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History and Clinical Findings: A 54-year-old man was hospitalised because hypercalcaemia and associated renal failure were suspected. He had a history suggesting gastric ulcer, with nonspecific back and shoulder pain and spontaneously passed kidney stone. On admission the patient reported reduction in physical fitness, fatigue, headache and nausea without vomiting. Physical examination was unremarkable except for pain on pressure over the thoracic and lumbar vertebrae., Investigations: Hypercalcaemia of 3.9 mmol/l was found while parathormone was low. Serum creatinine concentration was 2.8 mg/dl. Malignancy was excluded after extensive tests. A florid gastric ulcer was demonstrated, together with Helicobacter pylori infection. Computed tomography revealed stippled calcifications in the kidneys., Treatment and Course: Renal function markedly improved, the hypercalcaemia disappeared and the parathormone level rose within four days of the administration of sodium chloride (2.51 daily of a 0.9% solution) and of furosemide (40 mg daily). Repeat questioning of the patient revealed that because of stomach pains he had for four years been taking up to 6 g calcium carbonate daily in the form of a prescription-free antacid. He was thereupon treated for a milk-alkali syndrome. Calcium concentration became normal, while renal function has remained slightly impaired a year later. The ulcer has healed without recurrence on eradication of the Helicobacter pylori infection with amoxicillin and omeprazole., Conclusions: The danger of some "over the counter" prescription-free medications should not be underestimated and patients should be routinely questioned about them. Absorbable antacids should no longer be taken in the treatment of peptic complaints now that effective antacids, H2-receptor antagonists and proton-pump inhibitors have become available.

Functional deficits of elderly patients are often not recognized during routine treatment in acute hospital care. In Germany, there are only limited experiences with the use of standardized assessment-scales in this health care setting. In this study, 112 patients were recruited for a very broad geriatric assessment focused on methodological and practical questions. There were 38.8% with deficits in the ADL and 12.6% with depressive symptoms. Many patients showed low motivational factors such as energy, efficacy and will. Geriatric syndromes such as malnutrition were also very common. In general, many patients in acute care hospitals have functional deficits which are not recognized by the physicians. For many patients, short instruments are sufficient for screening purposes. The effectiveness of a complete geriatric assessment depends mostly on the use of good selection criteria.

Upper gastrointestinal bleeding occurred in a 64-year-old woman who was being treated with 1,000 mg acetylsalicylic acid and three times 5,000 IU heparin daily previous to a planned embolectomy because of occlusion of a lower leg artery. Radiology demonstrated multiple areas of osteolysis of the left thorax which were interpreted as recurrence of carcinoma of the breast, treated by mastectomy and radiotherapy 15 years previously. Acute renal failure, recurring severe back and abdominal pain, paraplegia of both legs and finally death from circulatory failure were explained as having been caused by multiple embolisation in the course of arteriosclerosis or a paraneoplastic increase in clotting activity. Autopsy revealed complete occlusion of the descending thoracic aorta by a malignant fibrous histiocytoma which had been the site of multiple emboli of thrombotic material and tumour tissue to spleen, kidneys, liver, intestinal segments, spinal cord and the artery to the left lower leg. Adrenal metastasis and osteolysis of the ribs were due to the histiocytoma and not the previously known carcinoma of the breast.

The following is an outline of one typical case of chronic eosinophilia-myalgia syndrome (EMS). In 1987 a 62-year-old woman began taking L-tryptophan, 1.5 g nightly, due to sleeping difficulty. During the months preceding the appearance of EMS she continued to take L-tryptophan, derived from the biosynthetic production of the Japanese manufacturer "Showa Denko". She has suffered increasingly from severe myalgia and a proximal muscle weakness since July of 1989. In November, 1989 her white blood cell count measured 12.1 X 10(9)/l with 3.6 X 10(9) eosinophil cells/l. The bone marrow exhibited an increased granulopoesis and an extreme increase in the amount of eosinophil cells. The muscle biopsy specimen indicated an inflammation with perivascular distribution. The eosinophil cell count of the blood was quickly normalized via the introduction of prednisone over a short period. In the absence of further immunosuppressive therapy a slow improvement can be seen in the myalgia and in her general condition. Since the beginning of 1990 there has been a slow development of hyperpigmented scleroderma-like skin changes with distal distribution.

We report a case of human pentastomiasis in a 28-year-old man who emigrated to Canada from Nigeria in 1982 and died as a result of a motor vehicle accident in 1989. At autopsy, in addition to trauma, numerous small cystic nodules (3 to 9 mm in diameter) were discovered in the liver, pleura, lungs, and mesentery and under the intestinal and parietal peritoneum. The parasites were diagnosed as well-preserved, encysted Armillifer armillatus nymphs. Neither degenerative nor inflammatory granulomatous reactions were observed in the adjacent tissue. To our knowledge, this is the first reported case of human infection with encysted nymphs of A armillatus and the eighth reported case of pentastomiasis in North America.

63 inpatients with duodenal ulcer disease were treated with either depot-secretin or placebo. Two different secretin-regimens were used. In group I 18 patients were given secretin twice daily. 11 ulcers from a total of 19 ulcers healed within 3 weeks. In group II 23 patients were given secretin once daily. 21 out of 28 ulcers healed within 3 weeks. In the placebo-treated group 24 ulcers were observed in 22 patients. Of these 15 healed within 3 weeks. There was no statistical difference in the healing rate between the 3 groups. However, depot-secretin significantly improved typical symptoms. Analgetics were used less frequently. Serious side effects did not occur.

In 8 outpatients with duodenal ulcer the effect of a single dose of 50 mg pirenzepine is compared to a 3-7 days treatment with 2x50 mg. Basal and peptone-stimulated acid output is measured. A single dose of 50 mg pirenzepine reduced basal acid output by 39,9% and the stimulated acid secretion by 21,3%. Treatment for 3-7 days with 2x50 mg pirenzepine is significantly more effective. Basal acid output is reduced by 75,1% and stimulated acid output by 54,0%. No acid inhibition can be demonstrated 12 hours after the last drug administration. Basal serum gastrin levels are little but significantly increased after chronic treatment.

In six healthy male subjects the duodenum was perfused with phosphate buffer and peptone respectively via a double balloon tube. During peptone perfusion secretion of gastrin into the duodenal lumen and serum gastrin rose simultaneously and significantly compared with buffer control. There was a significant but delayed increase of gastric acid secretion. 60 % of the gastrinlike immunoreactivity in duodenal perfusates corresponded to gastrin 1-34 and 40 % to gastrin 1-17 when separated by starch gel electrophoresis and gel filtration.

Gastrin 1--17 protected against physiological proteolysis does not change gastric acid secretion and serum gastrin level even if present in the duodenal and gastric lumen in excessive amounts. Consequently gastric juice gastrin has no local effect on the parietal cell. There is no measurable resorption of gastrin from the gastric or duodenal lumen. Gastrin 1--17 does not liberate endogenous gastrin from the antral and duodenal mucosa. Thus, an indirect systemic influence of gastric juice gastrin on the function of the parietal cell can be excluded. Gastric juice gastrin seems to be a waste-product of a bidirectional G-cell secretion. Gel filtration and starch block electrophoresis revealed considerable amounts of immunoreactive material in the duodenal perfusate resembling gastrin 1--34. Thus, the duodenal G-cells seem to liberate gastrin into the duodenal lumen.

Various amounts of hydrochloric acid (50, 100 and 200 ml) of two different concentrations (70- and 140 mmol/l) were rapidly instilled into the duodenum of eight healthy subjects and five duodenal ulcer patients. Secretin, gastrin and bicarbonate output were measured. Secretin release and bicarbonate secretion are dependent on acid load and not on acid concentration. There is a linear correlation between the amount of acid instilled into the duodenum and pancreatic bicarbonate output. After duodenal acidification duodenal ulcer patients released equal amounts of secretin and secreted as much bicarbonate as healthy subjects.

In 16 healthy male subjects the effects of natural and synthetic secretin on the function of the exocrine pancreas were compared. Following; stimulation with secretin in all cases pancreozymin was injected to ascertain normal pancreatic secretory capacity. The methods applied corresponded to those used in the multicenter study of the European Pancreatic Club. No significant differences were found between the results concerning volume of secretion, maximal bicarbonate concentration, maximal bicarbonate output and enzyme secretion rates after stimulation with natural and synthetic secretin, respectively. It is concluded that the synthetic peptide can be utilized in the same way as the natural product in the secretin-pancreozymin-test.

H2-receptor-antagonists inhibit pentagastrin-stimulated acid secretion for a longer period than basal secretion. Anticholinergic drugs and pirenzepine are less effective and act differently by reduction of volume. Acid concentration is reduced to 95% by cimetidine compared to 20% by atropine and pirenzepine. By increasing electrical vagal stimulation there is a decreasing effect of cimetidine. In contrast, atropine and pirenzepine inhibit vagally transmitted acid secretion by about 45%, even when vagally stimulated acid secretion amounts to more than 50% of the pentagastrin-stimulated secretion. These results support the hypothesis of histaminergic and cholinergic receptors in man.

Studies on isolated gastric glands and parietal cells suggest that calcium plays a role in the stimulus-secretion coupling of acid secretion. To determine which stimulants of human gastric secretion depend on calcium-mediated receptors, the effect of the calcium antagonist verapamil on gastric secretion was studied. Gastric secretion was stimulated by intravenous infusion of 50 micrograms/kg/h bethanechol, 10 micrograms/kg/h impromidine, 0.5 micrograms/kg/h pentagastrin, 4 mg/kg/h Ca++, or by sham feeding. Each type of stimulation was tested twice in six healthy subjects, alone and together with verapamil. Verapamil was administered as an intravenous bolus of 200 micrograms/kg followed by an infusion of 150 micrograms/kg/h. Six subjects had 2 step tests in which 4 doses of pentagastrin were administered consecutively in increasing dosage. Pentagastrin was given either alone or superimposed on a verapamil bolus followed by an intravenous infusion. Verapamil left gastric secretion stimulated by bethanechol, impromidine, or sham feeding unaffected. During Ca++ infusion verapamil caused a significant drop in volume, but not acid output. Pentagastrin-stimulated acid and volume output were significantly inhibited by intravenous verapamil, the inhibition resembling an uncompetitive pattern. Pentagastrin-stimulated gastric secretion was also inhibited by the calcium antagonist diltiazem. The results confirm earlier reports that calcium is involved in the stimulus-secretion coupling of the human gastric mucosa. Calcium appears to mediate the stimulation of acid secretion by gastrin.

Gastrin is a peptide hormone originating from G-cells of the antrum, the duodenum and the proximal jejunum. From extracts of gastrinomas and from sera of hypergastrinaemic subjects several gastrin molecules could be isolated which were nominated as "mini gastrin" (G13), "little gastrin" (G17), "big gastrin" (G34) and "big big gastrin". Antisera used for radioimmunological gastrin determinations should be characterized with respect to their specificity, as differeing affinity towards the various gastrins and towards CCK-PZ influences the results of the assay and thus the comparability with values of other laboratories. Gastrin is released by direct vagal stimulation of the antral G-cells and by local chemical and physical stimuli in the antrum and duodenum; probably an oxynto-pyloric reflex also exists. Gastrin stimulates in physiologic doses gastric acid secretion and, as shown in dogs and cats, reveals a trophic action on parietal cell growth. H+-secretion and gastrin release are connected by a feed back mechanism, insofar, as a decrease of intragastric pH below 3 inhibits endogenous gastrin release. Hypergastrinaemia has been demonstrated in patients with gastric anacidity or hypo-secretion, benigne pyloric stenosis, uraemia, short bowel-syndrome, gastric and duodenal ulceration and in patients with gastrinomas (Zollinger-Ellison-syndrome). Hypergastrinaemia in combination with hypersecretion exhibits clinical significance in patients suffering from Zollinger-Ellison-syndrome or excluded antrum syndrome which are due to autonomous gastrin release. The differential diagnosis between these syndromes and other diseases, in which hypergastrinaemia is not associated with gastric hypersecretion, can be achieved by several tests using calcium infusion or intravenous application of secretin and glucagon. The significance of elevated gastrin levels in patients with duodenal ulceration (DU) is pointed out. In DU-patients basal and postprandial hypergastrinaemia has been observed. In these patients gastrin release from gastric and extragastric sites is increased. In these patients hypergastrinaemia due to extragastric gastrin release could cause gastric hypersecretion at a time, when the stomach already has emptied. Furthermore parietal cell hyperplasia could be the result of chronic hypergastrinaemia.

The effectiveness of omeprazole (20 mg orally each morning) or ranitidine (150 mg orally twice daily) in the treatment of gastric ulcer was compared in 184 out-patient in a randomized, endoscopically controlled multi-centre double-blind ("double dummy") trial. Healing rates with omeprazole after two, four and eight weeks were 43, 81 and 95%, respectively, those with ranitidine were 45, 80 and 90%, a statistically not significant difference. Independently of medication, small ulcers (less than 8 mm diameter) healed more quickly than larger ones. Ulcers in the body of the stomach responded poorest to both drugs. Smoking had no statistically significant effect on healing rate. Omeprazole and ranitidine had similarly favourable effects on symptoms. Neither side effects nor changes in biochemical parameters could be ascribed to omeprazole. Both drugs had equivalent effects on the healing of gastric ulcers in the stated dosages.

Gastrin analogues are known to stimulate acid secretion with higher potency the more amino acids prolong the peptid chain towards the N-terminal end. In order to compare the response of pentagastrin (Gastrodiagnost, Merck, Darmstadt) and Heptagastrin (HOE 293, Hoechst AG, Frankfurt/M.) in 12 healthy subjects the two peptides were given subcutaneously in doses of 1 microgram/kg, 3 microgram/kg and 6 microgram/kg body weight. Additionally in 8 subjects 1 microgram/kg/h and 2 microgram/kg/h of the gastrins were given intravenously. Gastric content was aspirated under basal and stimulated conditions in portions of 15 minutes, volume (ml) and acid concentration (meq/l) of each fraction was measured and acid secretion (meq/90'), BAO and PAO were calculated. As compared with pentagastrin the dose response curve was shifted to the left, when heptagastrin was given subcutaneously. The amount of acid secretion over a time period of 90 min. was about 17% higher after heptagastrin than after pentagastrin. There was no difference between the peak acid outputs (PAO). Stimulation of acid secretion was prolonged after heptagastrin as compared to pentagastrin. Both gastrins acted similarly on all parameters measured when administered intravenously. Side effects as nausea and dizziness were observed in two subjects of each group.

Results obtained with stools preserved in a simple, stable and relatively nontoxic fixative (SAF) composed of sodium acetate, acetic acid and formalin, suggest that this fixative is a suitable alternative to other fixatives for the preservation and recovery of intestinal parasites by diphasic concentration methods and permanent staining.

Gastric acid secretion and gastrin-like immunoreactivity in serum and gastric juice of six healthy subjects were measured during an increasing intravenous administration of pentagastrin and compared with basal values obtained during intravenous infusion of 0.9% NaCl. Gastric acid secretion and gastrin-like immunoreactivity in the serum increased significantly during infusion of pentagastrin. Gastrin-like immunoreactivity released into the gastric lumen was unchanged from the NaCl control. This is a further evidence for direct secretion of gastrin into the lumen of the stomach from antral G-cells.

Atropine and an eightfold greater amount of pirenzepine inhibit pentagastrin-stimulated secretion to nearly the same extent (70-75%). Neither drug influences acid concentrations markedly (18%). Atropine and pirenzepine decrease the potassium concentration of gastric juice. By increasing electrical vagal stimulation the inhibitory effect of cimetidine decreases. In contrast, inhibition of vagally stimulated secretion by pirenzepine or by atropine averages 45%, when vagally stimulated secretion amounts to more than 50% of the pentagastrin-stimulated secretion. Thus pirenzepine inhibits gastric secretion similarly to atropine. These results support the hypothesis of a histamine and a cholinergic receptor.

Using Gastrin 14-17 as immunogen it was possible to raise an antiserum, which showed a high sensitivity for the C-terminal octapeptide of CCK in a radioimmunoassay with 125J-gastrin as tracerhormon. High immuno-reactivity could be demonstrated in the grey and white matter of the human cortex as well as in the putamen and nucleus caudatus using this assay. By comparing the unknown brain substance with different peptides in different physico-chemical systems, the brain substance was shown to be homogenous and being similar to CCK-8.

To determine the average diameter and the upper normal limit of the common bile duct in healthy man, 830 blood donors were examined by ultrasound. The mean diameter was 2.5 +/- 1.1 mm (SD) at the porta hepatis and 2.8 +/- 1.2 mm (SD) at the widest point, the regression coefficient between both diameters being r = 0.84. None of the healthy subjects had a diameter larger than 7 mm at any site, and in 95% of all subjects the diameters were less than 4 mm at both sites of measurement. The diameters were significantly correlated with age (r = 0.16) and weight (r = 0.11), but not with sex, height, and body surface area. In 73 patients with cholelithiasis and in 55 patients after cholecystectomy, all of whom lacked clinical or laboratory signs of biliary obstruction, the average diameters at the porta hepatis were 3.8 +/- 2.0 mm and 5.2 +/- 2.3 mm, and at the widest point 4.8 +/- 2.2 mm and 6.2 +/- 2.5 mm, respectively. It is concluded that a common bile duct with any sonographic diameter larger than 4 mm should be followed closely and evaluated further with clinical examinations such as intravenous cholangiography unless cholecystectomy has been performed.

185 patients with endoscopically proven duodenal ulcers were randomly allocated to treatment with either famotidine 40 mg nocte, 20 mg bid, 40 mg bid or ranitidine 150 mg bid for 2-8 weeks in a prospective double-blind study. The four groups were similar with regard to age, sex, duration of ulcer disease, smoking habits etc. After 2 weeks treatment 28/42 patients (66.7%) healed on famotidine 40 mg nocte, 24/42 patients (57.1%) on famotidine 20 mg bid, 26/41 patients (63.4%) on famotidine 40 mg bid and 28/43 patients (65,1%) on ranitidine 150 mg bid. The corresponding healing rates after 4 weeks were 90.5%, 83.3%, 90.2% and 93%, respectively. After 8 weeks more than 93% of the patients had healed ulcers. At each time there was no statistical difference between the different famotidine regimens and the ranitidine group. All treatments were well tolerated and severe adverse events were rare. Famotidine 40 mg at night, therefore, appears to be as good as conventional ranitidine.

Inhibition of acid secretion was investigated in 5 patients with Zollinger-Ellison syndrome and 12 patients with duodenal ulcer after administration of 200 mg cimetidine alone and combined with 50 mg methanthelinebromide. A preinvestigation of 5 patients had not shown any significant decrease of acid secretion after 50 mg methanthelinebromide alone. Compared with a single dose of 200 mg cimetidine, combined drugs' use (200 mg cimetidine and 50 mg methanthelinebromide) led to significant increase of inhibition of secretion both as regards degree and duration. In 6 patients with duodenal ulcer basal secretion of more than 2.0 mmol H+/h 200 mg cimetidine led to inhibition of secretion by 91.4% over 120 min compared to 96.4% over 225 min after combined administration. Similar results were obtained in 6 patients with a basal secretion of less than 2.0 mmol H+/h.

The diagnosis of benign recurrent intrahepatic cholestasis was made in a 40 year old female. Seven episodes of jaundice persisting up to 6 months in lengths lead to 3 laparotomies, numerous peritoneoscopies and needle biopsies of the liver. Elevation of conjugated serum bilirubin and alkaline phosphatase levels and histopathological confirmation of intrahepatic cholestasis without cholangitis were the main characteristics during the episodes of cholestatic jaundice. However, hepatic histology and liver function were normal in remission periods. Drug induced cholestasis was ruled out by careful history. A sister also suffered from 4 episodes of intrahepatic cholestasis. The etiology of the disease is probably of a genetic origin. The pathogenesis remains unclear. There is no specific treatment to prevent or shorten the occurrence of cholestatic episodes. The patients are advised to avoid pregnancy and oral contraceptives, since both will induce icteric phases.

Dientamoeba fragilis was found in 4.2% of approximately 43,000 individuals who submitted stools for parasitological examination during 1970 to 1974. The parasite was more frequently found in the younger age group (less than 20 years) than in older age groups, and more often in females than in males. Symptoms in 255 of patients in whom D. fragilis was the only parasite found and for whom detailed symptoms had been supplied, included: diarrhea, abdominal pains, anal pruritus, and loose stools. Analysis of mixed infections of D. fragilis with intestinal helminths suggests that such infections are random except for the combination of D. fragilis and Enterobius vermicularis. This combination occurred 9 times more often than theoretically expected. Daily periodicity and distribution of D. fragilis within stools of one patient were studied over a period of 6 months. More than twice as many organisms per ml of stool were present in the last than in the first portion evacuated. The total number of organisms excreted fluctuated markedly from day to day.

50 mg pirenzepine inhibit basal acid secretion by 39.9% and peptone-stimulated acid output by 21.3%. The percentage of inhibition is nearly doubled if the same dose is given after a treatment with 50 mg pirenzepine twice daily for 3 to 7 days. No acute effect on serum gastrin levels can be demonstrated by a single dose of pirenzepine. After pretreatment only a small increase of basal gastrin levels is observed, serum gastrin does not change during stimulation. On the bases of these results the effect on ulcer healing by high doses of pirenzepine is probably due to a much more pronounced acid inhibition. One reason for stronger inhibition of acid secretion after pretreatment with pirenzepine is probably accumulation of the drug, other reasons may be distribution space or receptor binding. The effect of anticholinergic drugs on serum gastrin concentrations is probably dose-dependent.

Histamine H2-receptor antagonists metiamide and cimetidine were used in the treatment of severe peptic ulceration in Zollinger-Ellison syndrome. The ulcerations were completely healed in all four patients after treatment lasting from six weeks to four-and-a-half-months. Two patients developed recurrent ulcer after the treatment had stopped, but responded to a second course. One patient developed hepatitis B during cimetidine treatment and it is possible that the course of the hepatitis was unfavourable affected by cimetidine. But no other side effects were noted nor was there a significant change in basal serum-gastrin concentration or an increase in H+ secretion. Total gastrectomy remains the treatment of choice in Zollinger-Ellison syndrome, but cimetidine should be considered if the patient refuses operation or operation is not feasible because of a poor general state.