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Biomedical subjects

E G Hahn

Publications and source records attributed to E G Hahn.

At least 253 records · Page 14Linked to original sources
PubMed1999

Helicobacter pylori associated gastric pathology.

Helicobacter pylori (HP), undoubtedly, the most common world-wide infection plays an important role in pathogenesis of peptic ulcer. Proof for a causal role for HP in peptic ulcer rests in two major points; 1) the majority of ulcer patients are HP infected and the prevalence of this infection for both gastric ulcer (GU) and duodenal ulcer (DU) is much higher than for gender- and age-adjusted controls and 2) the cure of HP infection dramatically reduces ulcer recurrence. Conclusions regarding the mechanisms by which HP induces peptic ulcer are restricted mainly to studies observing the consequences of its eradication by antibiotics combined with gastric inhibitors or bismuth agents. Several specific virulence factors such as cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) as well as other noxious substances including ammonia, lipopolysaccharide (endotoxin), platelet activating factor (PAF), nitric oxide (NO) and others have been implicated in gastritis and were found to be significantly more frequent in gastric cancer than in gender- and age-matched controls, especially in younger generation. Chronic inflammation, atrophic gastritis, intestinal metaplasia, impaired defense mechanisms combined with hypergastrinemia, deficiency of vitamin C in the stomach , excessive oxygen metabolites and epithelial cell proliferation have been associated with gastric cancer. This multi-step pathway originally proposed by Correa and his colleagues, long before the HP was discovered in the stomach, leads to cancer but may be reversed by eradication of HP. This is, however, a controversial issue because gastric atrophy and intestinal metaplasia may be also caused by other factors such as bile reflux, dietary irritants, and autoimmunity. The implication of HP in MALT-lymphoma is based on the observations that eradication of HP in early stage of low-grade of this tumor leads to complete remission. The significance of HP in non-ulcer dyspepsia remains questionable and requires further studies.

Animals↗
PubMed1999

Role of gastrin in gastric cancerogenesis in Helicobacter pylori infected humans.

Numerous epidemiological studies demonstrated the association between Helicobacter pylori (H. pylori) infection and gastric cancer but the mechanism of the involvement of H. pylori in gastric cancerogenesis remains virtually unknown. This study was designed to determine the seropositivity of H. pylori and cytotoxin associated gene A (CagA), serum gastrin and gastric lumen gastrin levels under basal conditions and following stimulation with histamine in gastric cancer patients and controls. 100 gastric cancer patients aging from 21 to 60 years and 300 gender- and age-adjusted controls hospitalized with non-ulcer dyspepsia (NUD) entered this study. 13C-Urea Breath Test (UBT), serum immunoglobulin (IgG) antibodies to H. pylori and CagA were used to assess the H. pylori infection and serum levels of IL-1beta, IL-8 and TNFalpha were measured by enzyme-linked immunosorbent assay (ELISA) to evaluate the degree of gastric inflammation by H. pylori . Gastrin-17 mRNA and gastrin receptors (CCK(B)) mRNA expression in gastric mucosal samples taken by biopsy from the macroscopically intact fundic and antral mucosa as well as from the gastric tumor was determined using RT-PCR. The overall H. pylori seropositivity in gastric cancer patients at age 21-60 years was about 92%, compared, respectively, to 68%, in controls. A summary odds ratio (OR) for gastric cancer in H. pylori infected patients was about 5.0 . The H. pylori CagA seropositivity in gastric cancer patients was about 58.5% compared to 32.4% in controls, giving the summary OR for gastric cancer in CagA positive patients about 8.0. The prevalence of H. pylori- and H. pylori CagA-seropositivity was significantly higher in cancers than in controls, irrespective of the histology of gastric tumor (intestinal, diffuse or mixed type). Median IL-1beta and IL-8 reached significantly higher values in gastric cancer patients (9.31 and 30.8 pg/ml) than in controls (0.21 and 3.12, respectively). In contrast, median serum gastrin in cancers (as total group) was several folds higher (62.6 pM) than in controls (19.3 pM). Also median luminal gastrin concentration in gastric cancer patients was many folds higher (310 pM) than in controls (20 pM). This study shows for the first time that cancer patients are capable of releasing large amounts of gastrin into the gastric lumen to increase luminal hormone concentration to the level that was recently reported to stimulate the growth of H. pylori. There was no any correlation between plasma gastrin levels and gastric luminal concentration of gastrin suggesting that: 1) luminal gastrin originates from different source than plasma hormone, most probably from the cancer cells, 2) cancer cells are capable of expressing gastrin and releasing it mainly into the gastric juice and 3) the gastric cancer cells are equipped with gastrin-specific (CCK(B)) receptor so they exhibit the self-growth promoting activity in autocrine fashion. This notion is supported by direct detection of gastrin mRNA and gastrin receptor (CCK(B)-receptors) mRNA using RT-PCR in cancer tissue. To our knowledge this is the first study showing an important role of gastrin as self-stimulant of cancer cells in patients infected with H. pylori. Basal and histamine maximally stimulated acid outputs were significantly lower in gastric cancer patients than in controls despite of enhanced gastrin release, particularly in cancer patients and this might reflect the mucosal inflammatory changes (increased serum levels of proinflammtory interleukins - IL-1beta and IL-8), that are known to increase gastrin release. We conclude that: 1) H. pylori infected patients, particularly those showing CagA-seropositivity, are at greatly increased risk of development of gastric cancer, 2) H. pylori-infected cancer patients produce significantly more IL-1beta and IL-8 that might reflect an H. (ABSTRACT TRUNCATED)

Adult↗
PubMed1998

Base variant of human pancreatic secretory trypsin inhibitor in healing of stress-induced gastric lesions in rats.

Pancreatic secretory trypsin inhibitor (PSTI) is an inhibitor of serine-proteinases including pancreatic trypsin that prevents excessive digestion of the gastrointestinal mucus, but its role in the mechanism of mucosal defense has been little studied. This study was designed to determine the effect of base variant of human PSTI (R44S-PSTI) on gastric secretion, healing of gastric lesions induced by stress and the expression of PSTI during mucosal recovery from stress lesions. Recombinant R44S-PSTI was obtained using by site-directed mutagenesis due to replacement of arginine by serine that led to longer half life of this peptide than its natural form. Stress ulcerations were induced by exposure of rats to a standard 3.5 h of water immersion and restraint stress with or without pretreatment with vehicle or R44S-PSTI (0.1 mg/kg) applied s.c. 30 min before and immediately after the end of stress. Rats were then sacrificed immediately (time 0) and at 6 h or 12 h after the termination of stress. The gastric blood flow (GBF) was measured by H2-gas clearance technique at each time period and gastric mucosal samples were excised for assessment of PSTI immunohistochemical expression and PSTI messenger RNA by reverse transcriptase polymerase chain reaction (RT-PCR) and Southern hybridization. Stress produced numerous gastric lesions and decreased the GBF by about 30% as compared to the respective value in vehicle-treated non-stressed gastric mucosa. R44S-PSTI given s.c. in graded doses (0.01-1 mg/kg) inhibited dose-dependently gastric acid and pepsin outputs, in rats with gastric fistula and accelerated the healing of stress-induced gastric lesions significantly. The healing effects of R44S-PSTI (0.1 mg/kg s.c.) recorded at 6 h and 12 h after the end of stress were accompanied by a significant rise in the GBF. The expression of PSTI mRNA in the intact mucosa was weak, but following exposure to stress it was significantly augmented to reach the highest observed value at 6 h after the stress. We conclude that (1) base variant of human PSTI accelerates healing of stress-induced gastric lesions probably due to its antisecretory activity and enhancement of mucosal blood flow and (2) the expression of genes for PSTI plays an important role in the mechanism of mucosal recovery from gastric lesions induced by stress.

Animals↗
PubMed1998

[Diagnostic procedure in cholecystolithiasis. Diagnostic approach, repeat examinations and (incidental) findings].

If non-surgical methods are to be taken into account in the therapeutic decision-making process in cholecystolithiasis, an expanded diagnostic work-up including not only stone parameters but also gallbladder function, is needed. In 2270 patients (1649 women, 621 men; age: 47.2 +/- 14 years) with (suspected) "cholecystolithiasis" attending the special gallstone outpatient clinic at a university medical department within a period of 5 years the diagnostic procedures most commonly used in both the doctor's office and hospital were abdominal ultrasonography (52%/78%), laboratory investigations (28%/39%) and plain films of the biliary tract (27%/39%). In the doctor's office gallbladder function testing took the form of an cholecystogram (17% of the patients); in the hospital ultrasonography to determine gallbladder contractility (38%). With decreasing frequency, the following additional procedures were carried out (office/hospital): CT 3%/19%, esophagogastroduodenoscopy 7%/3%, intravenous cholegram 6%/0.6%, abdominal X-ray 1%/0.4%, ERCP 1%/0.4%, chest X-ray 0.8%/1.6%. Duplicated examinations showed a relevant frequency only for ultrasonography (39% of the cases), laboratory investigations (18%) and plain films of the gallbladder (4%). Pathologic secondary findings were established in 22% of the cases.

Adolescent↗
PubMed1998

[Changes in and acceptance of surgical and noninvasive therapy procedures in cholecystolithiasis].

BACKGROUND: The treatment of cholecystolithiasis has changed fundamentally in recent years due to the development of non-surgical techniques (extracorporeal shockwave lithotripsy [ESWL], oral litholysis) and the implementation of laparoscopic cholecystectomy. PATIENTS AND RESULTS: Retrospective analysis of 2270 patients (1649 women, 621 men; age: 47.2 +/- 14 years) presenting with gallstone disorders in a university medical outpatients department between 1988 and 1992 in order to be instructed as to the most suitable therapy method bear witness to the rapid change in therapeutic procedure. Laparoscopic removal of the gallbladder has virtually supplanted conventional cholecystectomy, and within 5 years the proportionate role of ESWL has declined from 21 to 12%. Over the years, the proportion of patients requiring no therapeutic intervention remained constant (at about 20%). The therapeutic recommendations of the "experts" were implemented in almost 80% of cases. The majority of patients were satisfied with the chosen therapeutic approach (surgery: 93.0%, ESWL: 77.6%), although 44% of ESWL-patients and 36% of surgically managed patients reported complaints which persisted even after completion of therapy. Despite unsuccessful ESWL (residual fragments or recurrent stones) 58/95 (61%) of interviewed patients would again give preference to this non-invasive modality in the event of a renewed therapeutic decision. CONCLUSION: Only a few years after its introduction, laparoscopic cholecystectomy has asserted itself as the predominant treatment option. But as far as acceptance and preference by the patient are concerned extracorporeal shockwave lithotripsy--as a non-invasive treatment modality--also enjoys high popularity and can be recommended as an alternative to surgery in suitable patients chosen according to the currently established stringent selection criteria.

Adolescent↗
PubMed1998

Involvement of ornithine decarboxylase and polyamines in epidermal growth factor-induced recovery of gastric mucosa from gastric lesions provoked by stress.

Polyamines such as spermine or putrescine, resulting from increased activity of ornithine decarboxylase (ODC), are known for gastroprotective and mucosal growth promoting effects but little information is available about their role in the acceleration of the healing of stress-induced gastric lesions by epidermal growth factor (EGF). In this study, rats with intact or suppressed ODC activity by alpha-difluoromethylornithine (DFMO, 400 mg/kg i.p.) were subjected to 3.5 h of water immersion and restraint stress (WRS) without or with intragastric (i.g.) administration of spermine and putrescine or with subcutaneous (s.c.) injection of EGF. At 0, 2, 6, 12 and 24 h after stress, rats were killed and the number of gastric lesions was counted, gastric blood flow (GBF) was recorded by the H2-gas clearance technique, the gene expression of ODC mRNA using reverse-transcriptase polymerase chain reaction (RT-PCR) and the ODC activity in this mucosa were determined in oxyntic mucosa. Stress produced gastric lesions combined with decreased GBF (by approximately 43%), but at 2, 6, 12 and 24 h after stress, these lesions and the fall in GBF were gradually attenuated. Healing of stress lesions was accompanied by strong stimulation of ODC mRNA expression and by an immediate increase in enzyme activity, with a peak occurring about 6 h after stress. Pretreatment with DFMO or salivectomy (which resulted in a marked fall in luminal EGF levels and mucosal DNA synthesis) delayed significantly the healing of stress lesions. EGF or spermine significantly accelerated the ulcer healing and raised the GBF. Suppression of endogenous generation of prostaglandins (PGs) with indomethacin (5 mg/kg i.p.) almost completely reversed the EGF- and spermine-induced acceleration of the healing of stress lesions and the accompanying rise in GBF. DFMO significantly reduced the enhancement in healing and the rise in the GBF induced by EGF, but failed to influence those induced by exogenous spermine. The acceleration of the healing induced by spermine or EGF and accompanying hyperemia were not affected by salivectomy. We conclude that (1) upregulation of the ODC transcript, increased ODC activity and polyamines play an important role in mucosal recovery from stress lesions due to acceleration of mucosal repair and an increase in gastric microcirculation, (2) increased ODC activity and resulting excessive polyamine release appear to act as primary mediators of EGF-induced acceleration of healing of stress lesions and (3) endogenous PGs cooperate with EGF and polyamines in mucosal repair from stress ulcerations.

Animals↗
PubMed1998

[Tsutsugamushi fever. Rare rickettsiosis after a stay in the Philippines].

HISTORY AND CLINICAL FINDINGS: After returning to his native Germany from a holiday in the Philippines a 37-year-old man was admitted because of high fever, cervical lymphadenopathy, pharyngitis and conjunctivitis, transient skin rash, nausea and vomiting, leukocytosis with shift to the left, atypical lymphocytes, as well as increased transaminases, LDH and cholestasis-indicating enzymes. INVESTIGATIONS: Stool, sputum and urine cultures were negative. The chest radiogram showed bilateral mild interstitial infiltration. Antibody titres against Rickettsia tsutsugamushi were markedly raised (IgG 1:128, IgM 1:2048). DIAGNOSIS, TREATMENT AND COURSE: Empirical antibiotic treatment with ciprofloxacin (200 mg twice daily intravenously) had no effect. As the mild signs of interstitial pneumonia progressed, clarithromycin (500 mg twice daily orally) was substituted with rapid fall in fever and gradual improvement. Tsutsugamushi infection was diagnosed serologically and the antibiotic changed to doxycycline (100 mg twice daily orally), continued for 14 days. Full remission occurred. CONCLUSIONS: Tsutsugamushi fever should be included in the differential diagnosis if, in addition to a history of a visit to an endemic area, there is the clinical triad of skin necrosis at the site of a mite bite, regional lymphadenopathy and skin rash (in this case, no skin lesion). The infection can be lethal without adequate treatment. Tetracyclines and possibly also macrolide antibiotics are effective against the causative organism.

Adult↗
PubMed1998

[Secondary obstructive sleep apnea syndrome in a patient with tracheal stenosis and bilateral recurrent paresis. Successful treatment with nasal continuous positive airway pressure therapy].

HISTORY AND ADMISSION FINDINGS: A 67-year-old woman complained of marked daytime sleepiness, as well as loud snoring and apnoeas during sleep. She was known to have had 3 thyroidectomies for goitre 41, 23 and 12 years ago, with known tracheal stenosis and recurrent nerve palsy for 11 years. Physical examination revealed marked stridor, hoarse voice and slightly enlarged and palpable recurrent right thyroid. INVESTIGATIONS: Polysomnography demonstrated a clearly elevated obstructive sleep apnoea activity (apnoea index: 34/h, apnoea-hypopnea index: 40/h, desaturation index: 31/h, minimal saturation: 63%). Selective tracheal imaging showed subglottic tracheal stenosis with an inspiratory luminal diameter of 4 mm and an expiratory luminal diameter of 8 mm. Lung function analysis revealed marked flattening of the flow-volume curve as sign of a functionally effective tracheal stenosis. These findings indicated a secondary obstructive sleep apnoea (OSA) due to tracheal stenosis and bilateral recurrent nerve palsy. The patient declined further studies, such as bronchoscopy. TREATMENT AND COURSE: As the patient did not want any surgical treatment, nasal continuous positive airway pressure therapy (CPAP) was instituted as a trial. No apnoea occurred at a pressure of 12 mm H2O and this was well tolerated. She has now continued CPAP at home for 12 months and her vigilance was markedly improved. CONCLUSIONS: Tracheal stenosis or recurrent nerve palsy is a rare cause of OSA which can be effectively treated by nasal CPAP.

Aged↗
PubMed1998

Activation of genes for growth factors and cyclooxygenases in rat gastric mucosa during recovery from stress damage.

Growth factors and prostaglandins protect the gastric mucosa against stress-induced lesions but their role in the recovery of the mucosa from these lesions has been little studied. We evaluated gastric mucosa lesions, gastric blood flow, mucosal generation of prostaglandin E2 and mucosal gene expression of epidermal growth factor (EGF) and transforming growth factor alpha (TGF alpha) as well as constitutive prostaglandin cyclooxygenase-1 and inducible cyclooxygenase-2 and the effect of the inhibition of these enzymes on the recovery of mucosa from the stress-induced lesions. Rats were exposed to 3.5 h of water immersion and restraint stress and killed at 0, 2, 4, 6, 8, 12 and 24 h after stress. The number of gastric lesions was determined and gastric blood flow was measured by H2-gas clearance. Gastric acid secretion was tested in separate gastric fistula rats. Gastric mucosa biopsies were taken for determination of immunoreactive EGF and TGF alpha. Expression of EGF and TGF alpha mRNA and cyclooxygenase-1 and cyclooxygenase-2 mRNA was also determined by reverse-transcriptase polymerase chain reaction. The number of gastric lesions induced by 3.5 h stress averaged approximately 20 per rat and declined significantly at 2, 4, 6, 8 and 12 h, to disappear almost completely after 24 h. This was accompanied by a gradual rise in gastric blood flow, mucosal generation of prostaglandin E2 and mucosal EGF and TGF alpha contents, while the increased gastric acid secretion returned to normal. In the intact mucosa, EGF mRNA was not detected but TGF alpha mRNA was found in measurable amounts. Following exposure to stress, the expression of both these factors was significantly increased. Similarly, the expression of cyclo-oxygenase-1 and cyclooxygenase-2 mRNA was detected in the oxyntic mucosa at all time intervals after exposure to stress. Indomethacin (5 mg/kg i.p.), an inhibitor of cyclooxygenase-1 and cyclooxygenase-2, and meloxicam (1 mg/kg i.p.), an inhibitor of cyclooxygenase-2, both prolonged the healing of stress lesions and reduced the gastric blood flow, while enhancing gastric acid secretion at all times tested. We conclude that healing of stress lesions results in the restoration gastric blood flow and mucosal prostaglandin generation and that these effects are accompanied by overexpression of EGF and TGF alpha as well as cyclooxygenase-1 and cyclooxygenase-2 mRNA and by increased biosynthesis of gastroprotective prostaglandin.

Animals↗