The association of duodenal diverticula and pancreatitis is rare. Various types of such diverticula are reviewed, especially intra- and extraluminal Vaterian diverticula in which common and pancreatic duct terminate. The pathogenesis of the pancreatitis in case of interposed Vaterian diverticula is thought to be mechanical by means of the creation of a closed Vaterian pouch in which higher pressures produce reflux of bile and pancreatic enzymes. Two patients with this particular type of duodenal diverticula are presented.
In an isolated rat liver perfusion system the effects of normothermal ischemia on hepatic functions were investigated. After 30 minutes of anoxy bile production and BSP elimination capacity of the liver are significantly reduced. The quantity of secreted "ascites" from the surface of the liver several times high after anoxic damage, while oxygen consumption, portal venous pressure and ammonia elimination do not differ significantly from the controls. Pretreatment with insulin plus glucose, isoproterenol, hypoxanthine, chlorpromazine and glucagon (5 micrograms/100 g i.v., or 0.2 mg/100 g s.c.) does not reduce noticeably the normothermal anoxic lesion of the liver Glucagon (50 micrograms/100 g i.v.), allopurinol, dibenzyline, ATP-MgCl2 and aspartic acid enhance significantly the ischemia-tolerance of liver in vitro.
Perfusion of mouse pancreatic slices revealed that continuous exposition with cholecystokinin-pancreazymin (CCK-PZ) provokes an initially high peak of amylase secretion, which is followed by a slow decline in enzyme discharge. A return to the basal secretory level is noticed after about 45 min. Repeated pulse stimulations with CCK-PZ result in a more efficient stimulation of pancreatic amylase release, compared to a continuous stimulation. In the presence of CCK-PZ for 45 min, as well as during a post-stimulatory period of 45 min, a significant depression of L-(U-14C) leucine incorporation into amylase as well as total protein is recorded. In conclusion, in vitro incubated mouse pancreatic slices thus seem to be unable to increase their rate of protein synthesis during and after stimulation of secretion.
In six healthy volunteers the interdigestive motor activity and the secretory pattern were recorded in the duodenum by open tip catheters and intraluminal titration, respectively. The duodenal part of the interdigestive myoelectric complex (IDMEC) was regularly associated with a significantly increased alkali load to the duodenum amounting to 2.4 +/- 0.4 mmol per IDMEC. Thus, the intestinal "housekeeper" function of the IDMEC may be brought about by a coupled action of propagated motility and flushing secretion.
Fasting gastrinemia in cirrhotics (48.35 +/- 2.77 pg/ml) was higher than in normal controls (32.93 +/- 0.75 pg/ml; P less than 0.001). After insulin-induced hypoglycemia, the mean increase of gastrin above basal level was 42.29 +/- 1.92 pg/ml in controls and 10.85 +/- 5.05 pg/ml in cirrhosis (P less than 0.001). BAO was 2.53 +/- 0.36 mEq/h in controls and 0.42 +/- 0.004 mEq/h in cirrhotics (P less than 0.001). After i.v. insulin, TAO was 8.42 +/- 0.72 mEq/h in controls and 3.06 +/- 0.26 mEq/h in cirrhotics (P less than 0.001). The authors suggest that the lack of an adequate gastrin and acid response to the hypoglycemic stimulus in cirrhotics might be accounted for by a decreased insulin sensitivity.
The results of 99 histologically examined liver biopsy samples--14 of them also examined under the electron microscope--taken from 68 insulin-treated diabetic children of both sexes at an age from 2-14 years. most of them with long-standing diabetes, are presented, thus giving a survey of morphologic liver findings of diabetes mellitus in this age group. Apart from metabolic changes, such as amount of fat and glycogen storage--including the nuclear glycogen of the liver--secondary diseases of inflammatory nature were found to play a prominent role in one third of the children. There are definite correlations with the degree of metabolic decompensation, demanding preventive and therapeutic measures.
Encephalopathic patients with cirrhosis of the liver consistently showed elevated levels of the aromatic amino acids, phenylalanine, tyrosine and free tryptophan as well as methionine in serum, whereas levels of the branched chain amino acids, valine, leucine and isoleucine, were depressed. Comatose patients with fulminant hepatitis had markedly elevated levels of all amino acids, the results being greatly different from those of cirrhotic patients. Molar ratios of (valine + leucine + isoleucine)/(phenylalanine + tyrosine) decreased both in cirrhotics with and without encephalopathy and in cases with fulminant hepatitis. Infusion of a commercially available L-amino acid solution in a cirrhotic patient induced a strikingly abnormal aminogram documented in hepatic encephalopathy. Therefore, effects of branched chain amino acid infusion on the deranged amino acid pattern were primarily studied for the purpose of improvement in hepatic encephalopathy by normalization of serum amino acid patterns. Elevated levels of the aromatic amino acids and methionine could be apparently depressed in a cirrhotic patient by this type of infusion but not in a case of fulminant hepatitis probably because of the poor utilization of these amino acids in severely impaired liver.
For a long time, it has been assumed that stagnation of active estrogens in the blood gives rise to liver injury and causes a severe inflammatory process in the liver as well as affecting the clinical course of chronic aggressive hepatitis in women. During reproductive years, estrogen production, as gaged by the values of urinary excretion, follows a cyclic pattern. As the menopause is approached, urinary excretion of estrogens gradually diminishes and the cyclic fluctuation becomes more shallow. The titer continues to fall progressively in the post-menopausal years although some estrogen may be found even in aged women. Even though it must be assumed that estrogens are rarely produced in bilaterally ovariectomized women, chronic aggressive hepatitis is rather frequently encountered in practice in women after ovariectomy. To find a solution to the question of whether stagnation of active estrogen in the blood actually gives rise to liver injury, estrogen levels in the blood must be estimated in these patients. It will be desirable to estimate not the metabolites of estrogens in the urine but the estrogens or estrogenic substances themselves in the blood. The authors have estimated estrogens in the blood by means of radioimmunoassay and revealed a decrease in quantity of the estrogen values in the blood. Therefore, it can be stressed that the lack of estrogens in the blood must be taken into consideration because it has been pointed out that estrogens exert some form of liver-protecting influence against infection as well as the protracting factors of hepatitis.
Immunoreactive serum gastrin from portal and peripheral veins was determined in five controls and in five cirrhotic patients with indwelling portal catheters in basal conditions, during and after 30 min arginine infusion, in order to assess whether the human liver is involved in gastrin metabolism. A significant difference was found between portal and peripheral gastrin concentrations in controls at 0, 60 and 90 min; no significant differences were found in cirrhotics. Our findings support the hypothesis of an at least partial breakdown of endogenous gastrin in the human liver.
A 73-year-old female patient developed beside aortic stenosis angiodysplasia in the caecum, which gave rise to serious, repeated intestinal bleedings. As a result, the patient was admitted to hospital 32 times. Over a period of 8 years she was given 178 litres of blood. The vascular disorder which was the source of bleeding, was detected by mesenterial angiography. After resection of the colonic section concerned, the bleeding stopped. The diagnosis of angiodysplasia of the caecum was confirmed by pathological examination.
Intravenous administration of endotoxin in doses, 1.0 mg/kg, 0.1 mg/kg or 0.01 mg/kg caused activation (in the sense of nucleolar RNA synthesis) of the lymphocytes in peripheral blood, kidney and liver in rabbits. The evaluation of the ratio of lymphocyte count to the number of organ tissue cells leads to the conclusion that the accumulation of endotoxin activated lymphocytes occurs in liver.
Twelve patients with Crohn's disease (C.D.), in whom there was no improvement of symptoms and signs under protracted corticosteroid and salicylazosulphapyridine medication, were treated with 1 000 mg metronidazole (M.) daily. Crohn's Disease Activity Index (CDAI) was used as a criterion of therapeutic response. Seven patients showed improvement of symptoms with a concomitant fall of the CDAI from 300 +/- 84 to 56 +/- 32 (mean +/- SD) after 10 to 45 days. In one patient, therapeutic success was judged to be doubtful, a negative result being obtained in 4 patients. During follow-up, which was maximally 21 months, patients failed to relapse while receiving a maintenance dose of 250 and 500 mg of M. per day. -- Judicious attempts at drug withdrawal were undertaken during the first 6 months but were invariably followed by a relapse. -- Metronidazole given over a protracted period did not give rise to side-effects. -- A reduction of anaerobic bacterial invaders of the intestine is suggested to underlie the favourable therapeutic effect of M.
In six healthy volunteers pure pancreatic juice was obtained by endoscopic cannulation of the main pancreatic duct. Following a 20-min basal period, secretin (0.03 CU/kg, h) was intravenously infused alone for 20 min and then with caerulein 15 ng/kg, h for further 20 min. From a basal level of 28 +/- 13 mu mol/5 min, secretin by itself significantly increased pancreatic bicarbonate to 182 +/- 24 mu mol/5 min. A further significant two-fold increase to 396 +/- 50 mu mol/5 min was observed during caerulein. The increment in plasma secretin of 2.1 +/- 0.3 pmol/l is comparable to the rise that may be observed post-prandially. It is concluded that secretin in combination with cholecystokinin may indeed play a physiological role in the regulation of duodenal pH.
