Evidence for mast cell activation in collagenous colitis.
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Publications and source records attributed to E G Hahn.
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BACKGROUND & AIMS: The first therapeutic experiences with the conventional photosensitizer dihematoporphyrinester in the treatment of Barrett's esophagus show the curative potential of photodynamic therapy (PDT). The aim of this study was to test 5-aminolevulinic acid (5-ALA)-induced protoporphyrin IX, a photosensitizer with a high mucosa specificity without phototoxic side effects on the skin, as a new form of PDT. METHODS: Thirty-two patients (mean age, 68.5 years) with histologically proven high-grade dysplasia (n = 10) and mucosal cancer (n = 22) in Barrett's esophagus were treated. Four to 6 hours after oral ingestion of 5-ALA (dose, 60 mg/kg body wt), irradiation was conducted with a dye laser system (635 nm) with a light dose of 150 J/cm2. The patients received 20-80 mg omeprazole daily after PDT. RESULTS: High-grade dysplasia was eradicated in all patients (10 of 10), and mucosal cancer was eliminated in 17 of 22 patients (77%) at a mean follow-up of 9.9 months (range, 1-30 months). All tumors < or = 2 mm in thickness were completely ablated (17 of 17). The method-related mortality and morbidity was 0%. CONCLUSIONS: Severe dysplasia and thin (< or = 2 mm) mucosal cancer of Barrett's esophagus can be completely ablated. PDT might offer a minimally invasive treatment modality as an alternative to esophagectomy.
BACKGROUND: NSAIDs, such as aspirin (ASA), cause widespread mucosal damage, but repeated ASA insults appear to induce mucosal tolerance (adaptation) to this injury. The mechanism of the gastric adaptation to the damage induced by ASA has not been fully explained. AIM: To determine the role of the mucosal gene expression for spasmolitic peptide (SP) (a member of trefoil peptides) and transforming growth factor alpha (TGF alpha) as well as for cyclooxygenase (COX)-1 and COX-2 during gastric adaptation to ASA in rats. METHODS: Gastric lesions were produced by ASA (100 mg/kg in 1.5 mL of 0.2 M HCl) applied intragastrically (i.g.) as a single dose. every day for 5 days. Control rats were given 1.5 mL of vehicle (0.2 M HCl i.g.) as a single dose, during 5 consecutive days. Gastric blood flow (GBF) was measured by H2-gas clearance technique and gastric mucosal specimens were taken for the assessment of cell proliferation rate in gastric mucosa by bromodeoxyuridine (BrdU) uptake, mucosal generation of prostaglandin E2 measured by radioimmunoassay, and for expression of SP, TGF alpha COX-1 and COX-2 mRNA as determined by RT-PCR. To quantify the relative amounts of mRNA for SP and TGF alpha, southern blotting analysis of the PCR products was performed and the intensity of PCR products was compared with that of beta-actin used as a standard. RESULTS: ASA applied once produced numerous gastric erosions, but with repeated ASA doses the adaptation to this NSAID developed, the area of gastric lesions being reduced by 86% after six consecutive ASA insults. This adaptation to ASA was accompanied by approximately a 90% reduction in prostaglandin E2 biosynthesis, by a significant rise in BrdU uptake by glandular cells predominantly in the neck region of gastric glands and by expression of SP (SP/beta-actin ratio; 0.96 +/- 0.08 in ASA-adapted mucosa vs. 0.38 +/- 0.05 in the control mucosa) and TGF alpha (TGF alpha/beta-actin ratio: 0.97 +/- 0.07 in ASA-adapted mucosa vs. 0.77 +/- 0.06 in the control mucosa). COX-1 expression was detected in vehicle-control gastric mucosa and after single exposure to ASA or after six consecutive ASA insults, while COX-2 mRNA was not detected in vehicle-control gastric mucosa, but appeared after single ASA insult and was sustained after subsequent ASA doses. CONCLUSIONS: (i) Gastric adaptation to aspirin injury involves enhanced cell proliferation which appears to be mediated by increased expression of SP and TGF alpha, and (ii) rapid upregulation of COX-2 expression following single and repeated ASA insults may represent a compensatory response to suppression of prostaglandin generation by this NSAID.
PURPOSE: Sonographically-guided Radio-Frequency Tissue Ablation-applied with a percutaneously placed needle can be used for the palliative treatment of primary or secondary liver tumours. In vitro experiments were carried out to establish the relations of the coagulation zone to histologic findings and sonographic appearance. METHOD: Fresh bovine livers were obtained and radio-frequency was applied under ultrasound guidance. The coagulation zone was dissected and examined by determining its three-dimensional diameters (macroscopically) and the histologic appearance of the coagulation margin to the surrounding tissue. In our series of 50 experiments the application time ranged from 30 seconds to 10 minutes. RESULTS: The coagulation zone increased with increasing application time in a way that can be described as a negative logarithmic function. The largest volume was 4 x 5 x 5 cm (length, width, depth) approximating 50 ml. It was no problem to judge the coagulation zone sonographically. The macroscopically and sonographically determined width and length correlated with coefficients of 0.90 and 0.96. Microscopically the coagulation necrosis showed sharply outlined margins without any vital cells. CONCLUSION: Radio-Frequency Tissue Ablation applied under sonographic guidance has certain features which seem to make it a promising method for the palliative treatment of primary and secondary tumours of the liver.
BACKGROUND AND STUDY AIMS: The aim of the study was to investigate the evolution of endoscopic sphincterotomy (EST) over a period of 25 years at its birthplace in Erlangen, Germany. PATIENTS AND METHODS: A total of 3498 consecutive ESTs between 1973 and the end of 1997 were reviewed with respect to indications, technology, success, complications, therapy of complications and mortality. In order to demonstrate changes in the course of time, the results have been compiled separately for four time periods (A-D). RESULTS: During the 25 years' practice of EST in Erlangen the frequency of ETSs has increased constantly and significant changes have been observed concerning the spectrum of indications: Bile duct stones (total 55.1%) decreased continuously from 91.1% (period A) to 35.7% (period D). In contrast, the proportion of ESTs applied for malignant obstruction (total 22.1%) rose successively from 1.1% (period A) to more than 25% (periods B-D). Chronic pancreatitis as an indication for EST was established in period B (1.0%) and accounted for 20.2% of all procedures in period D (total 8.0%). Several new indications (summarized as "others") increased from 1.8% in period A to 11.9% in period D (total 6.7%) whereas biliary pancreatitis and scarred papillary stenosis remained constantly below 5%. Whereas the "Erlangen sphincterotome" was the only sphincterotome used in period A, it was almost completely replaced by guide-wire sphincterotomes in period D. With the introduction of the needle knife the precut technique became popular and was used with increasing frequencies: period B 31.9%, period C 34.1%, period D 41.9%. The success rate in total was 95.2%. For each time period the highest success rate of EST was obtained for bile duct stones (96-98%), whereas EST appeared to be more difficult in case of malignant obstruction (93.3%) or chronic pancreatitis (90.2%), but for both indications growing experience resulted in an increase in the success rates (85.7% to 94.9% and 90.9% to 94.0%, respectively). Complications occurred in 7.9% of cases. The complication rate declined significantly from 10.5% in period A over 7.6% in period B to 6.3% in period C. Prospective data acquisition in period D revealed a significant increase in the detection of mild forms of acute pancreatitis, resulting in a slight increase of the complication rate (8.4%). Needle-knife papillotomy did not significantly increase the complication rate. Whereas in period A 41% of all complications were managed by surgery, this value dropped over 28% (period B) and 7.5% (period C) to ultimately 1.6% in period D. The method-related mortality was nearly constant over the whole period of time (0.6%). CONCLUSIONS: Despite a continuous shift of indications and a changing mixture of learning endoscopists and EST experts over 25 years, the practice of EST at its birthplace in Erlangen has shown a constantly high success rate, a decreasing complication rate and an acceptable but mainly unchanged mortality rate. Currently, nearly all complications can be successfully managed nonoperatively.
BACKGROUND: Epidermal growth (EGF) and transforming growth factor alpha (TGFalpha) are potent gastric secretory inhibitors, mitogens, and mucosal protectors, but the impact of Helicobacter pylori infection on their mucosal expression and luminal release has not been clarified. METHODS: In this study, gene and immunoreactive and immunohistochemical expressions of EGF and TGFalpha were assessed in the gastric mucosa of 15 H. pylori-negative healthy normals, in 22 H. pylori-positive duodenal ulcer patients (DU) and in 24 H. pylori-positive non-ulcer dyspepsia patients (NUD). All studies in DU and NUD patients were repeated after 2 weeks of triple therapy (amoxicillin + clarithromycin + omeprazole) and 4 weeks and 2 years later. RESULTS: Immunohistochemical expression of EGF and TGFalpha in H. pylori-positive DU and NUD was significantly higher than in H. pylori-negative normals, and this increase persisted at 2 and 4 weeks after therapy but normalized 2 years later. EGF mRNA was detected in the gastric mucosa of H. pylori-positive DU before and at 2 and 4 weeks after H. pylori eradication, but it was not found 2 years after the eradication of H. pylori or in gastric mucosa of H. pylori-negative control subjects. TGFalpha mRNA was detected in the gastric mucosa independently of H. pylori status, with the stronger expression observed in the gastric mucosa of H. pylori-positive DU and NUD before eradication than after this procedure. Plasma gastrin, which was significantly increased in H. pylori-positive DU, normalized already after 2 weeks of triple therapy. The eradication rate as determined by histology after triple therapy reached 86.3% in DU patients and 90.5% in NUD patients. Two years after the eradication the H. pylori reinfection rate was 4.5% among DU patients and 4.2% among NUD. Treatment of DU patients with triple therapy resulted in complete ulcer healing. CONCLUSIONS: 1) Chronic H. pylori infection and resulting antral gastritis are associated with increased plasma gastrin and increased mucosal cell proliferation, probably due to enhanced expression of EGF and TGFalpha, and 2) the H. pylori eradication results in a decrease in plasma gastrin, but the increase in gastric TGFalpha and EGF content is sustained, suggesting that they may be involved in ulcer healing.
BACKGROUND: Lipopolysaccharide (LPS) has been proposed to act as one of the pathogens in endotoxemia-induced gastric lesions, but its action on mucosal integrity has not been fully clarified. METHODS: We compared the effects of LPS originating from Escherichia coli and the chemical donor of nitric oxide (NO), S-nitroso-acetylpenicillamine (SNAP), on acute gastric lesions induced by 100% ethanol, mucosal blood flow (GBF), and mucosal generation of prostaglandin E2 (PGE2) and examined the expression of constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) mRNA in the gastric mucosa of rats treated with LPS, by using reverse transcription polymerase chain reaction (RT-PCR). RESULTS: LPS (0.01-1.0 mg/kg) or SNAP (0.37-3.0 mg/kg) given intraperitoneally, dose-dependently prevented ethanol-induced mucosal lesions, and these protective effects were accompanied by a significant increase in the GBF and excessive mucosal release of NO. Suppression of NOS activity by NG-nitro-L-arginine methyl ester (L-NAME) (20mg/kg intravenously) or L-NG-(1-iminoethyl)-lysine (L-NIL) (30mg/kg intraperitoneally) and NOS induction by treatment with dexamethasone (2 mg/kg intraperitoneally) reversed the protective and hyperemic effects of LPS, and this reversal by L-NAME was significantly antagonized by addition of the substrate for NOS, L-arginine, but not D-arginine. Both LPS and SNAP increased PGE2 generation significantly, and this effect was reduced by pretreatment with L-NAME, L-NIL, or dexamethasone. Expression of cNOS was detected by RT-PCR in the intact mucosa, but intense signals for expression of both cNOS and iNOS were detected in the mucosa of LPS-treated rats. CONCLUSIONS: Parenteral LPS, similarly to the chemical NO donor, SNAP, protects the gastric mucosa against ethanol-induced damage via an increase in GBF mediated by NO due to the activation of arginine-NO system and possibly also enhanced generation of PGE2.
Polyamines such as spermine or putrescine, resulting from increased activity of ornithine decarboxylase (ODC), are known for gastroprotective and mucosal growth-promoting effects. EGF exhibits similar effects, but little is known about the involvement of polyamines in 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-difluoromethy-ornithine (DFMO, 400 mg/kg i.p.) were subjected to 3.5 h of water immersion and restraint stress (WRS) without or with addition of spermine or EGF. At 0, 2, 6, 12, or 24 h after stress, rats were sacrificed. The number of gastric lesions was determined and gastric blood flow (GBF) was recorded by the H2 gas clearance technique. Stress produced gastric lesions (mean number 18+/-2 per stomach) and decreased GBF (by approximately 43%), but at 2, 6, 12, and 24 h after stress, these lesions and the decrease in GBF were gradually attenuated. Pretreatment with DFMO or removal of an endogenous source of EGF by salivectomy resulted in a marked decrease in mucosal DNA synthesis and significantly delayed the healing of stress lesions. EGF or spermine significantly accelerated ulcer healing and increased the GBF in rats with intact or removed salivary glands. DFMO significantly reduced the enhancement of healing and the increase in GBF induced by EGF, but failed to influence those induced by exogenous spermine. We conclude that polyamines play an important role in mucosal recovery from stress lesions due to acceleration of mucosal repair and increase in gastric microcirculation and that increased ODC activity and resulting excessive polyamine release appear to act as primary mediators of EGF-induced acceleration of the healing of stress lesions.
Duodenal fat such as oleate is known to influence gut functions by release of cholecystokinin (CCK), but the contribution of CCK endogenously released by duodenal fat or by diversion of pancreatic juice from the duodenum in the mechanism of mucosal integrity and gastroprotection has been little studied. This study was designed to compare the effect of CCK-8 and intraduodenal (i.d.) instillation of sodium oleate, or diversion of the pancreatic biliary secretions that are known to release CCK, on the gastric mucosal lesions induced by topical application of 100% ethanol or acidified aspirin (ASA) in rats with or without the pretreatment with a CCK-A receptor antagonist, loxiglumide, or with L-365,260 to block CCK-B receptors. In addition, the effect of suppression of prostaglandin (PG) biosynthesis by indomethacin (5 mg/kg i.p.), inhibition of nitric oxide (NO)-synthase by L-NAME (5 mg/kg i.v.), or blockade of sensory nerves by capsaicin (125 mg/kg s.c.) on the protective activity of sodium oleate was determined. Sodium oleate (50-200 mM i.d.), or diversion of pancreatic juice from the duodenum for 3 h that produced significant rise in plasma CCK levels, significantly reduced gastric lesions induced by 100% ethanol to an extent similar to that induced by exogenous CCK-8 (5 nmol/kg s.c.). The protective effect of oleate or diversion of pancreatic juice was accompanied by an increase in gastric blood flow (GBF). Both protection and accompanying hyperemia were completely abolished by blockade of CCK-A receptors with loxiglumide, whereas L-365,260, an antagonist of CCK-B receptors, had no effect. Oleate given i.d. significantly attenuated acidified ASA-induced gastric lesions and gastric secretion while increasing the luminal concentration of somatostatin. These effects were significantly reduced by loxiglumide but not by L-365,260. In contrast, CCK-8, which stimulated gastric acid secretion, failed to affect the lesions induced by acidified ASA and the decrease in the GBF produced by this ulcerogen. Indomethacin, which suppressed PG generation by approximately 90%, failed to influence the protective activity of oleate or CCK-8 against ethanol-induced lesions, whereas L-NAME, vagotomy, or sensory denervation significantly attenuated this protection and accompanying hyperemia. Addition to L-NAME of L-arginine, but not D-arginine, restored the protective and hyperemic effects of CCK-8 and duodenal oleate against gastric lesions induced by ethanol or acidified ASA. We conclude that endogenous CCK released by oleate or diversion of pancreatic secretion exerts a potent gastroprotective action on the stomach involving predominantly CCK-A receptors and depending on vagal activity, and hyperemia mediated by NO and sensory nerves but unrelated to acid secretory effects and endogenous PG.
In this study, cytokine patterns produced by CD4(+) T cells isolated from antrum or corpus gastral biopsy specimens of 10 patients with Helicobacter pylori-positive gastritis were compared. To this end, expression of intracellular cytokines (interleukin-4 [IL-4] and gamma interferon) and of CD4 was assessed by flow cytometry. Ten to 60% of the isolated CD4(+) T cells produced gamma interferon upon stimulation. With the exception of one patient, IL-4-positive CD4(+) cells were not detected. Therefore, CD4(+) cells infiltrating antrum and corpus stomach mucosa during H. pylori infection show a Th1 phenotype. This polarized Th1-type response may contribute to the inability of the immune system to eradicate H. pylori infection.
BACKGROUND: Radical surgical treatment has been the first choice for early gastric cancer, but high resolution endosonography allows in situ diagnosis with a high sensitivity and specificity and in consequence the option of local endoscopic treatment. AIMS: To evaluate photodynamic therapy (PDT) using meso-tetrahydroxyphenyl-chlorin (mTHPC) as the photosensitiser in superficial gastric cancer. METHODS: Twenty two patients with superficial early gastric cancer received mTHPC (0.075 mg/kg intravenously) and were treated 96 hours later with red light at 652 nm (20 J/cm2). Tumour response was assessed by endoscopy and extensive biopsy. RESULTS: Endoscopies performed two to three days after PDT showed a haemorrhagic fibrinoid necrosis of the mucosal layer. Complete remission was achieved in 16/22 (73%) patients: 13/16 (80%) with intestinal type cancer and 3/6 (50%) with a diffuse Lauren's carcinoma. The mean follow up period was 12 months and 20 months, respectively. An average of 1.8 treatment sessions was required. Severe side effects were not observed. Seven patients had mild to moderate skin photo-sensivity reactions; 12 had local pain after PDT for 1-10 days. CONCLUSION: PDT using mTHPC as the photosensitiser represents a safe and efficient method for topical treatment of early gastric cancer, especially of Lauren's intestinal carcinoma. If the preliminary results can be verified in larger patient series and during long term follow up, local treatment of early cancers of the stomach by PDT could be considered as a therapeutic option for selected patients.
INTRODUCTION: Laser lithotripsy of bile duct stones has become a widely accepted endoscopic treatment modality for giant, impacted, or very hard stones. The procedure is usually carried out under direct endoscopic control in view of the potential risk of bile duct injuries in "blind" laser application. AIMS: To investigate the use of a rhodamine 6G laser lithotriptor with an integrated optical stone tissue detection system (oSTDS). METHODS: From 1 September 1991 to 7 March 1997, 60 patients with giant or impacted common bile duct stones refractory to endoscopic papillotomy stone extraction, and mechanical lithotripsy were treated via the endoscopic retrograde route using a rhodamine 6G dye laser (595 nm, 2.5 micros, 80-150 mJ pp, Lithognost Telemit/Baasel Corp., Germany) with integrated oSTDS. In case of tissue contact oSTDS cuts off the laser pulse after 190 ns (transmission of 5-8% of the total pulse energy). 47 patients (78.3%) were subjected to x ray targeting (oSTDS) alone, five (8.3%) to choledochoscope targeting alone, and eight (13.3%) to both techniques. RESULTS: At the end of treatment 52 (87%) patients were completely stone-free. The only major complications included transient haemobilia, cholangitis, and pancreatitis in five patients. All five were successfully treated by conservative methods. CONCLUSIONS: Laser lithotripsy using the described rhodamine 6G dye laser with oSTDS seems to be safe and effective and allows "blind" fragmentation of difficult common bile duct stones under radiological control only.
BACKGROUND: Auto-CPAP machines used in the treatment of obstructive sleep apnoea (OSA) are designed to vary the treatment pressure automatically in order always to apply the actually needed pressure. Consequently they should be able to achieve at least identical therapeutic effects as conventional constant pressure CPAP with a lower mean treatment pressure. The present study was designed to evaluate the therapeutic efficacy and the treatment pressure of an auto-CPAP machine (REM + auto, SEFAM) in comparison with a conventional CPAP device. METHODS: Following CPAP titration, 16 patients with OSA were allocated to receive conventional CPAP and auto-CPAP treatment under polysomnographic control in a randomised order. After each treatment the patients were asked to assess the therapy using a questionnaire; a vigilance test was also carried out and subjective daytime sleepiness was evaluated using the Epworth Sleepiness Scale (ESS). RESULTS: The mean (SD) apnoea/hypopnoea index (AHI) during auto-CPAP treatment was comparable with that during conventional CPAP treatment (4.2 (5.1) versus 3.6 (4.0)). Neither an analysis of sleep architecture nor the arousal index (7.4 (4.1) versus 7.0 (4.3)) revealed any significant differences. Daytime sleepiness measured with the ESS was also comparable (5.3 (3.4) versus 6.5 (4.2)). The vigilance test showed normal values after both treatments in all patients with no significant differences. The mean pressure during auto-CPAP treatment (8.1 (2.9) mbar), however, was significantly higher than that employed in conventional CPAP treatment (7.6 (2.7) mbar; mean difference 0.5 mbar; 95% CI 0.1 to 0.9 mbar; p < 0.05). CONCLUSIONS: Auto-CPAP was equally as effective as conventional CPAP with respect to therapeutic efficacy. The aim of reducing the treatment pressure with auto-CPAP, however, was not achieved.
Overexpression of transforming growth factors (TGF) in acute pancreatitis (AP) suggested that these substances play an important role in pancreatic repair and remodeling but the contribution of epidermal growth factor (EGF), that is well known to promote cell growth and regeneration, has not been investigated. The aim of this study was to compare the gene and immunohistochemical expression of EGF and TGF-beta1, cell proliferation, and biochemical parameters in AP induced by infusion of a supramaximal dose of caerulein in rats. The rats were sacrificed at 0, 12, 24, 48, 72 h, 5 and 10 days after the termination of caerulein infusion. Pancreatic tissue DNA synthesis, cell proliferation, histological and immunohistochemical assessments and plasma amylase were estimated following induction of AP. The mRNA expression for EGF and TGF-beta1 was evaluated by reverse transcription-polymerase chain reaction. During 10 days of the study after induction of AP a gradual normalization of biochemical and histological parameters was observed. DNA synthesis and cell proliferation which were significantly decreased at 0 and 24 h, increased significantly at 48 and 72 h, and then gradually decreased reaching at day 10 the values similar to those of vehicle-treated control rats. In these control rats the EGF mRNA or immunohistochemical expression was not detected, while the TGF-beta1 expression was weak. After induction of AP, the mRNA and immunohistochemical expression of EGF showed an increase during the initial 5 days, while those of TGF-beta1 showed a marked increase between 0 and 48 h and then again at day 10. We confirm that: (1) the expression of TGF-beta1 during AP is biphasic with an initial increase probably related to pancreatic damage and inhibition of cell proliferation and with the later phase of increase accompanied by the stimulation of the synthesis of extracellular matrix components and (2) AP is accompanied by an induction of synthesis of EGF that occurs in the initial phase of AP, probably limiting the extent of AP, and enhancing the stimulation of the pancreatic repair and regeneration.
Knowledge of conditions associated with an increased prevalence of obstructive sleep apnoea (OSA) may help to identify patients with OSA and might give some insight into the pathogenesis of OSA and its sequelae. A number of earlier, smaller studies hinted at an association between diabetic cardiovascular autonomic neuropathy (AN) and OSA. The present study was, therefore, conducted with the aim of establishing the prevalence of OSA in diabetics with AN and of determining whether OSA is more prevalent in diabetics with AN, than in those without. We studied two groups of diabetic patients: 23 with and 25 without AN. All patients were evaluated for possible OSA (apnoea/hypopnoea index > or = 10) using initial ambulatory screening followed by polysomnography. Six patients with AN (26%) were found to have OSA, but none of the patients without AN met the diagnostic criteria (p<0.01). When the patients with OSA were compared to those without, no differences were found in terms of age, sex, body mass index or diabetes type or duration. In conclusion, about one in four diabetic patients with autonomic neuropathy suffers from OSA. Thus, obstructive sleep apnoea is more prevalent in diabetic patients with autonomic neuropathy, than in those without.
INTRODUCTION: Photodynamic therapy (PDT) is a new local, endoscopically controlled therapeutic concept based on the selective sensitization of malignant and precancerous lesions prior to light-induced tissue destruction. 5-aminolaevulinic acid (5-ALA) appears to be a promising alternative photosensitizer with a high mucosa specificity without phototoxic side effects on the skin. We report on our experience with this new form of PDT in 24 patients. PATIENTS AND METHODS: Five females and 19 males (aged 50 to 79 years) with histologically proven high-grade dysplasia (n = 9) and early cancer (normal EUS or uTlNOMO, n = 15) of the esophagus were included in this study. Four to six hours after oral ingestion of 5-ALA (dosage of 60 mg/kg b.w.) laser light irradiation was conducted with a dye laser system (XP 800 KTP/YAG, Laserscope, San José, USA) at a wavelength of 635 nm. With a light dose of 150 J/cm2. RESULTS: The length of the segment with severe dysplasia or mucosal cancer varied between 0.5 and 9 cm (mean length: 3.6 cm). High-grade dysplasia was eradicated in all patients (9/9). In addition, 16 mucosal carcinomas in 15 patients were successfully treated in 8/16 cases with an average of 1.8 treatment sessions and a mean follow-up of 14.5 months (range: 3-31 months). A method-related mortality and morbidity was not observed. CONCLUSIONS: Severe dysplasia and superficial (< or = 2 mm) mucosal cancer of the esophagus can be completely ablated by 5-ALA-PDT. Patients with early carcinoma thicker than 2 mm are not suitable for 5-ALA-PDT. PDT with 5-ALA has few side effects and might offer an alternative to esophagectomy or radio-chemotherapy.
The reprocessing of flexible gastrointestinal endoscopes is time-consuming and expensive. Endoscopically transmitted infections due to insufficient disinfection are already of clinical importance. A new developed prototype of a flexible, fiberoptic gastroscope was tested in a prospective open randomized trial to evaluate the function. reprocessing and hygienical safety of this disposable, sheathed endoscopic system and was compared with a standard gastroscope. This new endoscopical system utilizes a disposable sheath to cover and protect all working surfaces of the endoscope from contamination. A prospective, randomized trial was performed in our unit to compare the disposable gastroscope (G-F100) with a standard-gastroscope of the newest Generation (GIF-Q 30). Visual analog rating scales were used to record evaluations of endoscope performance and reprocessing by endoscopists and reprocessing personnel. We recorded the time of reprocessing, the time to perform the procedures, depth of insertion, total instrument downtime and any problems which occurred during the procedure. Microbiological swabs were taken from each endoscope. 40 procedures (20 standard, 20 sheathed) were performed. The sheathed gastroscope 8.9 min versus 7.1 min. The overall instrument downtime was significantly shortened by the endosheath (9.8 min versus 47.5 min with the standard gastroscope). The disposable gastroscope-system permits an increase of procedure-frequency up to a factor of 2.9. The standard gastroscope was preferred by the endoscopists and the reprocessing personnel. No microbiological contaminations of the sheathed or the standard gastroscopes could be demonstrated, and no leak of the sheaths was recorded after gastroscopy. The disposable gastroscope has important advantages of decreased instrument turn-around time and potentially increased staff and patient safety.
Helicobacter pylori (Hp) is a major risk factor of peptic ulcer but studies on the relation between Hp infection and gastric pathology are limited due to lack of convenient models resembling Hp infection in humans. We studied the effects of inoculation of conventional BALB/c mice with toxigenic type I Hp (cagA+ and vacA+) and non-toxigenic type II Hp (cagA- and vacA-) vs administration of vehicle on gastric secretion and healing of gastric ulcers. The gastric secretion studies were performed on mice with chronic gastric fistula before and after inoculation with toxigenic or non-toxigenic Hp strain or administration of vehicle (saline). Gastric ulcers were produced in mice inoculated with toxigenic and non-toxigenic Hp strain or vehicle and then sacrificed at day 0 and after 2, 4, 7, 14 and 28 days. Ulcer area and gastric blood flow (GBF), plasma gastrin and gastric luminal somatostatin were determined. Gastric mucosal biopsy specimens were also taken for the assessment of the presence of viable Hp using rapid urease test, the Hp-culture and the reverse transcriptase--polymerase chain reaction (RT-PCR) analysis of the signal for Hp CagA. Gastric acid output was reduced by over 50% immediately after Hp inoculation and this effect persisted during all time intervals tested, being significantly more pronounced in type I Hp-infected stomach. The area (7 mm2) of ulcers in control mice decreased gradually and then continued to decline during 14 days to disappear almost completely after 28 days. In contrast, the ulcers were present till day 28 in all mice infected with type I or type II Hp strain being significantly larger especially with type I Hp-infection. The GBF in control mice showed gradual rise with decreasing ulcer size being significantly higher at the ulcer margin than the ulcer crater and reached after 14 and 28 days the value not significantly different from that in vehicle-administered mice. In contrast, the GBF in type I Hp-infected mice but to a lesser extent, in type II Hp infected mice was significantly lower than in the vehicle controls, both at the ulcer margin and the crater of ulcers at all tested days. Hp-infection was accompanied by significant increment in plasma gastrin and the fall in gastric somatostatin contents observed at all test days, particularly in mice infected with type I Hp strain. Edema of surface epithelium appeared after 7 days and wak but significant mucosal inflammatory infiltration occurred after 14 days to further increase after 28 days, especially in type I Hp and less in type II Hp infected mice. We conclude that conventional mice with gastric ulcers can be successfully infected by both toxigenic and non-toxigenic Hp strains and this infection markedly reduces gastric acid secretion and delays healing of ulcers probably due to the fall in mucosal microcirculation in ulcer area, mucosal inflammation and impairment in gastric-somatostatin link.