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H G Beger

Publications and source records attributed to H G Beger.

At least 55 records · Page 3Linked to original sources

Anti-ICAM-1 antibody modulates late onset of acinar cell apoptosis and early necrosis in taurocholate-induced experimental acute pancreatitis.

The hallmark of severe acute pancreatitis (SAP) is massive acinar cell death by necrosis. However, programmed, apoptotic acinar cell death has also been observed. Little is known about the dynamics, localization, and inductive factors of acinar cell apoptosis in SAP. We therefore induced SAP in rats by retrograde infusion of 3% sodium taurocholate. Starting as early as 5 minutes after taurocholate administration, small scattered groups of acinar cells showed zymogen degranulation, loss of cell polarity, cytoplasmic microvacuolization, and nuclear shrinkage, but no DNA degradation, thus featuring necrosis. The areas of necrotic acini extended at later time points giving rise to larger areas of complete parenchymal breakdown after 6 hours. Parenchymal degradation was paralleled by neutrophil infiltration and significant tumor necrosis factor (TNF)-alpha mRNA up-regulation. Up to the 12-hour interval, apoptotic acinar cells detected by TUNEL were as rare as in healthy pancreata. At 24 hours, however, the acinar apoptotic rate in nonnecrotic parenchyma had dramatically increased. Pretreatment of rats with anti-ICAM-1 antibody prior to pancreatitis induction led to a significant reduction of neutrophil infiltration along with decreased TNF-alpha mRNA expression throughout the 24-hour observation period without affecting the presence and dynamics of necrosis. However, anti-ICAM-1 pretreatment decreased the extent of acinar cell damage by necrosis and extensively suppressed acinar cell apoptosis. We conclude that taurocholate induces two sequential patterns of acinar cell death in terms of very early necrosis followed by late apoptosis during the postacute phase of SAP. The progression of necrosis and the late apoptotic acinar cell death seem to be influenced by the local presence of neutrophils via a TNF-alpha-dependent mechanism. In addition to augmenting necrosis, neutrophils might have an apoptosis-inducing potential in SAP.

Acute Disease↗

Epidermal growth factor induces cyclin D1 in human pancreatic carcinoma: evidence for a cyclin D1-dependent cell cycle progression.

INTRODUCTION: We recently showed that cyclin D1 is overexpressed in human pancreatic carcinoma cells, and that this overexpression correlates significantly with a poor prognosis. AIMS: To assess the interrelations of epidermal growth factor (EGF), EGF receptor (EGFR), and cyclin D1 in human pancreatic carcinoma. METHODOLOGY AND RESULTS: In pancreatic carcinoma cell lines (BxPC-3, AsPC-1), cell cycle analysis revealed an increase in cells in the S/G1 phase between 18 and 30 hours after stimulation with 50 ng/mL EGF. Cyclin D1 mRNA increased after 2 hours, corresponding to an increase in cyclin D1 protein, with the maximum level between 7.5 and 10 hours after stimulation, as demonstrated by Western blot analysis. We performed immunohistochemical analysis on 61 adenocarcinoma tissues for the expression of EGF, EGFR, and cyclin D1 and demonstrated an overexpression in the tumor cells in 51%, 54%, and 62.3%, respectively, whereas normal human pancreas stained negative for all of the three factors. Interestingly, EGF and EGFR expression correlated significantly with the cyclin D1 expression in human pancreatic tumor cells (p < 0.001 and p < 0.01, respectively). CONCLUSION: These results demonstrate that cyclin D1 overexpression in the tumor cells of pancreatic carcinoma tissue is at least partly dependent on the mitogenic effects of EGF signaling through the EGFR.

Blotting, Western↗

Low serum levels of CD44, CD44v6, and neopterin indicate immune dysfunction in chronic pancreatitis.

INTRODUCTION: In autoimmune diseases, malignancies, and inflammatory conditions, a correlation of serum levels of CD44, interleukin-2 receptor (IL-2r), and neopterin with disease activity could be shown. AIMS: To assess the immune parameters in chronic pancreatitis in correlation to clinical data to evaluate the potential role of immune dysfunction as a risk factor. METHODOLOGY: Levels of IL-2r, sCD44, sCD44v6, and neopterin were measured using the enzyme-linked immunosorbent assay in 63 patients with chronic pancreatitis who underwent surgery between 1992 and 1995 in our institution. Clinical data were evaluated prospectively before surgery, and a follow-up investigation was conducted in 1997. RESULTS: Mean serum levels of CD44, CD44v6, and neopterin were significantly lower in patients with chronic pancreatitis compared with the control group. The mean level of IL-2r was also lower in chronic pancreatitis, but this difference was not significant. However, no influence of immunosuppressive factors such as alcohol consumption, cigarette smoking, or diabetes could be detected on the levels of IL-2r, CD44, CD44v6, and neopterin. CONCLUSION: In accordance with other diseases of reduced immunoreactivity, depressed serum levels of biomarkers in chronic pancreatitis are caused by reduced T-lymphocyte and macrophage activation. By ruling out a significant influence of concomitant immunosuppressive factors, we conclude that the inflammatory process itself is the source of the depressed immune function, which might be restored by surgical resection.

Alcohol Drinking↗

Management of patients with extended pancreatic necrosis.

BACKGROUND: Extended pancreatic necrosis pose a considerable therapeutic problem in patients with necrotizing pancreatitis. AIM: Factors that limit conservative treatment in patients with extended pancreatic necrosis were analyzed. METHODS: The clinical course of 61 patients with an extent of necrosis of more than 50% of the gland (according to contrast-enhanced CT scan) were analysed with special regard to systemic complications. Indications for surgical treatment were either persistent organ failure or pancreatic infection. RESULTS: 10 patients were managed by conservative treatment, 51 (84%) patients underwent operation. Indications for surgery were sepsis with or without organ failure in 17 patients, persistent organ failure in another 17 patients, persistent SIRS in 13 patients and local complications in 4 patients. Pancreatic infection was present in 25 patients. The incidence of systemic complications did not differ between infected and sterile necrosis, but they occurred earlier in sterile necrosis. CONCLUSIONS: Persistent organ failure is limiting conservative treatment during the early course in patients with sterile necrosis. The latter course is characterized by a high incidence of pancreatic infection and septic organ failure.

APACHE↗

Expression of the IIIc variant of FGF receptor-1 confers mitogenic responsiveness to heparin and FGF-5 in TAKA-1 pancreatic ductal cells.

BACKGROUND: Fibroblast growth factors (FGFs) contribute to angiogenesis and mitogenesis by binding to tyrosine kinase receptors termed FGF receptors (FGFRs). FGF-5 is a secreted FGF that is believed to preferentially act via the IIIc splice variant of FGFR-1. Human pancreatic ductal carcinoma cells express FGF-5 and FGFR-1IIIc, implying a potential for autocrine growth modulation. AIM: In this study we investigated the importance of FGFR-1 IIIc expression for FGF-5 mitogenic signaling in a pancreatic ductal cell line. METHODS: A cDNA encoding FGFR-1 IIIc was expressed in the well-differentiated TAKA-1 Syrian hamster pancreatic ductal cell line. RESULTS: TAKA-1 cells secrete FGF-5, but were found not to express FGFR-1 and to be unresponsive to exogenous FGF-5. In contrast, TAKA-1 clones expressing FGFR-1 IIIc were growth stimulated in the presence of FGF-5 and displayed enhanced mitogen-activated protein kinase (MAPK) activity in the presence of FGF-5. PD98059, an inhibitor of this pathway, inhibited FGF-5-induced growth in these clones. CONCLUSION: Our data demonstrate that FGFR-1 IIIc can mediate FGF-5-induced mitogenesis via the MAPK pathway in pancreatic ductal cells, and suggest that expression of FGFR-1 IIIc in conjunction with FGF-5 may contribute to the pathobiology of human pancreatic cancer.

Animals↗

[Infected necroses and pancreatic abscess: surgical therapy].

Infected pancreatic necrosis and pancreatic abscesses are severe complications of necrotizing pancreatitis. Compared to infected necrosis, pancreatic abscess is associated with lower mortality. Surgical treatment is the current standard. Necrosectomy is performed as a single-step operation in combination with postoperative drainage/lavage or as scheduled reoperation. In selected cases, pancreatic abscesses can be successfully drained by percutaneous interventional drainage. Mortality in infected necrosis is 20-30% and 5-10% in patients with pancreatic abscess.

Abscess↗

Glutathione depletion causes cell growth inhibition and enhanced apoptosis in pancreatic cancer cells.

BACKGROUND: Recent studies have demonstrated that various tumors express enhanced levels of the radical scavenger glutathione (GSH). Moreover, there are grounds for claiming that GSH plays a crucial role in cell proliferation and tumor resistance. In the current study, we investigated the relation between cell growth and GSH levels in the pancreatic adenocarcinoma cell line, AsPC-1, and the significance of GSH in tumor resistance to chemotherapy. METHODS: Cell growth in AsPC-1 was initiated through transforming growth factor-alpha (TGF-alpha) or fetal calf serum (FCS). Then, cell cycle, cell proliferation, and cellular GSH content were analyzed at different times in the presence or absence of buthionine sulfoximine (BSO). The impact of GSH on chemotherapy-induced apoptosis was studied using 5-fluorouracil or melphalan in the presence or absence of BSO. Finally, we compared the GSH content of 15 pancreatic tumor specimens with 10 normal pancreatic tissue specimens. RESULTS: Analysis of GSH in pancreatic tissues demonstrated increased GSH levels in cancerous compared with normal tissue (17.5 +/- 2.3 vs. 8. 8 +/- 1.4 nmol/mg protein; P < 0.004). Incubation of AsPC-1 with TGF-alpha or FCS resulted in cell proliferation and cell cycle activity, whereas GSH content was not altered. Incubation of GSH-depleted cells with TGF-alpha did not stimulate cell growth. In addition, GSH-depletion resulted in an increased rate of apoptosis after melphalan (6.3 +/- 0.3 % vs. 11.2 +/- 0.3 %; P < 0.001), but not after 5-fluorouracil treatment. CONCLUSIONS: Taken together, our results show enhanced GSH levels in pancreatic carcinoma and an essential role of GSH in cell proliferation and in resistance of AsPC-1 cells. Therefore, GSH-depletion may improve the efficacy of adjuvant therapy in pancreatic carcinoma.

Adult↗

[Benign tumors of the Vater's papilla].

BACKGROUND AND OBJECTIVE: Villous adenoma is the most common tumour of the papilla of Vater, and transition from adenoma to carcinoma is now generally accepted as proven. It is thus essential for an adenoma to be removed. Methods of removal have ranged from endoscopic sling papillectomy to partial duodenopancreatectomy. It was the aim of this study to determine whether recurrence can be prevented by local resection. PATIENTS AND METHODS: 58 patients with a benign tumour of the papilla (26 men, 32 women; average age 59 [range from 18 to 81] years) were included. Depending on preoperative histology, intraoperative frozen-section diagnosis and macroscopic histopathology, some form of surgical intervention was undertaken, most often resection of the ampulla. The clinical course and findings at postoperative follow-up were recorded and the absence of recurrence checked by endoscopy. RESULTS: Ampullectomy was performed in 49 of the 58 patients, papillectomy in three. Although frozen-section examination had failed to reveal any malignancy, resection of the head of the pancreas with preservation of the pylorus was done in six patients, carcinoma having been suspected macroscopically. There were no operative deaths. An adenoma had been found in 44 patients, one quarter of them showing severe dysplasia: follow-up examinations after a mean interval of 45 months (range of 6-180 months) failed to find any recurrence. CONCLUSION: Ampullectomy provides an adequate surgical treatment of benign adenoma of the ampulla of Vater. Accurate surgical technique and pre-, intra- and final histopathological diagnosis by an experienced pathologist are decisive factors in determining the ultimate outcome. If the histological findings as to benignity are unclear, resection of the head of the pancreas with preservation of the pylorus by an experienced surgeon is indicated.

Adenoma↗

Thymidylate synthase quantitation and in vitro chemosensitivity testing predicts responses and survival of patients with isolated nonresectable liver tumors receiving hepatic arterial infusion chemotherapy.

BACKGROUND: Patients with isolated, nonresectable liver tumors may receive regional hepatic arterial infusion (HAI) chemotherapy with response rates of about 50%. The objective of this study was to investigate the value of thymidylate synthase (TS) determination in combination with in vitro chemosensitivity testing to predict the responses and survival of patients receiving HAI. METHODS: TS mRNA expression was quantitated using a reverse transcription-polymerase chain reaction technique with beta-actin as the internal standard. In vitro chemosensitivity testing was performed with tumor cell suspensions using the human tumor colony-forming assay (HTCA). RESULTS: An analysis of the test combination in 24 consecutive patients revealed that 77% (10 of 13) of the sensitive and 9% (1 of 11) of the resistant patients had complete or partial clinical responses. Sensitive patients were 8.5-fold more likely to respond (P = 0.0036) and displayed with 32 months (range, 5-75 months) a longer median survival than resistant patients with 17 months (range, 3-28 months, P = 0.003). Analysis of the Kaplan-Meier curves revealed that sensitive patients had a higher overall survival probability, as determined by the log rank test (P = 0.044). CONCLUSIONS: These results suggest that the clinical outcomes of patients receiving HAI therapy may be predictable with TS quantitation and HTCA. It is possible, therefore, that this combination may be used in the future to select patients with liver tumors who will benefit from HAI before the start of regional chemotherapy.

Adult↗

Early prediction of severity in acute pancreatitis by urinary trypsinogen activation peptide: a multicentre study.

BACKGROUND: There is a pressing clinical requirement for an early simple test of severity in acute pancreatitis. We investigated the use of an assay of trypsinogen activation peptide (TAP). METHODS: We undertook a multicentre study in 246 patients (172 with acute pancreatitis [35 with severe disease], 74 controls). We assessed the predictive value of urinary TAP concentrations measured by a validated competitive immunoassay. We compared the results with those for plasma C-reactive protein and three clinicobiochemical scoring systems. TAP and C-reactive protein concentrations were analysed at set times after symptom onset and compared with the clinicobiochemical systems scores at key times during hospital stay. FINDINGS: At 24 h after symptom onset, the median urinary TAP concentration was 37 nmol/L (IQR 17-110) for severe and 15 nmol/L (5-35) for mild disease (p<0.001). The respective values for plasma C-reactive protein were 24 mg/L (3-34) and 25 mg/L (6-75; p=0.208). The sensitivity, specificity, positive predictive, and negative predictive values of the test to show severe acute pancreatitis compared with mild acute pancreatitis at 24 h were: for TAP (>35 nmol/L), 58%, 73%, 39%, and 86%, respectively, and for C-reactive protein (>150 mg/L), 0%, 90%, 0%, and 75%. 48 h after admission the values for the clinicobiochemical scoring systems were: APACHE II (> or =8), 56%, 64%, 30%, and 85%; Ranson score (> or =3), 89%, 64%, 38%, and 96%; and Glasgow score (> or =3), 77%, 75%, 44%, and 93%. At 48 h, the values for C-reactive protein were 86%, 61%, 37%, and 94% and for TAP were 83%, 72%, 44%, and 94%. Combined testing of C-reactive protein and TAP was not superior to TAP alone for accuracy. INTERPRETATION: Urinary TAP provided accurate severity prediction 24 h after onset of symptoms. This single marker of severity in acute pancreatitis deserves routine clinical application.

Acute Disease↗

[Stage-adapted reconstruction of the stomach after gastrectomy].

The only realistic chance of a cure for cancer of the stomach is gastrectomy with a wide margin of clearance. The question as to what constitutes the ideal reconstruction of a substitute stomach, however, remains unanswered. A number of prospective randomized studies show that patients operated on in curative intent and with a good long-term prognosis, should be given a substitute stomach in the form of a pouch constructed from small bowel, with restoration of duodenal passage. On account of the shorter operating time, patients receiving palliative surgery should be treated with a simple oesophagojejunostomy without such a small-bowel pouch substitute stomach.

Anastomosis, Roux-en-Y↗

Aggregation substance promotes colonic mucosal invasion of Enterococcus faecalis in an ex vivo model.

BACKGROUND: Bacterial translocation through the gastrointestinal tract is the crucial step in the pathogenesis of intraabdominal infections. We assessed whether aggregation substance (AS), a bacterial adhesin and virulence factor of Enterococcus faecalis, promotes bacterial translocation and colonic mucosal invasion in an ex vivo experiment. METHODS: Colonic mucosa of male Wistar rats was placed in a modified Ussing system. The mucosal side of the chamber was filled with a suspension of E. faecalis OG1X:pAM721 (AS-positive) or E. faecalis OG1X (AS-negative). The serosal side was filled with sterile Dulbecco's modified Eagle's medium. For assessment of colonic mucosal invasion the mucosal side was incubated for 2.5 h with a suspension of AS-positive or AS-negative enterococci. After being washed, a solution of gentamicin and penicillin G in tissue culture medium was added on both sides in order to kill extracellular bacteria. Subsequently, the mucosa was removed from the system, washed, lysed with Triton X-100, and homogenized. Viable intramural bacteria were quantified by plating serial dilutions of the homogenate on Todd-Hewitt broth agar plates. To quantify bacterial translocation samples which were taken at various time points from the serosal side were plated on Todd-Hewitt broth agar plates and colony forming units (CFU) were determined. RESULTS: Invasion of the AS-positive E. faecalis strain OG1X:pAM721 into the colonic mucosa was significantly higher than invasion rates of the AS-negative strain OG1X (2.88 log(10) CFU/ml vs 1.73 log(10) CFU/ml; P = 0.02). However, none of the tested strains was found to translocate from the mucosal to the serosal side within the incubation time of 4 h. CONCLUSIONS: The aggregation substance promotes invasion of E. faecalis into colonic mucosa.

Animals↗

[Necrosectomy or anatomically guided resection in acute pancreatitis].

Necrotizing pancreatitis is still associated with considerable morbidity and mortality. Formerly, surgical treatment with early and extensive pancreatic resection has been the standard. Improvements in our understanding of the pathogenesis of the disease and progress in the field of intensive care therapy have made conservative therapy the initial standard in the treatment of necrotizing pancreatitis. A considerable percentage of patients with sterile necrosis can be managed with low morbidity and mortality by conservative treatment without operation. Nevertheless, surgical treatment is indicated in patients with infected necrosis and in sterile necrosis if multiorgan failure persists over a limited period of time despite maximum intensive care therapy. Pancreatic resection should be abandoned for surgical treatment of pancreatic necrosis, as results with regard to morbidity, mortality and long-term outcome are unsatisfactory. Today the surgical standard is careful digital necrosectomy, which must be followed by either postoperatve drainage, repeated open lavage or continuous closed lavage. In experienced hands, all three procedures provide similar results with regard to morbidity and mortality.

Debridement↗

Release of endotoxin-binding proteins during major elective surgery: role of soluble CD14 in phagocytic activation.

Our previous study demonstrated that soluble CD14 (sCD14) modulates the biologic activity of circulating endotoxin, which appears after surgery. In this study, we examined the behavior of endotoxin-binding proteins, such as sCD14, lipopolysaccharide-binding protein (LBP), and bactericidal/permeability-increasing protein (BPI), in patients' plasma after major abdominal surgery and the phagocytic secretion of sCD14 from peripheral blood mononuclear cells (PBMCs) throughout the observation period. In a prospective study, 15 patients undergoing major abdominal surgery (gastrectomy, n = 3; pancreatectomy, n = 10: colectomy, n = 2) were involved in this study. The endotoxin-binding proteins were perioperatively (preoperatively; postoperative hour 6; days 1, 2, 3, 4, 5, 7, and 10) measured by an enzyme-linked immunosorbent assay (ELISA). To exclude the hemodilution effect of samples, each parameter was corrected by dividing the respective value by the albumin concentration. The phagocytic activity at each time point was tested as an ex vivo sCD14 secretion from PBMCs in the presence and absence of exogenously added endotoxin, Escherichia coli 055B5 (1 ng/ml). Significant endotoxemia (0.35 +/- 0.13 EU/ml; p < 0.05) was observed 6 hours after the beginning of surgery. The sCD14/albumin value rapidly increased at 6 hours after surgery, peaked on day 1, and sequentially declined, whereas the BPI/albumin and LBP/albumin ratios increased more gradually and peaked on day 2. The secretion of sCD14 from 2 x 10(6) PBMCs was significantly enhanced from 6 hours after operation. The increased plasma level of sCD14 may be explained by the parallel-enhanced sCD14 PBMC production. Activated secretion of these endotoxin-binding proteins may play a role in regulating the biologic activity of circulating endotoxin.

Acute-Phase Proteins↗

Sphincter-saving treatment in epidermoid anal cancer: cooperative analysis of 142 patients in five German university surgical centers.

Five southern German university centers cooperated in comparing the effect of surgical vs. nonsurgical therapy strategies on survival and sphincter preservation in the treatment of anal cancer. A standardized questionnaire was used to evaluate retrospectively (mean follow-up 30 months) treatment strategy and outcome (survival, colostomy rate, colostomy-free survival) in patients treated between 1987 and 1996. Of the 142 patients 65% had squamous cell, 20% basaloid, 6% adeno-, and 1% undifferentiated carcinoma (8% histology not recorded); 9% were classified in UICC stage I, 37% in stage II, 25% in stage III, and 4% in stage IV (25% not recorded). Primary treatment consisted of local excision (10%), excision plus radio- and/or chemotherapy (17%), radiotherapy (20%), radiochemotherapy (28%), or colostomy with or without resection, radiotherapy, and chemotherapy (23%). We observed no difference between these treatment groups in overall (P = 0.43) or colostomy-free survival (P = 0.14, log-rank). Primary colostomy was prevented in 77% of cases and decreased over the years. Mean overall survival (in months) was 42 in stage I, 38 in stage II, and 25 in stage III (P = 0.0013); mean colostomy-free survival was 36 in stage I, 26 in stage II, and 16 in stage III (P = 0.0021, log-rank). Outcome was not significantly related to therapeutic strategy (surgery or radio-chemotherapy. Primary surgical and nonsurgical strategies in treating anal cancer thus produced similar results, although radiochemotherapy is usually recommended for sphincter-endangering anal cancer. Challenges to be met in the future include the prevention of metastasis and long-term preservation of anal sphincter function.

Adenocarcinoma↗

Follow-up in colorectal cancer: cost-effectiveness analysis of established and novel concepts.

BACKGROUND: Follow-up programs in colorectal cancer have been under question recently due to their low efficacy. Some meta-analyses found a survival benefit and four randomized studies suggested the opposite. Therefore, this paper analyzes existing and proposed follow-up programs for costs and efficacy. METHODS: One thousand and fifty-four colorectal cancer patients intensively followed-up in Ulm (endoscopy, chest radiography, abdominal ultrasound, computed tomography (CT) pelvis) were prospectively evaluated for recurrence, salvage surgery rate, survival and costs. Costs were compared among existing and proposed international follow-up programs retrieved by a MedLine search. RESULTS: A total of 350/1,054 colorectal cancer patients (33.2%) relapsed asymptomatically, as detected by follow-up. 56/350 (local 47%, distant 53%) recurrences were resectable (16%), 21/350 patients survived (6%). The efficacy of follow-up was 21/1,054 patients (2%). Costs were, per patient, 2,220 euros (colon) or 4,851 euros (rectum). Costs in five randomized studies varied between 616 euros for minimal and 5,049 euros for intensive follow-up. Four proposed follow-up concepts include risk-adaption, which claim to reduce costs by 50-60% and range between 889 (colorectal) and 5,910 (high-risk, rectum) euros. The recommended German follow-up guideline costs 610 euros (low-risk, colorectal), 1,120 euros (high-risk, colon) or 2,252 euros (high-risk, rectum). CONCLUSION: Follow-up concepts for colorectal cancer should aim at the identification of curable patients with recurrence. Evidence-based concepts, including life quality tests, remain to be defined, but currently abdominal ultrasound, endoscopy and carcino-embryonic antigen (CEA) determination at 6-month intervals for 2 years and annual intervals for 3 years seem to identify this patient sub-group.

Carcinoembryonic Antigen↗

Fluorescence detection of small gastrointestinal tumours: principles, technique, first clinical experience.

Photodynamic therapy (PDT) is a form of cancer treatment based on the selective accumulation of a photosensitizer in neoplastic tissue. The fluorescent properties of a photosensitizer permit diagnostic localization of primary tumours and/or metastasis. Occult lesions are hard to detect and can easily be missed during routine laparoscopy. Fluorescence observation offers additional optical information and the ability to detect these occult tumours. Clinically, we used 5-aminolevulinic acid for peritoneal staining and tumour demarcation via tumour-specific fluorescence induced by protoporphyrin IX. For laparoscopic observations, a "D-Light" system was used; the conventional white light source was equipped with an optical blocking filter that transmits at the excitation wavelength (380-450 nm) and blocks all other parts of the spectrum. With the aid of a suitable observation filter, the relevant fluorescence was detectable. With the help of this fluorescence we increased the capacity to detect occult tumours, that were missed with white-light observation (9/26). In the gastrointestinal tract, we used a krypton laser at 405 nm for PP IX fluorescence induction. Although there were high sensitivity rates for neoplasms (81% peritoneal carcinomas, 60% gastric cancer), no exact histopathological statement could be achieved at because of false-positive fluorescence, mainly caused by inflammation (6/32). Current clinical goals and the future perspectives of photodynamic diagnostic are discussed.

Aminolevulinic Acid↗