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PubMed2001

Hepatic dysfunction associated with moderate ovarian hyperstimulation syndrome. A case report.

BACKGROUND: Liver dysfunction is a rare complication of severe ovarian hyperstimulation syndrome (OHSS). Based on a MEDLINE search from 1966 to September 2000, we report the second case of liver dysfunction associated with moderate OHSS. In addition, this is the first report of moderate OHSS with serum progesterone levels during the first trimester of pregnancy higher than the upper limit of normal for a third-trimester gestation. CASE: A 33-year-old nulligravida with a history of infertility had previously undergone three failed cycles of assisted reproduction. During her fourth attempt at in vitro fertilization and intracytoplasmic sperm injection, she developed moderate OHSS 11 days after embryo transfer. She was managed on an outpatient basis. Her serum progesterone and liver enzyme levels were significantly elevated, as is unusual for the moderate picture of OHSS in this patient. CONCLUSION: Hepatic dysfunction is not limited to the severe forms of OHSS. Liver function should be analyzed even in moderate cases. Further study is needed to understand the role of elevated liver function tests and serum progesterone in the pathogenesis of OHSS.

Adult↗
PubMed1988

Prevalence and causes of long-lasting hepatic dysfunction after heart transplantation: a series of 80 patients.

The long-term follow-up of 80 heart transplant patients (70 men, 10 women) from January 1982 to July 1985 who had received cyclosporine (CsA) showed a high incidence of mild to severe liver dysfunction. Fifty patients (62.5%) had long-lasting postoperative biological disturbances (alanine amino transferase greater than 2N and/or alkaline phosphatase greater than 1.5N for 3 months or more). Most patients were asymptomatic; eight were icteric, and one had arthralgia. The most common biological feature consisted of isolated elevation of ALAT (27 cases). Assessment of causes led to a definite etiology in 42 patients: 7 cardiac failure, 13 HBsAg-positive liver disease (26%) (chronic persistent hepatitis 8, chronic active hepatitis 2, subacute necrosis 2). Fourteen patients (28%) sustained non-A, non-B (NANB) hepatitis (chronic persistent hepatitis 5, chronic active hepatitis 1, cirrhosis 1), and 7 (14%) sustained a drug-related hepatitis. Liver biopsy and complete virus screening was contributive to the diagnosis in nearly all patients. Additionally, prolonged impairment of liver function tests occurred in 62% of heart transplant recipients, mostly during the first 6 postoperative months. Hepatitis B virus (HBV) and NANB hepatitis accounted for 26% and 28% of the cases of liver dysfunction, respectively; drug-induced hepatitis may have been involved in 14% of the cases. Complete hepatitis virus screening should be performed before heart transplant and in any case of abnormal liver function posttransplantation. HBV vaccination prior to heart transplant is recommended in HBsAg- and HBcAb-negative candidates for heart replacement. Long-term follow-up of these patients is mandatory to assess the severity of these liver dysfunctions.

Adolescent↗
PubMedDate not supplied

Histopathology of the liver in pediatric patients following transplantation.

Recognition of rejection and other hepatic complications by needle biopsy plays a significant role in the management of liver allograft recipients. In this report, 22 pediatric patients (below 18 years old) were selected from the 37 liver transplants. Seven of the 22 cases have an uneventful posttransplant course. The most common cause of allograft injury in these patients appeared to be acute cellular rejection. It occurred in 7 (31.8%) of the 22 cases and was the primary process in 8 of the 25 episodes of liver dysfunction. Other etiologies, such as opportunistic viral infection (3 cases), biliary obstruction (2 cases), preservation injury (1 case), and vascular obstruction (1 case) were less common. Acute graft rejection causing liver dysfunction was associated with a mixed portal inflammation, destruction of the interlobular bile ducts, and varied degree of venous endotheliitis, followed by centrilobular hepatocyte necrosis. Chronic rejection was not seen in our pediatric cases. Cold ischemic injury causing transient graft dysfunction as seen in one of our patients demonstrated focal, limited areas of hepatocyte necrosis, mild centrilobular hepatocyte ballooning, and cholestasis without evidence of bile duct damage. More severe ischemic injury resulted from vascular complication causing diffuse hepatocyte necrosis was seen in one patient with hepatic vein thrombosis. The histologic patterns observed were not pathognomic; however, liver biopsies were helpful in suggesting the probable cause of liver dysfunction and in predicting subsequent allograft recovery when used in conjunction with clinical information, radiologic, and other laboratory tests.

Adolescent↗
PubMed1995

Tacrolimus analysis: a comparison of different methods and matrices.

We determined the through blood and plasma concentrations of tacrolimus from the day of transplantation through 30 days posttransplantation in four liver and four kidney transplant patients by three different methods. The first method involved a solid phase extraction of the blood or plasma using Sep-Pak columns (SPs) followed by quantitation of tacrolimus using an enzyme-linked immunosorbent assay (ELISA); the second method involved a liquid-liquid extraction using methylene chloride (MC) followed by quantitation of tacrolimus using the ELISA, and the third method involved a high-performance liquid chromatography (HPLC) fractionation of the extract obtained from the solid-phase extraction and quantitation of tacrolimus in the fractions by ELISA. The trough plasma tacrolimus concentrations ranged from 0.1 to 5.2 ng/ml. While the trough plasma concentrations of tacrolimus were similar and independent of the method of analysis in kidney transplant patients and in liver transplant patients with normal biochemical profile, in patients with liver dysfunction, tacrolimus plasma concentrations were higher when measured by SP-ELISA and MC-ELISA methods as compared to the HPLC-ELISA method. In plasma samples obtained from liver transplant patients with liver dysfunction, the presence of some metabolites that cross-reacted with the antibody used in the ELISA could be documented in the HPLC fraction corresponding to the metabolites. This indicates that while tacrolimus metabolites that cross-react significantly with the antibody used in the ELISA do not accumulate in kidney transplant patients, they can appear in the plasma of patients, they can appear in the plasma of patients with liver dysfunction. The trough blood tacrolimus concentrations in patients were significantly higher than the corresponding plasma concentrations and ranged from 1.4 to 107 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Chromatography, High Pressure Liquid↗
PubMed2005

[Clinical and laboratory screening studies on urea cycle defects].

OBJECTIVE: To investigate the incidences of urea cycle defects (UCDs) in the patients with hyperammonemia and study their etiology, clinical and laboratory features. METHODS: In the past 7 years, 26 cases (10.2%) of UCDs were detected from 254 patients with hyperammonemia. The etiological diagnoses were made by blood amino acids analysis, urinary organic acid analysis and blood acylcarnitine profile analysis. Three patients with citrullinemia type II were further confirmed by liver pathological analysis and gene diagnosis. RESULTS: Among 26 cases with UCDs, 15 had ornithine transcarbamylase (OTC) deficiency, 5 had citrullinemia type I, 3 had citrullinemia type II and 3 patients had arginemia. The age of onset of the patients ranged from 3 days to 13 years. Three cases (11.5%) developed hyperammonemic encephalopathy during neonatal period. Thirteen (50.0%), 7 (26.9%) and 3 (11.5%) cases developed clinical symptoms at the age of 1 to 12 months, 1 to 3 years and 6 to 13 years, respectively. Positive family history was found in 11 cases (42.3%). Among 26 patients with UCDs, 9 (34.6%) were hospitalized with the complains of seizures, psychomotor retardation, vomiting and unconsciousness, 8 (30.8%) with recurrent vomiting, headache and coma, 6 due to liver dysfunction. Intrahepatic cholestatic jaundice was found in 3 patients with citrullinemia type II. Blood ammonia ranged from 58 to 259 micromol/L on their first visit to our hospital. Twenty cases (76.9%) had liver dysfunction, 4 patients (15.4%) were diagnosed postmortem. Twenty-one patients got treatment and were followed up. Among them, 7 cases died of hyperammonemic encephalopathy or upper alimentary tract bleeding. Clinical improvement was observed in 14 cases. A boy with OTC deficiency who received a partial liver transplant from his mother showed normal general condition for two years. CONCLUSIONS: UCDs are the most frequent causes of congenital hyperammonemia. In this study, 26 patients (10.2%) with UCDs were identified from 254 patients with hyperammonemia resulting in encephalopathy and liver dysfunction. Early diagnosis and treatment can contribute a lot to improve the prognosis of the patients. Blood ammonia assay and further etiological analysis should be considered in the differential diagnosis of neurological and hepatic abnormality.

Adolescent↗
PubMed2004

Contralateral portal vein embolization for hepatectomy in the setting of hepatic steatosis.

Portal vein embolization is evolving as an important adjunctive tool in hepatic surgery. In select patients, preoperative hypertrophy of the future remnant liver via contralateral portal vein embolization decreases postoperative liver dysfunction. Hepatic steatosis is the most common liver parenchymal disorder in Western populations. Moderate and severe degrees of hepatic steatosis convey an increased risk of postoperative liver dysfunction following major hepatic resections, but no studies exist examining the role of preoperative portal vein embolization in patients with hepatic steatosis. In this manuscript, we review the indications for portal vein embolization currently supported by the literature and present a patient with moderate to severe steatosis who successfully underwent portal vein embolization and a subsequent major liver resection.

Embolization, Therapeutic↗
PubMed1996

Depletion of mitochondrial deoxyribonucleic acid in a family with fatal neonatal liver disease.

We describe a family in which three children of consanguineous parents died of hepatic failure before the age of 3 months. The first child had clinical symptoms of liver disease with hypoglycemia that were evident at birth. The second child was healthy and has normal development. The third child had severe liver dysfunction noted a few days after birth. Liver failure also developed in the fourth child soon after birth. Recently a mitochondrial disorder was considered as a possible cause. Deficiency of respiratory chain enzymes that contain polypeptides encoded by mitochondrial DNA (mtDNA) and depletion of mtDNA were found in the liver of the fourth child, but mitochondrial abnormalities were absent in muscle of the third child. The similarities in clinical presentation suggest that liver-specific depletion of mtDNA was the cause of the hepatic failure in all three children. We conclude that liver dysfunction with onset in the perinatal period can be caused by depletion of mtDNA.

Autoradiography↗
PubMed1999

Serum IFN-inducible protein-10: a new clinical prognostic predictor of hepatocyte death in biliary atresia.

PURPOSE: The aim of this study was to determine whether chemokines such as serum IP-10 levels in patients with biliary atresia (BA) correlate with liver function and histology and assess its value as a medium to long-term prediction of prognosis in postoperative BA patients. METHODS: Thirty postoperative BA patients (mean age, 10.8+/-3.5 years) and eight normal controls (mean age, 10.3+/-3.3 years) were studied. The BA patients were divided into three groups according to liver function. Group I (n = 8) was jaundice free, had normal liver function and no evidence of severe cholangitis or portal hypertension. Group II (n = 12) had moderate liver dysfunction. Group III (n = 10), had severe liver dysfunction. Hepatic histology was assessed using conventional needle biopsy. Serum IP-10 levels were determined using a specific enzyme-linked immunosorbent assay (ELISA). RESULTS: Serum levels of IP-10 in group III (458.0+/-240.0 pg/mL) were significantly higher than those in group II (233.6+/-126.9 pg/mL; P < .0001). Levels in group II were also significantly higher than those in group I (144.8+/-23.4 pg/mL; P < .05), but there was no significant difference between group I and controls (107.9+/-34.0 pg/mL). Liver biopsy findings showed a progression of fibrosis and mononuclear cell infiltration from group I to group III. There was intimal hyperplasia and swelling of endothelial cells of branches of the hepatic artery in the portal area in group III. CONCLUSION: Because IP-10 levels correlate closely with histological findings in postoperative BA patients, it would appear to play a specific role in hepatocyte death and hepatic artery changes, thus providing important information about progressive fibrosis in BA patients that facilitates treatment decision making and prediction of prognosis.

Biliary Atresia↗
PubMed2000

Organ survival after primary dysfunction of liver grafts in clinical orthotopic liver transplantation.

In a retrospective analysis of 632 orthototopic liver transplant procedures performed between 1982 and 1997, the incidence of primary dysfunction (PDF) of the liver and its influence on organ survival were studied. Graft function during the first 3 postoperative days was categorized into four groups: (1) good (GOT max < 1000 U/l, spontaneous PT > 50%, bile production > 100 ml/day); (2) fair (GOT 1000-2500 U/l, clotting factor support < 2 days, bile < 100 ml/day); (3) poor (GOT > 2500 U/l, clotting factor support > 2 days, bile < 20 ml/day); (4) primary non-function (PNF; retransplantation required within 7 days). The aim of this study was to evaluate graft survival comparing organs with PDF (poor function) and PNF vs organs with initial good or fair function. After a median follow-up of 45 months, initially good and fair function of liver grafts resulted in a significantly better long-term graft survival compared with grafts with initially poor function or primary non-function (if re-transplanted) (P < 0.01). The Cox model revealed primary function as a highly significant factor in the prediction of long-term graft survival (P < 0.0001). We conclude that these results confirm the hypothesis that primary graft function is of major importance for the long-term survival of liver transplants. Patients with a poor primary function have the worst survival prognosis, which leads to the interpretation that these patients may be candidates for early retransplantation.

Adolescent↗
PubMed1993

Absence of hepatic uptake of Tc-99m phytate in a man with chronic toluene hepatotoxicity.

The case reported here is of a 28-year-old man diagnosed as having toluene hepatotoxicity. He had a 5-year history of exposure to toluene and was admitted to hospital complaining of two episodes of loss of consciousness. The high total bilirubin and the low prothrombin time suggested serious liver dysfunction. Based on histologic examination of a liver biopsy specimen, the diagnosis of toxic liver dysfunction caused by toluene poisoning was made. Hepatic images were not present in Tc-99m phytate scintigrams, but they were present in hepatobiliary scintigrams done with the Tc-99m N-pyridoxyl-5-methyltryptophan. The diagnosis of hepatic reticuloendothelial failure was made.

Adult↗
PubMed2001

[Tricuspid valve replacement using right heart bypass in patient with liver cirrhosis].

A successful case with liver cirrhosis underwent re-tricuspid valve replacement (TVR) using right heart bypass is reported herein. A 59-year-old lady previously undergone tricuspid valve replacement with bioprosthetic valve had suffered from exertional fatigue as the feature of congestive heart failure. She also presented severe liver dysfunction owing to chronic hepatitis and cardiac liver cirrhosis. She was diagnosed with structural deterioration of bioprosthesis in tricuspid position. She underwent re-TVR with right heart bypass consisted of centrifugal pump, heparin coating circuit and blood reservoir. This system lacked of membranous oxygenator in order not to activate various kinds of chemical mediator which leads to postoperative liver dysfunction. Postoperative course was uneventful and she is doing well 1 year after the operation. Although the mortality of the TVR in the patient with cirrhosis remains still high, this new technique seems to provide better outcome in this kind of patients.

Bioprosthesis↗
PubMed1991

Fosinopril pharmacokinetics and pharmacodynamics in chronic ambulatory peritoneal dialysis patients.

The pharmacokinetics and pharmacodynamics of fosinoprilat, the diacid of fosinopril sodium, a new angiotensin-converting enzyme (ACE) inhibitor, were investigated after the oral administration of 10 mg of fosinopril sodium to 6 chronic ambulatory peritoneal dialysis (CAPD) patients. The results from 1 patient are reported separately because of the presence of concomitant liver dysfunction. The mean t1/2, Cmax, tmax, and AUC values for 5 of the CAPD patients were 19.5 h, 202 ng.ml-1, 4.8 h, and 3.19 micrograms.h.ml-1, respectively. Values for 1 CAPD patient with liver dysfunction were t1/2 of 65.4 h, Cmax of 182 ng.ml-1, tmax of 9 h, and AUC of 18.1 micrograms.h.ml-1. Peritoneal clearance of fosinoprilat was negligible, ranging from 0.07 to 0.23 ml.min-1. Serum ACE activity remained significantly suppressed at 24 and 48 h after fosinopril sodium administration with mean decreases from baseline of 94.2% and 70.6%, respectively. ACE activity was suppressed to an even greater degree in the patient with liver dysfunction, remaining 97% inhibited 72 h after drug administration. Plasma renin activity (PRA) increased and plasma aldosterone concentrations decreased following drug administration. Mean arterial pressure did not change appreciably throughout the study. Dosage reductions may not be necessary in the majority of dialysis patients.

Adult↗
PubMed1996

Adjuvant oral chemotherapy to prevent recurrence after curative resection for hepatocellular carcinoma.

Adjuvant oral chemotherapy was studied in 67 patients with stage II hepatocellular carcinoma who underwent curative resection between May 1988 and December 1990. Patients were stratified into two groups according to preoperative liver dysfunction: 55 had stage I disease (mild dysfunction) and 12 had stage II (moderate dysfunction). A randomized controlled study of postoperative oral administration of 1-hexylcarbamoyl-5-fluorouracil (HCFU) was conducted in each group. From October 1994 HCFU administration was suspended because of side-effects in nine patients with stage I liver dysfunction and in three with stage II dysfunction who had received the drug for more than 4 weeks. Cumulative survival and recurrence-free survival rates of patients with stage I disease in the treatment group were higher (P = 0.08 and P = 0.04 respectively) than those in the control group. However, in patients with stage II disease no significant difference was observed (P = 0.77 and P = 1.0 respectively). This study suggests that the potential benefits of HCFU on tumour recurrence should be weighed against the risk of adverse reactions in patients with mild liver dysfunction.

Antineoplastic Agents↗
PubMed2000

alpha-Glutathione-s-transferase as a new sensitive marker of hepatocellular damage in biliary atresia.

Early identification of patients likely to deteriorate post-hepatic portoenterostomy for biliary atresia (BA) would be beneficial. alpha-Glutathione-s-transferase (alpha-GST) is a serologic marker of reactive hepatocellular damage because of its low molecular weight, uniform hepatic distribution, high cytosol concentration, and short half-life. We evaluated whether serum alpha-GST in post-surgical BA patients correlates with liver function (LF) and investigated its potential as a medium- to long-term marker of prognosis. Postoperative BA patients (n = 30; mean age: 11.8 +/- 3.7 years) were divided into three groups based on average LF over the 3 months prior to this study. Group I (n = 8) were jaundice-free and had normal LF. Group II (n = 12) had moderate liver dysfunction, and group III (n = 10) had severe liver dysfunction. Serum alpha-GST was determined using a specific ELISA. Tissue alpha-GST was determined immunohistochemically, using liver needle-biopsy specimens. Bile lakes were found in 5 group II patients and 5 group III patients. Serum alpha-GST was significantly higher in group II (20.7 +/- 8.4 ng/ml) than in groups I (4.7 +/- 1.3 ng/ml) and III (8.0 +/- 1.2 ng/ml) (P < 0.0001) and was highest in group II subjects with bile lakes. In control liver specimens alpha-GST distribution was weak but uniform throughout normal liver lobule hepatocytes. In group II there was strong staining in centrilobular hepatocytes, and in group III alpha-GST was only found in regenerative nodules. We conclude that alpha-GST may be a more sensitive indicator of hepatocellular damage in BA because its distribution is correlated to the proportion of functioning liver tissue present. This is the first report of this relationship, which has great implications for group II subjects because a sudden shift in concentration of alpha-GST may be a better predictor of impending hepatic dysfunction than conventional LF tests.

Adolescent↗
PubMed1990

Pulsatile portal vein flow: a sign of tricuspid regurgitation on duplex Doppler sonography.

Sonography and duplex Doppler frequently fail to identify a cause for right upper quadrant pain, liver dysfunction, or ascites. The aim of our study was to describe and analyze the pulsatile portal venous waveform in which minimum velocity dropped to or below zero on duplex Doppler sonography and to investigate its possible association with tricuspid regurgitation, one of the causes of liver dysfunction. We correlated the findings in 15 patients in whom this duplex Doppler waveform was seen with the findings on Doppler echocardiography (n = 14) or ultrafast CT (n = 1). All patients had biochemical liver abnormalities or sudden onset of ascites, rapid weight gain, increased abdominal girth, and hepatomegaly. They were referred for sonography to rule out liver metastases, biliary disease, portal vein thrombosis, or Budd-Chiari syndrome. All examinations were done with a 3-MHz phased-array sector transducer with duplex Doppler capability. Seventeen volunteers with no known liver or heart disease served as a control group. We correlated maximum and minimum flow velocities on the portal venous Doppler waveform with the portal vein diameters of the study and control groups. Thirteen patients were later proved to have tricuspid regurgitation, one patient had an aortic-right atrial fistula owing to rupture of an aneurysm of the sinus of Valsalva, and one patient was proved to be normal. In none of the 17 control subjects was this pulsatile portal venous waveform seen. Our study shows that detection of a pulsatile portal venous waveform on duplex Doppler sonography in patients with liver dysfunction should raise the possibility of tricuspid regurgitation.

Adult↗
PubMed2006

Hypomorphic mutation of PGC-1beta causes mitochondrial dysfunction and liver insulin resistance.

PGC-1beta is a transcriptional coactivator that potently stimulates mitochondrial biogenesis and respiration of cells. Here, we have generated mice lacking exons 3 to 4 of the Pgc-1beta gene (Pgc-1beta(E3,4-/E3,4-) mice). These mice express a mutant protein that has reduced coactivation activity on a subset of transcription factors, including ERRalpha, a major target of PGC-1beta in the induction of mitochondrial gene expression. The mutant mice have reduced expression of OXPHOS genes and mitochondrial dysfunction in liver and skeletal muscle as well as elevated liver triglycerides. Euglycemic-hyperinsulinemic clamp and insulin signaling studies show that PGC-1beta mutant mice have normal skeletal muscle response to insulin but have hepatic insulin resistance. These results demonstrate that PGC-1beta is required for normal expression of OXPHOS genes and mitochondrial function in liver and skeletal muscle. Importantly, these abnormalities do not cause insulin resistance in skeletal muscle but cause substantially reduced insulin action in the liver.

Animals↗
PubMed1997

Hepatic arterial resistance index--an indicator of diffuse liver disease in children treated with bone marrow transplantation.

AIM: To describe the relationship between the resistance index of the common hepatic artery and liver function tests in children undergoing bone marrow transplantation. MATERIALS AND METHODS: We analysed prospectively the results of 106 Doppler ultrasound examinations of the common hepatic artery from 31 bone marrow transplant patients, 16 of whom had normal liver function. The aetiology of the liver dysfunction in the other 15 patients was veno-occlusive disease (n = 7), unknown (n = 3), hepatic graft-versus-host disease (n = 2), hepatitis (n = 2), or cholestasis (n = 1). We assessed the relationships between the hepatic arterial resistance index (HART) and the results of the serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase (SGPT), alkaline phosphatase (ALK), lactate dehydrogenase (LDH) and serum albumin (ALB) assays and calculated HARI break-point values that might distinguish patients with liver disease from patients with the normal liver function. RESULTS: The significant break point (P < 0.05) of the HARI was 0.55 for SGOT, SGPT and ALK. LDH was associated with a break point of 0.53. Resistance indices for the common hepatic artery below the break-point values predicted liver dysfunction with specificities of 81%, 80%, 92% and 93%, respectively. There was no significant relationship between liver function tests and ALB levels. CONCLUSION: If below 0.55, the hepatic arterial resistance index is a non-invasive indicator of liver dysfunction in children undergoing bone marrow transplantation.

Adolescent↗
PubMed2000

Factors predicting for efficacy and safety of docetaxel in a compassionate-use cohort of 825 heavily pretreated advanced breast cancer patients.

PURPOSE: To identify predictive factors for efficacy and safety in advanced breast cancer (ABC) patients treated in the French compassionate-use docetaxel program. PATIENTS AND METHODS: A total of 825 ABC patients treated with docetaxel (100 mg/m(2) every 3 weeks) were source-reviewed and analyzed for prognostic factors associated with overall response rate (ORR), time to treatment failure (TTF), overall survival (OS), febrile neutropenia, mucositis, and severe fluid retention syndrome by univariate and multivariate analysis. RESULTS: The ORR was 22.9% (95% confidence interval, 20.2% to 26.2%). The median TTF and OS were 4.0 and 9.8 months, respectively. By multivariate analysis, secondary anthracycline-resistant disease was significantly associated (P <. 05) with lower ORR and shorter TTF and OS, whereas anthracycline-refractory disease was associated with shorter OS. Poor performance status was associated with lower ORR, shorter TTF, and shorter OS. Liver dysfunction (transaminase levels > 1.5 times the upper limit of normal [ULN] and alkaline phosphatase [AP] level > three times ULN) and time since first relapse less than 24 months were associated with shorter TTF and OS. Other significant correlations included the following: elevated CA 15-3 serum level with lower ORR; more than two involved sites, and minor transaminase and AP level abnormalities with shorter OS; and no previous chemotherapy for ABC with shorter TTF. According to multivariate analysis, ORR, TTF, and OS were not decreased in patients with liver metastases but without liver dysfunction. CONCLUSION: Docetaxel activity was maintained in heavily pretreated ABC patients and in those with liver metastasis; docetaxel must be used cautiously, however, in patients with liver dysfunction in whom high morbidity risk necessitates strict adherence to dose-adaptation guidelines.

Anthracyclines↗