Nitinol esophageal stents: new designs and clinical indications.

PURPOSE: To evaluate the clinical use of covered and noncovered, knitted nitinol stents in patients presenting new stent indications. METHODS: Self-expandable, knitted nitinol stents were implanted in four patients for treatment of dysphagia. In two patients who had malignant strictures and had esophago-respiratory fistulae and in one patient with an esophagocutaneous fistula, polytetrafluoroethylene (PTFE)-covered stents were implanted. One patient received a noncovered stent, but a retrograde approach through a percutaneous endoscopic gastrostomy (PEG) fistula had to be chosen for recanalization of an esophageal occlusion. Two patients received stents for treatment of benign strictures. RESULTS: Recanalization of the stricture and stent implantation were performed under fluoroscopic control without any procedure-related morbidity or mortality. Dysphagia improved in all patients and the esophageal fistulae could be sealed off by covered stents. During a maximum follow-up of 18 months, there was no stent migration or esophageal perforation. Complications observed were stent stenosis due to food impaction (1/4) and benign stent stenosis (2/2). Most complications could be treated by the interventional radiologist. CONCLUSION: Self-expandable, covered Nitinol stents provide an option for the treatment of dysphagia combined with esophageal fistulae. In combination with interventional radiology techniques, even complex strictures are accessible. For benign strictures, the value of stent treatment has not yet been proven.

Acupuncture inhibits vagal gastric acid secretion stimulated by sham feeding in healthy subjects.

In a prospective randomised study, the effect of acupuncture on sham feeding stimulated gastric acid secretion was investigated. In eight healthy volunteers (five men, three women, mean (SEM) age 26.3 (4.7) years) various methods of acupuncture were performed. Apart from the sham procedure, the acupuncture was performed at the classic acupuncture points. Electroacupuncture reduced gastric acid secretion expressed as median (range) significantly during the first 30 minute period to 1.6 (0-5.2) mmol compared with 3.8 (2.3-14.5) mmol (p < 0.05) during control period (sham feeding without acupuncture). Inhibition of gastric acid secretion by electroacupuncture was also significant during the second 30 minute period (0.2 (0-5.6) v 3.6 (0.3-9.1) mmol; p < 0.05) and for peak acid output (0.8 (0.2-5.1) v 7.6 (3.4-12.1) mmol; p < 0.05). Transcutaneous electrical nerve stimulation also resulted in significant reduction of gastric acid secretion during the first 30 minute period (1.0 (0-3.6) mmol v 3.8 (2.3-14.5) mmol; p < 0.05), and peak acid output (3.6 (1.2-12.0) v 7.6 (3.4-12.1) mmol; p < 0.05). The classic needle acupuncture, laser acupuncture, and sham acupuncture had no significant effect on gastric acid secretion. This study shows firstly that in healthy volunteers, only the versions of acupuncture using more pronounced stimulation (electroacupuncture, transcutaneous electrical nerve stimulation), but not those with only mild stimulation of the nerves (classic needle acupuncture, laser acupuncture), and secondly only acupuncture performed at defined points lead to significant reduction in gastric acid secretion.

Free fatty acids in serum of patients with acute necrotizing or edematous pancreatitis.

Serum concentrations of free fatty acids (FFA) were assayed in 20 patients with acute necrotizing pancreatitis (ANP). Pancreatic and peripancreatic fat necrosis was verified on operation and/or by contrast-enhanced computed tomography. For comparison, 20 patients with acute edematous pancreatitis (AEP) were examined. On admission, FFA serum levels were 1.14 +/- 0.12 (SEM) mmol/L in ANP and, thus, significantly (p < 0.03) higher than in AEP (0.78 +/- 0.09 mmol/L). The two groups also differed in the later course: in ANP, the FFA values remained raised (d 5-11:0.86 +/- 0.13 mmol/L; p > 0.05 vs day 1), whereas in AEP, the FFA concentrations normalized within 1 wk (d 2-4:0.52 +/- 0.11 mmol/L; d 5-11:0.39 +/- 0.05 mmol/L; p < 0.05 vs day 1 and p < 0.01 vs ANP). Serum FFA correlated positively with C-reactive protein levels (rs = 0.42; p < 0.01), but has less discriminating potency between ANP and AEP. In AEP, the initial peak may correspond to the disease outburst itself and to unspecific stress. In ANP, the higher and sustained elevation of FFA may predominantly mirror the ongoing pancreatic parenchymal and extrapancreatic fat necrosis, and be pathophysiologically relevant, especially in view of significantly reduced serum albumin levels in ANP.

Longer relapse-free period after sucralfate than after H2-blocker treatment of duodenal and gastric ulcers.

In a prospective investigation of 2,045 patients with recurrent peptic ulcer disease, the relapse-free period after acute treatment with sucralfate was evaluated over 1 year. This remission period was compared retrospectively with that achieved by previous treatment with a histamine-H2-blocker in the same patients. Only patients who had a symptomatic relapse within 1 year after H2-blocker therapy were included. Patients with no relapses within 1 year after sucralfate were assumed to have a relapse on day 366, in order to compare the two periods. In 73% of the evaluable 2,045 patients, remission after sucralfate was longer than after H2-blocker, and 23% of these patients had no symptomatic relapse at all within 1 year after sucralfate. The average relapse-free period after sucralfate was 212 days, as compared with 132 days after H2-blockers (difference = 80 days; p less than 0.0001). Elderly and nonsmoking patients and those experiencing their first recurrence, or who had a duodenal ulcer, benefited especially from acute treatment with sucralfate. It can be concluded that peptic ulcer patients with a relapse after treatment with an H2-blocker are suitable candidates for sucralfate therapy. There is a high probability that the relapse-free period after sucralfate is longer than after H2-blocker treatment in both gastric and duodenal ulcer patients.

[Parameters of connective tissue metabolism as markers in acute and chronic pancreatitis. A retrospective study with a cohort of normal subjects]. / Parameter des Bindegewebsstoffwechsels als Marker bei akuter und chronischer Pankreatitis. Eine retrospektive Studie mit Erhebung eines Normalkollektivs.

It is suggested that during active phases of acute and chronic pancreatitis (aP and cP) a major breakdown of extracellular matrix occurs. Since our group previously established that serum levels of the precollagen-III-peptide (P-III-P) are good markers for changes in the extracellular matrix in liver disease (e.g. fibrosis and cirrhosis), we investigated whether this would also serve as a possible marker for pancreatitis. A total of 52 patients with pancreatitis were studied (aP = 17; cP = 35) and compared to 194 controls. Diagnosis of pancreatitis was done on the basis of established classifications. Concomitant diseases, e.g. of the liver, were excluded. Serum levels of P-III-P (three assays with polyclonal and monoclonal antibodies and Fab-Fragments), hyaluronic acid (HA) and laminin (LAM) were measured by RIA or IRMA. Patients with pancreatitis displayed elevated levels in all groups, when compared with the controls. Since the P-III-P-Fab RIA measures the Col1-fragment by 50%, which is considered to be a degradation product of P-III-P, this could mean that neogenesis of collagen is paralleled by degradation during the initial course of an acute episode of pancreatitis. The ratio (quotient) of P-III-P-Fab and P-III-PMoAb (nl = 127.3 +/- 27) is changed in patients with pancreatitis towards P-III-P-Fab (aP: 115.4 +/- 84.7*, cP: 94.9 +/- 21.8*, cP-I: 89.3 +/- 9.2*; * = p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of CA 72-4 with CA 19-9 and carcinoembryonic antigen in the serodiagnostics of gastrointestinal malignancies.

Serum levels of the new tumor-associated marker CA 72-4 were measured in healthy controls (n = 64) and patients with benign (n = 410) or malignant (n = 199) gastrointestinal diseases. A cut-off limit of 4 U/ml was established. Tumor-indicating sensitivity was compared with that of the conventional markers carcinoembryonic antigen (CEA) and CA 19-9. In serodiagnostic evaluations CA 72-4 was clearly inferior to CA 19-9 in pancreatic carcinomas (22% versus 82%; all stages) and to CEA in colorectal cancer (32% versus 58%; all stages), with no appreciable diagnostic gain from combined determination. However, in gastric carcinoma CA 72-4 identified 59% of all patients (CA 19-9, 52%; CEA, 25%), and a combination of CA 72-4 and CA 19-9 detected as many as 70%. Positive results correlated roughly with tumor size. Compared with the other two tumor markers, CA 72-4 had a very high specificity (98%) in benign diseases of the gastrointestinal tract, including inflammatory processes, so that elevated serum levels of CA 72-4 should always be taken seriously.

Exocrine pancreatic function after gastrectomy. Specificity of indirect tests.

We compared intraindividually the specificity of indirect pancreatic function tests before and after total (n = 4; Roux-en-Y) or subtotal (n = 6; Billroth II) gastrectomy. Before gastrectomy only 1 patient showed a falsely pathological result with the pancreolauryl test (90% specificity), while the results of all the other tests were correctly normal (100% specificity using the usual cutoff limits). After gastrectomy the respective specificities were as follows: pancreolauryl test 10%, bentiromide test 70%, fecal chymotrypsin 70%, and plasma amino acid consumption test 100%. There was no obvious difference in the reduction of specificity between subtotal and total gastrectomy. The respective preoperative to postoperative changes in the median test data were as follows: plasma amino acid consumption test +21%, bentiromide test -12%, fecal chymotrypsin -51%, and pancreolauryl test -53%. It is concluded that after gastrectomy only the plasma amino acid consumption test is unaffected by postoperative anatomic alterations.

Coeliac sprue: abnormalities of the hormone profile of gastroduodenal mucosa.

To further characterize coeliac sprue, the hormonal content of routine endoscopic biopsies of gastroduodenal mucosa was estimated in 5 coeliac sprue patients and in 8 volunteers without upper gastrointestinal disease. Levels of cholecystokinin-like immunoreactivity tended to be lower in duodenal mucosa of coeliac sprue patients, while the mucosal map of GIP and somatostatin exhibited no peculiar profile. Gastrin was markedly elevated in the antral mucosa of coeliac sprue patients (3013 +/- 760 versus 1048 +/- 392 pmol/g), while basal plasma gastrin was normal. The mucosal VIP content of the descending duodenum was significantly higher in coeliacs than in controls (409 +/- 161 versus 81 +/- 16 pmol/g) and tended to be increased also in the remaining upper small intestine. This rise may be a reaction to mucosal irritation and a reason for enhanced fluid secretion. Even in antral mucosa of coeliac sprue patients, VIP levels were elevated when compared to controls (82 +/- 14 versus 40 +/- 8 pmol/g) and may have some impact, e.g. on local mucosal blood flow or mucus secretion. The mucosal concentration of another putative neurotransmitter, substance P, also showed a tendency to be raised in the mucosa of upper small intestine of coeliac sprue patients.

Gut hormone release by intraduodenal stimulation in duodenal ulcer patients.

After an overnight fast, plasma levels of gut peptide hormones were determined before and after intraduodenal stimulation (IDS) with glucose and citric acid in 8 patients with a recent endoscopically proved duodenal ulcer (DU) attack and in 8 healthy volunteers. The DU patients had a hyperacidic mean BAO of 6.6 and an average PAO of 41.8 mEq/h. In DU, basal secretin levels were similar to those in controls, and after IDS secretin release was not impaired. There was no defect of VIP liberation or of the neurotensin response (basal 21 +/- 7 vs 16 +/- 3, after IDS 68 +/- 28 vs 35 +/- 5 pmol/l) which could account for gastric acid hypersecretion. Although fasting GIP levels were significantly lower than in controls (16 +/- 2.5 vs 25 +/- 1.4 pmol/l), they did not correlate negatively with BAO. In contrast to former studies with oral test meals, integrated GIP release was rather reduced after IDS. Basal plasma levels of gastrin were significantly lower in DU (4.0 +/- 0.4 vs 12 +/- 2 pmol/l) and were inversely related to BAO (r = -0.82, p less than 0.02). From the present data, there is insufficient evidence for abnormal plasma levels of gut hormones as major etiologic factors for basal hyperchlorhydria in ordinary DU disease.

Chronic pancreatitis and diabetes mellitus: plasma and gastroduodenal mucosal profiles of regulatory peptides (gastrin, motilin, secretin, cholecystokinin, gastric inhibitory polypeptide, somatostatin, VIP, substance P, pancreatic polypeptide, glucagon, enteroglucagon, neurotensin).

A disturbed intraduodenal milieu and pancreatic scarring in advanced chronic pancreatitis (CP) may lead to changes of gut and pancreatic hormones. In the present study, the gastroduodenal mucosal content of several regulatory peptides was determined in 8 patients with severe calcific CP and 8 healthy volunteers. In addition, hormone release into the bloodstream was estimated after intraduodenal acid/glucose stimulation in the control subjects and 8 CP patients each with or without secondary diabetes mellitus (DM), and in 8 patients with juvenile DM, so that disturbed gut hormone release could be attributed either to CP or DM. While VIP release into the circulation was similar in all participants, mucosal levels of VIP and substance P were significantly elevated in the duodenal bulb and descending duodenum of CP patients. The somatostatin content of gastroduodenal mucosa in CP was at least as high as in normals. Gastrin was significantly more abundant only in the duodenal bulb of CP patients, while plasma gastrin was normal. Duodenal CCK concentrations tended to be elevated in the duodenal bulb, but not significantly. The release of secretin seemed to be higher in type-1 diabetics than in CP patients. The mucosal pattern of GIP was nearly identical in CP patients and controls. Compatible with this finding, the GIP release did not show any peculiarities in CP with or without DM or in DM. Basal and stimulated plasma levels of motilin were abnormally high in CP. Pancreatic polypeptide plasma levels were normal in DM, but significantly reduced in CP, especially in CP with DM. Fasting PP and stimulated pancreatic enzyme outputs were linearly related.(ABSTRACT TRUNCATED AT 250 WORDS)

[Amino acid level in plasma--expressed as alpha-amino-nitrogen--reaction to stimulation of the exocrine pancreas: approaches to a new pancreatic function test]. / Aminosäurespiegel im Plasma--dargestellt als alpha-Amino-Stickstoff--reagieren auf Stimulation des exokrinen Pankreas: Ansätze für einen Pankreasfunktionstest.

We determined by the ninhydrin method the plasma amino acid (AA) levels prior to, during and following, a 1-hour i.v. infusion of 1 U/kg body weight each of secretin and pancreozymin in patients with normal (n = 74) or reduced (n = 39) exocrine pancreatic function, as assessed by the duodenal aspiration test. The results of the two tests correlated significantly with each other (p less than 0.001). A maximum AA decrease of greater than or equal to 12% was observed in all patients with a normally functioning pancreas (specificity 100%), and of less than 12% in all patients with medium to high-grade impairment of pancreatic function (sensitivity 100%). Since, however, low-grade pancreas insufficiency (20-40% of the mean normal enzyme output) is recognized in fewer than one-half of the cases, the overall sensitivity of the AA-consumption test decreases to 69%. The results can, however, be improved by: 1) Calculating the mean percentage AA decrease with a limit value of 5% (sensitivity 90%); 2) determining individual AA with pancreas-specific absorption, such as serine (sensitivity 92%); 3) dropping the lower normal value of exocrine pancreatic function to 25% of the normal mean enzyme output (sensitivity 96%). Diseases that may be associated with the most common condition that causes pancreatic insufficiency--chronic pancreatitis--and which have an influence on AA metabolism, such as cirrhosis of the liver and diabetes mellitus, have no influence on the accuracy of the AA consumption test, which, considered overall, represents a competitive alternative to other tubeless tests of pancreatic function.

[Gastroduodenal lesions caused by drugs]. / Gastroduodenale Läsionen durch Medikamente.

Nonsteroidal analgetics (NSA), in particular, can cause acute gastroduodenal erosions. Acid NSA, especially acetylsalicylic acid (ASA), damage gastric epithelium and mucosal capillary endothelium directly. In addition, gastric mucosa is made more prone to attack by aggressive factors like acid, when prostaglandin biosynthesis is inhibited by NSA. Useful studies on the relationship between these acute lesions and peptic ulceration are rare. For the greatest offender, unbuffered ASA, an increased risk for gastric ulceration is documented after prolonged use of higher doses. Major bleeding from peptic ulcers and erosions seems likewise to be fostered. With newer NSA, the damaging potency is, in general, smaller.

NMR spectrometry. A new method for total stool fat quantification in chronic pancreatitis.

In the present investigation, suitability of nuclear magnetic resonance (NMR) spectrometry for total stool fat quantification in patients with normal or impaired exocrine pancreatic function (chronic pancreatitis) has been analyzed in comparison with a conventional chloroform-methanol extraction technique. Basic temperature-dependence studies of NMR spectrometry (90 degrees/180 degrees radiofrequency pulse sequence) on 21 chloroform-methanol extracted pure total stool lipid standards (weight range: 0.05-1.6 g) revealed significantly (P less than 0.05) improving correlations between NMR signal amplitudes and corresponding weights at increasing temperatures (r = 0.952/40 degrees C, r = 0.965/60 degrees C, r = 0.988/80 degrees C), thus indicating 80 degrees C as optimal temperature for NMR spectrometric total stool fat quantification. In subsequent comparative measurements of lyophilized stool samples, NMR spectrometry (at 80 degrees C) and conventional chloroform-methanol extraction provided significantly (P less than 0.001) correlated results with respect to total fecal fat contents/day of quantitatively collected and homogenized stools in 93 patients with known exocrine pancreatic function (secretin-pancreozymin test), irrespective of whether correlations were determined for all 93 patients (r = 0.983) or separately for patients with normal (N = 45; r = 0.867), moderately reduced (N = 31; r = 0.946), or highly reduced (N = 17; r = 0.992) exocrine pancreatic function and correspondingly increased total fecal fat excretions.

Whipple's procedure plus intraoperative pancreatic duct occlusion for severe chronic pancreatitis: clinical, exocrine, and endocrine consequences during a 3-year follow-up.

The present investigation provides follow-up data (up to 36 months) of exocrine and endocrine pancreatic function, inflammatory activity, pain, and body weight in 23 chronic pancreatitis patients submitted to Whipple's procedure plus intraoperative Ethibloc occlusion of the remaining pancreatic duct system between January 1983 and February 1984. Clinically, Whipple's procedure plus intraoperative pancreatic duct occlusion resulted in almost complete and continuous cessation of pain as well as significant (p less than 0.05) increase in body weight. With regard to exocrine pancreatic function (Secretin-Pancreozymin test, plasma amino acid consumption test, Pankreolauryl test, fecal chymotrypsin determination), intraoperative pancreatic duct occlusion was shown to induce high-grade insufficiency and thus exocrine parenchymal atrophy in all patients. Simultaneously, the inflammatory process (represented by serum levels of trypsin, lipase, and pancreatic isoamylase) was terminated in all 23 patients. Endocrine pancreatic function, evaluated by serum levels of insulin and C-peptide measured under fasting conditions and subsequent maximal combined beta-cell stimulation as well as corresponding integrated hormone releases, was reduced by partial pancreas resection by about 50%, while there was no further impairment during the 36-month follow-up period in consequence of additional intraoperative pancreatic duct occlusion. Altogether, Whipple's procedure plus intraoperative Ethibloc occlusion of the residual pancreatic duct system seems suitable for termination of the inflammatory process and thus preservation of residual endocrine pancreatic function in chronic pancreatitis.