Orthotopic liver transplant with hepatic artery occlusion and portal vein thrombosis.
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Adult↗
Biomedical subjects
H Solomon
Publications and source records attributed to H Solomon.
Is hepatitis G/GB virus-C virus hepatotropic? Detection of hepatitis G/GB virus-C viral RNA in liver and serum.
The recently identified hepatitis G virus (HGV, also named GB virus-C, GBV-C) appears to have similarities to hepatitis C virus and other flaviviridae. To better understand its clinical significance and hepatotropism, we collected liver tissue and matched serum samples from 56 patients undergoing liver transplantation. HGV/GBV-C RNA was detected by reverse transcription-nested PCR, using primers from the relatively conserved 5' noncoding region of the genome to detect HGV/GBV-C RNA and the amount was semiquantitatively estimated by serial 10-fold endpoint dilution. The presence and amount of HCV RNA was estimated by the same methodology. Seventeen patients (30%) had HGV/GBV-C RNA detectable either in liver or in serum, including two of three with cryptogenic liver disease. Interestingly, 5 of 17 (29%) patients had HGV/GBV-C RNA in serum but not liver, even with repeated testing of hepatic RNA from different portions of the liver. Furthermore, the titer of HGV/GBV-C RNA was significantly lower in liver than in serum in most samples (mean log titer, 1.33 vs. 2.56, P < 0.05). In contrast, all 21 patients with HCV RNA in serum also had the virus detectable in liver. In five patients coinfected with HCV and HGV/GBV-C, the mean titer of HCV RNA in liver was higher than that in serum (log titer, 2.8 vs. 3.0, P > 0.05). Thus, our results suggest that HGV/GBV-C is probably not hepatotropic and may replicate predominantly in sites other than the liver. These findings brings into question the role of HGV in causing significant liver disease.
5' Untranslated Regions↗
Management and outcome of patients with combined bile duct and hepatic artery injuries.
BACKGROUND: Major bile duct injury is an important therapeutic problem that can be associated with simultaneous injury to the hepatic artery. Limited information exists regarding the course of patients who have combined bile duct and arterial injuries. OBJECTIVE: To compare the management and outcome of isolated bile duct injuries with bile duct and hepatic artery injuries. PATIENTS AND METHODS: Since 1991, 13 patients have undergone reconstruction of right and left hepatic confluence or proximal bile duct injuries. At the time of bile duct injury, 4 of these patients had simultaneous occlusion or extirpation of the right hepatic or common hepatic artery. All patients underwent reconstruction of the biliary tract with hepaticojejunostomies. The immediate and long-term outcomes of the patients with and without hepatic artery injury were compared. RESULTS: In the immediate postoperative period, 3 of 4 patients with combined injuries had hepatic necrosis and/or abscesses with 2 patients requiring transcutaneous or operative drainage. This problem was not diagnosed in patients with isolated bile duct injuries. None of the biliary anastomoses have failed in the patients with isolated bile duct injuries while 50% of the anastomoses in patients with combined injuries have caused recurrent problems following reconstruction. CONCLUSION: Patients with major bile duct injuries should be evaluated for concomitant hepatic arterial injury as management and outcome may be influenced by the absence of arterial blood flow to the injured bile ducts and to the liver.
Adult↗
Role of neutrophils in hepatotoxicity induced by oral acetaminophen administration in rats.
Acetaminophen (APAP) is a common analgesic and antipyretic compound which, when administered in high doses, has been associated with significant morbidity and mortality, secondary to hepatic toxicity. To date, the mechanism(s) whereby APAP induces liver injury remains to be delineated. This study investigated the potential role of neutrophils as contributors to liver injury in rats administered sublethal doses of APAP. Oral APAP administration (650 mg/kg) was associated with increases in serum alanine transaminase (ALT) levels indicating biochemical evidence of significant liver damage. Furthermore, histological analyses verified significant hepatocellular necrosis as well as enhanced myeloperoxidase staining in these liver specimens. However, if animals were pretreated with antineutrophil sera prior to APAP administration, neutrophil counts remained depressed, ALT levels were significantly decreased, and the degree of liver injury was attenuated on a histological level. Taken together these data suggest that neutrophils mediate, at least in part, the hepatotoxic effects of oral acetaminophen administration in rats.
Acetaminophen↗
Clostridium difficile colitis requiring subtotal colectomy in a renal transplant recipient: a case report and review of literature.
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Adult↗
Estradiol regulates estrogen receptor mRNA stability.
Previous studies suggest that post-transcriptional events play an important role in estrogen-induced loss of estrogen receptor expression. The present study shows that treatment of MCF-7 cells with estradiol resulted in a six-fold decrease in estrogen receptor mRNA half-life from 4 h in control cells to 40 min in estradiol treated cells. To determine the role of protein synthesis in the regulation of estrogen receptor mRNA stability, several translational inhibitors were utilized. Pactamycin and puromycin, which prevent ribosome association with mRNA, inhibited the effect of estradiol on receptor mRNA stability, whereas cycloheximide, which has no effect on ribosome association with mRNA, had no effect on estradiol regulation of estrogen receptor mRNA stability. In control cells, the total cellular content of estrogen receptor mRNA was associated with high molecular weight polyribosomes. Treatment with estradiol resulted in a 70% decrease in estrogen receptor mRNA associated with polyribosomes but had no effect on the polyribosome distribution of estrogen receptor mRNA. In an in vitro degradation assay, polyribosomes isolated from estradiol-treated cells degraded ER mRNA faster than polyribosomes isolated from control cells. The nuclease activity associated with the polysome fraction appeared to be Mg2+ independent and inhibited by RNasin. Freeze-thawing and heating at 90 degrees C for 10 min resulted in the loss of nuclease activity. These studies suggest that an estrogen-regulated nuclease activity associated with ribosomes alters the stability of estrogen receptor mRNA.
Breast Neoplasms↗
Microsatellite instability in human hepatocellular carcinoma: relationship to p53 abnormalities.
AIMS/BACKGROUND: Microsatellite instability was sought in 10 human hepatocellular carcinomas (HCCs) to determine whether defective DNA mismatch repair might be implicated in the multiple genetic alterations observed in the p53 tumor suppressor gene in some of these patients' tumors. METHODS: Genomic DNA from HCCs and adjacent nontumorous livers was subjected to PCR with primers for nine microsatellites, and PCR products were resolved in a denaturing gel. Microsatellite instability was defined as the presence of band shifts or additional bands for at least two microsatellite sequences in an HCC compared to the nontumorous liver tissue from the same patient. RESULTS: Microsatellite instability was detected in four of ten HCCs. Three of these four HCCs did not have p53 exon mutations. However, one HCC had microsatellite instability as well as multiple p53 exon mutations and multiple intron alterations. Four other patients with multiple p53 intron alterations in HCC (compared to their own nontumorous liver), three of whom also had a mutation in the exons, had no microsatellite instability. CONCLUSIONS: Defective DNA mismatch repair, as indicated by microsatellite instability, might have played a role in hepatocarcinogenesis in four of the ten patients, but in general it was not associated with p53 alterations. In one of the ten patients, defective DNA mismatch repair might have been the cause of multiple mutations in both the coding and intron sequences of the p53 gene.
Adolescent↗
Prognostic value of dipyridamole thallium-201 screening to minimize perioperative cardiac complications in diabetics undergoing kidney or kidney-pancreas transplantation.
To minimize perioperative cardiac events, we utilize a screening protocol consisting of intravenous dipyridamole thallium-201 myocardial imaging (DPT), with the selective use of coronary angiography based on the presence of reversible defect(s) on DPT test. A retrospective study was performed to determine the prognostic value of this protocol and to identify any clinical parameters predictive of an abnormal DPT test. To accomplish this, a detailed chart analysis of 176 consecutive kidney (n = 89) and kidney-pancreas (n = 87) transplant recipients who had undergone pretransplant DPT testing was performed. The results of the DPT test were interpreted as normal in 111, fixed defect in 15, and reversible defect(s) in 50 patients. Forty-two of the 50 patients with reversible defect(s) underwent coronary angiography. Twelve of the 27 patients with significant coronary artery disease (CAD, > 50% stenosis in one or more coronary arteries) underwent pretransplant revascularization and the remaining 15 were treated medically. Cardiac events (documented acute myocardial infarction or sudden cardiac death) within 6 wk of transplant were stratified by the results of this protocol. Also, various clinical parameters were compared between patients with normal and abnormal (fixed and reversible defect) DPT tests. Only one of the 111 (0.9%) transplant recipients with a normal DPT test had a perioperative cardiac event. None of the 15 (0%) patients with a fixed defect and none of the 15 (0%) patients with reversible defect(s), but a nonsignificant (< 50% narrowing) coronary angiogram, had a perioperative cardiac event. Three of the 27 (11.1%) patients with reversible defect(s) and significant disease on coronary angiography, who had undergone pre-transplant revascularization or were managed medically, had a perioperative coronary event. Of 14 recipients parameters analyzed, age > 50 yr was the only variable predictive of an abnormal DPT test. We conclude that the incidence of perioperative cardiac events in patients with a normal or fixed defect, or reversible defect(s) but a nonsignificant (< 50% narrowing) coronary angiogram is very low, indicating the high correlation of these findings on DPT and an uneventful (cardiac) post-transplant course. The incidence of perioperative cardiac complications amongst the high-risk transplant recipients with reversible defect(s) and significant CAD on coronary angiogram may be minimized by appropriate preoperative medical management or revascularization. None of the clinical variables except age > 50 yr was predictive of an abnormal DPT test.
Adult↗
Renoprotective effects of the 21-aminosteroid U74389G in ischemia-reperfusion injury and cold storage preservation.
Free radical mediated lipid peroxidation (LPO) has been implicated in the pathogenesis of ischemic-reperfusion injury (IRI). To address the renoprotective effect(s) of LPO inhibition, the efficacy of the 21 aminosteroid U74389G was evaluated in three IRI models. In Model 1 51 unilateral nephrectomized rats that underwent 60 min of warm ischemia followed by a 72-hr reperfusion interval were treated with the test vehicle only, or 3, 6, or 12 mg/kg of U74389G intravenously, 5 min pre- or postischemia. In Model 2 Sprague-Dawley rats underwent sham operation (n=9), or 45 min of warm ischemia and 10 min of reperfusion with U74389G (6 mg/kg; n=10) or test vehicle only (n=10) administered intravenously over 10 min beginning 5 min prior to clamp release. After reperfusion, LPO was determined by assay of snap frozen tissue for thiobarbituric acid (TBA) concentrations (nmol/g tissue weight). In Model 3 domestic lean maid pigs (14-18 kg) underwent left nephrectomy with 30 min of warm ischemia, Collins C-4 flush, and 24 hr of cold storage preservation. Heterotopic autotransplantation and immediate contralateral nephrectomy was then performed in Group A-nonischemic controls (n=4), Group B-ischemic controls (n=5), and Group C-U74389G (6 mg/kg) administered preischemia and at autotransplantation (n=5). In Model 1 maximal renoprotection was demonstrated with the 6 mg/kg dose of U74389G administered after ischemia (ischemic control 72-hr serum creatinine (Cr) = 8.01+/-1.1 mg% vs. 3.32+/-0.96 mg%; ischemic control creatinine clearance = 0.069+/-0.03 ml/min vs. 0.206+/-0.04 ml/min; P<0.05). In Model 2 TBA levels were significantly lower in U74389G treated animals (88.5+/-10.0 vs. ischemic controls = 296.8+/-81.4; P=0.02). In Model 3 graft survivals were 100%, 0%, and 60% respectively. Peak Cr and BUN (mg%) were significantly greater in Group C vs. Group A, (Group A Cr = 8.59+/-0.63 vs. Group C = 12.8+/-1.01; Group A BUN = 64.1+/-2.73 vs. Group C = 104.9+/-12.21)--however, by day 10, thee were no significant differences in renal function: (Group A Cr = 2.15+/-0.3 vs. Group C = 2.10+/-0.06; Group A BUN = 27.0+/-6.0 vs. Group C = 31.1+/-6.4). These results support the beneficial effects of LPO inhibitors in models of ischemia-reperfusion, as well as preservation/transplantation, and suggest that this renoprotection correlates with decreased membrane lipid peroxidation.
Animals↗
Effects of low-intensity AC and/or DC electromagnetic fields on cell attachment and induction of apoptosis.
Rat tendon fibroblast (RTF) and rat bone marrow (RBM) osteoprogenitor cells were cultured and exposed to AC and/or DC magnetic fields in a triaxial Helmholtz coil in an incubator for up to 13 days. The AC fields were at 60 and 1000 Hz and up to 0.25 mT peak to peak, and the DC fields were up to 0.25 mT. At various combinations of field strengths and frequencies, AC and/or DC fields resulted in extensive detachment of preattached cells and prevented the normal attachment of cells not previously attached to substrates. In addition, the fields resulted in altered cell morphologies. When RTF and RBM cells were removed from the fields after several days of exposure, they partially reattached and assumed more normal morphologies. An additional set of experiments described in the Appendix corroborates these findings and also shows that low-frequency EMF also initiates apoptosis, i.e., programmed cell death, at the onset of cell detachment. Taken together, these results suggest that the electromagnetic fields result in significant alterations in cell metabolism and cytoskeleton structure. Further work is required to determine the relative effect of the electric and magnetic fields on these phenomena. The research has implications for understanding the role of fields in affecting bone healing in fracture nonunions, in cell detachment in cancer metastasis, and in the effect of EMF on organisms generally.
Animals↗
Rapid development of hepatic alpha1-antitrypsin globules after liver transplantation for chronic hepatitis C.
A 37-year-old man undergoing liver transplantation for cirrhosis caused by chronic hepatitis C and alcoholism developed large numbers of alpha1-antitrypsin (AAT) globules within hepatocytes of the transplanted liver during a 5-month period. This finding occurred simultaneously with severe recurrent hepatitis C. The AAT phenotype of this patient changed from MM before transplantation to MZ after transplantation; AAT levels in serum did not change significantly. After a second liver transplantation 6 months after the first, the AAT phenotype reverted to MM and globules were not detectable in the second transplanted liver. Severe recurrent hepatitis C and the appearance of AAT globules within the liver allograft of a heterozygous donor may be related. The recurrent infection may have induced accumulation of AAT protein, or, alternatively, the MZ liver may have been more susceptible to injury from recurrent viral infection.
Adult↗
A new autosomal dominant disorder of pyogenic sterile arthritis, pyoderma gangrenosum, and acne: PAPA syndrome.
OBJECTIVE: To describe a multigenerational family with transmission of an autosomal dominant disorder characterized by pyogenic arthritis, pyoderma gangrenosum, and severe cystic acne. MATERIAL AND METHODS: We present a detailed case report of a 39-year-old man with arthritic changes in several joints, pyoderma gangrenosum, and cystic acne. Several relatives from three generations of his family underwent clinical and genetic investigations. The findings in this kindred are reported. RESULTS: Ten affected family members in three generations manifested variable expression of a pauciarticular, nonaxial, destructive, corticosteroid-responsive arthritis that began in childhood; pyoderma gangrenosum; and severe cystic acne in adolescence and beyond. Other less commonly associated features included adult-onset insulin-dependent diabetes mellitus, proteinuria, abscess formation at the site of parenteral injections, and cytopenias attributable to sulfonamide medications. Laboratory evaluation was nondiagnostic. Genetic studies excluded linkage to the major histocompatibility locus. CONCLUSION: The acronym of PAPA syndrome (pyogenic sterile arthritis, pyoderma gangrenosum, and acne) is suggested for this newly recognized pleiotropic autosomal dominant disorder. The nature of the genetic alteration in PAPA syndrome is unknown.
Acne Vulgaris↗
Risk of wrist injury from repetitive use of ultrasound transducers.
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Allied Health Personnel↗
Evaluation of the thromboxane A2 synthetase inhibitor OKY-046 in a warm ischemia-reperfusion rat model.
The pathophysiology of ischemia-reperfusion renal injury is mediated, in part, by the generation of the vasoconstricting prostanoid thromboxane A2 (TXA2). This study was undertaken to evaluate the renoprotective effects, as well as the optimal timing and dosage, of a selective thromboxane synthetase inhibitor, OKY-046, in a unilateral nephrectomized, 60 min ischemia, 72 hr reperfusion, rodent model. Forty-one rats were subjected to right nephrectomy only (group A), or right nephrectomy with 60 min of left renal ischemia and treatment with inactive vehicle only (group B), or 2 mg/kg or 4 mg/kg of OKY-046 administered intravenously before (groups C and D) or after (groups E and F) pedicle clamping. Outcome variables included animal survival; change in kidney weight; 0, 24, and 72 hr plasma creatinine (CR); urea nitrogen (BUN); thromboxane B2 (TXB2) and 6-keto prostaglandin F(1alpha) (6 kPGF(2alpha)) levels; creatinine clearance (CRCL); and histologic evidence of renal injury. Animal survival and postperfusion kidney weight were not significantly different among the groups. However, renal functional parameters were significantly improved with the 2 mg/kg dose of OKY-046 administered after renal ischemia. (group B 72 hr Cr= 8.01 +/- 1.1 mg% vs. group E=3.99 +/- 1.5 mg%, and group B 72 hr BUN=241.3 +/- 32.8 mg% vs. group E=52.6 +/- 22.5 mg%). The CRCL was also improved in group E vs. group B, although these results did not reach statistical significance (group B=0.069 ml/min vs. group E=0.194 ml/ min). The 24 hr TXB2 levels were significantly increased in group B (0 hr=754.1 +/- 219.4 pg/ml vs. 24 hr=2055.9 +/- 550.0 pg/ml), and pre- or posttreatment with OKY-046 abrogated this increase (group C 0 hr=517.1 +/- 80.9 pg/ml vs. 24 hr=384.7 +/- 251.5 pg/ml, and group E 0 hr=781.6 +/- 390.4 pg/ml vs. 24 hr=183.0 +/- 81.4 pg/ml). The 24 hr 6 kPGF(1alpha) levels decreased in all groups, whereas 72 hr 6 kPGF(1alpha) levels increased above baseline in groups A, C, and E, but not in group B. These data demonstrate the beneficial effects of thromboxane A2 synthesis inhibition in the setting of ischemia-reperfusion injury and suggest that this renoprotection correlates with late vasodilatory prostanoid synthesis.
6-Ketoprostaglandin F1 alpha↗
Exocrine effects of the CCK antagonist L-364,718 in canine pancreatic autografts.
This study evaluated the effect of the cholecystokinin antagonist L-364,718 on exocrine secretion in canine pancreatic autografts with pancreaticocystostomies. Urinary (autograft) amylase (U/min) and bicarbonate (mmole/min) secretion, over a 6 hr interval, were determined in the basal state (Group A), after a bolus injection of 20 nmoles/kg of L-364,718 (Group B), during a continuous cholecystokinin octapeptide (OP-CCK) infusion at 125 ng/kg/hr either alone (Group C), with a bolus injection of 20 nmoles/kg (Group D), or 30 nmoles/kg (Group E), of L-364,718 1 hr before initiating OP-CCK, or 20 nmoles/kg of L-364,718 1 hr after initiating OP-CCK (Group F). L-364,718 had no effect on basal or OP-CCK-stimulated secretion of bicarbonate. Basal amylase secretion was decreased 1 hr after L-364,718 and remained significantly lower than controls throughout the study interval. When compared to Group C (280.3 +/- 48.6), OP-CCK-stimulated amylase secretion was significantly lower for the first hour after L-364,718 in both Group D (157 +/- 46.7) and Group E (31.9 +/- 11.6). In Group E, 2, 3, and 4 hr post-L-364,718 amylase releases were 60.2 +/- 19.7, 77.7 +/- 25.1, and 87.2 +/- 28.3 compared to 335.5 +/- 85.9, 291.0 +/- 21.8, and 289.9 +/- 45.7 in Group C indicating a sustained significant inhibition of stimulated autograft amylase secretion with the higher L-364,718 dosage. In Group F, no significant change in amylase secretion was demonstrated, indicating that L-364,718 must be administered prior to CCK stimulation to be effective. These studies demonstrate that L-364,718 has a dose dependent, inhibitory effect on basal, and OP-CCK-stimulated amylase secretion in a denervated autograft model. The therapeutic potential of L-364,718 and other CCK receptor antagonists in pancreatic transplantation warrants further study.
Amylases↗
Prognostic value of the monoethylglycinexylidide liver function test in assessing donor liver suitability.
BACKGROUND: Liver graft assessment prior to transplantation continues to be controversial. Various donor organ parameters must be evaluated to ensure that the transplanted organ will function and that the number of organs discarded will be minimized. Recent attempts to quantify liver function have utilized the metabolism of lidocaine to monoethylglycinexylidide (MEGX), and the MEGX test has been employed to evaluate the functional characteristics of donor livers prior to transplantation, with conflicting results. OBJECTIVE: To ascertain the role of quantitating the metabolic rate of lidocaine in predicting the results of liver transplantation. METHODS: Consecutive liver donors (N = 37) underwent quantitation of the amount of lidocaine converted to MEGX at 15 minutes. The donor patients were divided arbitrarily into efficient and poor lidocaine metabolizers, and the results of liver transplantation were evaluated. RESULTS: Patients who received livers that produced MEGX values of 80 ng/mL or less in 15 minutes had no definable alteration in transplantation outcome compared with patients who received livers that were more efficient lidocaine metabolizers. In a collected series, 46 patients who received livers that produced MEGX values of 80 ng/mL or less had a 1-month graft survival rate of 89% (41/46), while 74 patients who received livers that produced MEGX values greater than 80 ng/mL had a 1-month graft survival rate of 86% (64/74). CONCLUSIONS: The MEGX test had no practical utility in predicting liver graft functional status.
Humans↗
Effect of L-364,718 on pancreatic endocrine function following partial pancreatectomy.
This study was designed to determine the effect of a potent cholecystokinin antagonist, L-364,718, on canine pancreatic endocrine function following partial pancreatectomy. Plasma glucose, insulin, and glucagon were determined over a 2-hr interval following an intravenous bolus of 0.5 g/kg glucose in a 50% solution. The following groups were established: normal animals (group A, n = 5), normal animals pretreated with 20 nmole/kg L-364,178 (group B, n = 5), partially pancreatectomized animals (group C, n = 5), and partially pancreatectomized animals pretreated with 20 nmole/kg L-364,178 (group D, n = 5). In contrast to animals with an intact pancreas, pretreatment with L-364,718 following partial pancreatectomy resulted in a significant decrease in peak insulin (group C = 132.8 +/- 13.0 microU/ml vs Group D = 90.4 +/- 16.1 microU/ml, P < 0.05) and the basal-to-peak insulin difference (group C = 111.9 +/- 11.5 microU/ml vs group D = 77.5 +/- 16.6 microU/ml, P < 0.05). Despite this, the rate of glucose utilization (K value) was significantly increased in the partially pancreatectomized animals given the antagonist (group C = -1.22 +/- 0.22%/min vs group D = -2.79 +/- 0.427%/min) and there were no significant differences in basal or peak glucose when comparing the groups given L-364,718 with the groups given placebo (group A vs B and group C vs D). Thus, the CCK antagonist L-364,718 significantly decreases peak insulin in partially pancreatectomized animals but not in nonoperative control animals. There is a paradoxical increase in the rate of glucose utilization but no effect on glucose homeostasis. The effect of this antagonist in other models of reduced islet cell reserve (i.e., pancreas transplantation) remains to be determined.
Animals↗
The effect of prostanoids on hepatic bile flow in dogs with normal liver and bile duct cell hyperplasia.
Bile flow rates and composition are subject to a wide variety of neural, endocrine and paracrine influences. The effects of these multiple factors may be different in the diseased liver compared to the response produced in the normal liver. As prostanoids may have a therapeutic role in liver disease it was intended to evaluate the effects of two principal therapeutic prostanoids, prostaglandin E2 and prostacyclin, on bile flow in dogs with a normal liver and in dogs with hepatotoxin-induced liver injury. Initially, in awake animals with chronic biliary and gastric fistulas the bile flow response to prostaglandin E2 and prostacyclin was evaluated and compared to the response produced by bile salt infusion alone and to that produced by the standard choleretic hormones, secretin and glucagon. The animals were then fed alpha-naphthylisothiocyanate (ANIT) and the studies repeated. ANIT is a hepatoxin that produces bile duct cell hyperplasia which was confirmed in dogs by demonstrating that ANIT increased [3H]thymidine incorporation by isolated canine bile duct cells. In normal dogs, the prostanoids, secretin, and glucagon increased hepatic bile flow. 10 days of ANIT feeding produced a hypercholeresis. While secretin was able to stimulate the hyperplastic biliary epithelium and increase bile flow over values produced by the hyperplastic biliary epithelium alone, neither prostaglandin E2, prostacyclin, or glucagon appeared to stimulate the hyperplastic biliary epithelium. As ANIT produced evidence of cholestasis and hepatocellular damage, only secretin would seem to have a potential therapeutic role in increasing bile flow in cholestatic liver disorders associated with bile duct cell hyperplasia.
1-Naphthylisothiocyanate↗