Publications

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    B. A. Payer, P. Ferenci, C. Zauner
    Alimentary Pharmacology & Therapeutics 10/2014; 40(7). · 4.55 Impact Factor
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    ABSTRACT: Background and Aims Hypoxic hepatitis (HH) is a frequent and life-threatening complication associated with states of oxygen depletion in critically ill patients. Ischemia and reperfusion contribute to liver injury in HH. Experimental data suggest beneficial effects of statins in hepatic ischemia/reperfusion injury. This study was conducted to investigate whether statin treatment prior to intensive care unit (ICU) admission affects incidence rates and severity of HH. Methods Eight hundred fifty-one patients admitted consecutively to three medical ICUs between December 2008 and December 2009 were prospectively screened for new occurrence of HH within 48 hours following ICU admission. Statin treatment prior to ICU admission was assessed. 28-day-, 90-day- and 1-year-survival as well as new-onset of complications in HH patients were prospectively documented. Results Eighty-seven patients (10%) developed HH. Statin treatment prior to ICU admission was significantly associated with decreased incidence of HH within 48 hours after ICU admission in the multivariate analysis (adjustedOR=0.42 (95% CI 0.19-0.95); p<0.05). Cardiogenic shock (p<0.001), septic shock (p<0.001) and active alcohol consumption (p<0.01) were identified as independent risk factors for development of HH. 28-day-, 90-day- and 1-year-mortality rates in HH were 58%, 67% and 74%, respectively. Statins were associated with improved 28-day-survival in the total study cohort (p<0.05), but did not affect 90-day- and 1-year-mortality, respectively. Conclusions Cardiogenic shock, septic shock and active alcohol consumption were independent factors predisposing patients to new onset of HH. Statin treatment prior to ICU admission was the only protective factor regarding the new occurrence of HH in critically ill patients.
    Journal of Hepatology 06/2014; · 9.86 Impact Factor
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    ABSTRACT: Background/objectives:Women and men differ in substrate and energy metabolism. Such differences may affect energy requirements during the acute phase of critical illness.Subjects/methods:Data of 155 critically ill medical patients were reviewed for this study. Indirect calorimetry in each patient was performed within the first 72 h following admission to the medical intensive care unit after an overnight fast.Results:In overweight (body mass index (BMI)25 kg/m(2)) but not in normal-weight patients, resting energy expenditure (REE) adjusted for body weight (REEaBW) differed significantly between women and men (17.2 (interquartile range (IQR) 15.2-20.7) vs 20.9 (IQR 17.9-23.4) kcal/kg/day, P<0.01). Similarly, REE adjusted for ideal body weight (REEaIBW) was significantly lower in women compared with men (25.5 (IQR 22.6-28.1) vs 28.0 (IQR 25.2-30.0) kcal/kg/day, P<0.05). In overweight patients, gender was identified as an independent predictor of REEaBW in the multivariate regression model (r=-2.57 (95% CI -4.57 to -0.57); P<0.05), even after adjustment for age, simplified acute physiology score (SAPS II), body temperature, body weight and height.Conclusions:REEaBW decreases with increasing body mass in both sexes. This relationship differs between women and men. Overweight critically ill women show significantly lower REEaBW and REEaIBW, respectively, compared with men. These findings could affect the current practice of nutritional support during the early phase of critical illness.European Journal of Clinical Nutrition advance online publication, 15 January 2014; doi:10.1038/ejcn.2013.287.
    European journal of clinical nutrition 01/2014; · 3.07 Impact Factor
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    ABSTRACT: Ganciclovir is an antiviral agent that is frequently used in critically ill patients with cytomegalovirus (CMV) infections. Continuous venovenous haemodiafiltration (CVVHDF) is a common extracorporeal renal replacement therapy in intensive care patients. Aim of this study was to investigate the pharmacokinetics of ganciclovir in anuric patients undergoing CVVHDF. Population pharmacokinetic analysis was performed in nine critically ill patients, with proven or suspected CMV infection undergoing CVVHDF. All patients received a single dose of ganciclovir at 5 mg/kg of bodyweight intravenously. Serum and ultradiafiltrate concentrations were assessed by high performance liquid chromatography and this data was used for pharmacokinetic analysis. Mean peak and trough prefilter ganciclovir concentrations were 11.8 ± 3.5 mg/L and 2.4 ± 0.7 mg/L. As pharmacokinetic parameters elimination half-life (24.2 ± 7.6 h), volume of distribution (81.2 ± 38.3 L), sieving coefficient (0.76 ± 0.1), total clearance (2.7 ± 1.2 L/h) and clearance of CVVHDF (1.5 ± 0.2 L/h) were determined. Based on population pharmacokinetic simulations with respect to a target area under the curve (AUC) of 50 mg·h/L and a trough level of 2 mg/L a ganciclovir dose of 2.5 mg/kg once daily seems to be adequate for anuric critically ill patients during CVVHDF.
    Antimicrobial Agents and Chemotherapy 10/2013; · 4.57 Impact Factor
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    ABSTRACT: PURPOSE: Increased arterial ammonia levels are associated with high mortality in patients with acute liver failure (ALF). Data on the prognostic impact of arterial ammonia is lacking in hypoxic hepatitis (HH) and scarce in critically ill patients with cirrhosis. METHODS: The patient cohort comprised 72 patients with HH, 43 patients with ALF, 100 patients with liver cirrhosis and 45 patients without evidence for liver disease. Arterial ammonia concentrations were assessed on a daily basis in all patients and the results were compared among these four patient groups and between 28-day survivors and 28-day non-survivors overall and in each group. RESULTS: Overall 28-day mortality rates in patients with HH, ALF and cirrhosis and in the control group were 54, 30, 49 and 27 %, respectively. Peak arterial ammonia levels differed significantly between transplant-free 28-day survivors and non-survivors in the HH and ALF groups (p < 0.01 for both). Multivariate regression identified peak arterial ammonia concentrations as an independent predictor of 28-day mortality or liver transplantation in patients with HH and ALF, respectively (p < 0.01). There was no association between mortality and arterial ammonia in patients with liver cirrhosis and in the control group. Admission arterial ammonia levels were independently linked to hepatic encephalopathy grades 3/4 in patients with HH (p < 0.01), ALF (p < 0.05) and cirrhosis (p < 0.05), respectively. CONCLUSIONS: Elevated arterial ammonia levels indicate a poor prognosis in acute liver injury and are associated with advanced HE in HH, ALF and cirrhosis. Arterial ammonia levels provide additional information in the risk assessment of critically ill patients with liver disease.
    European Journal of Intensive Care Medicine 05/2013; · 5.17 Impact Factor
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    ABSTRACT: Hypoxic hepatitis (HH) is the most frequent cause of acute liver injury in critically ill patients. No clinical data exist about new onset of jaundice in patients with HH. This study aimed to evaluate the incidence and clinical effect of jaundice in critically ill patients with HH. Two hundred and six consecutive patients with HH were screened for the development of jaundice during the course of HH. Individuals with preexisting jaundice or liver cirrhosis at the time of admission (n = 31) were excluded from analysis. Jaundice was diagnosed in patients with plasma total bilirubin levels >3 mg/dL. One-year-survival, infections, and cardiopulmonary, gastrointestinal (GI), renal, and hepatic complications were prospectively documented. New onset of jaundice occurred in 63 of 175 patients with HH (36%). In patients who survived the acute event of HH, median duration of jaundice was 6 days (interquartile range, 3-8). Patients who developed jaundice (group 1) needed vasopressor treatment (P < 0.05), renal replacement therapy (P < 0.05), and mechanical ventilation (P < 0.05) more often and had a higher maximal administered dose of norepinephrine (P < 0.05), compared to patients without jaundice (group 2). One-year survival rate was significantly lower in group 1, compared to group 2 (8% versus 25%, respectively; P < 0.05). Occurrence of jaundice was associated with an increased frequency of complications during follow-up (54% in group 1 versus 35% in group 2; P < 0.05). In particular, infections as well as renal and GI complications occurred more frequently in group 1 during follow-up. Conclusion: Jaundice is a common finding during the course of HH. It leads to an increased rate of complications and worse outcome in patients with HH. (HEPATOLOGY 2012).
    Hepatology 06/2012; · 12.00 Impact Factor
  • Critical Care 03/2012; 16(1). · 4.93 Impact Factor
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    ABSTRACT: Critical illness leads to increased endogenous production of carbon monoxide (CO) due to the induction of the stress-response enzyme, heme oxygenase-1 (HO-1). There is evidence for the cytoprotective and anti-inflammatory effects of CO based on animal studies. In critically ill patients after cardiothoracic surgery, low minimum and high maximum carboxyhemoglobin (COHb) levels were shown to be associated with increased mortality, which suggests that there is an 'optimal range' for HO-1 activity. Our study aimed to test whether this relationship between COHb and outcome exists in non-surgical ICU patients. We conducted a retrospective, observational study in a medical ICU at a university hospital in Vienna, Austria involving 868 critically ill patients. No interventions were undertaken. Arterial COHb was measured on admission and during the course of treatment in the ICU. The association between arterial COHb levels and ICU mortality was evaluated using bivariate tests and a logistic regression model. Minimum COHb levels were slightly lower in non-survivors compared to survivors (0.9%, 0.7% to 1.2% versus 1.2%, 0.9% to 1.5%; P=0.0001), and the average COHb levels were marginally lower in non-survivors compared to survivors (1.5%, 1.2% to 1.8% versus 1.6%, 1.4% to 1.9%, P=0.003). The multivariate logistic regression analysis revealed that the association between a low minimum COHb level and increased mortality was independent of the severity of illness and the type of organ failure. Critically ill patients surviving the admission to a medical ICU had slightly higher minimum and marginally higher average COHb levels when compared to non-survivors. Even though the observed differences are statistically significant, the minute margins would not qualify COHb as a predictive marker for ICU mortality.
    Critical care (London, England) 01/2012; 16(1):R6. · 4.72 Impact Factor
  • Journal of Hepatology 03/2011; 54. · 9.86 Impact Factor
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    ABSTRACT: Khat is a drug widely used in the Horn of Africa and the Arabian Peninsula. Khat leaves contain, among other substances, the psychoactive alkaloid cathinone, which induce central nervous system stimulation leading to euphoria, hyperactivity, restlessness, and insomnia. However, it also could cause psychological adverse effects such as lethargy, sleepiness, psychoses, and depression necessitating pharmacologic treatment. Here we report the case of a 35-year-old man from Somalia who became unconscious and developed aspiration pneumonia and subsequent ARDS after excessive consumption of khat leaves. His unconsciousness was possibly caused by the sleepiness developed after khat consumption and a benzodiazepine intake by the patient himself. Thus, khat-induced adverse effects should not primarily be treated pharmacologically, but patients should be urged to quit khat consumption in order to eliminate or, at least, reduce the severity of present psychological adverse effects.
    Case Reports in Critical Care. 01/2011; 2011.
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    ABSTRACT: Paraneoplastic pemphigus (PNP) is a rare life-threatening autoimmune bullous skin disease which is an obligate paraneoplasma. A 34-year-old woman presented with recalcitrant stomatitis and a generalized lichenoid rash. A diagnosis of PNP was established based on clinical findings, immunofluorescence, histopathology and biochemistry. A localized mediastinal mass was found with CT imaging and excised. The histologic diagnosis was dendritic cell sarcoma. Despite removal of tumor and immunosuppressive therapy, the PNP progressed rapidly and the patient died of septic multiorgan failure.
    Journal der Deutschen Dermatologischen Gesellschaft 01/2009; 7(4):356-9. · 1.40 Impact Factor
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    ABSTRACT: Basophilic crisis and eosinophilia are well recognized features of advanced chronic myeloid leukaemia. In other myeloid neoplasms, however, transformation with marked basophilia and eosinophilia is considered unusual. We examined the long-term follow-up of 322 patients with de novo myelodysplastic syndromes (MDS) to define the frequency of basophilic, eosinophilic and mixed lineage (basophilic and eosinophilic) transformation. Of all patients, only one developed mixed lineage crisis (>or= 20% basophils and >or= 20% eosinophils). In this patient, who initially suffered from chronic myelomonocytic leukaemia, basophils increased to 48% and eosinophils up to 31% at the time of progression. Mixed lineage crisis was not accompanied by an increase in blast cells or organomegaly. The presence of BCR/ABL and other relevant fusion gene products (FIP1L1/PDGFRA, AML1/ETO, PML/RAR alpha, CBF beta/MYH11) were excluded by PCR. Myelomastocytic transformation/myelomastocytic leukaemia and primary mast cell disease were excluded by histology, KIT mutation analysis, electron microscopy and immunophenotyping. Basophils were thus found to be CD123+, CD203c+, BB1+, KIT- cells, and to express a functional IgE-receptor. Among the other patients with MDS examined, 4(1.2%) were found to have marked basophilia (>or= 20%) and 7(2.1%) were found to have massive eosinophilia ( >or= 20%), whereas mixed-lineage crisis was detected in none of them. Mixed basophil/eosinophil crisis may develop in patients with MDS but is an extremely rare event.
    European Journal of Clinical Investigation 07/2008; 38(6):447-55. · 3.37 Impact Factor
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    ABSTRACT: Critical illness is characterized by a hypermetabolic state associated with increased mortality, which is partly ascribed to the occurrence of hyperglycemia caused by enhanced endogenous glucose production and insulin resistance (IR). Insulin resistance is well described in patients after surgery and trauma. However, it is less clearly quantified in critically ill medical patients. In this clinical cohort study, IR (M value) was quantified in 40 critically ill medical patients and 25 matched, healthy controls by isoglycemic hyperinsulinemic clamps after an overnight fast on the day after admission to a medical intensive care unit. Energy and substrate metabolism were measured by using indirect calorimetry in the patients before and during the clamp. The severity of illness was assessed by the acute physiology and chronic health evaluation (APACHE) III score. M values of critically ill medical patients were significantly lower compared with healthy controls (2.29 +/- 1.0 and 7.6 +/- 2.9 mg/kg per minute, respectively; P < .001) and were closely related to APACHE III scores (r = -0.43, P < .01), body mass index (r = -0.41, P < .01), and resting energy expenditure (r = 0.40, P < .05). The M value was not associated with age, basal glucose concentrations, and respiratory quotient, and it did not differ among patients with various admission diagnoses. In conclusion, insulin sensitivity was found to be reduced by 70% in critically ill medical patients. The severity of IR was associated with the severity of illness, body mass index, and resting energy expenditure, but not with substrate oxidation rates. In addition, the severity of IR did not vary among patients with different admission diagnoses.
    Metabolism 01/2007; 56(1):1-5. · 3.10 Impact Factor
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    ABSTRACT: In critically ill patients, energy requirements are frequently calculated as a multiple of total body weight presuming a linear relationship between total body weight and resting energy expenditure (REE); however, it is doubtful if this estimation of energy needs should be applied to all patients, particularly to overweight patients, since adipose tissue has a low contribution to REE. This study was undertaken to test the hypothesis that REE adjusted for total body weight decreases with increasing body mass index in critically ill patients. Additionally, measured REE was compared with three predictive equations. Clinical study in a university hospital intensive care unit. One hundred critically ill patients admitted to the intensive care unit. Patients were included into four groups according to their body mass index (normal weight, pre-obese, obese, and morbidly obese). Measured REE was assessed using indirect calorimetry. Energy needs were calculated using the basal metabolic rate, the Consensus Statement of the American College of Chest Physicians (REEacs), and 25[Symbol: see text]kcal/kg of ideal body weight (REEibw). Adjusted REE was 24.8 +/- 5.5 kcal/kg in normal weight, 22.0 +/- 3.7 kcal/kg in pre-obese, 20.4 +/- 2.6 kcal/kg in obese, and 16.3 +/- 2.3 kcal/kg in morbidly obese patients (p < 0.01). Basal metabolic rate underestimated measured REE in normal weight and pre-obese patients. REEacs and REEibw over- and underestimated measured REE in overweight patients, respectively. Predictive equations were not able to estimate measured REE adequately in all the patients. Adjusted REE decreased with increasing body mass index; thus, a body mass index group-specific adaptation for the estimation of energy needs should be applied.
    Intensive Care Medicine 03/2006; 32(3):428-34. · 5.54 Impact Factor
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    ABSTRACT: Hyperglycemia and protein catabolism frequently occur in critically ill patients and both are associated with increased complication rates. These metabolic alterations can be improved by insulin administered exogenously. Since a wide range of insulin dosages have been used, this randomized, placebo-controlled, investigator-blinded, clinical study tests the hypothesis that a low-dose insulin regimen improves hyperglycemia and protein catabolism in critically ill medical patients. The day after their admission to a medical intensive care unit, forty consecutive, critically ill medical patients were randomized for receiving either a low-dose insulin regimen (i.e. 1 IU/h) (treatment group, n = 20) or placebo (control group, n = 20) continuously over 24 hours. The primary endpoint was the efficacy of the low-dose insulin regimen to decrease serum glucose concentrations; the secondary endpoint was its influence on protein catabolism. Serum glucose concentrations and protein catabolism, which was assessed by the urea nitrogen appearance rate, were determined at baseline and at 8 and 24 hours thereafter. Serum insulin concentrations were measured at baseline and after 24 hours. After 24 hours the low-dose insulin regimen increased serum insulin concentrations compared with baseline (16.8+/-13.3 microU/ml and 11.5+/-16.9 microU/ml, respectively; p<0.05). Hyperglycemia and the urea nitrogen appearance rate did not change within the two groups of patients and there was no difference between the groups at the different time points. Administration of the low-dose insulin regimen was safe. However, the short-term low-dose insulin regimen was inefficient in influencing mild hyperglycemia and protein catabolism in critically ill medical patients.
    Wiener klinische Wochenschrift 10/2004; 116(17-18):603-7. · 0.81 Impact Factor
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    ABSTRACT: To compare three scoring systems, the Acute Physiology and Chronic Health Evaluation (APACHE) II, the Simplified Acute Physiology Score (SAPS) II and a modified Mortality Probability Model II (ICU cancer mortality model, ICMM) for their prognostic value for mortality during hospital stay in a group of cancer patients admitted to a medical ICU. Prospective cohort study. Medical ICU of a tertiary care hospital. Two hundred forty-two consecutive cancer patients admitted to the ICU. Variables included in APACHE II, SAPS II and the ICMM scores as well as demographic data were assessed during the first 24 h of stay in the ICU. Hospital mortality was measured; it was 44%. Calibration for all three scoring systems was acceptable, SAPS II yielded a significantly superior discrimination between survivors and non-survivors. The areas under the receiver operating characteristic curves were 0.776 for APACHE II, 0.825 for SAPS II and 0.698 for the ICMM. The SAPS II was superior to APACHE II and ICMM. The newly developed ICMM does not improve mortality prediction in critically ill cancer patients.
    Intensive Care Medicine 04/2004; 30(3):430-6. · 5.54 Impact Factor
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    Diabetologia 07/2003; 46(6):871-3. · 6.49 Impact Factor
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    ABSTRACT: Hypoxic-ischaemic brain damage in cardiac arrest survivors is global, but postmortem histology could identify parts of the brain that are selectively vulnerable to ischaemia, comprising the thalamus and cortex. We hypothesized that hypoxic-ischaemic brain damage increases along the afferent sensory pathway with a stepwise decrease of detectable somatosensory evoked potential peaks. Somatosensory evoked potentials were recorded within 72 h after cardiac arrest in 305 comatose patients after cardiopulmonary resuscitation. We measured the short latency SEP peaks N9, P15, N20, P25 (reflecting the peripheral-thalamo-cortical pathway) and the long latency SEP peaks N35 and N70 (reflecting complex cortico-cortical interactions). Patients with a Cerebral Performance Category score > 2 at 1 year were defined as patients with hypoxic-ischaemic brain damage. Patients with hypoxic-ischaemic brain damage (n = 232) showed a statistically significant decrease of detectable peaks (P < 0.05) along the thalamo-cortical afferent pathway: N13, P15, N20, P25 and N70 peaks were detectable in 99%, 63%, 59%, 55% and 44% patients, respectively. In patients without hypoxic-ischaemic brain damage (n = 73) the N13, P15, N20, P25 peaks were detectable in all, and the N35 and N70 peaks in 98%. Furthermore, in patients with hypoxic-ischaemic brain damage and detectable SEP peaks, P15, N20, P25, N35 and N70, peak latencies were prolonged (P < 0.05) and N20 and N70 amplitudes were decreased (P < 0.05) compared with patients without hypoxic-ischaemic brain damage. Extent of hypoxic-ischaemic brain damage in cardiac arrest survivors increases along the afferent sensory pathway, with pronounced vulnerability of thalamic and cortical brain regions.
    European Journal of Clinical Investigation 04/2003; 33(4):283-7. · 3.37 Impact Factor
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    ABSTRACT: Sensory evoked potential (SEP) peak latencies were recorded in order to evaluate the incidence and severity of septic encephalopathy, testing the hypothesis that the occurrence of septic encephalopathy is more frequent than generally assumed. Prospective cohort study. Medical intensive care unit of a university hospital. Sixty-eight critically ill patients were studied within 48 hrs after the development of severe sepsis (n = 41) or septic shock (n = 27). None. Septic encephalopathy was defined as prolongation of SEP peak latencies beyond the upper limit of the reference range of subcortical (N13-N20 interpeak latency) and cortical SEP pathways (N20-N70 interpeak latency), as well as asymmetry of peak latencies marked by the presence of subclinical cerebral focal signs. Subcortical SEP pathways were impaired in 34% and cortical SEP pathways in 84% of all patients. The prolongation of the cortical SEP pathway correlated with the Acute Physiology and Chronic Health Evaluation III score (r = 0.23; p <.0001). SEP peak latencies did not differ in patients with severe sepsis compared with those with septic shock. Subclinical cerebral focal signs were present in 24% of the subcortical SEP pathways and in 6% of the cortical SEP pathways. Septic encephalopathy occurs more frequently than generally assumed, and its severity is associated with the severity of illness. The impairment of subcortical and cortical SEP pathways was not different between patients with severe sepsis and those with septic shock.
    Critical Care Medicine 06/2002; 30(5):1136-9. · 6.12 Impact Factor
  • A Schoeggl, K Kitz, M Reddy, C Zauner
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    ABSTRACT: The development of brain metastases represents an ominous event for patients with colorectal cancer. We evaluated results following stereotactic radiosurgery (SR) for patients with metastatic colorectal cancer to identify efficacy of SR and prognostic factors for survival. This is a retrospective study of 60 brain metastases from colorectal cancer in 35 consecutive patients who underwent SR from January 1993 to December 1996. Thirteen patients also underwent additional whole-brain radiation therapy (WBRT). The median dose delivered to the tumor margin was 20 Gray (range 16-28 Gy), in most cases the tumor enclosing the 50% isodose (range 40-60%). Patients were classified into two groups: SR with and SR without WBRT. Univariate and multivariate testing was performed to determine significant prognostic factors. The median survival time was 6 months after SR and 40 months after diagnosis of primary tumor. A Karnofsky performance scale >70 was a significantly favorable prognostic factor in uni- and multivariate testing. Post-SR imaging was evaluated in 32 patients and in 54 cerebral lesions. Local tumor control was revealed in 94% of patients and 96% of treated tumors. Two patients developed local recurrences, and remote brain disease was revealed in five. No patient experienced a new focal neurologic deficit due to SR. The addition of WBRT to SR did not improve survival and local tumor control rates. Distant control rate was borderline in univariate analysis and significantly improved for patients who received additional WBRT in multivariate analysis. SR for brain metastases from colorectal cancer results in a high local tumor control rate of 94% associated with few complications and therefore provides patients with a higher quality of their remaining life.
    International Journal of Colorectal Disease 05/2002; 17(3):150-5. · 2.24 Impact Factor

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