加味四逆散抗大鼠肝纤维化的实验研究

目的探讨加味四逆散抗大鼠肝纤维化的作用。方法采用二甲基亚硝胺（DMN）致肝纤维化的方法对健康雄性SD大鼠进行造模，以秋水仙碱为阳性对照组。经加味四逆散治疗4周后测血清丙氨酸转氨酶（ALT）、碱性磷酸酶（ALP）、谷氨酰转肽酶（GGT）、总蛋白（TP）、白蛋白（ALB）、透明质酸（HA）及Ⅳ型胶原（C—Ⅳ）水平，并检测肝组织羟脯氨酸（HyP），同时观察肝组织的病理改变。结果加味四逆散治疗后，可显著降低血清ALT（P〈0．01）、ALP（P〈0．01）、GGT（P〈0．05）、HA（P〈0．01）、C-Ⅳ（P〈0．05）及肝组织HyP（P〈0．01），升高TP（P〈0．05）及ALB（P〈0．01）。肝组织病理切片表明，用药后病理改变明显减轻。结论加味四逆散对实验性大鼠有明显的抗肝纤维化作用。     

The influence of l-methionine-d,l-sulfoximine on the labelling of acid soluble fraction and proteins of the brain cortex after intraperitoneal injection of 14c-leucine.

Methionine sulfoximine (MSO) inhibits the labelling of the acid soluble fraction and proteins of the brain cortex after the injection of 14C-leucine. The inhibition takes place even during the early stages after the injection of MSO, when no symptoms of paroxysms are observable. The action of MSO on the labelling of the acid soluble fraction and proteins in the brain cortex is obviously different from that in the kidney and liver. Whereas in the brain tissue MSO markedly influences the labelling of the free amino acid pool, in the kidney and liver it seems primarily affect the protein synthetic mechanisms. Also no decrease in labelling of the plasma acid soluble fraction was found on mice, treated with MSO. Experimental data support the idea, that the changes in the metabolism of proteins in the brain are not connected with the onset of the paroxysmal period.     

A prospective trial of colchicine for primary biliary cirrhosis

We entered 60 patients with primary biliary cirrhosis in a double-blind randomized controlled trial to determine whether colchicine is therapeutically effective. Thirty patients had early disease (Stages 1 and 2), and 30 had advanced disease (Stages 3 and 4). Fifteen patients with early disease and 15 with advanced disease received colchicine (0.6 mg twice daily), and the remainder received placebo. Patients were studied about every two months; those remaining in the blind phase at two years underwent repeat liver biopsy and were then placed on open-label colchicine (0.6 mg twice daily). With a few exceptions, the results in patients with early disease were similar to those in patients with advanced disease; hence, data on patients in all stages were combined in the main analysis. During the two-year study period the colchicine-treated patients, as compared with the placebo-treated patients, had improvement in levels of serum albumin, serum bilirubin, alkaline phosphatase, cholesterol, and aminotransferases. However, there was no such improvement in the severity of symptoms or physical findings; moreover, there was no significant difference in the histologic changes noted at liver biopsy in the two treatment groups. At four years after entry, the cumulative mortality from liver disease was 21 percent in patients given colchicine and 47 percent in those given placebo (P = 0.05). The only side effect of colchicine was diarrhea, noted in three patients. The consistent and significant improvement in a number of markers of liver disease and the apparent decreased mortality from liver disease suggest that colchicine may provide some long-term clinical benefit in patients with primary biliary cirrhosis. However, the failure of colchicine to reduce hepatic inflammation and fibrosis leaves uncertain the effect of the drug on the longterm outcome of this disease.     

Kinetics of amyloid deposition. II. The effects of dimethylsulfoxide and colchicine therapy

Amyloid (AA) protein, when deposition begins, is deposited in two stages--a rapid deposition period of 2 weeks and a plateau stage. The effect of dimethylsulfoxide (DMSO) and colchicine therapy on the kinetics of amyloid deposition was dependent on the stage of the disease at which therapy began. If given during the rapid deposition period, colchicine delayed the increase in amyloid but did not abolish it. Eventually, splenic and liver amyloid reached the level seen in untreated animals. On the other hand, DMSO given during the rapid deposition period led to significant resorption of both splenic and liver amyloid. By contrast, colchicine and DMSO given after the rapid deposition period were essentially without effect in promoting amyloid resorption. These results correlated well with the serum levels of SAA, the putative AA precursor. Colchicine given during the period of rapid AA deposition caused a transient decline in SAA levels, which eventually returned to levels seen in untreated animals. DMSO given during the rapid deposition period rapidly abolished the high SAA levels and maintained it at a level seen in normal animals. Both colchicine and DMSO therapy, if instituted after the rapid amyloid deposition period, failed to reduce SAA levels significantly below that of untreated controls.     

Colchicine in the treatment of cirrhosis of the liver

There is preliminary evidence that colchicine, an inhibitor of collagen synthesis, may be beneficial in the treatment of cirrhosis of the liver. To evaluate the use of colchicine (1 mg per day, five days per week) in the treatment of hepatic cirrhosis, we performed a randomized, double-blind, placebo-controlled trial in which 100 patients were followed for up to 14 years. Forty-five patients had alcoholic cirrhosis, 41 had posthepatitic cirrhosis, and the remaining 14 had cirrhosis with various other causes. Histologic studies were available for 92 percent of patients. Seventy-three patients were in Child-Turcotte class A, 26 were in class B, and one was in class C. Fifty-four patients received colchicine, and 46 received placebo. The overall survival in the colchicine group was markedly better than in the placebo group (median survival, 11 and 3.5 years, respectively; P less than 0.001). The cumulative 5-year survival rates were 75 percent in the colchicine group and 34 percent in the placebo group; the corresponding 10-year survival rates were 56 percent and 20 percent. Among the 30 patients treated with colchicine who underwent repeated liver biopsies, histologic improvement was seen in 9; the liver appeared normal in 2, and 7 had minimal portal fibrosis. No histologic improvement was observed in the 14 members of the placebo group who had two or more biopsies. Few side effects were observed in either group.     

Endocytosis of particulate and soluble IgG immune complexes: differential effects of cytoskeletal modulating agents.

We determined the ability of cytoskeletal modulating agents to affect endocytosis of particulate and soluble immune complexes. Either immunoglobulin G-opsonized 51Cr-labelled erythrocytes (E) or 125I-labelled soluble IgG anti-dinitrophenyl immune complexes (IC) were added to adherent murine peritoneal macrophages and the extent of internalization was measured. Either intracellular 51Cr radioactivity or trichloroacetic acid soluble 125I radioactivity was monitored as an indication of uptake by the cell. In addition to cytochalasin B and colchicine, the phospholipid methylation inhibitors, 3-deazaadenosine and 3-deaza(+/-)aristeromycin, were used. Whereas incubation of macrophages with colchicine alone resulted in 50% inhibition of uptake of E-IgG, there was no effect on the degradation of soluble IC. Both cytochalasin B and colchicine produced a 95% inhibition of E-IgG uptake by macrophages, but these drugs only minimally inhibited (17%) the degradation of soluble immune complexes. Both inhibitors of methylation produced a 50% decrease in phospholipid methylation in treated cells. However, only 3-deazaadenosine inhibited phagocytosis (50% of control for E-IgG and 75% of control for soluble IC). These data suggest that an intact cytoskeleton is necessary for the uptake of a particulate immune complex and much less important for the internalization and degradation of these model soluble immune complexes. In addition, inhibition of phospholipid methylation reactions alone do not impare the uptake and degradation of either a soluble or a particulate immune complex.     

Association of African swine fever virus with the cytoskeleton

The association of African swine fever virus (ASFV) with the cytoskeleton was investigated. Immunofluorescent studies of ASFV infected cells with anti-ASFV serum showed a temporal and spatial development of viral inclusions which moved from a peripheral to a perinuclear location and fused to give a single large perinuclear factory. The migration and fusion of viral inclusions was inhibited by colchicine suggesting a function for microtubules in assembly site organization not previously described. Accumulation of virions outside the inclusions and inhibition of viral release was also observed in colchicine treated cells. Viral antigens and structural elements were retained on the cytoskeleton fraction of Triton X-100 extracted cells. Reorganization of cytoskeletal elements around the assembly sites was demonstrated by transmission electronmicroscopy and by immunofluorescent studies using monoclonal antibodies against actin, tubulin and vimentin. Intermediate filaments accumulated around the viral factories, microtubules were greatly decreased in number and microfilaments were reorganized in association with the plasma membrane. Bundles of 15 nm tubules of unknown origin were also observed around the assembly sites. The distribution of viral proteins in soluble, cytoskeleton and detergent insoluble nuclear fractions was studied by pulse-chase experiments with [35S]methionine. SDS-PAGE analysis showed the presence in the cytoskeletal and nuclear fractions of 150, 72, 38, 28, 19 and 15 kDa virus structural proteins which increased after a 5 h chase. Our results indicate a close association of ASFV replication with the cytoskeleton similar to events described during FV3 replication but which differ from those occurring in poxvirus-infected cells.     

Association of reovirus proteins with the structural matrix of infected cells

The interaction of reovirus with the cytoskeleton was investigated. The soluble components of infected cells were extracted with the nonionic detergent NP-40 in a physiological buffer, and a cytoskeletal extract was prepared from the detergent-insoluble fraction. We observed a selective association of viral-specified products with the cytoskeleton that was temporally controlled. Viral dsRNA appeared first on the framework but after several hours was found also in the soluble phase, encapsidated in mature virions. The initial viral translation products were associated exclusively with the soluble fraction, but concomitant with the appearance of dsRNA, viral proteins microNS and sigma 3 were detected on the cytoskeleton. Several hours later, all viral proteins were detected on the framework. Viral polypeptide microNS exhibited unique spatial distribution patterns that correlated with viral assembly: Before dsRNA replication, it appeared as diffusely distributed protein; a few hours later, it was detected in punctate foci interconnected by tiny filaments; several hours later, it appeared as an extensive fiber network that traversed the foci. The other viral proteins were detected only within viral foci. MicroNS remained bound to the matrix fraction after treatment with DNase, Mg2+, and high salt, treatments that released other viral proteins. This distribution pattern was virus-directed because passage of virus at high multiplicity of infection induced mutations that prevented assembly of the microNS-coated filament organization. A small fraction of the viral-specified products that included polypeptide microNS, but not viral dsRNA, was coprecipitated from cytoskeletal extracts with proteins of mol wt approximately 55K by monoclonal antibodies that recognized tubulin and vimentin. Disruption of this interaction by long exposure to colchicine did not prevent association of viral proteins or RNA with the matrix, indicating that viral products were not transported through these interactions. The results indicate that reovirus morphogenesis includes temporal and spatial controls not described previously.     

Subcellular localization of the 30K protein in TMV-inoculated tobacco protoplasts

We investigated the intracellular localization of the 30K protein in TMV-inoculated tobacco protoplasts by means of pulse-labeling and pulse-chase experiments with [35S]methionine. Protoplasts were lysed with a nonionic detergent and the extracts were centrifuged to yield soluble and crude nuclear fractions. Most of the 30K protein was found in the crude nuclear fraction. The nuclear fraction was further purified by centrifugation in a step-wise Percoll gradient. Nuclei and the 30K protein were found in the same fractions. The results of pulse-chase experiments indicated that the 30K protein is synthesized in the soluble fraction and then translocated to the crude nuclear fraction. The 30K protein of Ls1, a temperature-sensitive (ts) mutant affecting the cell-to-cell viral transport function, was also found in the nuclei, even at a nonpermissive temperature. These results suggested that the 30K protein has to be localized in the nuclei to function, and that impaired translocation of the 30K protein to the nuclei is not responsible for the ts lesion of mutant Ls1.     

The isolation of polynucleotide phosphorylase from animal tissues

Summary The presence of enzyme fractions isolated from the regenerating rat liver gives rise to the following changes during incubation with adenosinephosphates: increase in organic phosphorus content, reduction in easily hydrolyzed phosphorus and adeninenucleoprotein in the acid — soluble fraction and augmentation of the adeninenucleoprotein concentration in the acid-insoluble fraction.Presented by Active Member AMN SSSR N. N. Zhukov-Verezhnikov     

Evidence for exocytotic release of dopamine beta-hydroxylase from rabbit heart and of vasopressin from rat neurohypophyses during homogenization and fractionation. Effects of gadolinium ions, cytochalasin B, gallopamil and different temperatures

Isolated rabbit hearts were perfused according to a modified Langendorff method for 1 h (unstimulated hearts). In different hearts, release of dopamine beta-hydroxylase activity into the transmyocardial fluid draining the interstitium was evoked by electrical field stimulation for six periods of 1 min at 30 min intervals (stimulated hearts). The hearts were then homogenized and fractionated into 100,000 g supernatant and sedimented at 4 degrees C. In homogenates from unstimulated hearts, the soluble dopamine beta-hydroxylase (determined in the supernatant) accounted for 17% of the total dopamine beta-hydroxylase (determined in the homogenate). In stimulated hearts the soluble fraction of dopamine beta-hydroxylase was reduced by 65%. The dopamine beta-hydroxylase released into the transmyocardial fluid by electrical stimulation, expressed as fraction of the total activity, corresponded well to the loss of enzyme from the supernatant demonstrating that the soluble dopamine beta-hydroxylase determined from the supernatant represents the releasable pool. Gadolinium ions (Gd3+) added to the homogenization medium of unstimulated hearts reduced the soluble fraction of dopamine beta-hydroxylase up to 63%, with the maximum effect at 200 microM. Similarly, when neurohypophyses were homogenized and spun at 0-4 degrees C, the fraction of vasopressin in the soluble phase was about 50% of the total. Gd3+ reduced this fraction by maximally 60%, an effect which was accompanied by an increase of vasopressin in the sedimentable fraction. When cytochalasin B (10 microM) was present during the homogenization of the hearts the soluble fraction of dopamine beta-hydroxylase was reduced to the same extent as in the presence of Gd3+. However, cytochalasin B had no effect on the distribution of vasopressin in the soluble and sedimentable fractions of homogenates of neurohypophyses. Gallopamil, when present during the homogenization of the hearts at a maximum effective concentration of 1 microM, reduced the soluble fraction of dopamine beta-hydroxylase by only 40%. However, the electrically evoked noradrenaline release from perfused hearts was completely blocked at 100-300 microM gallopamil. When neurohypophyses were homogenized and fractionated at room temperature only 13% of the total vasopressin was found in the soluble fraction and Gd3+ did not further reduce this fraction. When unstimulated hearts were homogenized and fractionated at room temperature the fraction of soluble dopamine beta-hydroxylase was reduced by 40% compared to the experiments at 0-4 degrees C.(ABSTRACT TRUNCATED AT 400 WORDS)     

Hepatic triacylglycerol and fatty-acid biosynthesis during hypoxia in vivo

Hepatic fatty acid biosynthesis and the activity of phosphatidate phosphohydrolase, the rate-limiting enzyme of triacylglycerol biosynthesis, were studied after hypoxic periods of 1 and 7 days under hypo-bark conditions at 40.8 kPa. Phosphatidate phosphohydrolase activity increased 2-fold in the soluble fraction of the liver after one day at 40.8 kPa, but had returned to normal by 7 days. This was accompanied by a significant increase in liver triacylglycerol and sn-glycerol-3-phosphate. The phosphatidate phosphohydrolase activity increased continuously over 7 days in the pair-fed controls, probably due to the restriction on food. Measured as in vivo incorporation of ³H₂O into lipids, the hepatic fatty acid synthesis rate increased somewhat in acute hypoxia, but returned to normal values during 7 days of hypoxia. Plasma free fatty acids increased markedly after 24 h in the fasting controls (90 %) with a smaller increase in the hypoxic group (50%) due to peripheral lipolysis. Hepatic glycogen stores decreased in the hypoxic and fasting animals both after 1 and 7 days. It Is concluded that hypoxia induces the accumulation of fat into the liver at least partly as a consequence of an increase in phosphatidate phosphohydrolase activity in the soluble fraction of the liver.     

Trans-synaptic modulation of Purkinje cell plasma membrane organization by climbing fiber axonal flow

Summary Destruction of the inferior olivary nucleus in the rat by thermocoagulation results in the degeneration of climbing fibers in the cerebellar cortex. Under these conditions the plasma membrane of Purkinje cells was selectively affected at the level of the spines on large dendrites (LD spines), the postsynaptic targets for climbing fibers. The number of small (< 10 nm) non-junctional intramembrane particles (IMP) was significantly decreased in E-faces during the first 3 days following the lesion (47% of control IMP values). Later, the number of IMPs progressively recovered to reach 67% of the control IMP values 1 month following the lesion. IMP numbers in the P-face and in the postsynaptic junctional aggregates of the E-face were unaffected by destruction of climbing fibers. Following injection of colchicine into the inferior olivary nucleus, a treatment that inhibits axonal transport in climbing fibers, a selective decrease in IMP numbers on the E-faces of LD spines was also found. The maximal decrease was found during the first 10 days after injection (48% of control values), and then the number of IMPs gradually increased to reach control values by 90 days post-injection. In the case of colchicine treatment also, the reduction in the number of IMPs affected selectively a class of non-junctional small IMPs, less than 10 nm in diameter. These data show that there is a similar selective modification in the membrane structure of Purkinje cells, not only following destruction of climbing fibers by thermocoagulation, but also following inhibition of axonal flow in climbing fibers by colchicine injection. The results are consistent with the hypothesis that Purkinje cell membrane structure is modulated by the presence of a trophic factor(s) associated with climbing fibers.Supported by the Swiss National Science Foundation, grant 3.370.82 and by C.S.I.C., Spain     

Evaluation of the colchicine-like activity of Gloriosa superba-extracted fractions for mosquito (Diptera: Culicidae) cytogenetic study

Four fractions of Gloriosa superba L., i.e., hexane fraction, dichloromethane fraction 1, dichloromethane fraction 2, and methanol fraction, were investigated for colchicine-like activity using a mosquito cytogenetic assay. The results revealed that the latter three fractions yielded promisingly high colchicine-like activity, whereas the hexane fraction yielded very low activity compared with 1% colchicine in a 0.85% sodium chloride solution. The metaphase rates and average number of metaphase chromosomes per positive brain ganglion (range) of Aedes aegypti L. larvae after incubation with 0.25-2% solutions of dichloromethane fraction 1, dichloromethane fraction 2, 0.5-2% solutions of methanol fraction, and 1% colchicine solution were 90-100% and 7 (2-19) to 22 (7-47); 90-100% and 4 (1-11) to 30 (4-73); 95-100% and 11 (1-28) to 17 (2-62); and 100% and 6 (2-11), respectively. The temperature stability tests of the three promising fractions were performed by heating 0.5% working solution at 121 degrees C for 15 min and preparing 0.5% working solution from stock frozen at -20 degrees C for 10 mo. These fractions also yielded satisfactory outcomes of metaphase rates and an average number of metaphase chromosomes per positive brain ganglia compared with 1% colchicine solution.     

The Effect of Regular Colchicine Treatment on Biomarkers Related with Vascular Injury in Newly Diagnosed Patients with Familial Mediterranean Fever

We aimed to evaluate some of the vascular biomarkers in newly diagnosed, colchicine naive familial Mediterranean fever (FMF) patients. Our primary aim was to investigate the effect of regular colchicine treatment on these variables. Twenty-four (12 males [M] and 12 females [F], 33.3?±?13.4?years) newly diagnosed FMF patients were included in the study. These patients were started on colchicine treatment following the initial assessment and were studied again no earlier than 2?months. Five patients were lost to follow-up, and assessment of the on-treatment patients was performed on the remaining 19 patients (8 M and 11 F, 33.6?±?11.8?years). There were 19 healthy subjects (11 M and 8 F, 32.2?±?7.2?years) who served as a control group. Cellular adhesion molecules (CAMs; soluble intercellular adhesion molecule-1 [sICAM-1] and soluble CD146 [sCD146]), plasminogen activator inhibitor-1 (PAI-1), fetuin-A and hs-CRP were studied. Examinations were performed on attack-free periods. The levels of hs-CRP, fetuin-A, sICAM-1, and PAI-1 were significantly higher in newly diagnosed patients compared to those of controls (P??0.05). On-treatment sCD146 was found significantly lower than the controls (P??0.05). Administration of therapeutic doses of colchicine markedly reduces vascular injury parameters and normalizes the values in FMF.     

Pharmacokinetic, biochemical and histological study of the carbamazepine-josamycin interaction in the rat following chronic administration

The determination of possible modifications of pharmacokinetic parameters of carbamazepine by josamycin in an experimental study after chronic administration of the drugs in the rat was undertaken to assay, or not, the enzymatic inhibition hypothesis which is supported in human clinical studies. Our data do not show any alteration in the Cmax, Tmax and AUC parameters of carbamazepine (total and unbound fraction) in case of conjunction with josamycin, but an earlier increase of plasmatic concentrations. The biochemical parameters are not modified, but a significant decrease of total bilirubin compared with controls and carbamazepine alone. The histological study does not show any liver lesion.     

Effect of colchicine on urinary phosphate and regulation by parathyroid hormone.

The possible role of cytoplasmic microtubules in the renal handling of phosphate and its regulation by parathyroid hormone (PTH) was evaluated with colchicine, a microtubule-disrupting agent. Colchicine-treated rats were thyroparathyroidectomized (TPTX) and subsequently infused with PTH. Treatment with a total dose of 1 mg colchicine had no effect on glomerular filtration rate or fractional excretions of sodium and potassium. Fractional excretion of phosphate in colchicine-treated TPTX rats was significantly higher compared with TPTX controls. After PTH infusion, control rats responded with increases in fractional excretion of phosphate and urinary cyclic AMP but colchicine-treated rats had variable and insignificant changes in both parameters. Fractional excretion of sodium and potassium did not change significantly after PTH. Renal cortical activities of cyclic AMP phosphodiesterase, soluble alkaline phosphatase, cytochrome oxidase, leucine aminopeptidase, or basal adenylate cyclase were not significantly affected by colchicine treatment. On the other hand, stimulation of adenylate cyclase by a submaximal dose of PTH was markedly decreased in colchicine-treated rats, and the activity of membrane-bound alkaline phosphatase was also significantly decreased. The binding of radioactive colchicine in renal cortical extracts from rats treated with colchicine was significantly diminished. These results suggest that disruption of cytoplasmic microtubules in renal cortical cells interferes with phosphate transport and its regulation by PTH.     

Specific, high affinity colchicine binding monoclonal antibodies: development and characterization of the antibodies

Nine colchicine specific monoclonal antibodies have been developed by immunizing BALB/c mice with a colchicine-keyhole limpet hemocyanin (Col-KLH) conjugate prepared using a bishydroxysuccinimide coupling reagent. Of four immunization procedures examined, intraperitoneal injection of the antigen attached to acid treated E. coli resulted in the maximum antigen specific antibody titers. A colchicine bovine serum albumin (Col-BSA) conjugate, prepared using a water soluble carbodiimide coupling technique, formed the basis of an enzyme linked immunosorbent assay used for screening hybridomas for colchicine specific antibody secretion and for determining the relative affinity and specificity profile of the monoclonal antibodies. All antibodies demonstrated high affinity, saturable binding to colchicine and low cross-reactivity with a panel of compounds structurally related to colchicine. The IC50 for the highest affinity antibody, C44, was 3.6 +/- 0.84 nM colchicine in the competitive enzyme immunoassay. The affinity of this antibody determined from Scatchard analysis of antibody binding to tritiated colchicine was 0.66 +/- 0.11 nM. Antibody C44 has the level of specificity and affinity suitable for a sensitive and selective immunoassay of colchicine for monitoring therapeutic drug levels. In addition, this antibody provides a specific pharmacologic antagonist for studies of colchicine's therapeutic mechanism and has the potential to reverse colchicine toxicity.     

Features of the destructive and reparative processes of the liver in various types of acute experimental peritonitis

In experiments on 135 albino rats, present-day techniques were used to examine the time-course of hepatic destructive and reparative processes during various courses of acute experimental peritonitis (AEP). The magnitude of destructive changes in the liver was found to be directly related to the severity of peritoneal lesion, degree of intoxication, and immunologic reactivity of the body. Within the first 4-5 days of AEP, the liver was regenerated mainly by intracellular hyperplasia. On days 3-4 the mitotic activity of hepatocytes markedly increased, reaching its maximum on day 5 of the experiment. Destructive and suppurative changes predominated over reparative ones in the organ in AEP treated with the immunodepressant azathioprine. In contrast, the administration of the cellular immunity stimulant, levamisole++, to the experimental animals was followed by drastically increased mononuclear infiltration, hepatic stromal cell proliferation and reparative hepatocyte regeneration.     

A case of pseudolymphoma of the liver

A case of pseudolymphoma (reactive lymphoid hyperplasia) of the liver in a 66 year old female is presented. A tumor-like lesion was incidentally discovered in the liver during clinical follow up of diabetes mellitus. The hepatic lesion was resected because malignant lymphoma was suspected after a needle biopsy. Grossly, the lesion was well-deflned and measured 1.0 × 1.5 × 1.0 cm. Microscoplcally, the lesion consisted of hyperplastic lymphoid follicles with distinctive germinal centers and interfollicular areas consisting of mature lymphocytes and plasma cells. An immunohistologlcal study revealed that the lymphoid cells of the lesion were polyclonal in immunophenotypes. These histological and immunohistochemical findings strongly suggested a pseudolymphoma and not hepatic inflammatory pseudotumor. Thls case was diagnosed as pseudolymphoma of liver. Only a few cases of hepatic pseudolymphoma have so far been reported In the English literature.