Biomedical subjects
Publications and source records attributed to M van Blankenstein.
Five patients suffered from dysphagia due to breast carcinoma. Several aspects of diagnosis and therapy are discussed. It is recommended to start the therapy based on the clinical diagnosis and not to wait until the diagnosis is histologically confirmed.
Endoscopic papillotomy may not be possible in patients who have previously undergone gastric surgery. We describe the successful treatment of such a patient with ultrasound-guided, percutaneous transhepatic biliary drainage, followed by balloon dilatation of the sphincter of Oddi and extracorporeal shock-wave lithotripsy. Combinations of new treatment forms may be necessary and effective when single forms of treatment fail.
Recently extracorporeal shockwave lithotripsy (ESWL) has been introduced as a nonoperative treatment for gallstone disease. Except for lung damage, no significant adverse effects of ESWL of gallbladder stones have been observed in animals. In clinical use ESWL of gallbladder stones is now confined to 15% to 30% of symptomatic patients. To achieve complete stone clearance, ESWL of gallbladder stones must be supplemented by an adjuvant therapy. ESWL of bile duct stones is highly effective and can be considered in patients in whom primary endoscopic or surgical stone removal fails. Second generation lithotriptors allow anesthesia-free (outpatient) treatments, but the clinical experience with most of these ESWL devices is still limited. The likelihood of gallbladder stone recurrence is a major disadvantage of ESWL treatment, which raises the issue of cost-effectiveness. ESWL for cholelithiasis is a promising treatment modality with good short-term and unknown long-term results.
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A patient with Crohn's disease of the colon developed severe abdominal pain after salicylicazosulfapyridine and after disodium azodisalicylate therapy. Raised serum and urinary amylase levels were found after disodium azodisalicylate. Rechallenge with disodium azodisalicylate caused a recurrence of the pain and of the elevated amylase levels. The time course of these episodes was compatible with 5-aminosalicylate-induced pancreatitis.
Protein-losing gastroenteropathy is a well-recognized entity in systemic sclerosis, for which several mechanisms have been postulated. Acquired intestinal lymphangiectasia as a cause of increased intestinal protein loss has not previously been described in the literature. We report the first case of acquired intestinal lymphangiectasia in systemic sclerosis.
Using autoradiography after 1 h of pulsed labeling with tritiated thymidine in endoscopic biopsy specimens from normal-appearing mucosa, cell proliferation was determined at six predetermined sites of the whole colon in patients with neoplastic disease of the large bowel and was compared with that of subjects without macroscopic colonic pathology. The labeling index (the percentage of cells incorporating [3H]thymidine) was 8.6 +/- 0.5 (mean +/- SEM) in 13 patients with colon carcinoma (p less than 0.001 vs. 16 control patients whose labeling index was 4.9 +/- 0.2) and 9.1 +/- 0.4 in 11 patients with a large adenoma in the colon (p less than 0.001 vs. controls). Twenty-one patients with one or more small adenomas (diameter less than 1 cm) had a moderately increased cell proliferation compared with controls (labeling index 6.2 +/- 0.3, p less than 0.02 vs. controls). In patients with neoplastic disease an enlargement of the proliferative compartment was found, whereas 6 patients with Crohn's colitis had values for labeling index and a distribution of labeled cells along the crypt comparable to that of control subjects. An increased cell proliferation was found along the entire colon under each of the neoplastic conditions studied. These findings indicate that although neoplastic lesions develop in a limited area of the colon, the entire large bowel may be at risk for tumor growth.
The results of the secretin-CCK test were compared with the histological findings of pancreatic tissue resected in 25 patients with chronic pancreatitis. Secretin-CCK test results were interpreted with the use of discriminant analysis, yielding a quantitative score for each patient. Histological findings were recorded according to a semiquantitative scale. Fairly high correlation coefficients were found between secretin-CCK test results and severity of acinar atrophy and small dilatation. These findings emphasize the importance of the secretin-CCK test for diagnostic and follow-up purposes in chronic pancreatitis.
A method for disinfecting fibreoptic endoscopes with povidone-iodine and a simple cleaning device, consisting of a curved glass pipe and a peristaltic pump is described. If properly employed the system produces satisfactory results.
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Using cutaneous electrodes an electrogastrographic study was made of gastric myoelectrical activity in both the fasting and postprandial states in 48 patients with unexplained nausea and vomiting and in 52 control subjects. A gastric emptying study, using a radio-labelled solid phase meal, was carried out in 30 of these 48 patients. A follow up study was done after one year. In 48% of the patients abnormal myoelectrical activity was found which was characterised by: instability of the gastric pacemaker frequency; tachygastrias in both the fasting and postprandial states; the absence of the normal amplitude increase in the postprandial electrogastrogram. This last characteristic was correlated with a delayed gastric emptying of solids. The present study shows that with electrogastrography in a heterogeneous group of patients with unexplained nausea and vomiting a subgroup can be discerned with abnormal myoelectrical activity. Our findings suggests that this abnormal myoelectrical activity is related to these symptoms.
Discriminant analysis was used to interpret the results of the secretin-cholecystokinin (CCK) test in the diagnosis of chronic pancreatitis. An allocation rule based on the use of two test variables--mean chymotrypsin concentration and peak bicarbonate output--was constructed to distinguish between 63 patients with chronic pancreatitis and 68 patients without organic disease. These latter patients had signs and symptoms similar to those of the patients with chronic pancreatitis and were used as controls. The allocation rule was applied to a larger set of individuals, including 105 patients with various other diseases. The sensitivity of the test was 83%, and the specificity was 89%. With a prevalence of chronic pancreatitis of 27% in this set of individuals, the positive predictive value was 73%, the negative predictive value was 93%, and the accuracy rate 87%. This diagnostic performance of the secretin-CCK test gives the test a meaningful place in the examination of patients suspected of having chronic pancreatitis.
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The effects of intragastric prostaglandin E2 (PGE2) on the occurrence of acute GI hemorrhage in intensive care patients were investigated in a prospective, double-blind, placebo-controlled study. Ninety patients with two or more risk factors (major surgery, multiple trauma, respiratory insufficiency, renal insufficiency, jaundice, hypotension, peritonitis, sepsis) were randomized for treatment with either PGE2 (0.5 mg) or placebo, administered every 4 h via a nasogastric tube. Blood loss in gastric aspirates was measured by 51Cr-erythrocyte labeling and a peroxidase test (orthotolidine). Of 57 patients who could be evaluated, 29 received PGE2 and 28 received placebo. Hemorrhage occurred in nine PGE2 patients and 13 placebo-treated patients, not a significant difference. The occurrence of hemorrhage was related to the number of risk factors, and GI hemorrhage was rarely the major factor determining mortality. Results of the orthotolidine test were not positively correlated with those of erythrocyte labeling, indicating that peroxidase tests should not be relied upon to detect blood in gastric aspirates.
A double-blind controlled trial was conducted in which the efficacy of cimetidine in a dosage of 20 mg/kg/24 h in preventing upper gastrointestinal hemorrhage was tested in 34 critically ill patients on assisted ventilation. In 28 patients, 14 on cimetidine and 14 on placebo, gastric pH measurements and blood loss measured by 51Cr-labelled erythrocytes could be analyzed. Although cimetidine produced a markedly lower number of days with a gastric pH below 3.5 (17.4% vs. 72.2%) 5 patients on cimetidine bled as against 1 on placebo. These results do not suggest that cimetidine was effective in preventing stress-induced upper gastrointestinal bleeding.
Recurrent upper gastrointestinal haemorrhage arising from the pancreatic duct presents diagnostic difficulties. Bleeding can be secondary to pancreatic disease (pancreatitis, pseudocysts) or vascular disorders (aneurysms of the splanchic arteries). Of the 5 cases reported here, 3 involved a ruptured aneurysm of the splenic artery and 2 chronic pancreatitis. Attacks of colicky pain in the left epigastric region associated with haematemesis and/or melaena were characteristic symptoms. Pancreatectomy controlled the bleeding in 4 and ligation of the splenic artery and the pancreatic duct in one. Fifty-five patients with similar pathology have been previously reported, suggesting that this syndrome should be borne in mind when gastrointestinal haemorrhage of obscure origin is encountered. If routine endoscopy does not reveal the site of the haemorrhage and there are no signs of cholestasis, endoscopic retrograde pancreatography (ERP) and selective coeliac arteriography should be performed to evaluate the possibility of haemorrhage from the pancreatic duct. Surgical management depends on the site of the causative lesion.
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