Stellar cross sections for 33S(n, alpha )30Si, 36Cl(n,p)36S, and 36Cl(n, alpha )33P and the origin of 36S.
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Biomedical subjects
Publications and source records attributed to R Steininger.
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OBJECTIVE: Interventional treatment of biliary sludge in liver transplant recipients includes transhepatic biliary drainage and saline irrigation, catheter chemolysis and/or basket extraction, and endoscopic intervention. The purpose of this study was to compare these interventional procedures with oral chemolysis and with surgical treatment of biliary sludge in order to evaluate the effectiveness of interventional procedures as an alternative to surgery in the treatment of this complication. MATERIALS AND METHODS: We retrospectively evaluated the outcome of several forms of treatment for biliary sludge occurring after liver transplantation in 49 cases. Treatments included oral chemolysis with chenodeoxycholic acid (n = 35), percutaneous transhepatic biliary drainage (n = 13) followed by irrigation with heparinized saline solution (n = 4), intraluminal chemolysis with glycero-octanoate-carnosine and bile salts-EDTA (n = 3) and/or basket extraction (n = 5), and endoscopic intervention (n = 2) or surgery (n = 26). Oral chemolysis was attempted in all cases of biliary sludge if no other complications were present. If this conservative treatment failed and the sludge was limited to the main bile ducts, interventional procedures were attempted. Surgical removal of the sludge (n = 15) or retransplantation (n = 5) without any attempt at prior nonsurgical treatment was performed if concomitant complications were present (n = 14) or if the extent of the sludge was considered too time-consuming for an interventional attempt (n = 6). The six patients in whom nonsurgical treatment failed underwent surgery. Treatment was considered successful if cholangiograms obtained after therapy showed no more evidence of sludge. Treatment was considered a failure if biliary sludge was shown after therapy by means of cholangiography, surgery, or autopsy. RESULTS: Complete disappearance of biliary sludge as a result of oral chemolysis was achieved in 14 (40%) of 35 cases. Interventional procedures were performed in 15 of the patients in whom oral treatment failed. After percutaneous transhepatic biliary drainage, the sludge was successfully removed by chemolysis with glycero-octanoate-carnosine in three cases, by basket extraction in one case, and by a combination of chemolysis and basket extraction in three cases. In two other cases, underlying recurrent tumor was treated palliatively with percutaneous transhepatic biliary drainage or endoscopic stenting. Irrigation with heparinized saline solution failed in four cases, and percutaneous or endoscopic basket extraction failed in one case each. Surgical treatment was successful in 18 (86%) of 21 cases, and retransplantation was successfully done in five patients. In all, interventional techniques were used in 43% of the patients with biliary sludge who could not be treated successfully with oral chemolysis, and the overall success rate was 60%. CONCLUSION: Interventional techniques are effective therapeutic alternatives for treating biliary sludge occurring after liver transplantation and should be considered before surgical procedures. An indication for interventional procedures in biliary sludge is lack of success of oral chemolysis and an absence of other complications that require surgery or retransplantation.
OBJECTIVE: Biliary sludge (inspissated, thickened bile or collective collagen tissue from destroyed [or necrotic] bile duct walls) can be found a few days to several years after liver transplantation, mainly in the common and main hepatic bile ducts. The purpose of this study was to review the imaging findings of biliary sludge occurring after liver transplantation and to determine the relative merits of various imaging procedures (cholangiography, CT, and sonography) for establishing the diagnosis. MATERIALS AND METHODS: Cholangiograms, sonograms, and CT scans obtained in 352 patients with 400 liver transplants were reviewed retrospectively for evidence of biliary sludge. In all patients, T-tube cholangiograms were routinely obtained 7 and 30 days and 3 months after transplantation. Thereafter, in the absence of findings, the T-tube was removed. In all patients, sonograms were obtained immediately, 2 and 7 days after transplantation. Additional cholangiograms were obtained when biliary complications were suspected (T-tube cholangiograms in 215 patients, percutaneous transhepatic cholangiograms in 79 patients, and endoscopic retrograde cholangiograms in five patients after T-tube removal). Additional sonograms were obtained in 289 patients and CT scans in 238 patients when complications were suspected. The findings of these various imaging studies were analyzed and compared with each other, with the clinical course of the patient, and with surgical and histologic findings to determine the relative merits of each imaging method for the diagnosis of biliary sludge. Criteria for the diagnosis of biliary sludge were filling defects or pluglike obstruction seen on cholangiograms or material filling the bile ducts seen on sonograms or CT scans. The radiologic diagnosis of biliary sludge was certified by gross specimens obtained at surgery (n = 21) or autopsy (n = 2) or by complete disappearance of the radiologic findings with specific oral or interventional treatment (n = 28). RESULTS: Biliary sludge was diagnosed on the basis of radiologic findings in 51 (13%) of 400 transplanted livers. Cholangiograms (T-tube in 34, percutaneous transhepatic cholangiography in seven, a combination of T-tube and percutaneous transhepatic cholangiography in eight, and a combination of endoscopic retrograde and percutaneous transhepatic cholangiography in two cases) showed biliary sludge in all 51 cases. Cholangiographic findings included filling defects in 34 (67%) and obstruction of the bile duct with pluglike appearance in 17 (33%) of the 51 cases. Dilatation of bile ducts was present in 32 (63%) of the 51 cases. The presence of biliary sludge was certified in 50 of these cases, with one case turning out to be a sutural granuloma at autopsy. On sonograms, biliary sludge was shown as echogenic material in the main bile ducts in only 16 (31%) of the 51 cases, with dilatation of bile ducts in 12 of them. In 10 others (20%), sonograms showed dilatation of the bile ducts but did not show the sludge itself. CT scans did not show the sludge in any of the 12 cases in which they were obtained. CONCLUSION: Our results show that cholangiography is the only accurate imaging method for diagnosing biliary sludge after liver transplantation. Sonography is limited and CT is of no value for this purpose. In the absence of a T-tube, endoscopic retrograde or percutaneous transhepatic cholangiography should be used. Otherwise, T-tube cholangiography is the method of choice. Filling defects and obstruction of the bile ducts with pluglike material are characteristic findings of biliary sludge seen on cholangiograms.
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OBJECTIVE: To see if it was possible to predict the development of infection after liver transplantation from concentrations of endotoxin, tumour necrosis factor-alpha (TNF-alpha), or interleukin-6 (IL-6) in plasma. DESIGN: Prospective open study. SETTING: University hospital, Austria. SUBJECTS: 46 Consecutive patients who underwent liver transplantation for end stage liver disease, 1989-90. INTERVENTIONS: Samples of 4 ml blood were taken in endotoxin free tubes, and of 10 ml into heparinised tubes at the beginning of the operation, during hepatectomy, at the beginning and end of the anhepatic phase, 10 minutes after reperfusion, and at the end of the operation. MAIN OUTCOME MEASURES: Correlation between development of infections postoperatively and operative release of endotoxin, TNF-alpha, and IL-6. RESULTS: There was no correlation between development of postoperative infections and operative concentrations of endotoxin, and of TNF-alpha and IL-6 up to the end of the anhepatic phase. There was, however, a sixfold increase in TNF-alpha and IL-6 concentrations between the end of the anhepatic phase and the end of the operation in patients who subsequently developed infections (p = 0.01). CONCLUSION: The increase in the concentrations of these two cytokines in the blood after reperfusion of the transplanted liver seems to predict the development of subsequent bacterial infection.
Many transplant centers are reluctant to accept alcoholic patients for OLT because of their supposed potential for alcoholic recidivism and poor compliance with the required immunosuppressive regimen, both of which result in graft failure. Only inconclusive data related to these arguments are available. From May 1982 to January 1993, 58 patients received OLT at our institution for end-stage cirrhosis, where alcohol was the only toxic component. The indication for OLT in these patients was considered with particular attention to recidivism and compliance. Overall survival in this group was 71% and 63% at 1 and 5 years, respectively, with an average survival time of 78 months. Actuarial survival of patients transplanted since January 1989 (n = 37) was 86% and 83% at 1 and 2 years (average survival 42 months). Nonfatal clinical endpoints were analyzed in those patients surviving at least 3 months (n = 44). Return to alcohol abuse has been documented in 14 persons at routine short-term outpatient checkups. The estimated risk for alcoholic recidivism amounts to 31%, with a median follow-up of 33 months. Compliance with immunosuppressive regimen was expressed as a dependent value of acute rejection episodes (0.3 per patient, median follow-up 33 months), chronic rejection (occurred in none of the patients), and measurements of CsA HPLC blood trough level (92.2% within the target range). The preversus postoperative improvement of employment, marital, and social status after OLT showed a statistically significant difference. Unwillingness to offer OLT to individuals with alcoholic liver disease because of failure to demonstrate 100% long-term abstinence appears difficult to defend in the face of good results in survival, compliance, and social rehabilitation.
Several studies have shown that the postoperative course of cytokines such as TNF-alpha or IL-6 is predictive of rejection and infection after human orthotopic liver transplantation (OLT). The aim of this prospective clinical trial was to evaluate the impact of transhepatic metabolism of endotoxin (ET), tumor necrosis-factor-alpha (TNF-alpha), and interleukin-6 (IL-6) after hepatic ischemia/reperfusion on the postoperative graft function. In 13 consecutive elective adult OLT patients with primary grafts, we determined concentrations of ET, TNF-alpha, and IL-6 in the radial artery, portal vein, and right hepatic vein at 1, 4, 7, 10, and 13 min after reperfusion. Of the 13 patients, four had ET levels below the detection limit (< 10 ng/L), and one patient had extremely high ET concentrations (151 ng/L in the hepatic vein). In the remaining patients the mean ET levels were 26 +/- 14, 26 +/- 15, and 24 +/- 14 ng/L in the portal vein, hepatic vein, and in the radial artery, respectively. These values indicate that in patients with a moderately elevated ET level, no transhepatic concentration differences of ET exist. However, in the patient with severe endotoxemia, the liver was apparently an ET-producing organ (HV-P: 29 +/- 13 ng/L). TNF-alpha levels were not measurable in four patients, and varied between 15 and 72 pg/ml (portal vein) in the remaining patients. The transhepatic concentration differences (HV-P and HV-A, respectively) of patients with PNF or dysfunction were higher than in those with "good" or "excellent" graft function (HV-P: 160 +/- 122 pg/ml vs. 7.3 +/- 9.7 pg/ml; P < 0.01 and HV-A: 137 +/- 101 pg/ml vs. 3.9 +/- 12 pg/ml; P < 0.01, respectively). Arterial IL-6 levels were below 88 pg/ml (mean value: 31 +/- 20 pg/ml) at the beginning of the operation, and increased considerably in three patients during the anhepatic phase and after reperfusion. No clinical correlation was found with the transhepatic concentration differences of IL-6. We conclude that in OLT patients without infection no transhepatic ET exchange was documented. However, a stimulated hepatic TNF-alpha release seems to be predictive of the beginning of liver dysfunction.
L-Arginine plays an important role in protecting animals against ammonia intoxication, enhances immune function, stimulates wound healing, and is the precursor for the endothelium-derived relaxing factor, recently recognized as nitric oxide (NO). In this study, we investigated the influence of hepatic reperfusion on amino acid metabolism after human OLT. After 10 sec of reperfusion, the arterial plasma levels of L-arginine dropped from 105 +/- 12 mumol/L to 3.8 +/- 0.6 mumol/L (P < 0.001), whereas plasma ornithine increased from 40 +/- 5.5 mumol/L to 129 +/- 15 mumol/L (P < 0.001). The reduced L-arginine levels remained subnormal for several hours after OLT. This drop in plasma L-arginine was due to an arginase release from the implanted graft. Immediately after reperfusion, the plasma concentrations of arginase increased from pretransplantation values of 18 +/- 13 IU/L to 2384 +/- 1456 IU/L (P < 0.01). Measurement of plasma nitrite (NO2-) and nitrate (NO3-), which are the stable end products of NO, revealed that NO2- decreased about 50% after reperfusion (from 1.64 +/- 0.32 mumol/L to 0.80 +/- 0.17 mumol/L; P < 0.001), whereas NO3- levels remained unchanged (76 +/- 23 mumol/L vs. 63 +/- 8 mumol/L). We conclude that hepatic reperfusion causes L-arginine deficiency by liberating high amounts of arginase from the implanted graft. This L-arginine depletion may influence the NO synthesis in patients after OLT.
Sensory evoked potentials are markedly changed in patients with fulminant liver failure. It is unknown, however, whether serial recordings of sensory evoked potentials provide useful prognostic informations for patient management in fulminant liver failure. Ninety recordings of bilateral median nerve-stimulated short- and long-latency sensory evoked potentials were performed in 25 patients with fulminant liver failure (9 patients spontaneously recovered and survived, 8 patients were referred to emergency liver transplantation and 8 patients died). In all nine survivors the cortical long-latency sensory evoked potential N70 peak was constantly detectable between 74 and 162 ms. In all eight patients who subsequently underwent liver transplantation and in seven of eight patients who died, loss of the N70 peak developed during the course of fulminant liver failure. In 4 of 15 patients who were selected for liver transplantation according to the King's College criteria, the N70 peak was constantly detectable. All four transplantation candidates spontaneously recovered and survived without transplantation. In contrast, eight patients never did fulfill the criteria for liver transplantation. Five of them with constantly detectable N70 peak recovered spontaneously. However, in the remaining three patients loss of the N70 peak developed, and they ultimately died. The probability of correct outcome prediction by sensory evoked potentials is superior to that based on clinical criteria alone (0.96 vs. 0.72). Therefore serial recording of sensory evoked potentials may help identify (a) a subgroup among liver transplantation candidates who may spontaneously recover without transplantation and (b) a subgroup of patients with severe brain dysfunction who should undergo early liver transplantation even though they do not fulfill King's College criteria.
Many transplant centres are reluctant to accept alcoholic patients because of their supposed potential for alcoholic recidivism, resulting in graft failure and recurrence of alcoholic liver cirrhosis. From May 1982 to January 1993 80 patients received orthotopic liver transplantation (OLT) at our institution either for alcoholic cirrhosis exclusively (n = 58) or for a hepatoma in an alcoholic cirrhosis (n = 22). The outcome of these patients was analysed with particular attention to recurrence of liver disease. Overall survival in this group was 67% and 49% at 1 and 5 years, respectively, with a median follow-up of 45 months. Actuarial survival of patients transplanted since January 1989 (n = 46) and 84% and 82% at 1 and 2 years (median follow-up 31 months). Non-fatal clinical endpoints were analysed in those patients surviving for at least 3 months (n = 61). Return to alcohol abuse was documented in 16 patients at routine short-term out patient check-ups. All patients except one admitted to taking alcohol and showed changes in their laboratory test results. A specific pattern of liver function test values related to alcohol abuse was not detected and at the end of a relapse the liver function values usually returned to pre-event values. Only in one case was toxic injury of the liver related to alcoholic recidivism diagnosed on percutaneous liver needle biopsy or post-mortem examination. Compliance with the required immunosuppressive regimen and social rehabilitation after OLT were excellent. Unwillingness to offer OLT to individuals with alcoholic liver disease because of failure to demonstrate 100% long-term abstinence appears difficult to defend in the face of results showing good survival, compliance and social rehabilitation. The hypothesis of a higher sensitivity of the transplanted liver to a drinking episode and the redevelopment of alcoholic diesease in the new liver was not confirmed in our study population.
Evaluation of graft quality remains a major problem in liver transplantation. The aim of this retrospective analysis was to examine the impact of donor criteria on postoperative graft function. Between June 1986 and September 1993 324 liver transplantations were performed at our institution. Criteria for exclusion from analysis were postoperative thrombosis of graft vessels, retransplantation, death prior to the 5th postoperative day or missing donor criteria. For the eligible 255 transplantations the impact of the following donor criteria were examined: age (range 1-62 years, median 28 years), size/body weigt index, duration of intensive care, cause of death, circulatory condition, need for vasopressive support and liver function tests (bilirubin, GOT, GPT, GGT, LDH, ALP, prothrombin time (PT), creatinine, sodium). The following intraoperative factors were also assessed: type of protective solution, cold ischaemic time (CIT), anhepatic period and blood transfusions. Graft function during the first 5 postoperative days was categorized into four groups: (1) good function (GOT max < 1000 U/l, spontaneous PT > 50%, bile production > 100 ml/day); (2) fair function (GOT 1000-2500 U/l, clotting factor support < 2 days, bile < 100 ml/day); (3) poor function (GOT > 2500 U/l, clotting factor support > 2 days, bile < 20 ml/day); (4) primary non-function (retransplantation required within 7 days). A univariate analysis revealed duration of intensive care (P = 0.001), circulatory condition (P = 0.005), anhepatic period (P = 0.0004), blood transfusions (P = 0.03) and CIT (P = 0.039) as significant risk factors for postoperative graft function. Entering these factors in a multivariate regression model we identified creatinine (P = 0.007), duration of intensive care (P = 0.009) and the size/body weight index (P = 0.03) as donor-related factors of high significance. Analysis of the intraoperative data revealed the anhepatic period as the factor of highest significance (P = 0.0004) together with CIT (P = 0.02) and intraoperative blood transfusions (P = 0.008). A doubling of the number of days of intensive care resulted in a threefold increased risk of postoperative graft failure. Prolonged intensive care is a variable representing multiple risk factors. Accepting donors with a longer history of hypotension or who show signs such as elevated creatinine should be carefully considered. In patients with expected surgical difficulties resulting in an extended anhepatic period and a higher blood loss, transplantation of organs retrieved from donors with a long duration of intensive care and a long CIT should be avoided.
Up to the present the histological diagnosis of rejection through biopsy is still the only possibility for a definite rejection diagnosis. We searched for a reliable non-invasive marker of renal graft rejection. By means of a highly sensitive enzyme-linked immunosorbent assay we investigated the changes in the concentration of serum soluble TNF receptor in kidney graft recipients with different clinical courses according to their graft tolerance. sTNF-R in 19 patients with stable graft function (5.3 +/- 3.2 ng/ml) did not differ significantly from those detected in 22 healty volunteers (4.1 +/- 2.2 ng/ml). In contrast 17 patients suffering from acute graft rejection showed highly significantly increases (23 +/- 8.3 ng/ml, P < 0.0001). These elevated concentrations returned to prerejection rejection values after a 3-day anti-rejection therapy with high-dose methylprednisolone. In 18 patients with an irreversible, chronic kidney graft rejection we could demonstrate significantly increased sTNF-R values (20 +/- 7.9 ng/ml); eight of those patients did not reflect on the anti-rejection therapy, so that the elevated concentrations remained even after the administration of high-dose corticosteroids and ATG. Additionally we found soluble TNF receptor concentrations to be increased earlier than other commonly used biochemical parameters such as creatinine. Soluble TNF-R also proved to be useful for the differentiation of cyclosporin nephrotoxicity. Therefore we believe that the soluble TNF-R and its concentration course may be of diagnostic and prognostic value in kidney graft rejection, as it supports the diagnosis of transplant rejection, indicates the rejection event very early, and reflects the response to anti-rejection therapy.
The elevated incidence of large bowel carcinoma after cholecystectomy has long been controversial. The pathomechanism of this entity, however, is still unclear. Many authors have demonstrated a correlation between cholecystokinin (CCK) and gastrin levels and the occurrence of colorectal cancer. As yet, no clear data are available on the potential impact of cholecystectomy on CCK level alterations. Moreover, no reports have yet been published on CCK receptors. We have investigated the role of CCK-8 and gastrin plasma levels in patients with prior cholecystectomy and CCK receptor levels in patients with colorectal cancer. 125 patients entered a prospective study. Of these, 45 served as controls. 40 patients had prior cholecystectomy, 5 patients underwent cholecystectomy during the ongoing trial. 35 patients had a colorectal cancer, 5 of these had prior cholecystectomy. No patient had elevated CCK-8 plasma levels. Gastrin levels were slightly elevated in 2 patients. There was no correlation between large bowel carcinoma and CCK-8 and gastrin levels. Elevated CCK-8 levels following cholecystectomy occur neither immediately after surgery nor on a long-term basis. Immunohistochemical studies in patients with colorectal cancer showed no CCK receptors in the normal colonic or tumor tissue. These findings are contrary to gastrin receptor data.
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