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Biomedical subjects

Hyun Jin Kim

Publications and source records attributed to Hyun Jin Kim.

At least 19 recordsLinked to original sources

Synthesis and characterization of poly (amino ester) for slow biodegradable gene delivery vector.

Many therapeutic carrier materials were exploited for human gene therapy from viral to polymeric vectors. This research describes the evaluation of two biodegradable ester-bonded polymers synthesized by double-monomer polycondensation for a non-viral cationic polymer-based gene delivery system. The backbone was constructed to include inner tertiary amines and outer primary amines. Self-assembly with DNA resulted in the production of regularly nano-sized spherical polyplexes with good transfection efficiency, especially in the presence of serum. The polymers showed a relatively slow degradability for an amine-containing ester polymer, as they maintained DNA/polymer complex for 7 days in physiological buffer conditions. Finally, the low toxicity and slow degradation concluded these polymers reliable for long-term therapeutic applications.

Buffers↗

Epigallocatechin gallate inhibits nitric oxide-induced apoptosis in rat PC12 cells.

Nitric oxide (NO) is associated with many pathophysiology of the central nervous system including brain ischemia, neurodegeneration and inflammation. Epigallocatechin gallate (EGCG) is a major compound of green tea polyphenol that has shown the protective activity against neuronal diseases. This study examined the effect of EGCG on NO-induced cell death in PC12 cells. The administration of sodium nitroprusside (SNP), a NO donor, decreased the cell viability and induced apoptosis showing characterization such as cell shrinkage and chromatin condensation as well as subG1 fraction of cell cycles. EGCG inhibited the cytotoxicity and apoptotic morphogenic changes induced by SNP. EGCG attenuated the production of reactive oxygen species (ROS) by SNP, and ameliorated the SNP-induced Bax to Bcl-2 expression ratio leading to apoptosis. In addition, EGCG prevented the release of cytochrome c from the mitochondria into the cytosol as well as the upregulation of the voltage-dependent anion channel (VDAC), a cytochrome c releasing channel, in the mitochondria of SNP-treated cells. EGCG abrogated the activation of caspase-9, caspase-8 and caspase-3 induced by SNP. These results demonstrate that EGCG has a protective effect against SNP-induced apoptosis in PC12 cells by scavenging ROS and modulating the signal molecules associated with cytochrome c, caspases, VDAC and the Bcl-2 family. These findings suggest that EGCG might be a natural neuroprotective substance.

Animals↗

Calpain-resistant fragment(s) of alpha-synuclein regulates the synuclein-cleaving activity of 20S proteasome.

Alpha-synuclein is a pathological component of Parkinson's disease by participating in Lewy body formation. Imbalance in protein turnover could result in the abnormal protein aggregation responsible for eventual neuronal cell death. This in vitro digestion study showed that both m-calpain and 20S proteasome preferentially hydrolyzed the N-terminal half of alpha-synuclein, which made the hydrophobic NAC and following acidic C-terminal region resistant against the proteolyses. Since the acidic C-terminal region contains the PEST segment-a protein degradation signal enriched with amino acids of proline (P), glutamate (E), serine (S), and threonine (T)-, the PEST segment has not been processed or even required for the proteolyses. Alpha-synuclein would be recognized primarily by m-calpain since the common substrate was processed by m-calpain five times more effectively than 20S proteasome with k(cat)/K(m) of 1.64 x 10(4)M(-1)s(-1) and 0.32 x 10(4) M(-1)s(-1), respectively. The N-terminally truncated protease-resistant C-terminal fragment of alpha-syn61-140 was demonstrated to stimulate the 20S proteasome-mediated breakdown of alpha-synuclein and its mutant forms of Ala53Thr and Ala30Pro. The stimulation for Ala53Thr, however, was noticeably less efficient than those for the other proteins, which might support the previous observation of the prolonged intracellular life span of Ala53Thr by 1.5-fold compared to that of wild-type form. We have hypothesized that the N-terminally truncated C-terminal fragment derived from the abundant alpha-synuclein through intracellular proteolyses could be involved in various physiological or pathological effects which might be related to the formation of abnormal protein aggregation and subsequent neuronal degeneration by influencing the intracellular protein turnover or directly participating in the aggregate formation.

Amino Acid Sequence↗

Characterization of surface-confined alpha-synuclein by surface plasmon resonance measurements.

Urea-driven denaturation and renaturation of surface-bound alpha-synuclein are monitored by surface plasmon resonance (SPR) spectroscopy. The differential SPR angle shift (Delta Theta(SPR))(Net) enables us to estimate the Gibbs free energy change (DeltaG(o)) for the denaturation of the supported alpha-synuclein. DeltaG(o) for the denaturation of the supported alpha-synuclein, which is indirectly related to its biological activity can be increased significantly by the mixed self-assembled monolayers of 11-mercaptoundecanoic acid and 1,6-hexanedithiol. These SPR measurements of surface-bound biomolecules suggested herein can be further utilized to design effective biological scaffold for biosensor, biocatalyst, and possible diagnosis.

Coated Materials, Biocompatible↗

Aortoiliac hemodynamic and morphologic adaptation to chronic spinal cord injury.

BACKGROUND: Reduced lower limb blood flow and resistive hemodynamic conditions potentially promote aortic inflammation and aneurysmal degeneration. We used abdominal ultrasonography, magnetic resonance imaging, and computational flow modeling to determine the relationship between reduced infrarenal aortic blood flow in chronic spinal cord injury (SCI) subjects and risk for abdominal aortic aneurysm (AAA) disease. METHODS: Aortic diameter in consecutive SCI subjects (n = 123) was determined via transabdominal ultrasonography. Aortic anatomic and physiologic data were acquired via magnetic resonance angiography (MRA; n = 5) and cine phase-contrast magnetic resonance flow imaging (n = 4) from SCI subjects whose aortic diameter was less than 3.0 cm by ultrasonography. Computational flow models were constructed from magnetic resonance data sets. Results were compared with those obtained from ambulatory control subjects (ultrasonography, n = 129; MRA/phase-contrast magnetic resonance flow imaging, n = 6) who were recruited at random from a larger pool of risk factor-matched individuals without known AAA disease. RESULTS: Age, sex distribution, and smoking histories were comparable between the SCI and control groups. In the SCI group, time since injury averaged 26 +/- 13 years (mean +/- SD). Aortic diameter was larger (P < .01), and the prevalence of large (> or = 2.5 cm; P < .01) or aneurysmal (> or = 3.0 cm; P < .05) aortas was greater in SCI subjects. Paradoxically, common iliac artery diameters were reduced in SCI subjects (< 1.0 cm; 48% SCI vs 26% control; P < .0001). Focal preaneurysmal enlargement was noted in four of five SCI subjects by MRA. Flow modeling revealed normal flow volume, biphasic and reduced oscillatory flow, slower pressure decay, and reduced wall shear stress in the SCI infrarenal aorta. CONCLUSIONS: Characteristic aortoiliac hemodynamic and morphologic adaptations occur in response to chronic SCI. Slower aortic pressure decay and reduced wall shear stress after SCI may contribute to mural degeneration, enlargement, and an increased prevalence of AAA disease.

Aorta, Abdominal↗

Comparison of forward shift of posterior corneal surface after operation between LASIK and LASEK.

PURPOSE: To compare the forward shift of the posterior corneal surface as a function of time after surgery between successful laser in situ keratomileusis (LASIK) and laser-assisted subepithelial keratectomy (LASEK). METHODS: Twenty-two eyes from 14 patients who underwent LASIK and 19 eyes from 10 patients who underwent LASEK were reviewed retrospectively. The uncorrected visual acuity, spherical equivalent and pachymetry were obtained before and 1 or 2 weeks and 2, 6, 12, and 24 months after surgery. The change in the elevation of the posterior corneal surface was assessed using the difference map of an Orbscan II (Bausch and Lomb, Salt Lake City, Utah, USA), which was generated from the preoperative and subsequent postoperative elevation map. RESULTS: One or 2 weeks after LASIK and LASEK, the posterior corneal surface had shifted forward by 18.00 and 25.90 microm, respectively (p = 0.008). However, the mean posterior corneal surface reduced by 3.05 microm from 1 or 2 weeks to 2 years in the LASIK group (p = 0.359). In contrast, the mean posterior corneal surface had reduced by 12.40 microm in the LASEK group (p = 0.004). This forward shift did not return to the corneal normal elevation observed prior to surgery in the two groups. CONCLUSIONS: Refractive surgery induced a forward shift of the posterior corneal surface early postoperatively in the LASIK and LASEK groups, and this change after LASEK was significantly larger than that observed after LASIK. The posterior corneal surface gradually shifted backwards depending on the time course in both groups, but they did not return to the preoperative levels.

Adult↗

Surgical management of bilateral exudative retinal detachment associated with central serous chorioretinopathy.

PURPOSE: To report a case of bilateral bullous exudative retinal detachment in central serous chorioretinopathy (CSC) which was attached by vitrectomy and internal drainage of the subretinal fluid. METHODS: A 47-year-old man affected by bilateral atypical CSC with a bullous retinal detachment with subretinal exudate. A fluorescein angiogram (FAG) showed multiple points of leakage and staining of subretinal fibrosis. A tentative diagnosis of Vogt-Koyanagi-Harada (VKH) syndrome was made and the patient was treated with systemic corticosteroids and immunosuppressive agents. However, the subretinal fluid was not absorbed. He was then treated with vitrectomy and internal drainage of subretinal fluid. RESULTS: The retina was attached successfully in both eyes. Visual acuity improved to 20/50 in his left eye but did not improve in the right eye due to subretinal fibrotic scarring and atropic changes on the macula. CONCLUSIONS: Our case suggests that the surgical management of bullous exudative retinal detachment is safe and necessary.

Choroid Diseases↗

Assessment of the therapeutic response of hepatocellular carcinoma treated with transcatheter arterial chemoembolization: comparison of contrast-enhanced sonography and 3-phase computed tomography.

OBJECTIVE: The purpose of this study was to compare contrast-enhanced sonography with 3-phase computed tomography (CT) in assessing the therapeutic response of hepatocellular carcinomas (HCCs) treated with transcatheter arterial chemoembolization (TACE). METHODS: Twenty-nine nodular HCCs treated with TACE were examined with contrast-enhanced sonography, 3-phase helical CT, and conventional angiography. Contrast-enhanced sonographic and CT findings were interpreted separately and prospectively for the presence or absence of contrast enhancement in the treated HCCs. Conventional angiography served as the reference standard. RESULTS: Intratumoral enhancement was seen in 19 HCCs (61%) on contrast-enhanced sonography and 12 HCCs (39%) on CT. Enhancement patterns on sonography were blush in 8 (42%), branching in 2 (11%), nodular in 4 (21%), and stippled in 5 (26%). Of the 19 HCCs with intratumoral enhancement on contrast-enhanced sonography, 13 (68%) showed tumor staining on angiography. Of the 12 HCCs without intratumoral enhancement on sonography, 1 (8%) showed tumor staining on angiography. The sensitivity and specificity of contrast-enhanced sonography in depicting flow in HCCs treated with TACE were 93% and 65%, respectively. The sensitivity and specificity of 3-phase CT were 64% and 100%. CONCLUSIONS: Contrast-enhanced sonography is a more sensitive imaging method than 3-phase CT in depicting vascularity in HCCs treated with TACE.

Adult↗

Dequalinium-induced protofibril formation of alpha-synuclein.

alpha-Synuclein is the major constituent of Lewy bodies, a pathological signature of Parkinson disease, found in the degenerating dopaminergic neurons of the substantia nigra pars compacta. Amyloidosis generating the insoluble fibrillar protein deposition has been considered to be responsible for the cell death observed in the neurodegenerative disorder. In order to develop a controlling strategy toward the amyloid formation, 1,1'-(1,10-decanediyl)-bis-[4-a-mino-2-methylquinolinium] (dequalinium), was selected and examined in terms of its specific molecular interaction with alpha-synuclein. The protein was self-oligomerized by dequalinium, which gave rise to the ladder formation on N-[2-hydroxy-1,1-bis(hydroxymethyl)ethyl]glycine/SDS-PAGE in the presence of a coupling reagent of N-(ethoxycarbonyl)-2-ethoxy-1,2-dihydroquinoline. The double-headed structure of dequalinium with the two cationic 4-aminoquinaldinium rings was demonstrated to be critical for the protein self-oligomerization. The dequalinium-binding site was located on the acidic C-terminal region of the protein with an approximate dissociation constant of 5.5 mum. The protein self-oligomerization induced by the compound has resulted in the protofibril formation of alpha-synuclein before it has developed into amyloids. The protofibrils were demonstrated to affect the membrane intactness of liposomes, and they have also been shown to influence cell viability of human neuroblastoma cells. In addition, dequalinium treatment of the alpha-synuclein-overexpressing cells exerted a significant cell death. Therefore, it is pertinent to consider that dequalinium could be used as a molecular probe to assess toxic mechanisms related to the amyloid formation of alpha-synuclein. Ultimately, the compound could be employed to develop therapeutic and preventive strategies toward alpha-synucleinopathies including Parkinson disease.

Amyloid↗

Solubility engineering and crystallization of human apolipoprotein D.

Human apolipoprotein D (ApoD) is a physiologically important member of the lipocalin protein family that was discovered as a peripheral subunit of the high-density lipoprotein (HDL) but is also abundant in other body fluids and organs, including neuronal tissue. Although it has been possible to produce functional ApoD in the periplasm of Escherichia coli and to demonstrate its ligand-binding activity for progesterone and arachidonic acid, the recombinant protein suffers from a pronounced tendency to aggregate and to adsorb to vessel surfaces as well as chromatography matrices, thus hampering further structural investigation. Here, we describe a systematic mutagenesis study directed at presumably exposed hydrophobic side chains of the unglycosylated recombinant protein. As a result, one ApoD mutant with just three new amino acid substitutions--W99H, I118S, and L120S--was identified, which exhibits the following features: (1) improved yield upon periplasmic biosynthesis in E. coli, (2) elution as a monomeric protein from a gel permeation chromatography column, and (3) unchanged binding activity for its physiological ligands. In addition, the engineered ApoD was successfully crystallized (space group I4 with unit cell parameters a = 75.1 A, b = 75.1 A, c = 166.0 A, alpha = beta = gamma = 90 degrees), thus demonstrating its conformationally homogeneous behavior and providing a basis for the future X-ray structural analysis of this functionally still puzzling protein.

Apolipoproteins↗

Highly effective and slow-biodegradable network-type cationic gene delivery polymer: small library-like approach synthesis and characterization.

Over the past years, macromolecular biodegradable polymers have been attracting considerable attention as gene delivery vehicles due to their safety and many potential applications. In the process of developing such biopolymers, we synthesized a biodegradable, network-type poly(amino ester) polymer (nt-PAE), which showed desirable chemical properties and a mechanical durability with high transfection efficiency. A small library-like approach to polymer synthesis using melt polycondensation followed by surface modification with aminohexanoic acid resulted in the final polymer, nt-PAE. The network-type structure of nt-PAE consists of biodegradable ester linkages and tertiary amines embedded in the backbone, and primary amines positioned at the surface. Unlike other rapidly degrading ester polymers, the nt-PAE exhibited fairly slow degradation, as the polymer sustained its DNA complexing ability for 10 days under physiological buffer conditions. In addition, the transfection efficiency of the nt-PAE could be increased to the same level comparable with that of PEI even in the presence of serum. Low toxicity and high transfection efficiency with a slow degradation profile implies that the nt-PAE can be used as a valuable nonviral gene delivery system.

Biocompatible Materials↗

A case of tubulointerstitial nephritis and uveitis syndrome with severe immunologic dysregulation.

Idiopathic tubulointerstitial nephritis and uveitis (TINU) syndrome is an uncommon condition, characterized by acute tubulointerstitial nephritis (TIN) with a favorable course and uveitis with a chronic relapsing course. The pathogenesis remains unclear, but a lymphocyte-mediated immune mechanism has been suggested. A 9-year-old boy was evaluated for fatigue and 2 kg of weight loss. Renal glucosuria, elevated urine beta(2)-microglobulin (MG), progressive renal dysfunction, polyclonal hypergammaglobulinemia, various autoantibodies and abnormal lymphocyte phenotypes were found. A renal biopsy revealed acute TIN. After 2 months of treatment with prednisolone, renal function and polyclonal hypergammaglobulinemia were normalized. While tapering prednisolone, anterior uveitis developed, which was improved with topical steroid. But abnormal lymphocyte phenotypes and autoantibodies persisted on low-dose prednisolone. Uveitis became aggravated, and urine beta(2)-MG increased again. The second renal biopsy (7 months later) was normal except for minimal focal interstitial fibrosis. Uveitis was not responsive to systemic steroids, but improved with additional cyclosporin. Abnormal lymphocyte phenotypes improved, and most autoantibodies disappeared. We report a rare case of idiopathic TINU syndrome with severe immunologic dysregulation, which correlated with the clinicopathological and biochemical parameters. The information about lymphocyte phenotypes and autoantibodies may provide more insight into the pathophysiology and the clinical course of uveitis in this rare disorder.

Acute Disease↗

Desensitization of canonical transient receptor potential channel 5 by protein kinase C.

The classic type of transient receptor potential channel (TRPC) is a molecular candidate for Ca(2+)-permeable cation channel in mammalian cells. TRPC5 is desensitized rapidly after activation by G protein-coupled receptor. Herein we report our investigation into the desensitization of mTRPC5 and localization of the molecular determinants of this desensitization using mutagenesis. TRPC5 was initially activated by muscarinic stimulation using 100 microM carbachol (CCh) and then decayed rapidly even in the presence of CCh (desensitization). Increased EGTA or omission of MgATP in the pipette solution slowed the rate of this desensitization. The protein kinase C (PKC) inhibitors, 1 microM chelerythrine, 100 nM GF109203X, or PKC peptide inhibitor (19-36), inhibited this desensitization of TRPC5 activated by 100 microM CCh. When TRPC5 current was activated by intracellular GTPgammaS, PKC inhibitors prevented TRPC5 desensitization and the mutation of TRPC5 T972 to alanine slowed the desensitization process dramatically. We conclude that the desensitization of TRPC5 occurs via PKC phosphorylation and suggest that threonine at residue 972 of mouse TRPC5 might be required for its phosphorylation by PKC.

Adenosine Triphosphate↗

Small (<or= 2 cm) hepatic lesions in colorectal cancer patients: detection and characterization on mangafodipir trisodium-enhanced MRI.

OBJECTIVE: The purpose of this study was to evaluate whether mangafodipir trisodium (MnDPDP)-enhanced MRI improves the detection and characterization of small ( 2.0 cm). The differences between MnDPDP-enhanced MRI and helical CT with regard to the detection rates for hepatic lesions and metastases and with regard to the false-positive rates for hepatic metastases were analyzed using the McNemar test. The performances of MnDPDP-enhanced MRI and helical CT in indicating metastases of focal liver lesions were analyzed using receiver operating characteristic curves. RESULTS: No statistically significant differences were seen between MnDPDP-enhanced MRI and helical CT in the detection of all hepatic lesions (p = 0.383) and small lesions (p = 0.210). However, concerning the differentiation between benign and metastatic lesions, MnDPDP-enhanced MRI was superior to helical CT both for all hepatic lesions (p = 0.023) and for small lesions (p = 0.015), and remained better when the analyses were restricted to patients with histopathologic confirmation (p = 0.023 for both). MnDPDP-enhanced MRI changed the diagnosis of hepatic metastasis in nine (13.0%) of 69 patients. Of 12 metastases that were found on MnDPDP-enhanced MRI and missed on helical CT, 11 lesions (91.7%) were small. MnDPDP-enhanced MRI showed a significantly greater detection rate than helical CT for small hepatic metastases (p = 0.022). MnDPDP-enhanced MRI was better when the analyses were restricted to patients with histopathologic confirmation (p = 0.043). CONCLUSION: Although MnDPDP-enhanced MRI is equal to helical CT in detection of both all hepatic lesions and small lesions in patients with colorectal carcinoma, it is superior to CT in characterization of the lesions.

Adult↗

[The clinical study on spontaneously ruptured hepatocellular carcinoma].

BACKGROUND/AIMS: Spontaneous rupture of hepatocellular carcinoma (HCC) is known as a rare but life- threatening condition because of massive blood loss into the peritoneal cavity. In the countries with high prevalence, the reported incidence of spontaneous rupture and hemorrhage ranged from 10.2% to 14.5% of patients with HCC. This study was aimed to analyze the risk factors for spontaneous rupture and prognosis in the patients with ruptured HCC. METHODS: Among 642 consecutive patients with HCC who had admitted to Gyeongsang National University Hospital from January 1998 to September 2003, spontaneous rupture of HCC occurred in 83 patients (12.9%). The medical records of the 83 patients were reviewed retrospectively, and the clinico-laboratory parameters and radiologic findings were analyzed. RESULTS: Sixty-nine out of the 83 patients were male, the mean age was 57.7 +/- 13.2 years (male, 56.8 +/- 12.9 years; female, 62.3 +/- 13.5 years). Location of tumor, Child-Pugh class and Okuda stage were the risk factors influencing spontaneous rupture of HCC, whereas the TNM stage, presence of portal vein thrombosis, and size of the tumor were not. Among the 83 patients with ruptured HCC, 51 were treated by transarterial embolization (TAE), 31 by supportive measures, and 1 by operation. The median survival time was 3.4 +/- 4.5 months in all patients with ruptured HCC, 4.9 +/- 5.1 in successful TAE, and 2.1 +/- 3.4 in supportive measure groups. CONCLUSIONS: Advanced Child-Pugh class, advanced Okuda stage, and peripheral location were the risk factors for spontaneous rupture of HCC. The prolonged survival could be achieved in patients eligible for successful transarterial embolization rather than supportive measures.

Aged↗

Five subtypes of muscarinic receptors are expressed in gastric smooth muscles of guinea pig.

Muscarinic receptors play key roles in the control of gastrointestinal smooth muscle activity. However, specific physiological functions of each subtype remain to be determined. In this study, the nonselective cation channel activated by carbachol (I(CCh)) was examined in circular smooth muscle cells of the guinea pig gastric antrum using patch-clamp technique. 4-DAMP inhibited I(CCh) dose-dependently with IC(50) of 1.1 0.1 nM (n = 6). GTPgS-induced current, however, was not inhibited by 10 nM 4-DAMP. I(CCh) was not recorded in pertussis-toxin (PTX)-pretreated smooth muscle cells of gastric antrum. I(CCh) values in response to 10 mM CCh at a holding potential of 60 mV were -330 32 pA (n=4) and -15 3 pA (n = 6) in the control and PTX-treated cells, respectively (P 0.01). Sensitivities to nanomolar 4-DAMP and PTX suggest the possible involvement of m4 subtype. Using sequence information obtained from cloned guinea pig muscarinic receptor genes, it is possible to amplify the cDNAs encoding m1-m5 from guinea pig brain tissue. Single cell RT-PCR experiments showed that all five subtypes of muscarinic receptor were present in circular smooth muscle cells of the guinea pig gastric antrum. Together with our previous results showing that G(o) protein is important for activation of ACh-activated NSC channels, our results suggest that I(CCh) might be activated by acetylcholine through m4 subtype as well as m2 and m3 subtypes in guinea-pig stomach.

Animals↗

TRPC5 as a candidate for the nonselective cation channel activated by muscarinic stimulation in murine stomach.

We investigated which transient receptor potential (TRP) channel is responsible for the nonselective cation channel (NSCC) activated by carbachol (CCh) in murine stomach with RT-PCR and the electrophysiological method. All seven types of TRP mRNA were detected in murine stomach with RT-PCR. When each TRP channel was expressed, the current-voltage relationship of mTRP5 was most similar to that recorded in murine gastric myocytes. mTRP5 showed a conductance order of Cs(+) > K(+) > Na(+), similar to that in the murine stomach. With 0.2 mM GTPgammaS in the pipette solution, the current was activated transiently in both NSCC in the murine stomach and the expressed mTRP5. Both NSCC activated by CCh in murine stomach and mTRP5 were inhibited by intracellularly applied anti-G(q/11) antibody, PLC inhibitor U-73122, IICR inhibitor 2-aminoethoxydiphenylborate, and nonspecific cation channel blockers La(3+) and flufenamate. There were two other unique properties. Both the native NSCC and mTRP5 were activated by 1-oleoyl-2-acetyl-sn-glycerol. Without the activation of NSCC by CCh, the NSCC in murine stomach was constitutively active like mTRP5. From the above results, we suggest that mTRP5 might be a candidate for the NSCC activated by ACh or CCh in murine stomach.

Animals↗

Preoperative evaluation of hepatocellular carcinoma: combined use of CT with arterial portography and hepatic arteriography.

OBJECTIVE: This study was undertaken to determine the usefulness of combined CT during arterial portography and CT hepatic arteriography in the preoperative evaluation of patients with known or suspected hepatocellular carcinoma and to describe the findings on CT during arterial portography and CT hepatic arteriography by which hepatocellular carcinomas may be differentiated from pseudolesions. SUBJECTS AND METHODS: This study included 137 patients who underwent combined CT during arterial portography and CT hepatic arteriography for the preoperative evaluation of known or suspected hepatocellular carcinoma. The images were prospectively evaluated to identify focal hepatic lesions and their differential diagnoses (hepatocellular carcinoma versus pseudolesion). We assessed the diagnostic accuracy of our prospective interpretation by comparing the interpretations with the results of histopathology or follow-up imaging. We also retrospectively analyzed imaging features seen on CT during arterial portography and CT hepatic arteriography-the size, shape, and location of the lesion within the liver; attenuation of the lesion; and opacification of the peripheral portal vein branches on CT hepatic arteriography. RESULTS: One hundred and forty-nine hepatocellular carcinomas (75 lesions confirmed at histopathology and 74 lesions on follow-up imaging) were found in 120 patients, and 104 pseudolesions (15 lesions confirmed at histopathology and 89 lesions on follow-up imaging) were found in 91 patients. The sensitivity of our prospective interpretations was 98.7%, and the specificity of our prospective interpretations was 90.4%. Our positive and negative predictive values were 93.6% and 97.9%, respectively. We found that hepatocellular carcinomas were larger, more frequently nodular, and more likely to be located intraparenchymally than were the pseudolesions (p < 0.01). Opacification of the peripheral portal vein branches on CT hepatic arteriography was detected in 36 pseudolesions (34.6%) but in none of the hepatocellular carcinomas (p < 0.01). CONCLUSION: Combining CT during arterial portography and CT hepatic arteriography is useful for the preoperative evaluation of patients with known or suspected hepatocellular carcinoma. Familiarity with the imaging features of hepatocellular carcinomas and pseudolesions can help in the accurate differentiation of hepatocellular carcinomas from pseudolesions.

Adult↗