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Biomedical subjects

E Elias

Publications and source records attributed to E Elias.

At least 19 recordsLinked to original sources

Favourable medium term outcome following hepatic vein recanalisation and/or transjugular intrahepatic portosystemic shunt for Budd Chiari syndrome.

BACKGROUND: We report our experience with management of patients with Budd Chiari syndrome over the past two decades. In 1996 we described a novel approach involving recanalisation of hepatic veins by combined percutaneous and transvenous approaches. This was incorporated into an algorithm published in 1999 in which our preferred treatment for all cases of Budd Chiari syndrome with short segment occlusion or stenosis of the hepatic veins involves recanalisation of the hepatic veins by transvenous or combined percutaneous-transvenous approaches. In symptomatic Budd Chiari syndrome where recanalisation is not possible, we perform transjugular intrahepatic portosystemic shunts (TIPS) because TIPS decompresses the portal circulation directly in an adjustable way. In this series of patients with Budd Chiari syndrome treated with radiological interventions alone, we assess their medium term outcome using two independent objective prognostic indices. METHODS: We retrospectively studied 61 patients with non-malignant Budd Chiari syndrome treated by radiological intervention alone in our centre. RESULTS: Actuarial survival for the entire cohort at one year and five years was 94% and 87%, respectively. Survival of our patients with mild disease (according to the Murad classification) was 100% at one year and at five years, with intermediate disease severity 94% at one year and 86% at five years, and with severe disease 85% at one year and 77% at five years. CONCLUSION: Management of Budd Chiari syndrome by interventional radiology resulted in excellent medium term survival for patients in all categories of disease severity.

Adolescent↗

Pharmacological thrombolysis in Budd Chiari syndrome: a single centre experience and review of the literature.

BACKGROUND/AIMS: To review our experience of thrombolytic therapy in patients with acute Budd Chiari syndrome (BCS). METHODS: Records of 10 patients with BCS, treated by thrombolysis over a 12-year period were retrospectively analysed for demographics, clinical presentation/duration, primary disease, thrombolytic regimen, and follow-up. The same characteristics were also studied in previously reported patients. The agent used was recombinant tissue plasminogen activator (tPA) in all patients. RESULTS: Thrombolysis was used 12 times in 10 patients. Infusion was made systemically in three patients, into the hepatic artery in one patient, locally into a hepatic vein and/or IVC in four patients and locally within TIPS/portal vein in two patients. Only one infusion made systemically was partially successful. Adjunctive balloon angioplasty and/or stent insertion was undertaken for all eight procedures (in six patients) where local infusion was into the hepatic vein or TIPS. Six of these were ultimately successful (in five patients) and two were unsuccessful. Thrombolysis was more likely to be successful in the presence of a short history of thrombosis, when the thrombolytic agent was locally infused and when it was combined with a successful radiological procedure. Mean follow-up was 4.5 years (range 1-10 years). No serious bleeding complication occurred. CONCLUSIONS: We observed no benefit from thrombolysis when delivered systemically or arterially except in one case. Thrombolysis was useful in adjunctive management of BCS when the drug was infused locally into recently thrombosed veins that had appreciable flow following partial recanalisation. Thrombolysis was clearly of benefit in the repermeation of occluded/partially occluded hepatic veins/TIPS when early detection of new thrombus followed interventional procedures such as balloon angioplasty or stenting of hepatic veins.

Adolescent↗

Revealing the cause of cryptogenic cirrhosis by posttransplant liver biopsy.

INTRODUCTION: Because of the tendency for preexisting diseases to recur following liver transplantation, studying the course of patients who were transplanted for their cryptogenic cirrhosis may reveal features of the original cause. We examined the clinicopathological posttransplant progression of patients transplanted due to cryptogenic cirrhosis with emphasis on the detection of posttransplant steatosis and steatohepatitis. METHODS: The data on all patients transplanted for cryptogenic cirrhosis and their routine 1-year posttransplant liver biopsies were compared to a control group of a randomized sample of patients transplanted for other indications matched for length of follow-up. The posttransplant histological diagnosis was based on the latest available biopsy. RESULTS: Among 1710 patients, 39 present with cryptogenic etiology survived at least 1 year after transplantation. The control group consisted of 78 patients. The mean ages of the two groups were 50.7 and 49.3 years and the mean follow-up periods 6.2 and 5.7 years, both of which were similar. There was a significantly greater prevalence of posttransplant steatosis and steatohepatitis among the cryptogenic group (37.5 vs 16.7%, P = .048). The difference in patients with at least moderate steatosis was more pronounced (18.8 vs 3.3%, P = .035). Half of these cases progressed to fibrosis and cirrhosis after 48 months. CONCLUSIONS: This study found a greater incidence of allograft steatosis and steatohepatitis among patients transplanted for cryptogenic cirrhosis compared with a control group. A significant proportion of these patients developed a picture resembling nonalcoholic steatohepatitis, which progressed to fibrosis and cirrhosis.

Adult↗

Bone mineral density and markers of bone turnover in patients with glycogen storage disease types I, III and IX.

Patients with glycogen storage disease (GSD) types I, III and IX show reduced bone mineral content, but there is scarce data on new serum and urine markers of bone turnover or their relationship to bone densitometry. Six GSD I, four GSD III and four GSD IX patients underwent bone mineral density (BMD) measurement by dual-energy X-ray absorptiometry. Free pyridinoline (fPYD):creatinine and free deoxypyridinoline (fDPD):creatinine ratios were analysed on random urines. Procollagen type I C-terminal propeptide, procollagen type I N-terminal propeptide (PINP), carboxyterminal telopeptide of type I collagen and bone-specific alkaline phosphatase were analysed in serum. Some GSD I and GSD III patients had low or very low BMD. There was no difference in total body BMD z-score between the GSD types after adjusting for height (p=0.110). Bone marker analysis showed no consistent pattern. Urine fPYD:creatinine ratio was raised in four GSD I and two GSD III patients, while serum PINP was inappropriately low in some of these patients. There was no clear correlation between any markers of bone destruction and total body z-score, but the patient with the lowest total body z-score showed the highest concentrations of both urinary fPYD:creatinine and fDPD:creatinine ratios. We conclude that some GSD I and GSD III patients have very low bone mineral density. There is no correlation between mineral density and bone markers in GSD patients. The inappropriately low concentration of PINP in association with the raised urinary fPYD:creatinine and fDPD:creatinine ratios seen in two GSD I patients reflect uncoupling of bone turnover. All these findings taken together suggest that some GSD I and GSD III patients may be at an increased risk of osteoporosis.

Absorptiometry, Photon↗

Nodular regenerative hyperplasia of the liver and coeliac disease: potential role of IgA anticardiolipin antibody.

Nodular regenerative hyperplasia (NRH) of the liver is a rare disorder that is often associated with connective tissue disorders, haematological malignancy, or drugs, and is a cause of non-cirrhotic portal hypertension. We describe two cases of NRH in individuals with adult coeliac disease and IgA anticardiolipin antibodies. We discuss the potential impact of this observation on the understanding of the pathogenesis of NRH.

Adult↗

Antidepressant induced cholestasis: hepatocellular redistribution of multidrug resistant protein (MRP2).

BACKGROUND: We report two cases of antidepressant induced cholestasis. CASE REPORTS: We describe the first reported case of acute cholestasis due to citalopram (selective serotonin reuptake inhibitor) occurring in a patient who also experienced obstetric cholestasis in association with each of three pregnancies; in a second patient cholestasis developed due to dothiepin (tricyclic antidepressant), and six years later due to paroxetine. In both cases liver biopsies showed features of a "pure" cholestasis with total resolution within 1-6 months after withdrawal of the causative drug. Immunostaining for the canalicular transporter, multidrug resistant protein 2 (MRP2), responsible for biliary secretion of several organic anions including bilirubin glucuronides, showed sustained expression in both biopsies as well as relocalisation with appearance of strong staining of the basolateral membrane of the hepatocyte. This finding has also not been reported previously. CONCLUSIONS: We postulate that intracellular redistribution of MRP2 may reflect an adaptive compensatory mechanism which helps in the elimination of the drug or its cholestatic metabolites from the hepatocyte back to the sinusoidal space and subsequent excretion in urine. Changes seen in these two patients differ from findings previously reported in rats where downregulation of mrp2 occurs in response to experimentally induced cholestasis. We speculate that the rat is more advanced than humans in its ability to downregulate canalicular transporter expression as protection against progressive intrahepatic cholestasis.

Acute Disease↗

Two new species of Heligmoptera Nadtochiy, 1977 (Nematoda: Trichostrongylina: Heligmosomoidea) from myospalacine rodents in China (Gansu), with a redefinition of the genus.

Two species, Heligmoptera giraudouxi n. sp. and H. querei n. sp., are described. These are co-parasites of the small intestine of Myospalax fontanierii in China (Gansu). H. giraudouxi is closely related to the only existing species of the genus, H. myospalaxi (Nadtochiy, 1970), a parasite of Myospalax psilurus in the Primor'e Region of Russia. It is distinguished by the pattern of the left lateral lobe. H. querei differs from the two other species by possessing a long dorsal ray and from H. giraudouxi by the length of the left ala. From a phylogenetic point of view, these three species may form a small clade, adapted to Myospalax spp., derived from related forms in Insectivora, this capture resulting in the appearance of monodelphy.

Animals↗

Hepatoprotection with tauroursodeoxycholate and beta muricholate against taurolithocholate induced cholestasis: involvement of signal transduction pathways.

BACKGROUND: Tauroursodeoxycholate (TUDC) provides partial protection against taurolithocholate (TLC) induced cholestasis, possibly by inducing a signalling cascade activating protein kinase C (PKC). The potential protective effects of beta muricholic acid (beta-MC), another 7-beta-hydroxylated bile salt, have not previously been studied in TLC cholestasis. AIMS: To study the effect of beta-MC on TLC induced cholestasis and also to investigate further the effects of agents affecting intracellular signalling, notably DBcAMP (a cell permeable cAMP analogue) and several protein kinase inhibitors. METHODS: Functional studies were carried out analysing the proportion of hepatocyte couplets able to accumulate the fluorescent bile acid analogue cholyl-lysyl-fluorescein (CLF) into their sealed canalicular vacuole (cVA of CLF assay). RESULTS: It was found that both beta-MC and DBcAMP were as effective as TUDC in protecting against TLC induced cholestasis. The PKC inhibitors staurosporin and H7 but not the specific protein kinase A (PKA) inhibitor KT5720 abolished the protective effects of TUDC and beta-MC. BAPTA/AM, a chelator of intracellular Ca(2+), significantly decreased the protective effect of both bile salts, and that of DBcAMP. PKC and PKA inhibitors had no effect on protection with DBcAMP. CONCLUSIONS: Beta-MC was as effective as TUDC in protecting against TLC cholestasis. Mobilisation of Ca(2+) and activation of PKC, but not of PKA, are involved in the anticholestatic effect of the two 7-beta-hydroxylated bile salts. The hepatoprotective effects of DBcAMP involved Ca(2+) mobilisation, but not PKC or PKA activation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Effect of tauroursodeoxycholate and S-adenosyl-L-methionine on 17beta-estradiol glucuronide-induced cholestasis.

BACKGROUND/AIMS: S-adenosyl-L-methionine (SAMe) and tauroursodeoxycholate (TUDC) exert an additive ameliorating effect on taurolithocholate (TLC)-induced cholestasis. The aims were to investigate the protective effect of SAMe on 17beta-estradiol-glucuronide (17betaEG) cholestasis and to find out whether SAMe and TUDC may exert an additive, ameliorating effect. METHODS: Hepatocyte couplet function was assessed by canalicular vacuolar accumulation (cVA) of cholyllysylfluorescein (CLF). Cells were co-treated with 17betaEG and SAMe, TUDC, or both (protection study), or treated with 17betaEG and then with SAMe, TUDC or both (reversion study) before CLF uptake. Couplets were also co-treated with SAMe and dehydroepiandrosterone (DHEA), a competitive substrate for the sulfotransferase involved in 17betaEG detoxification. The effects of 17betaEG, SAMe and TUDC were also examined on intracellular distribution of F-actin. RESULTS: Both SAMe and TUDC significantly protected against, and reversed, 17betaEG-induced cholestasis, but their effects were not additive. DHEA abolished the protective effect of SAMe. 17BetaEG did not affect the uptake of CLF into hepatocytes at the concentrations used, and also, it did not affect the intracellular distribution of F-actin. CONCLUSIONS: 17BetaEG does not affect the uptake of CLF into hepatocytes. SAMe and TUDC protect and reverse 17betaEG-induced cholestasis, but without an additive effect. Protection by SAMe may involve facilitating the sulfation of 17betaEG.

Actins↗

Visualization of the transport of primary and secondary bile acids across liver tissue in rats: in vivo study with fluorescent bile acids.

BACKGROUND/AIMS: Lysyl fluorescein conjugated bile acid analogues (LFCBAA) closely parallel their natural counterparts. To assess LFCBAA as a tool for the visualization of bile acid transport within liver tissue. METHODS: Wistar rats were administered physiological concentrations of the primary bile acid analogue cholyllysyl fluoroscein (CLF) and of the secondary bile acid analogue lithocholyllysyl fluorescein (LLF) and serial liver biopsies were taken at fixed intervals. Both compounds were also injected retrogradely into the biliary tree. Frozen sections were examined by fluorescence microscopy. RESULTS: Both CLF and LLF were rapidly taken up from sinusoidal blood but differed significantly in their hepatic handling. CLF was rapidly transported into bile, whereas LLF transport was slower and produced significantly more bile duct fluorescence. LLF clearance showed a lobular gradient with last remaining bile acid being confined largely to zone 3. Both compounds were avidly taken up by cholangiocytes after injection intravenously or retrogradely into the biliary tree. CONCLUSIONS: Visualization of LFCBAA by fluorescence microscopy may yield further information regarding hepatobiliary bile acid localization during studies of physiological and pathological mechanisms involved in transport of bile acids. The presence of both compounds within cholangiocytes strongly suggests that they may undergo a degree of chole-hepatic recirculation.

Animals↗

Liver transplantation for polycystic liver disease.

Polycystic liver disease (PLD) may provoke massive hepatomegaly and severe physical and social handicaps. Data on orthotopic liver transplantation (OLT) for PLD are rare and conflicting. Conservative surgery (resection or fenestration) is indicated for large single cysts, but its value for small diffuse cysts is questionable. In addition, conservative surgery is not devoid of morbidity and mortality. OLT offers the prospect of a fully curative treatment, but controversy remains because those patients usually have preserved liver function. Thus, we reviewed our experience with OLT for PLD. Sixteen adult women underwent OLT for small diffuse PLD between 1990 and 1999. Mean age was 45 years (range, 34 to 56 years). Fourteen patients had combined liver and kidney cystic disease, but only 1 patient required combined liver and kidney transplantation, whereas 13 patients underwent OLT alone. Two patients had isolated PLD. Indications for transplantation were massive hepatomegaly causing physical handicaps (n = 16), social handicaps (n = 16), malnutrition (n = 4), and cholestasis and/or portal hypertension (n = 5). OLT caused no technical difficulty in 15 of 16 patients (surgery duration, 6.8 hours; range, 5 to 8 hours), with blood transfusions of 7.9 units (range, 0 to 22 units). One patient who underwent attempted liver-mass reduction pre-OLT died of bleeding and pulmonary emboli. Native liver weight was 10 to 20 kg. Posttransplantation immunosuppression consisted of cyclosporine or FK506, azathioprine, and steroids (discontinued at 3 months). Morbidity included biliary stricture (2 patients), revision for bleeding and hepatitis (1 patient), pneumothorax and subphrenic collection (1 patient), and tracheostomy (1 patient). One patient died of lung cancer 6 years posttransplantation. Both patient and graft survival rates are 87.5% (follow-up, 3 months to 9 years). Of 15 patients who underwent OLT alone, only 1 patient needed a kidney transplant 4 years after OLT. Kidney function has remained satisfactory in the other patients despite the use of cyclosporine or FK506 (last follow-up creatinine level, 1.55 mg/dL; range, 0.80 to 2.85 mg/dL). OLT had a dramatic impact on daily quality of life, enabling these patients to go back to a fully active life style. OLT offers the chance of a definitive treatment in patients with extensive, small, diffuse PLD that has evolved into severely handicapping hepatomegaly. In contrast to previous studies, combined liver and kidney transplantation is rarely needed. Patient symptoms and chances of definitive palliation offered by OLT must be balanced against the risks of transplantation and lifelong commitment to immunosuppression.

Adult↗

[Laparoscopic treatment of symptomatic calculous diverticulum of the calyx].

Treatment of urinary stones in a caliceal diverticulum may be indicated when they are symptomatic. Operative techniques for the kidney are continuing to improve. After open surgery and percutaneous surgery, laparoscopy occupies an increasingly important place in the urological therapeutic armamentarium over recent years. The authors report the case of a woman with a stone in an inferior caliceal diverticulum, discovered in the context of acute pyelonephritis, and effectively treated by transperitoneal laparoscopy. The details of the operative technique are described and discussed in relation to the techniques reported in the literature.

Diverticulum↗

Lamivudine without HBIg for prevention of graft reinfection by hepatitis B: long-term follow-up.

BACKGROUND: This open, multicenter study was conducted to evaluate the efficacy and safety of lamivudine prophylaxis given to chronic hepatitis B virus-(HBV) infected patients before and after orthotopic liver transplantation (OLT). We now present long-term data that follow our previous short-term report. METHODS: Twenty-three patients were treated with lamivudine (100 mg orally, daily); 13 (57%), were serum HBV DNA positive (Abbott Genostics, Abbott Laboratories, Chicago, IL) at study entry. Patients received lamivudine for at least 4 weeks before OLT, and for up to 50 months (median 25 months) after OLT. RESULTS: Of the 23 treated patients, 17 survived to undergo OLT. Eleven patients (65%) survived up to 4 years (median 36 months) after OLT. One of the survivors stopped lamivudine because of a possible adverse reaction 9 months post-OLT, and prophylaxis with HBV immune globulin was then established. Ten survivors continue lamivudine. Eight long-term survivors have normal liver function without evidence of HBV reinfection. Of the 17 transplanted patients, 6 died. Four patients died (3 days to 5 months post-OLT) without evidence of graft reinfection. Two further patients died at 19 and 23 months post-OLT from graft failure. Both patients had YMDD variant detected at 12 months post-OLT. Two other patients with YMDD-variant HBV remain alive on lamivudine, 9 and 15 months after development of the variant. CONCLUSIONS: Lamivudine, given before and after OLT, prevents significant graft reinfection for the majority of treated patients. The study has also shown that lamivudine is extremely well tolerated by liver failure patients and for a prolonged period after transplantation.

Biopsy↗

Increased incidence of chronic rejection in adult patients transplanted for autoimmune hepatitis: assessment of risk factors.

BACKGROUND/AIM: It remains uncertain whether autoimmune hepatitis (AIH), as an original indication for orthotopic liver transplantation (OLTX), predisposes to the development of chronic rejection (CR) after surgery and published reports on heterogeneous groups of patients provided conflicting data. In this work we analyzed the incidence and risk factors for CR in a large cohort of adult patients transplanted for AIH in our unit. RESULTS: A total of 1190 adult patients received OLTX in our center between 1982 and 1998. A total of 77 patients (6.5%) were transplanted for AIH and 12 (15.6%) patients from this group developed clinical and histological features of CR within a median time of 3.5 months after OLTX. Patients with AIH who developed CR were younger than other AIH patients at OLTX (32 vs. 44.2 ys; P=0.015) and more often had histological features of moderate or severe acute rejection (83 vs. 34%; P=0.002) on early post-OLTX biopsies. The incidence of CR in AIH patients was significantly higher than in subjects transplanted for other indications such as primary biliary cirrhosis (8.2%; P<0.05), primary sclerosing cholangitis (5.2%; P<0.05) or alcoholic cirrhosis (2.0%; P<0.001). Also, we observed a tendency to decreased incidence of CR with time in all transplanted subjects. CONCLUSIONS: Apart from younger age at OLTX and higher incidence of severe acute rejection, patients with AIH who developed CR did not differ from other subjects transplanted for this indication. Unlike other studies, not stratified by diagnosis, recipient CMV negative status, young donor age, and HLA DR matching were not identified as risk factors for CR in AIH.

Adult↗

Heterozygous MDR3 missense mutation associated with intrahepatic cholestasis of pregnancy: evidence for a defect in protein trafficking.

Intrahepatic cholestasis of pregnancy (ICP) is a liver disease of pregnancy with serious consequences for the mother and fetus. Two pedigrees have been reported with ICP in the mothers of children with a subtype of autosomal recessive progressive familial intrahepatic cholestasis (PFIC) with raised serum gamma-glutamyl transpeptidase (gamma-GT). Affected children have homozygous mutations in the MDR3 gene (also called ABCB4 ), and heterozygous mothers have ICP. More frequently, however, ICP occurs in women with no known family history of PFIC and the genetic basis of this disorder is unknown. We investigated eight women with ICP and raised serum gamma-GT, but with no known family history of PFIC. DNA sequence analysis revealed a C to A transversion in codon 546 in exon 14 of MDR3 in one patient, which results in the missense substitution of the wild-type alanine with an aspartic acid. We performed functional studies of this mutation introduced into MDR1, a closely related homologue of MDR3. Fluorescence activated cell sorting (FACS) and western analysis indicated that this missense mutation causes disruption of protein trafficking with a subsequent lack of functional protein at the cell surface. The demonstration of a heterozygous missense mutation in the MDR3 gene in a patient with ICP with no known family history of PFIC, analysed by functional studies, is a novel finding. This shows that MDR3 mutations are responsible for the additional phenotype of ICP in a subgroup of women with raised gamma-GT.

ATP Binding Cassette Transporter, Subfamily B↗

Reduced hepatic content of dehydroepiandrosterone sulphotransferase in chronic liver diseases.

AIMS/BACKGROUND: Dehydroepiandrosterone sulphotransferase (DHEA ST) is the enzyme responsible for sulphation of lithocholic acid and other potentially hepatotoxic steroids. We have previously shown that DHEA ST activity is reduced in cytosol of liver from miscellaneous patients with chronic liver disease. The aim of this study was to investigate the cause of diminished sulphotransferase activity in order to further our understanding of whether a reduction in the ability to sulphate potentially hepatotoxic bile acids might play a role in the aetiology of primary cholestatic liver disease. METHODS: We quantified DHEA ST in human liver cytosol from groups of patients with chronic liver diseases and normal subjects using a semiquantitative sodium dodecyl sulphate/polyacrylamide gel electrophoresis (SDS-PAGE)/ immunoblotting method, and an enzyme-linked immunosorbent assay (ELISA). We determined DHEA ST enzyme activity and correlated it with its immunoreactive concentration in 87 samples of human liver tissue. RESULTS: DHEA ST activity and concentration were significantly reduced in primary biliary cirrhosis, primary sclerosing cholangitis, chronic active hepatitis and alcoholic cirrhosis but not in cryptogenic cirrhosis when compared to normal liver. There were no significant differences among disease groups. In all groups enzyme activity and cellular concentration correlated, suggesting that no aberrant non-functional enzyme was produced. CONCLUSION: These results confirm that DHEA ST activity is diminished in liver disease and that the reduction is due to diminished enzyme presence. Further studies are required to show whether the reduction has any pathogenetic significance or is merely a consequence of disease.

Adult↗

Plasma elimination of cholyl-lysyl-fluorescein (CLF): a pilot study in patients with liver cirrhosis.

BACKGROUND: Cholyl-lysyl-fluorescein (CLF) is a fluorescein-labelled bile acid whose biological behaviour closely resembles that of naturally occurring cholyl glycine. AIM: The aim of this study was to analyze the CLF plasma elimination in patients with liver cirrhosis. METHODS: A dose of CLF at 0.02 mg/kg b.w. was administered i.v. in 26 patients with liver cirrhosis and 9 healthy volunteers. Blood samples were collected before injection and then at 10 min intervals over 60 min. Plasma fluorescence was measured by a luminescence spectrometer and residual fluorescence over the time of the study was compared in each group. Routine liver function tests (rLFTs) were performed before each injection. RESULTS: Plasma elimination of CLF was significantly impaired in patients with cirrhosis compared to healthy subjects with p values <0.0001 at each analyzed time point. CLF test showed 100% sensitivity for liver cirrhosis when residual fluorescence was measured 30, 40, 50 and 60 min after injection. Routine LFTs showed 85% sensitivity for bilirubin, 84% for total bile acids, 69% for aspartate aminotransferase 62% for albumin and 50% for alkaline phosphatase. CLF elimination measured 60 min after injection correlated with Child-Pugh score (r=0.3945; p<0.05) and albumin (rs=0.6451; p<0.001). No adverse reaction or side effects of CLF were observed. CONCLUSIONS: CLF test clearly distinguished between the two analyzed groups and was more sensitive than routine liver function tests. The test appears safe, simple to perform and analyze and after validation in larger cohorts of patients may have the potential to become a useful dynamic test of liver function.

Adult↗