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Biomedical subjects

K Miyanishi

Publications and source records attributed to K Miyanishi.

At least 19 recordsLinked to original sources
PubMed2007

Effects of a p38 MAP kinase inhibitor on bone ingrowth and tissue differentiation in rabbit chambers.

The effects of an oral p38 mitogen-activated protein kinase (MAPK) inhibitor and polyethylene particles separately and together on tissue differentiation in the bone harvest chamber (BHC) in rabbits over a 3-week treatment period were investigated. The harvested tissue was analyzed histomorphometrically for markers of bone formation (percentage of bone area), osteoblasts (alkaline phosphatase staining), and osteoclasts (CD51, the alpha chain of the vitronectin receptor). Polyethylene particles decreased the percentage of bone ingrowth and staining for alkaline phosphatase. The p38 MAPK inhibitor alone decreased alkaline phosphatase staining. When the oral p38 MAPK inhibitor was given and the chamber contained polyethylene particles, there was a suppression of bone ingrowth and alkaline phosphatase staining. In contrast to oral non-steroidal anti-inflammatory drugs (NSAIDs) and local Interleukin-1 receptor antagonist (IL-1ra) administration, the oral p38 MAPK inhibitor alone did not suppress bone formation when given during the initial phase of tissue differentiation. Particle-induced inflammation and the foreign body reaction were not curtailed when the p38 MAPK inhibitor was given simultaneously with particles. Additional experiments are needed to establish the efficacy of p38 MAPK inhibitor administration on mitigating an established inflammatory and foreign body reaction that parallels the clinical situation more closely.

Administration, Oral↗
PubMed2006

Hepatitis C virus core protein promotes proliferation of human hepatoma cells through enhancement of transforming growth factor alpha expression via activation of nuclear factor-kappaB.

BACKGROUND: Hepatitis C virus (HCV) infection is a major cause of human hepatocellular carcinoma (HCC). The precise mechanism of hepatocarcinogenesis in humans by HCV is currently unclear. It was recently shown, however, that transgenic mice with the HCV core gene often develop HCC, suggesting tumorigenic activity of the HCV core protein. Further, the HCV core protein expressed in HepG2 cells transfected with the core gene was shown to stimulate proliferation of transfectants through activation of nuclear factor-kappaB (NF-kappaB). The downstream target molecule(s) of NF-kappaB activated by the HCV core protein to evoke cell proliferation is not yet identified. Transforming growth factor (TGF) alpha, which is often overexpressed in various tumour tissues such as HCC, has been shown to stimulate hepatocyte proliferation through activation of the mitogen-activated protein kinase or extracellular signal-related protein kinase (MAPK/ERK) cascade. AIMS: To explore the possibility that TGFalpha might be a target molecule for NF-kappaB activated by the HCV core, and that TGFalpha participates in the growth promotion of the core transfectants in an autocrine manner, activating the MAPK/ERK pathway. METHODS: A HCV core expression vector was transfected into human hepatoma Huh-7, HepG2 and Hep3B cells. NF-kappaB activity was examined by an electrophoretic mobility shift assay. TGFalpha transcription was assessed by a luciferase reporter assay. TGFalpha protein was determined by immunoblot and ELISA. MAPK/ERK activity was examined by an in vitro kinase assay. Cell proliferation was assessed by a water-soluble tetrazolium salt-1 assay. RESULTS: In the HCV core transfectants, NF-kappaB bound to the kappaB site in the TGFalpha proximal promoter region, resulting in an increase in TGFalpha transcription. Immunoblot as well as ELISA showed increased TGFalpha expression in the HCV core transfectants. SN50, a specific inhibitory peptide for NF-kappaB, cancelled HCV core-induced TGFalpha expression. HCV core protein increased cell proliferation as well as ERK activity of the HCV core transfectants as compared with the mock transfectants. The growth-promoting activity and activation of ERK by the HCV core protein were negated by treatment with anti-TGFalpha antibodies. CONCLUSIONS: These results suggest that the HCV core protein promotes proliferation of human hepatoma cells by activation of the MAPK/ERK pathway through up regulation of TGFalpha transcription via activation of NF-kappaB. Our finding provides a new insight into the mechanism of hepatocarcinogenesis by HCV infection.

Carcinoma, Hepatocellular↗
PubMed2006

Comparison of VEGF-producing cells in periprosthetic osteolysis.

The pro-angiogenic cytokine vascular endothelial growth factor (VEGF) has been implicated in periprosthetic osteolysis and subsequent aseptic loosening of implants following total hip arthroplasty (THA). The goal of this study was to investigate whether increased VEGF at the bone-implant interface is secondary to a greater number of VEGF-producing cells or to increased VEGF production by individual cells. Real time polymerase chain reaction (RT-PCR) techniques were used to assess the expression of VEGF mRNA (isoforms 121, 165, 189) in periprosthetic tissues from revision THAs. Immunofluorescence was used to determine both differences in overall cellularity and in VEGF-producing cell type (macrophages, fibroblasts, endothelial cells) between patients with periprosthetic osteolysis (OL) and a control group undergoing primary THA for osteoarthritis (OA). Quantitative analysis of VEGF release in periprosthetic membranes via RT-PCR demonstrated no significant difference in the per-cell mRNA production of VEGF isoforms 121 165, or 189 between OL and OA patient groups. Immunofluorescence showed both higher cellularity and higher overall VEGF expression in the OL group. Immunofluorescence also showed a significant increase in macrophages in the OL group, but no significant difference in the proportion of fibroblasts or endothelial cells between the OL and OA groups. Co-localization of CD68+ and CD11b+ macrophage fluorescent signals with VEGF signal was greater in the OL group than in the OA group. Our results demonstrate that increased VEGF in OL periprosthetic tissue compared to OA synovium is correlated to increased numbers of VEGF-producing CD68+ and CD11b+ macrophages. Impact statement: Aseptic loosening, caused in large part by OL, remains the major cause of failed THAs leading to revision surgery. At the bone-implant interface, we found increased numbers of macrophages-cellular mediators of OL-and increased VEGF expression. VEGF may be a possible target for therapeutic intervention in mitigating OL.

Aged↗
PubMed2006

Risk factors for dysbaric osteonecrosis.

OBJECTIVES: Dysbaric osteonecrosis (DON) is a complication of ineffective decompression following exposure to high-pressure environments. This study was designed to determine risk factors for the occurrence of DON in divers. METHODS: Fifty-six male divers received skeletal examinations by radiography to assess the occurrence of DON. A questionnaire was used to obtain clinical and diving information, including diving experience and maximum diving depth. Blood samples were collected to analyse the levels of plasminogen activator inhibitor (PAI)-1, cholesterol, triglyceride, low-density lipoprotein, very low-density lipoprotein, high-density lipoprotein, apolipoprotein A1 and apolipoprotein B. RESULTS: Lesions of DON were detected in 31 of the 56 (55%) divers. Multivariate logistic regression analysis showed that high levels of PAI-1, a coagulation marker (odds ratio 4.281; P=0.0296) and great maximum diving depth (odds ratio 5.627; P=0.0231) were independent predictors of DON. CONCLUSIONS: This study has shown the presence of coagulation abnormality in divers with DON. This result suggests that a pharmacological approach incorporating the use of an anticoagulant may represent a potential strategy for the prevention of DON.

Adult↗
PubMed2005

Involvement of transforming growth factor-beta and thrombopoietin in the pathogenesis of myelodysplastic syndrome with myelofibrosis.

We investigated the cause of myelofibrosis and proliferation of megakaryocytes in myelodysplastic syndrome with myelofibrosis (MDS-MF (+)). Plasma-transforming growth factor-beta1 (PTGF-beta1) concentrations closely correlated with myelofibrosis grade in MDS-MF (+) and were higher than those in idiopathic myelofibrosis (IMF), essential thrombocythemia (ET), idiopathic thrombocytopenic purpura (ITP), MDS-without MF (MDS-MF (-)) or healthy volunteers (HV). Peripheral blood mononuclear cells from MDS-MF (+) patients expressed more TGF-beta1 mRNA than those from IMF, MDS-MF (-) or HV. When we immunostained bone marrow specimens of MDS-MF (+) for TGF-beta, the intensity of blasts was apparently higher than that of megakaryocytes, while in MDS-MF (-), megakaryocytes were immunostained with a similar intensity as that in MDS-MF (+), but blasts were negative for staining. In IMF, megakaryocytes, monocytes and small mononuclear cells representing CD34+ cells were all similarly stained with a much lower intensity than that of blasts in MDS-MF (+). The number of bone marrow megakaryocytes were increased the most in MDS-MF (+), followed by ET, ITP, MDS-MF (-) and NHL and correlated with plasma thrombopoietin (TPO) levels or with plasma TGF-beta1 levels, respectively, in each disease. Thus, in MDS-MF (+), both myelofibrosis and the increased megakaryocytes were ascribed to overproduction of TGF-beta1 from blasts.

Adult↗
PubMed2004

Effects of different corticosteroids on the development of osteonecrosis in rabbits.

OBJECTIVES: Osteonecrosis (ON) of the femoral head is a devastating complication occurring in patients receiving corticosteroid treatment. This study examined the effect of three corticosteroids on the development of ON in rabbits. METHODS: Thirty-nine rabbits were injected once intramuscularly with either 25 mg/kg prednisolone sodium succinate (PSL; 13 rabbits), 20 mg/kg methylprednisolone acetate (MPSL; 13 rabbits) or 20 mg/kg triamcinolone acetonide (TR; 13 rabbits). Four weeks after corticosteroid injection, the bilateral femora and humeri were examined histopathologically for the presence of ON. Haematological examinations were performed before and after corticosteroid injection. RESULTS: MPSL treatment (17/26 proximal femora, 65%) significantly increased ON incidence in the proximal femora compared with the levels seen after TR (4/26, 15%) or PSL (3/26, 12%) treatment (P < 0.01). Although not significantly increased in comparison with rabbits receiving PSL treatment (1/26 proximal humeri, 4%), ON incidence within the proximal humeri was significantly increased in MPSL-treated rabbits (6/26, 23%) in comparison with those seen in rabbits receiving TR (0/26, 0%) treatment (P < 0.05). Serum levels of cholesterol, triglyceride and free fatty acid were significantly higher 1, 2 and 4 weeks after corticosteroid treatment in rabbits treated with MPSL relative to rabbits receiving TR and rabbits with PSL treatment (P < 0.05). CONCLUSIONS: MPSL treatment significantly increased ON incidence in rabbits over levels seen after TR or PSL treatment.

Animals↗
PubMed2002

Bone marrow fat cell enlargement and a rise in intraosseous pressure in steroid-treated rabbits with osteonecrosis.

The etiology of steroid-induced osteonecrosis (ON) is unclear. This study was designed to determine whether bone marrow fat cell size, intraosseous pressure, and blood flow rate differed between steroid-treated rabbits with ON and those without. Twenty-nine rabbits were intramuscularly injected once with 20 mg/kg of methylprednisolone acetate (MPSL), and five rabbits were injected once with physiologic saline (PS) as a control. Intraosseous pressure and blood flow rate in the proximal femur were determined before and at 2 weeks after the injection. After these measurements, both femora and humeri were histopathologically examined for the presence of ON, and size of bone marrow fat cells were morphologically examined. At 2 weeks after steroid injection, the intraosseous pressure was significantly higher in rabbits with ON than in those without (p = 0.0251), and the blood flow rate had decreased significantly more in rabbits with ON than in those without (p = 0.0051). The size of the bone marrow fat cells was significantly (p = 0.0004) larger in rabbits with ON (diameter, 63.5 +/- 5.8 microm) than in those without (diameter, 53.3 +/- 6.9 microm). Injection of PS (5 rabbits), 1 (10 rabbits), 5 (10 rabbits), and 20 (10 rabbits) mg/kg of body weight of MPSL showed that a larger dose of steroid increased both fat cell size and prevalence of ON. These results suggest that bone marrow fat cell enlargement and a rise in intraosseous pressure may be important when considering the pathophysiology of steroid-induced ON in rabbits.

Adipocytes↗
PubMed2001

Subchondral changes in transient osteoporosis of the hip.

OBJECTIVE: To review the subchondral changes on MR imaging in transient osteoporosis of the hip (TOH) and to consider the pathophysiology. DESIGN AND PATIENTS: MR images of 12 hips of 11 consecutive patients with TOH were retrospectively studied. The diagnoses of TOH were confirmed on the basis of previously published criteria, including decreased bone density of the femoral head and/or neck on radiographs, bone marrow edema (BME) pattern on MR images, spontaneous resolution of the symptoms and a return to normal radiodensity. RESULTS: All 12 hips showed a BME pattern in the femoral head and/or neck. Linear patterns of very low signal intensity were identified on T1-weighted images in the subchondral area within the diffuse low signal intensity area in all 12 hips. On T2-weighted images, a low signal intensity line was observed in the corresponding area in eight hips only. These linear patterns were thought to represent subchondral fracture lines. CONCLUSIONS: The presence of a subchondral fracture may be important when considering the pathophysiology of TOH.

Adult↗
PubMed2001

Osteonecrosis induced by a single administration of low-dose lipopolysaccharide in rabbits.

We succeeded in developing a novel rabbit model of nonsteroid and nontraumatic osteonecrosis (ON) by use of a single- and low-dose lipopolysaccharide (LPS) injection. This model is simple and highly reproducible for the frequent development of multifocal and widespread ON lesions. Male adult Japanese white rabbits intravenously injected with a single injection of 10 microg/kg body weight of LPS were histopathologically examined in the early phase (3 [n = 3], 5 [n = 3], and 24 h [n = 3]) and at 4 weeks (n = 22). Seventy-seven percent of the rabbits developed multifocal ON 4 weeks after LPS injection. ON was also observed in the femoral and humeral condyle. The average percentage of necrotic area/total area examined was 86.7 +/- 29.1% and 78.8 +/- 16.7% in the proximal one third of both the femoral and humeral bones, respectively. Organized thrombi in the intraosseous small-sized arteries and arterioles were frequently seen in and around the necrotic tissues. In the early phase, LPS treatment prominently induced thrombocytopenia, hyperlipidemia, and increased plasma levels of plasminogen activator inhibitor-1 (PAI-1). The plasma level of PAI-1 was significantly higher in the rabbits with ON than in those without ON (p < 0.01). The immunohistochemical expression of tissue factor was exaggerated in monocytes/macrophages and adipocytes in both the femoral and humeral bones of the LPS-treated rabbits. Histologically, marrow necrosis and fibrin thrombi could be observed at 24 h. In addition, pretreatment with an anticoagulant, warfarin potassium, significantly decreased the incidence of LPS-induced ON (33%, n = 9, p < 0.05) associated with elongation of prothrombin time. The results of our study show that a single administration of low-dose lipopolysaccharide induces multifocal and widespread ON characterized by the pathophysiological participation of hypercoagulability in ON development. Therefore, this model would be useful for elucidating the pathogenesis of nonsteroid ON in humans especially inflammatory hypercoagulability-induced as well as for developing preventive and therapeutic strategies.

Animals↗
PubMed2001

Vitamin D insufficiency in Japanese female college students: a preliminary report.

Vitamin D insufficiency, a risk factor for osteoporosis, has been well investigated in elderly women worldwide, but little information has been available for younger women. This study aimed to determine serum 25-hydroxyvitamin D [25(OH)D] levels in Japanese female college students, and to test whether there is an association between 25(OH)D and bone strength. Subjects were 77 Japanese female junior college students aged 19-24 years. Serum 25(OH)D was measured with high performance liquid chromatography. Bone strength of the calcaneus was evaluated using the osteo sono-assessment index (OSI), a combined index reflecting the bone mass, bone architecture, and elasticity, as measured by quantitative ultrasound densitometry (AOS-100, Aloka). The mean 25(OH)D concentration was 34.2 nmol/L (SD +/- 12.1). The proportion of subjects with 25(OH)D less than 30 nmol/L, a cut-off value for vitamin D insufficiency, was 31/77 (40.3%). Simple linear regression analysis showed that there was a significant linear relationship between 25(OH)D and OSI (R2 = 0.098, p = 0.0069). The association held even after adjusting for weight (partial R2 = 0.098, p = 0.0023). Body weight was also a significant predictor of OSI (partial R2 = 0.105, p = 0.0034). These results suggest that vitamin D insufficiency may be prevalent in healthy young women. Moreover, low levels of 25(OH)D in young women may adversely affect bone strength. An additional, newly designed epidemiological study with a sufficient sample size is needed to confirm the present findings.

Adult↗
PubMed2001

Analysis of K-ras, APC, and beta-catenin in aberrant crypt foci in sporadic adenoma, cancer, and familial adenomatous polyposis.

BACKGROUND & AIMS: We have previously shown that aberrant crypt foci (ACF) are the putative precursor lesions of colorectal adenomas and subsequent cancer in humans using magnifying endoscopy. The present study was designed to investigate these genetic alterations in ACF biopsy specimens from normal subjects, familial adenomatous polyposis (FAP) or sporadic patients. METHODS: The non-FAP cases included 34 normal subjects, 35 colorectal adenoma patients, and 19 colorectal cancer patients; there were 4 FAP patients. Biopsies were performed on ACF by magnifying endoscopy. K-ras mutations were analyzed by 2-step polymerase chain reaction and restriction fragment length polymorphism, APC mutations by in vitro-synthesized protein assay, and beta-catenin mutations by direct sequencing. Full-length APC and beta-catenin were detected by immunofluorescence. RESULTS: In non-FAP cases, K-ras mutations were detected in 82% (89/106) of nondysplastic ACF and 63% (17/27) of dysplastic ACF. APC mutation and beta-catenin accumulation were not detected in non-FAP ACF, whereas in adenoma of these patients, positivity of APC mutation and beta-catenin accumulation were 78% (24/31), and that of K-ras mutation was 65% (20/31). FAP patients showed K-ras mutations in only 13% (1/8) of dysplastic ACF, which is the predominant form of ACF found in FAP. In FAP patients, somatic APC mutations were found in 100% of dysplastic ACF, as they are in adenoma. The frequency of K-ras mutations was 73% (8 of 11) in FAP adenoma. CONCLUSIONS: The data suggest that in sporadic colorectal carcinogenesis, assuming the biological implication of ACF as a precursor of adenomas, there is a route where K-ras mutation mainly occurs during the formation of ACF, which then become adenomas wherein APC mutation occurs. In FAP, however, somatic mutation of APC predominantly occurs during ACF formation, followed by K-ras mutation.

Adenomatous Polyposis Coli↗
PubMed2001

Glutathione S-transferase-pi overexpression is closely associated with K-ras mutation during human colon carcinogenesis.

BACKGROUND & AIMS: In colorectal adenoma and carcinoma, glutathione S-transferase-pi (GSTP1-1) is highly expressed. K-ras mutation is also known to occur frequently in colorectal adenoma and carcinoma, as well as in the putative precursor of adenoma, aberrant crypt foci (ACF). Further, forced expression of v-H-ras in rat liver epithelial cells has been shown to enhance rat pi-class GST expression. The aim of the present study is, therefore, to investigate the causative relationship between GSTP1-1 overexpression and K-ras mutation in these lesions. METHODS: Twenty-seven specimens of colorectal carcinoma, 24 of adenoma, and 28 of ACF were examined in this study. The expression of GSTP1-1 or p21(K-ras) was examined by immunohistochemistry. The GSTP1-1 messenger RNA levels were measured by TaqMan reverse-transcription polymerase chain reaction (PCR). K-ras mutation was detected by two-step PCR restriction fragment length polymorphism. v-K-ras transfection to RPMI-4788 colon carcinoma cells was carried out by the lipofection method. Activities of GSTP1-1 promoters containing AP-1 and Sp1 responsive elements in the v-K-ras transfectants were measured by a secreted form of human placental alkaline phosphatase (SEAP) assay. Nuclear protein from these transfectants bound to the GSTP1-1 promoter was analyzed by electrophoretic mobility shift assay (EMSA). RESULTS: In human colorectal carcinoma, adenoma, and ACF, close association of increased expression of GSTP1-1 with K-ras mutation was observed. v-K-ras transfectants showed significantly higher SEAP activity than that of mock-transfectant activity. EMSA showed specific interaction of AP-1 with promoter of GSTP1-1. CONCLUSIONS: It is highly plausible that GSTP1-1 overexpression in ACF, colorectal adenoma, and carcinoma is induced by K-ras mutation via AP-1 activation.

Adenoma↗
PubMed2001

Comparison of postoperative early active mobilization and immobilization in vivo utilising a four-strand flexor tendon repair.

We evaluated a technique of four-strand double-modified locking Kessler flexor tendon repair in healing tendons. Seventy-two canine flexor digitorum profundus tendons in Zone 2 were repaired and evaluated following either active mobilization or immobilization at 0, 7, 14, 28 and 42 days after surgery. Fifty-six tendons were examined for gap and ultimate strength using a tensile testing machine and 16 were evaluated with standard hematoxylin and eosin, and Masson's trichrome staining. All tendons healed without rupture or gap formation of more than 1 mm, thus demonstrating that this repair technique has enough tensile strength to withstand early active mobilization. The gap and ultimate strength of actively mobilized tendons did not decrease significantly during the first 7 days, and were significantly greater than those of immobilized tendons throughout the 42-day study period. Actively mobilized tendons healed without the extrinsic adhesions and large tendon calluses that were found in immobilized tendons.

Animals↗
PubMed2001

A high low-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio as a potential risk factor for corticosteroid-induced osteonecrosis in rabbits.

OBJECTIVE: This study was designed to determine the potential risk factors for corticosteroid-induced osteonecrosis (ON) based on lipid metabolism, using a rabbit ON model. METHODS: Blood samples were obtained from 38 rabbits, which then received a single intramuscular injection of 20 mg/kg methylprednisolone acetate. Four weeks after the injection, the femora and humeri were examined histopathologically for the presence of ON, and the sizes of the bone marrow fat cells were also measured. RESULTS: Rabbits with and without ON differed significantly in the ratio of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol (LDL/HDL cholesterol ratio), which is considered to be a serological marker of lipid transport (P=0.026). The marrow fat cells were significantly larger in the rabbits with ON than in those without ON (P<0.0001). CONCLUSION: A higher LDL/HDL cholesterol ratio was significantly associated with the development of ON, and such an elevated ratio may partly contribute to the increased size of marrow fat cells.

Adrenal Cortex Hormones↗
PubMed2001

A case of successful management of portosystemic shunt with autosomal dominant polycystic kidney disease by balloon-occluded retrograde transvenous obliteration and partial splenic embolization.

We describe a patient with autosomal dominant polycystic kidney disease who was successfully managed for severe abdominal distension, impaired liver function and a portosystemic shunt by interventional therapies. The patient's intra-hepatic portal vein was compressed and narrowed by multiple liver cysts, which resulted in a decrease of the portal blood flow and portal hypertension due to a huge gastro-renal shunt These haemodynamic changes were assumed to contribute to insufficient protein synthesis in the liver. Therefore, we first repeatedly performed minocycline hydrochloride instillations to treat the multiple liver cysts. Then, we conducted a partial splenic embolization to prevent elevation of the portal vein pressure prior to balloon-occluded retrograde transvenous obliteration which was performed to increase the portal blood flow. The portal blood flow markedly increased, and protein synthesis in the liver also recovered and the clinical symptoms improved. The patient has been monitored for more than two years up to the present and her liver function parameters have remained within the normal range. Renal insufficiency is known to be a major prognostic factor in autosomal dominant polycystic kidney disease. In some cases, however, liver involvement with multiple cysts may result in a fatal outcome. In such cases, interventional therapies, as provided to this patient, should be considered.

Cysts↗
PubMed2001

Effect of transjugular intrahepatic portosystemic shunt formation on portal hypertensive gastropathy and gastric circulation.

OBJECTIVES: The aim of this study was to investigate the effect of a transjugular intrahepatic portosystemic shunt (TIPS) on portal hypertensive gastropathy (PHG) and gastric hemodynamics. METHODS: A total of 16 patients with cirrhosis and portal hypertensive gastropathy were prospectively studied. Of these, 12 patients underwent TIPS for esophageal varices and four for refractory ascites. Gastric mucosal blood flow (GMBF) was assessed by laser Doppler flowmeter, and total blood flow (TBF) in submucosa and mucosa by near-infrared endoscopy. Portal venous pressure was obtained by a transducer during the TIPS procedure. The severity of portal hypertensive gastropathy was classified as none, mild, or severe. The examinations were performed before and 2 wk after the procedure. RESULTS: TIPS significantly reduced portal venous pressure. PHG improved in all four patients with severe PHG and in five of 12 patients with mild PHG after treatment. Gastric mucosal blood flow increased from 49.0 to 55.6 ml/min/100 g after TIPS. In contrast, TBF decreased from 0.35/s to 0.27/s after treatment. Liver function tests showed no significant changes before and after the procedure. CONCLUSIONS: It is considered that TIPS may have a beneficial effect on PHG at least for a short time. The mechanism by which PHG improves may be closely related to the improvement of the injured gastric perfusion in cirrhotic patients with PHG.

Esophageal and Gastric Varices↗