, ASC concentrations in gastric mucosa, plasma and urine had increased in those groups receiving ASC and decreased in the group receiving ASA only. All differences were statistically significant and indicate an interaction with ASA. In gastric juice, differences in ASC concentrations between the treatment groups were not statistically significant between baseline and day 7. ASC concentrations in plasma were strongly correlated with corresponding ASC concentrations in gastric mucosa (r = 0.34) and urine (r = 0.83), as were ASC concentrations in gastric mucosa with ASC in urine (r = 0.28). CONCLUSIONS: The gastric mucosa is the largest depot of ASC in the human body with ASC concentrations 25 times higher than in plasma. In healthy subjects, clinically relevant doses of ASA reduced ASC concentrations in gastric mucosa by about 10% within 6 days resulting from antioxidative defense mechanisms. In patients with long-term ASA treatment or conditions with additional risks such as elderly subjects with unfavorable dietary conditions and impaired antioxidative protection, a protective adjunct administration of ASC appears to be beneficial.

Adolescent↗
PubMed2000

Eradication of H. pylori with pantoprazole, clarithromycin, and metronidazole in duodenal ulcer patients: a head-to-head comparison between two regimens of different duration.

BACKGROUND: The study was conducted to compare the efficacy and tolerability of two pantoprazole-based triple therapies of different length in the eradication of H. pylori. METHODS: In this double-blind, multicenter parallel group comparison, H. pylori-positive patients were randomly assigned to either the PCM-7 group (7 days of pantoprazole 40 mg bid, clarithromycin 500 mg bid, metronidazole 500 mg bid) or the PCM-14 m group (modified 14 day therapy of the same regimen with metronidazole only given for 10 days due to labeling reasons). H. pylori status was determined by urease test, histology, culture, and 13C-urea breath test. Treatment outcome was assessed 6 weeks after intake of the last study medication. RESULTS: The following eradication rates were achieved: for PCM-7 in the MITT population 83% (89/107), in the PP population 84% (81/97); for PCM-14 m in MITT 87% (92/106), in PP 88% (91/104). Ulcer healing rates were: for PCM-7 in MITT population 99% (106/107), in the PP population 99% (96/97); for PCM-14 m in MITT 99% (105/106), in PP 99% (103/104). Gastrointestinal symptoms and gastritis scores decreased in both treatment groups. Equivalence of treatment regimens could be proven for all populations. In total, 64 patients reported adverse events. Five serious adverse events occurred, all unrelated to the study medication. CONCLUSION: The two pantoprazole-based triple therapies tested in this study are equally effective in H. pylori eradication, ulcer healing and relief from ulcer pain. It is concluded that 7 days of triple therapy are generally sufficient.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1999

The effects of oral rabeprazole on endocrine and gastric secretory function in healthy volunteers.

AIM: To evaluate the short-term effects of rabeprazole 20 mg on endocrine parameters, in particular serum testosterone and cortisol, and on 24 h intragastric pH, H+ activity and nocturnal gastric acid secretion. METHODS: In this double-blind, two-period crossover study, 12 healthy young male volunteers were randomly given oral rabeprazole 20 mg o.m. or placebo for 14 days. There was a washout period of at least 1 week between the two studies. The effects of rabeprazole and placebo on cortisol and testosterone (primary criteria), and on tri-iodothyronine, thyroxine, 17beta-oestradiol, thyroid-stimulating hormone, thyroxine-binding protein, parathyroid hormone, insulin, glucagon, rennin, aldosterone, follicle-stimulating hormone, luteotrophic hormone, prolactin, somatotrophic hormone, dehydroepiandrosterone, cortisol-binding globulin and urinary 6-beta hydroxycortisol were compared. Intragastric 24 h pH, 24 h H+ activity and nocturnal gastric acid secretion were determined by pH probe and gastric aspiration. RESULTS: Rabeprazole produced no clinically relevant effects on endocrine function as assessed by measurement of serum testosterone, circadian serum cortisol levels, ACTH-stimulated serum cortisol levels and 17 other endocrine function tests. Rabeprazole significantly increased the 24 h median pH values compared to placebo (on Days 7 and 14 median values ranged from 3.92 to 6.88 with rabeprazole and from 1.48 and 4.22 with placebo, P < 0.001) and significantly decreased the integrated 24 h H+ activity (AUC08--08) from 343 mmol/L/h with placebo to 44 mmol/L/h with rabeprazole (P < 0.001). Following cessation of dosing, intragastric pH levels decreased and H+ activity increased, but acid secretion did not recover completely during the next 72 h. The mean value for nocturnal gastric acid secretion on Days 7 and 8 was 36 mmol/6 h with placebo and 5.6 mmol/6 h with rabeprazole (P < 0.001). Rabeprazole was well tolerated. CONCLUSION: Rabeprazole did not influence endocrine function in healthy young male volunteers during short-term dosing. Rabeprazole substantially increased intragastric pH over a 24 h period and significantly decreased intragastric acidity and nocturnal gastric acid secretion.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1999

Enteric coating of aspirin significantly decreases gastroduodenal mucosal lesions.

BACKGROUND: Low-dose aspirin (acetylsalicylic acid, ASA) increases the risk of developing peptic ulceration. AIM: To investigate the gastroduodenal mucosal tolerability of enteric-coated ASA (EC-ASA) 100 mg/day compared to either placebo (study 1) or plain ASA 100 mg/day (study 2) in healthy volunteers. METHODS: Study 1: In this double-blind study 18 volunteers received randomized dosing with either EC-ASA 100 mg or placebo for 15 days. Study 2: 41 volunteers underwent randomized 7-day dosing of either EC-ASA 100 mg or plain ASA 100 mg in this double-blind, parallel-group, comparison study. In both studies acute gastroduodenal mucosal lesions were assessed endoscopically before treatment, on the morning of day 1 after the first dose (only in study 2), and on the morning after the last dose of the test medication. RESULTS: Study 1 did not reveal any significant differences between the lesion scores of EC-ASA and placebo. In contrast, in study 2 significantly higher total gastroduodenal mucosal lesion scores were observed on day 1 after the first dose and after 7 days of dosing with plain ASA (mean sum of the lesion scores in the gastric fundus, body, antrum and in the duodenal bulb: day 1: plain ASA 3.95+/-3.38 vs. EC-ASA 1.43+/-1.91, P = 0.03; day 7: plain ASA 6.35+/-4.10 vs. EC-ASA 2.00+/-2.02, P = 0.0004). Tolerance of the test drugs was good, and no other adverse events were observed. CONCLUSIONS: Enteric-coated aspirin 100 mg/day causes significantly less gastroduodenal damage over 7 days than the same dose of plain aspirin, when given to healthy subjects. There was little gastric injury and no significant differences between EC-ASA and placebo in this respect.

Adult↗
PubMed1999

Impact of ELISA and immunoblot as diagnostic tools one year after eradication of Helicobacter pylori in a multicentre treatment study.

The performance of serological tests for Helicobacter pylori infections is hampered by the persistence of antibodies after eradication therapy or spontaneous healing. Detection of different antigens or immunoglobulin classes might have an impact on the validity of serodiagnosis. The aim of this study was to assess the decrease in IgA and IgG antibody levels after eradication of H. pylori. Serum samples of 242 patients with active duodenal ulcer were tested with the ELISA and the immunoblot (IB) techniques for H. pylori-specific IgA and IgG antibodies before therapy and 1 year after successful eradication. From a total of 81 patients paired sera were available. At the end of the follow-up period ELISA antibody titres from the IgA class had decreased from a mean value of 6.69 to 4.26 units (P = 0.0001), and IgG class antibody titres from a mean value of 21.9 to 12.1 units (P = 0.0001). Regarding seroreversion, from 34 initially IgA positive sera 16 (47%), and from 74 IgG positive sera 18 (24%), had definitively reverted to 'negative'. One year after eradication, when tested with the immunoblot, the antibody responses against specific antigens of 37% IgA-positive sera (23/62) and 8% IgG-positive sera (6/78) reverted to 'negative', compared to a seroreversion rate of 27% of the anti-CagA IgA-positive sera (18/67) and of 9% of the anti-CagA IgG-positive sera (7/79). In conclusion, despite an overall significant decrease of H. pylori antibodies, both tests cannot be recommended for monitoring treatment success.

Adult↗
PubMed1999

[Preferential COX-2 inhibition: its clinical relevance for gastrointestinal non-steroidal anti-inflammatory rheumatic drug toxicity].

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used in the treatment of arthritis and pain. These drugs tend to cause significant side effects, however, including gastric and intestinal toxicity. The mechanism of action of NSAIDs is through their inhibition of the key enzyme of prostaglandin biosynthesis, the cyclooxygenase. Recently, two forms of cyclooxygenase have been found to exist: COX-1 and COX-2, the constitutive and inducible forms, respectively. COX-1 exists in the stomach, intestine, kidneys and platelets, while COX-2, the inducible form, is expressed during inflammation. The therapeutic effects of NSAIDs are largely the result of inhibition of the enzyme cyclooxygenase-2 (COX-2), whereas the toxic effects (e.g., gastrointestinal, renal and platelet effects) are primarily due to the inhibition of COX-1. Individual NSAIDs show different potencies against COX-1 compared with COX-2 and this explains the variations in the side effects of NSAIDs at their anti-inflammatory doses. Drugs with high potency against COX-2 and a better COX-2-/COX-1 activity ratio will have anti-inflammatory activity with fewer gastrointestinal side effects. In contrast piroxicam and indomethacin, which drugs have a much higher potency against COX-1 than against COX-2, are amongst those with the highest gastrointestinal toxicity. Based on these findings, COX-2 seems to be an ideal target for the development of new anti-inflammatory drugs. Several compounds with preferential or specific COX-2 inhibiting properties have been synthesized and evaluated in pre-clinical and clinical studies i.e. Meloxicam, Celecoxib, MK-966, Flusolid and L-745, 337. The COX-2 selectivity of these novel NSAIDs relate well to their favorable gastrointestinal tolerability profile. Clinical trials have shown meloxicam and celecoxib to be as effective as currently available NSAIDs, but with an improved gastrointestinal tolerability profile. Further clinical trials and large-scale postmarketing surveillance programs are needed, however, to confirm the potential therapeutic benefits of these novel preferential or specific COX-2 inhibitors.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1999

Pantoprazole versus omeprazole: influence on meal-stimulated gastric acid secretion.

AIMS: To determine the influence of recommended therapeutic doses of pantoprazole and omeprazole on meal-stimulated acid secretion. METHODS: In this double-blind, placebo-controlled, three-period crossover study, 12 healthy male volunteers received 40 mg pantoprazole od, 20 mg omeprazole od or placebo at 08:00 h for 5 days in a randomized order. Meal-stimulated acid secretion was determined by means of a homogenized test meal, and intragastric titration on day 1, 4-6 h, 8-10 h, 16-18 h, and 24-26 h, and on days 3 and 5, 4-6 h after oral drug administration. RESULTS: On day 1 (4-6 h after oral drug administration), meal-stimulated acid secretion was decreased by 36% and 24% after administration of 40 mg pantoprazole or 20 mg omeprazole, respectively. After 3 and 5 days of dosing, the decreases were 88% and 85% with 40 mg pantoprazole, and 70% and 74% with 20 mg omeprazole. At all measuring points during the 5-day dosing periods, 40 mg pantoprazole proved superior to 20 mg omeprazole in inhibiting meal-stimulated gastric acid secretion. The differences were statistically significant for pantoprazole on day 1, 24-26 h after oral drug administration and on day 3 (P = 0.0425 and P = 0.0244, respectively). On day 1, only pantoprazole was significantly better than placebo (P = 0.0210, 4-6 h after dosing; P = 0.0093, 8-10 h after dosing and P = 0.0068, 16-18 h after dosing). CONCLUSION: Pantoprazole 40 mg is significantly more effective than omeprazole 20 mg in inhibiting meal-stimulated acid secretion. In addition, pantoprazole exhibits a more rapid onset of action.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Lansoprazole versus omeprazole: influence on meal-stimulated gastric acid secretion.

AIMS: To investigate, by means of meal-stimulated acid secretion, the extent to which differences in plasma half-life, bioavailability and the recommended therapeutic dose can influence the antisecretory potency of lansoprazole and omeprazole. METHODS: In this double-blind, placebo-controlled, crossover study, 10 healthy male volunteers received 15 mg or 30 mg lansoprazole, 20 mg or 40 mg omeprazole or placebo for 5 days, in a randomized order. Meal-stimulated acid secretion was determined by means of a homogenized test meal and intragastric titration. RESULTS: On day 1, meal-stimulated acid secretion was decreased by 35% and 45% after administration of 15 mg or 30 mg lansoprazole, and by 16% and 42% after 20 mg or 40 mg omeprazole. After 3 and 5 days of dosing the decreases were 53% and 48% with 15 mg lansoprazole, 82% and 82% with 30 mg lansoprazole, 43% and 39% with 20 mg omeprazole, and 76% and 83% with 40 mg omeprazole. At all measuring points during the 5-day dosing periods, lansoprazole 15 mg and 30 mg proved superior to 20 mg omeprazole in inhibiting meal-stimulated gastric acid secretion, but the differences were only statistically significant for the lansoprazole 30 mg dose, 30 mg lansoprazole and 40 mg omeprazole proved equipotent. On day 1 only 30 mg lansoprazole was significantly better than placebo. CONCLUSION: This study demonstrated the following order of antisecretory potency: 30 mg lansoprazole = 40 mg omeprazole > 15 mg lansoprazole approximately 20 mg omeprazole.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

[Helicobacter pylori eradication: triple therapy versus dual therapy].

For the eradication of Helicobacter pylori using dual therapy, the combination of a PPI with clarithromycin is clearly superior to PPI and amoxicillin. At the present time, a modified triple therapy, largely a PPI plus macrolide plus imidazole antibiotics, should be given preference as a cure of Helicobacter pylori infection. The short--one week--duration of the treatment means better tolerability, fewer side-effects and improved patient compliance. The high cure rate achieved with this form of treatment results in a favourable cost-benefit ratio. Overall, this form of therapy should overcome the reservations, still to be found, regarding the use of Helicobacter pylori eradication as optimal treatment of patients with peptic ulcer.

Amoxicillin↗
PubMed1995

Comparative trial of pantoprazole and ranitidine in the treatment of reflux esophagitis. Results of a German multicenter study.

In 249 patients with acute symptomatic reflux esophagitis grade II and III (Savary-Miller classification), we compared the efficacy and safety of pantoprazole, a newly developed proton pump inhibitor given at a once-daily dose of 40 mg, with a standard dose of the H2 receptor antagonist ranitidine (150 mg b.i.d.) in a randomized, double-blind, multicenter study. Complete healing was achieved after 4 and 8 weeks of therapy (protocol-correct) in 69 and 82% (pantoprazole) and 57 and 67% (ranitidine), respectively (p = 0.054 at 4 weeks and p < 0.01 at 8 weeks). The predominant symptoms of gastroesophageal reflux, i.e., heartburn and acid eructation, were more effectively reduced in pantoprazole- than in ranitidine-treated patients. The frequency of adverse events was low and did not differ between the two treatment groups. We conclude that pantoprazole is superior to ranitidine in the acute treatment of reflux esophagitis.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

[Effective prevention of indomethacin-induced gastroduodenal mucosal lesions with roxatidine acetate].

In this randomized single-blind cross-over study the gastroduodenal damaging effect of indometacin 75 mg bid alone and in combination with roxatidine acetate (CAS 78628-28-1, Roxit) 75 mg nocte or 75 mg bid was evaluated in 12 healthy male volunteers. Prior to the start of the three therapeutic periods subjects underwent endoscopic examination to exclude gastroduodenal mucosa lesions. On days 7 and 14 of therapy 2 h after the application of the last indometacin dose subjects underwent endoscopy again. The 7- and 14-days administration of indometacin 75 mg bid, indometacin 75 mg bid plus roxatidine 75 mg nocte and indometacin 75 mg bid plus roxatidine 75 mg bid led to gastroduodenal mucosa lesion scores of 1.67 +/- 0.40 and 2.00 +/- 0.35, 1.33 +/- 0.28 and 1.50 +/- 0.29, 0.42 +/- 0.23 and 1.00 +/- 0.33 (mean +/- SEM), respectively. These differences were statistically significant when comparing indometacin 75 mg bid versus indometacin 75 mg bid plus roxatidine 75 mg bid (p < 0.004 and < 0.008, respectively). This study shows that roxatidine acetate represents an effective alternative in the prophylaxis of NSAID-induced gastroduodenal mucosa lesions.

Adult↗
PubMed1994

Effects of pantoprazole on endocrine function in healthy male volunteers.

METHOD: In a randomized, double-blind, two-period crossover study, pantoprazole 40 mg or placebo were given orally to 12 male volunteers for 2 weeks each. There was a wash-out period of at least 1 week between the two treatment periods. The effects of pantoprazole or placebo on cortisol and testosterone (primary criteria), and tri-iodothyronine, thyroxine, thyroid-stimulating hormone, thyronine-binding protein, parathyroid hormone, insulin, glucagon, renin, aldosterone, follicle-stimulating hormone, luteotrophic hormone, prolactin and somatotrophic hormone were compared. In addition, intragastric 24-h pH, 24-h H(+)-activity, and volume of nocturnal gastric juice were determined by gastric aspiration technique. RESULTS: Pantoprazole did not influence plasma levels of testosterone, circadian cortisol concentrations or plasma cortisol levels after exogenous adrenocorticotropic hormone stimulation, as compared to placebo (P > 0.05, Koch's test). Furthermore, there were no clinically relevant changes with any of the other endocrine parameters. Pantoprazole significantly increased the median 24-h pH (group median 4.3 vs. 1.8; P < 0.001) and decreased 24-h H(+)-activity (4.0 vs. 22.6 mmol/L; P < 0.001). The volume of nocturnal gastric juice did not significantly differ between the two treatments. Pantoprazole was well tolerated and the frequency of adverse events was similar to placebo. No drug-related changes in laboratory values were observed. CONCLUSION: Pantoprazole did not influence endocrine function in healthy male volunteers during short-term treatment.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1993

The effects of lansoprazole, 30 or 60 mg daily, on intragastric pH and on endocrine function in healthy volunteers.

Seven days of dosing with either 30 mg or 60 mg of lansoprazole were compared with placebo in a double-blind, randomized, three-way cross-over study in 12 male healthy volunteers. Twenty-four-hour intragastric pH was measured after 7 days of dosing with each regimen, as well as 3 and 7 days after the end of dosing. During dosing with placebo, intragastric pH was above 4 for a median of 51 minutes. pH values were significantly raised to above 4 for 8.45 and 8.33 hours on Day 7 of dosing with lansoprazole 30 and 60 mg, respectively, but returned to normal by the third day after stopping dosing. No clinically relevant influence on endocrine function (serum concentrations of insulin, aldosterone, testosterone, parathormone, glucagon, T3, T4, TSH, LH, FSH, STH, prolactin, circadian cortisol profile, ACTH test) was observed. No serious adverse clinical or laboratory events were noted.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1993

Efficacy of continuous therapy for peptic ulcer in controlled clinical trials.

Long-term studies have confirmed unequivocally the clinical efficacy of continuous therapy with H2-receptor antagonists in reducing the incidence of ulcer recurrence. However, studies have also reported varying relapse rates as a result of differences in study design, particularly the frequency of endoscopy and hence the detection of asymptomatic ulcer relapse. Risk factors for ulcer relapse include smoking, stress, previous history of frequent ulcer relapses, duration of disease for more than 10 years and concomitant administration of non-steroidal anti-inflammatory drugs. In the prevention of relapse with H2-receptor antagonists, choice of agents also may influence the rate of relapse. A meta-analysis of data from direct comparative trials indicates that recurrence rates of duodenal ulcer are significantly lower after one year of treatment with ranitidine (150 mg nocte) than with cimetidine (400 mg nocte). It has been claimed that patients with peptic ulcer disease can be successfully managed by intermittent courses of treatment with H2-receptor antagonists which are taken in response to the development of symptoms. However, high relapse rates (64-100%) have been reported during the first year of follow-up of patients who were receiving intermittent treatment with H2-receptor antagonists. High complication rates (haemorrhage 11.4%, perforation 1.2%) have also been reported over a seven-year follow-up, while continuous treatment with H2-receptor antagonists significantly decreases the risk of haemorrhage in the event of ulcer recurrence.

Humans↗
PubMed1993

Differential effects of misoprostol and ranitidine on the pharmacokinetics of diclofenac and gastrointestinal symptoms.

1. The effects of oral misoprostol (800 microg day(-1)) and ranitidine (300 mg day(-1)) on the pharmacokinetics of diclofenac (100 mg) were assessed in a three-way randomized crossover study in 18 healthy male subjects. 2. Subjects were studied over three 8 day periods, during which they received twice-daily placebo, misoprostol, or ranitidine. A single dose of diclofenac was given orally on days 1 and 8, and plasma diclofenac concentrations were measured by h.p.l.c. over 24 h. 3. Misoprostol caused a non-significant 19% increase in the mean Cmax value of diclofenac on both days 1 and 8. After 8 days of dosing with misoprostol there was a significant (P = 0.04) 20% decrease in the AUC of diclofenac. 4. Ranitidine had no statistically significant effects on the pharmacokinetics of diclofenac. 5. Co-administration of misoprostol and diclofenac was associated with a higher frequency and severity of gastrointestinal symptoms and frequency of bowel opening, and a decrease in faecal consistency when compared with either placebo or ranitidine plus diclofenac (P < 0.01).

Administration, Oral↗
PubMed1992

[H2-blocker refractory ulcers: what can be done?].

H2-receptor antagonist refractory ulcers are seldom. Less than 5% of duodenal ulcers do not heal under H2-blockers. Today it is more and more accepted that duodenal ulcer is only H2-receptor antagonist refractory after a consequent therapy with H2-receptor antagonists in a standard dose or high doses for at least 2-3 months. The aims of therapy is refractory ulcers include as in non-refractory ulcers healing, pain relief and relapse prophylaxis. Often there is the choice to switch to a more potent antisecretory drug. E.g. ranitidine 300 mg/die was administered successfully in so-called cimetidine resistant ulcers. The specific acid inhibitory profile of omeprazole characterises this substance as a promising alternative in the treatment of H2-receptor antagonist refractory ulcers. In a large controlled clinical therapeutic trial with omeprazole 20 mg/die versus ranitidine 300 mg/die, however, no significant differences were observed in the 2- and 4-weeks healing rates. In two further controlled studies including 99 and 50 patients respectively treated with omeprazole 40 mg/die or cimetidine 800 mg/die and ranitidine 300 mg/die significantly higher healing rates were observed in favour of omeprazole. H2-blocker resistant ulcers are characterised by frequent and rapidly developing relapses. In this cases further treatment with H2-blockers in a two- or threefold daily dose has proved to be effective treatment. The administration of high omeprazole doses (40-60 mg/die) has also produced very convincing clinical results. If the above mentioned therapeutic measure do no provide adequate therapeutic results surgical procedures--usually resection--are indicated.

Anti-Ulcer Agents↗
PubMed1992

[Stages of grief in coping with diabetes?].

Forms of coping with diabetes were determined on the basis of self-ratings of emotions (depressive, sad, angry, anxious) and responses on a 30-item "stages of grief" questionnaire by 52 inpatients aged between 25 and 50 (diabetes duration 1 to 35 years) at the beginning of a 12 day diabetes education program. Psychometric qualities of the instruments were evaluated. To test empirically the notion of grief stages in coping with diabetes, the frequency of emphasis on one or more emotional areas or stages of grief was determined and tested to ascertain whether various conditions occurred more frequently than was expected by chance. Results indicated that shortly after diabetes manifestation scores on protest and depression with respect to diabetes were elevated. The majority of cases could not be assigned to a single emotion or stage of grief but displayed negative emotional reactions in different content areas simultaneously. Consequently the concept of grief stages for coping with diabetes as well as recommendations based on this concept are questioned.

Adaptation, Psychological↗