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Determination of the urinary excretion of sucrose after an oral dose has been used as a noninvasive test to measure gastric permeability in several clinical studies. Regarding different contact times of sucrose solution within the gastric mucosa, the present study investigates a possible influence of the gastric emptying rate on the sucrose permeability test. Urinary sucrose excretion and the gastric emptying rate of liquids using 13C-acetate breath test were determined in twelve healthy volunteers. Furthermore, in seven volunteers gastric emptying was accelerated by intravenous erythromycin and prolongated by oral anticholinergic propantheline in nine healthy controls. Breath samples were measured using infrared spectroscopy. The half-emptying time and Lag-phase were correlated with the urinary sucrose excretion. Erythromycin caused a significant (p = 0.02) reduction of the half-emptying time (median 35.0 min) compared with untreated controls (median 59.9 min), whereas propantheline significantly increased the half-emptying time (median 69.4 min, p = 0.01). After pharmacological increase of the half-emptying time the urinary sucrose excretion only slightly differs from the sucrose excretion of controls (median [range] 0.057 [0.034-0.106]% versus 0.031 [0.017-0.162]%), but there was an increase of urinary sucrose excretion in probands following reduction of the half-emptying time with erythromycin (0.077 [0.023-0.221]%. The present study shows that gastric motility has a possible influence on the sucrose permeability test. The sucrose permeability has to be interpreted critically concerning its clinical use especially in patients with altered gastric motility.

A 27-year-old woman was successfully treated with a highly dosed steroid therapy over several months during summer 1994 in the event of urticaria. In October 1994, when the patient was complaint free, therapy was abruptly terminated. In November 1994 jaundice, nausea and loss of appetite occurred. Biochemical results showed markedly elevated serum transaminases, negative hepatitis serology, normal immunoglobulins and inconspicious autoantibodies. Histology showed a florid hepatitis. In January 1995 the patient was hospitalized again in very low general and nutritional condition with a marked jaundice, high serum transaminases, insufficient liver synthesis function, established ANA(+), ASMA(+2) and normal immunoglobulins. This time histology painted out an active hepatitis going into liver cirrhosis. Evaluation in view of liver transplantation was carried out in this case of liver failure. At that time, tests showed a distinct gamma globulin fraction increase although the antibody pattern had remainded identical. An immunosuppressive therapy with azathioprine and steroids was decided upon under suspicion of an autoimmune hepatitis leading to a prompt positive response and therefore confirmation of the diagnosis. Complete biochemical remission was attained in April 1995 and a complete histological remission in March 1998.

During active inflammatory bowel disease (IBD) the respiratory burst of neutrophil granulocytes has been shown to be impaired using isolated circulating neutrophil granulocytes of patients with active disease. Using normal neutrophil granulocytes of healthy volunteers the present study examines the potential priming effect of sera of patients with active and quiescent IBD. The superoxide anion (O2-)-release of normal neutrophil granulocytes in response to N-formyl-methionyl-leucyl-phenylalanine (FMLP) has been investigated after incubation with sera of patients with active and inactive Crohn's disease and ulcerative colitis. O2(-)-release was measured using the superoxide dismutase inhibitable reduction of ferricytochrome c. The O2(-)-release of normal neutrophil granulocytes primed with sera of patients with inactive Crohn's disease (607.1 +/- 218.2 nmol/60 min, n = 10, p = 0.001) or cultured with sera of patients with quiescent ulcerative colitis (497.4 +/- 94.9 nmol/60 min, n = 3, p = 0.005) was significantly enhanced when compared with sera of normal controls (319.8 +/- 86.5 nmol/60 min, n = 10). There was no significant difference between priming with sera of patients with quiescent or active Crohn's disease (481.0 +/- 113.0 nmol/60 min, n = 5). Normal neutrophil granulocytes primed with sera of patients with active ulcerative colitis produce significantly larger amounts of O2- (809.5 +/- 256.9 nmol/60 min, n = 4, p = 0.001) when compared with sera of normal controls. The study shows that sera of patients with quiescent IBD as well as sera of patients with active disease have the potential to prime normal neutrophil granulocytes for an enhanced O2(-)-release in response to FMLP.(ABSTRACT TRUNCATED AT 250 WORDS)

The Crigler-Najjar-Syndrome type II is characterised by the decreased activity of the bilirubin-UDP-glucuronyltransferase. This fact leads to an increase of the indirect bilirubin to 6-10 mg/dl. The mode of hereditary transmission is autosomal dominant with variable penetrance. The age of manifestation varies from the first year to the second decade of life. The Crigler-Najjar-Syndrome type II of a 17-year-old girl is reported. The diagnosis was made on the basis of the pattern of laboratory parameters in combination with an uneventful morphology of the liver. Under treatment with Chlofibrat the decrease of the serum total bilirubin from 10.4 mg/dl to 2 mg/dl was achieved.

The case report on a 22-year-old female patient shows how the treatment with Imipenan/Cilastatin resulted in a severe intrahepatic cholestasis. The serum-bilirubin rapidly decreased after discontinuation of the antibiotic. The laboratory findings were no longer conspicuous four weeks after discharge from hospital.

The case report on an acute intrahepatic cholestasis caused by alcoholic intoxication in a 52-year-old medical laboratory assistant is given. In addition to extreme pathologic cholestasis parameters the increase of the tumor marker CA 19-9 was remarkable. By means of laparoscopy and histology, chronic fatty liver hepatitis due to alcoholic intoxication was found. The tumor marker CA 19-9 returned to normal following abstinence from alcohol parallel to the deline of the cholestasis parameters, which means the diagnostic importance of tumor markers in diseases with intrahepatic cholestasis is to be seen in relative terms.

Significantly decreased levels of serumcholinesterase (CHE) were found in acute Crohn's disease (= CD) (3.2 +/- 1.0 KU/L) and acute ulcerative colitis (= UC) (3.54 +/- 1.6 KU/L) as compared to patients with mild or quiescient disease (CD: 5.5 +/- 1.1 KU/L; UC: 5.59 +/- 0.94 KU/L) and healthy controls (5.69 +/- 1.3 KU/L). Suppression of CHE was most evident in Crohn's colitis (2.98 +/- 1.0 KU/L) and extensive UC (2.96 +/- 1.28 KU/L). Intraindividual comparison showed an increase of CHE-levels during treatment with steroids and salicylates. There was no significant correlation to the reduced bodyweight-levels in severe IBD. Best correlations were seen between CHE/albumin (CD: r = +0.61; UC: r = +0.73) and CHE/hematocrit (CD: r = +0.50; UC: r = +0.61) in severe inflammatory bowel disease. The results of a discriminant analysis showed that CHE-levels can predict the degree of activity correctly in the majority of patients with CD and UC. It is suggested that the decrease of serumcholinesterase reflects an inhibition of liver synthesis as an acute phase response-induced by endotoxins and cytokines.

Felson and Lessure 1964 (1) described varicosities involving the upper third of the esophagus in patients without portal hypertension. Several etiological factors causing these "downhill" varices, e.g. bronchogenic carcinoma, retrosternal thyroid adenoma or mediastinal fibrosis, have been described. Since September 1989 ectatic esophageal veins or "downhill" varices were diagnosed in nine patients with dysphagia and/or non cardiac chest pain. Intrathoracic masses as a possible cause of "downhill" varices could not be diagnosed in any of these patients. Endoscopy of the upper gastro-intestinal tract revealed spiral esophageal contractions as a potential sign of a esophageal motor disorder in seven patients. By means of esophageal manometry "nutcracker"-esophagus was seen in two patients and diffuse esophageal spasm in three patients. On the basis of these findings primary esophageal motor disorders should be considered as a possible cause of ectatic veins in the proximal esophagus and "downhill" varices.

We report the case of a 23-year old woman suffering from Crohn's ileocolitis for 14 years who died of a prolonged shock followed by hyperglycaemia. The post-mortem examination showed an acute pancreatitis. There was no hint for Crohn's disease of the duodenum or primary sclerosing cholangitis (PSC). Unexplained Pancreatitis coincident with Crohn's disease might be a possible extraintestinal manifestation of the disease. However such association remains speculative at the moment. Further studies based on morphological, functional, immunological and epidemiological data are required. Review of the literature and our own data show the necessity to look attentive for other causes of acute pancreatitis associated with Crohn's disease (PSC, pancreas divisum, drug induced-pancreatitis).

The development of hepatic encephalopathy and coma hepaticum in patients with acute gastrointestinal bleeding and hepatic cirrhosis is a serious problem. Since 1983 we perform a whole gut irrigation with mannite for cleansing the bowel via naso-gastric tube. The aim of this therapy is to reduce the severity of hepatic encephalopathy. The first 20 patients with the new therapeutic concept were compared with the last 20 patients with the prevailing therapy. We studied the effect of the new therapeutic concept as to reduction of hepatic encephalopathy and possible electrolyte loss. None of the patients in the mannite group had hepatic encephalopathy stage III or IV, whereas 75% of the patients without mannite showed clinical signs of stage III or IV. Serum potassium, sodium and chloride were not significantly different between both groups. In the group with mannite application no change in serum creatinine was observed, whereas in the other group a minute increase of serum creatinine was seen.

In a clinical study (1.1.1986-28.2.1988) the oro-cecal transit time of lactulose was studied in 45 patients with liver cirrhosis of different etiologies by hydrogen breath test. The results were compared to the transit time of 16 healthy volunteers. The oro-cecal transit time of patients with alcoholic cirrhosis (means = 154 +/- 29 min.) was significantly increased (P less than or equal to 0.001) while non alcoholic cirrhosis (means = 99 +/- 34 min.) did not differ from the control group (means = 98 +/- 16 min.) As an explanation of the increased oro-cecal transit time an alcoholic autonomic neuropathy (- greater than n. vagus) is discussed.