Effects of Lenvatinib on Skeletal Muscle Volume and Cardiac Function in Patients with Hepatocellular Carcinoma.

INTRODUCTION: Previously, we reported that the tyrosine kinase inhibitor (TKI) sorafenib decreases serum levels of carnitine and reduces skeletal muscle volume. Moreover, others reported that TKIs might lead to cardiomyopathy or heart failure. Therefore, this study aimed to evaluate the effects of lenvatinib (LEN) on skeletal muscle volume and cardiac function in patients with hepatocellular carcinoma (HCC). METHODS: This retrospective study included 58 adult Japanese patients with chronic liver diseases and HCC treated with LEN. Blood samples were collected before and after 4 weeks of treatment, and serum carnitine fraction and myostatin levels were measured. Before and after 4-6 weeks of treatment, the skeletal muscle index (SMI) was evaluated from computed tomography images and cardiac function was assessed by ultrasound cardiography. RESULTS: After treatment, SMI, serum levels of total carnitine, and global longitudinal strain were significantly lower, but serum levels of myostatin were significantly higher. Left ventricular ejection fraction showed no significant change. CONCLUSION: In patients with HCC, LEN decreases serum levels of carnitine, skeletal muscle volume, and worsens cardiac function.

Lenvatinib Might Induce Activation of Host Immunity in Patients with Hepatocellular Carcinoma.

INTRODUCTION: Atezolizumab, an immune checkpoint inhibitor, plus bevacizumab, a monoclonal antibody that binds to vascular endothelial growth factor (VEGF), is an approved first-line systemic treatment for unresectable hepatocellular carcinoma (HCC). Immune checkpoint inhibitors are more effective in patients with HCC when administered with anti-VEGF drugs; however, these drugs affect host immunity. Lenvatinib is an anti-VEGF agent used to treat HCC; therefore, this study evaluated the effect of treatment of HCC with lenvatinib on host immunity in patients with chronic liver disease (CLD). METHODS: We studied adult Japanese patients with CLD and unresectable HCC treated with lenvatinib at our hospital. Lenvatinib was administered for 4 weeks (8 mg/day for bodyweight <60 kg; 12 mg/day for bodyweight >60 kg). Blood samples were collected at baseline and at 4 weeks of treatment and examined for immune-related changes. RESULTS: Forty-three patients were enrolled in this study. We found a significant increase in T helper (Th) 1 cells following 4 weeks of lenvatinib treatment, although there was no significant difference in Th2 cells and regulatory T cells. We also found a significant increase in serum levels of TNF-alpha, soluble TNF-alpha receptor I, and endothelial growth factor following 4 weeks of lenvatinib treatment. Furthermore, an increase in Th1 cells and serum levels of TNF-alpha was found in patients with partial response. CONCLUSION: Lenvatinib might induce Th1-dominant host immunity in patients with CLD and unresectable HCC treatment in patients who showed a partial response. These changes in host immunity may be a biomarker in HCC patients treated with lenvatinib.

Usefulness of partial splenic embolization for left-sided portal hypertension in a patient with a pancreatic neuroendocrine neoplasm: a case report and review of the literature.

Left-side portal hypertension (LSPH) is caused by isolated obstruction of the splenic vein and is associated with esophagogastric varices that extend from the lower esophagus to the greater curvature of the gastric body. Here, we report on a 74-year-old man with a pancreatic neuroendocrine neoplasm (NEN) in the pancreatic tail with multiple liver metastases. We decided that partial splenic embolization (PSE) was the best course of treatment to prevent rupture of the gastric varices, which were classified as markedly enlarged, nodular, or tumor-shaped and showed erosion of the mucosa. After PSE, the patient had no major complications and was discharged. At 3 and 6 months after the procedure, esophagogastroduodenoscopy and enhanced computerized tomography showed that the gastric varices had improved. This case demonstrates the usefulness of PSE for LSPH in patients with unresected pancreatic NEN.

Adaptation of lenvatinib treatment in patients with hepatocellular carcinoma and portal vein tumor thrombosis.

PURPOSE: The aim of this study was to clarify the adaptation of lenvatinib treatment in patients with hepatocellular carcinoma (HCC) and portal vein tumor thrombosis (PVTT). METHOD: Fifty-three patients with HCC were treated with lenvatinib. Before and after treatment blood sampling, patients were examined by computed tomography and ultrasonography. In patients with portal trunk invasion (Vp4), the analysis focused on the degree of occlusion due to the tumor in the portal trunk. In patients without major PVTT {ie, invasion of the primary branch of the portal vein [Vp3] or Vp4}, portal blood flow volume was measured by Doppler analysis; however, Doppler analysis is difficult to perform in patients with major PVTT, so the time from administration of the contrast agent to when it reached the primary branch of the portal vein (portal vein arrival time) was evaluated with the contrast agent Sonazoid. RESULTS: Patients with Vp4 had a significantly worse prognosis than patients with Vp3 and a significant increase in Child-Pugh score at 2 months. Patients with major PVTT had a poor prognosis if the degree of occlusion of the portal trunk was 70% or more. In patients without major PVTT, portal blood flow was significantly decreased after administration of lenvatinib; and in patients with major PVTT, the hepatic artery and portal vein arrival times were significantly increased. CONCLUSION: Lenvatinib treatment should be avoided in patients with Vp4 with a high degree of portal trunk occlusion because of concerns about decreased portal blood flow.

Successful treatment of advanced pancreatic leiomyosarcoma treated with gemcitabine plus nab-paclitaxel: a case report and literature review.

Pancreatic leiomyosarcoma (PLMS) is an extremely rare tumor that accounts for 0.1% of pancreatic malignancies, and its chemotherapy has yet to be established. Generally, soft-tissue sarcoma chemotherapy is standard treatment with doxorubicin (DXR) alone. However, the effectiveness of gemcitabine (GEM) plus docetaxel (DOC) has been shown in uterine leiomyoma. In contrast, the GEM plus nab-paclitaxel (PTX) regimen has been established as first-line chemotherapy for unresectable pancreatic cancer. For this study, we selected the GEM plus nab-PTX regimen for patients with PLMS, achieving success in approximately 10 months. From a search on PubMed, we found only 12 cases of PLMS (including this case) that underwent chemotherapy. Our case is the first reported patient to have survived more than 2 years with chemotherapy alone. In a nude mouse model, the GEM plus DOC regimen was shown to significantly decrease tumor size when compared with DXR in leiomyosarcoma, and the GEM plus nab-PTX regimen was reported to significantly reduce necrosis when compared with DXR alone, GEM alone, DOC alone, nab-PTX alone and GEM plus DOC in soft-tissue sarcoma. GEM plus nab-PTX therapy might therefore be the first choice for soft-tissue sarcoma and leiomyosarcoma. This is the first reported case of PLMS treated with GEM plus nab-PTX.

Tivantinib Decreases Hepatocyte Growth Factor-Induced BCRP Expression in Hepatocellular Carcinoma HepG2 Cells.

Tivantinib, a mesenchymal-epithelial transition factor (cMET) inhibitor, is a molecular targeting drug that kills hepatocellular carcinoma (HCC) cells. Tivantinib alone does not affect the overall survival of patients with HCC, and combination treatment with tivantinib and other therapies has not been evaluated. This study was conducted to clarify the effect of the tivantinib in regulating breast cancer therapy-resistant protein (BCRP), a key transporter of 5-fluorouracil (5-FU), and dihydropyridine dehydrogenase (DPYD), a major metabolic enzyme of 5-FU. To this end, cMET gene expression was determined by RT-PCR in HepG2 (human hepatoma) cells. The transcriptional start sites of BCRP were determined by 5'-rapid amplification of cDNA ends (5'-RACE). BCRP and DPYD mRNA levels were determined by real-time RT-PCR, and promoter activities were measured by dual-luciferase assays. Results show that hepatocyte growth factor (HGF) upregulated the mRNA level of BCRP, but not DPYD, in HepG2 cells. The upregulation of BCRP expression by HGF was down-regulated by tivantinib. We also identified two transcriptional start sites (E1α, E1ß) in BCRP by 5'-RACE. The transcriptional activity of the region -287 to E1α of BCRP was upregulated by HGF, which was decreased by tivantinib, whereas activity of the region -297 to E1ßo f BCRP was not affected by tivantinib. Therefore, tivantinib regulates BCRP expression upstream of exon 1α. Combination treatment of tivantinib and 5-FU should be further evaluated for HCC therapy.

Sorafenib Might Induce Sarcopenia in Patients With Hepatocellular Carcinoma by Inhibiting Carnitine Absorption.

BACKGROUND/AIM: Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment of cancers. Sorafenib, an oral multi-target TKI, improves the median overall survival time in patients with hepatocellular carcinoma (HCC). It also inhibits the absorption of carnitine by down-regulating the human organic cationic transporter OCTN2 located largely in the small intestinal mucosa and skeletal muscle. The aim of the study was to determine, by assessing carnitine metabolism, whether sarcopenia is induced in patients with HCC who are receiving sorafenib. PATIENTS AND METHODS: This retrospective study included 110 adult Japanese patients with liver cirrhosis and HCC who received sorafenib. Sorafenib was administered at a dose of 200-800 mg/day for 4 weeks. Blood samples were collected before and after treatment, and serum carnitine fraction and myostatin levels were measured. Cross-sectional areas (cm2) of the skeletal muscles at the third lumbar vertebra level were determined by manually outlining computed tomography images before and after treatment. The cross-sectional areas were normalized for height [skeletal muscle index (SMI), cm2/m2]. RESULTS: Patients were allocated to two groups according to Child-Pugh (CP) class; 81 had CP-A liver function, and 29 had CP-B. SMI after treatment was significantly lower than that before treatment in both groups. Serum levels of total carnitine and free carnitine after treatment were significantly lower than those before treatment in both groups. There were no differences in serum levels of myostatin before and after treatment in either group. CONCLUSION: Sorafenib might decrease serum levels of carnitine by inhibiting carnitine absorption. Decreasing of serum levels of carnitine might lead to presarcopenia.

Influence of Sorafenib on Host Immunity in Patients with Liver Cirrhosis With Advanced Hepatocellular Carcinoma Stratified by Etiology.

AIM: We previously reported that sorafenib induces Th1 [interferon-γ (IFNγ)-positive interleukin 4 (IL4)-negative] dominance which prevents tumor cells from escaping the host immune system in patients with liver cirrhosis (LC) and advanced hepatocellular carcinoma (aHCC). However, in that study we did not assess the influence of sorafenib on host immunity according to the etiology of LC. Therefore, this study was retrospectively performed to evaluate the impact of sorafenib therapy for aHCC on host immunity in patients stratified according to the etiology of LC: Patients and Methods: A total of 116 adult Japanese patients with LC and aHCC received sorafenib therapy at our hospital. Blood samples were collected before and after treatment for 4 weeks. RESULTS: Twenty-two patients had hepatitis B virus (HBV)-related LC, 62 patients had hepatitis C virus (HCV)-related LC, 22 patients had alcoholic LC, and 10 patients had LC without these causative factors. In patients receiving sorafenib at a dose of 400 mg/day, patients in Child-Pugh class A, and patients with stage IVA aHCC, Th2 (IFNγ-negative/IL4-positive) cells decreased significantly after treatment, although there was no significant impact on the tumor response. In addition, Th2 cells decreased significantly in patients with HCV-related LC after treatment, while there were no significant changes in the other groups. CONCLUSION: Sorafenib might prevent tumor cells from escaping the host immune system in patients with aHCC and HCV-related LC, although it does not seem to do so in those with LC of other etiologies.

Flash Imaging Used in the Post-vascular Phase of Contrast-Enhanced Ultrasonography is Useful for Assessing the Progression in Patients with Hepatitis C Virus-Related Liver Disease.

Sonazoid is a commonly used contrast agent for characterizing liver tumors in ultrasonography (US). We performed flash imaging in the post-vascular phase of contrast-enhanced US (CEUS) to investigate associations between collapse of Sonazoid microbubbles (MB) and progression of liver disease. This study enrolled 409 patients (205 men, 204 women) with hepatitis C virus-related liver disease (CLD) between 2007 and 2017 (mean age 60 ± 14 y; range 20-90 y). In the post-vascular phase, 10 min after administering Sonazoid, flash imaging was performed to burst MB in the liver parenchyma; the range of bubble destruction was measured from the surface of the liver. The range of bubble destruction, stage of fibrosis, shear wave velocity (Vs), serologic markers and fibrosis-4 (FIB4) index were analyzed in 259 patients who underwent liver biopsy. Fibrosis stage was F0-1 in 108 patients, F2 in 73, F3 in 38 and F4 in 40. In 150 patients with cirrhosis, diagnosis was made based on imaging findings. The range of bubble destruction was 42.0 ± 10.4 mm in F0-1 patients, 42.9 ± 13.2 mm in F2, 51.5 ± 15.9 mm in F3 and 55.4 ± 17.3 mm in F4 and was significantly increased according to progression of fibrosis staging. The range of bubble destruction was positively correlated with Vs (r = 0.34; p < 0.01), total bilirubin (r = 0.25; p < 0.01) and FIB4 index (r = 0.38; p < 0.01). In contrast, the range of bubble destruction was negatively correlated with serum levels of albumin (r = -0.34; p < 0.01), platelet count (r = -0.35; p < 0.01) and prothrombin time (r = -0.36; p < 0.01). The results indicated that flash imaging in the post-vascular phase of CEUS was a non-invasive assessment and could predict disease progression in patients with CLD.

Coronary artery calcium score and CT angiography in asymptomatic elderly patients with high pretest probability for coronary artery disease.

PURPOSE: To evaluate the role of coronary artery calcium scoring (CACS) and/or coronary CT angiography (CCTA) in asymptomatic elderly patients with high pretest probability for coronary artery disease (CAD). MATERIALS AND METHODS: Forty-eight consecutive asymptomatic elderly (>65 years) subjects who had a high pretest probability and underwent CACS/CCTA were included. Each CCTA was evaluated for adequacy for assessment of coronary stenosis. Significant stenosis (>50% diameter narrowing) was assessed on evaluable CT images and by invasive catheter angiography (ICA). RESULTS: All subjects were men with mean CACS of 880 ± 1779. Among those with low (0-99), intermediate (100-399), and high (400-999) CACS, ICA-verified significant stenosis was present in 8% (1/13), 23% (2/13), and 67% (8/12), respectively. Among those with very high CACS (≥ 1000) (n = 10), 90% of CCTAs were not evaluable for stenosis. CONCLUSION: In asymptomatic elderly subjects with high pretest probability, CACS followed by CCTA may be considered for those with intermediate to high CACS.

Superficial siderosis of the central nervous system caused by hemorrhagic intraventricular craniopharyngioma: case report and literature review.

Superficial siderosis is a rare condition caused by hemosiderin deposits in the central nervous system (CNS) due to prolonged or recurrent low-grade bleeding into the cerebrospinal fluid (CSF). CNS tumor could be one of the sources of bleeding, both pre- and postoperatively. We report an extremely rare case of superficial siderosis associated with purely third ventricle craniopharyngioma, and review previously reported cases of superficial siderosis associated with CNS tumor. A 69-year-old man presented with headache, unsteady gait, blurred vision, and progressive hearing loss. Brain magnetic resonance (MR) imaging with gadolinium revealed a well enhanced, intraventricular mass in the anterior part of the third ventricle. T2*-weighted gradient echo (GE) MR imaging revealed a hypointense rim around the brain particularly marked within the depth of the sulci. Superficial siderosis was diagnosed based on these findings. The tumor was diffusely hypointense on T2*-weighted GE imaging, indicating intratumoral hemorrhage. The lateral ventricles were dilated, suggesting hydrocephalus. [(18)F]fluorodeoxyglucose positron emission tomography revealed increased uptake in the tumor. The whole brain surface appeared dark ocher at surgery. Histological examination showed the hemorrhagic tumor was papillary craniopharyngioma. His hearing loss progressed after removal of the tumor. T2*-weighted GE MR imaging demonstrated not only superficial siderosis but also diffuse intratumoral hemorrhage in the tumor. Superficial siderosis and its related symptoms, including hearing loss, should be considered in patients with hemorrhagic tumor related to the CSF space. Purely third ventricle craniopharyngioma rarely has hemorrhagic character, which could cause superficial siderosis and progressive hearing loss.

A novel GJA1 mutation in oculodentodigital dysplasia with progressive spastic paraplegia and sensory deficits.

Oculodentodigital dysplasia (ODDD) is a rare autosomal dominant inherited disorder mainly affecting the development of the face, eyes, dentition, limbs, hair and heart. GJA1 (the gap junction protein α-1) has been determined to be a causative gene of ODDD, mapped to chromosome 6q22-24 identified as the connexin 43 gene (Cx43). We found a novel GJA1 mutation (W25C) as the possible causative gene in this sporadic ODDD patient with neurological features of motor deficits by pyramidal tract signs, and sensory deficits due to peripheral nerve disturbance. It is also notable that the MRI of this patient demonstrated widespread aberrant signal lesions in the brain and brainstem.

Contrast- and non-contrast-enhanced ultrasonography (US) findings of hepatic metastasis from malignant pheochromocytoma/paraganglioma.

PURPOSE: To evaluate the findings of hepatic metastases from malignant pheochromocytoma/paraganglioma on non-contrast-enhanced and contrast-enhanced ultrasonography (US) and compare them with other imaging modalities. SUBJECTS AND METHODS: US was performed on eight patients with 65 hepatic metastases. Non-contrast computed tomography (CT), meta-iodo-benzyl-guanidine scintigraphy ((123)I-MIBG), and fluorine-18-fluorodeoxyglucose positron emission tomography (FDG-PET) were also performed. Magnetic resonance imaging, including diffusion-weighted imaging (DWI), was performed on six patients. RESULTS: Forty of the 65 lesions (61.5%) were detected on non-contrast-enhanced US: 27 were hyperechoic (67.5%), 10 were hypoechoic (25.0%), and 3 (7.5%) were isoechoic. Sixteen of 17 lesions appeared hypervascular in the arterial phase of dynamic contrast-enhanced US. On delayed images, contrast-enhanced US demonstrated 64 of 65 metastatic tumors (98.5%), and 51 of them were delineated as enhancement defects. Non-contrast-enhanced CT revealed 61 (93.8%) of 65, FDG-PET revealed 44 (67.7%) of 65, and DWI revealed 30 (90.9%) of 33. On (123)I-MIBG scintigraphy, seven patients had abnormal uptakes in the liver, suggesting metastases. There were no significant differences between the detectability of US and other modalities. CONCLUSION: On contrast-enhanced US, nearly all hepatic metastases were delineated. Most lesions showed hypervascularity on dynamic contrast-enhanced US, suggesting the usefulness of this technique.

Blood flow change quantification in cervical cancer before and during radiation therapy using perfusion CT.

The purpose of this study was to quantify the changes of tumor blood flow (BF) in cervical cancer after radiation therapy by using perfusion computed tomography (CT), and to examine the difference between maximum slope (MS) and single-input one-compartment model (SOCM) methods. Fourteen consecutive patients who received definitive radiation therapy for cervical cancer from October 2009 to February 2010 were enrolled in this study. Blood flow (BF) analyses were performed using both MS and SOCM methods. Quantitative BF maps were created using Body Perfusion (Toshiba Medical Systems, Co. Tokyo, Japan). Perfusion color maps were successfully created by the two analytical methods. BF of the tumors was clearly higher than that of normal cervix, making it possible to distinguish tumor tissue from normal cervical tissue. BF of the tumors after 20 Gy of radiation therapy calculated by the MS method was significantly larger than that before treatment (126.9 vs. 72.2 ml/min/100 ml, median; p < 0.05). Although BF calculated by the MS and SOCM methods showed a positive linear correlation (p < 0.001, r = 0.981), BF calculated by the MS method was lower than that obtained by the SOCM method (103.7 vs. 115.1 ml/min/100 ml, p < 0.01). The change of tumor BF in cervical cancer before and after radiation therapy can be monitored by conducting blood flow analysis using perfusion CT. BF by the MS method was lower than that by the SOCM method, but the two analytical methods correlated well. Perfusion CT may have potential in noninvasive monitoring of vascular and oxygenation status and for guiding adaptive therapy.

Hypertensive crisis due to contrast-enhanced computed tomography in a patient with malignant pheochromocytoma.

A 63-year-old man underwent computed tomography (CT) using intravenous low-osmolar iodine contrast medium (LOCM) 6 days after undergoing high-dose (131)I-MIBG therapy for metastatic pheochromocytoma. Immediately after the CT examination, his blood pressure increased to 260/160 mmHg (from 179/101 mmHg before the examination). Phentolamine mesilate was administered, and the blood pressure rapidly went back to normal. Although hypertensive crisis after administration of LOCM is rare, this case suggests that high-dose (131)IMIBG therapy may be a risk factor for hypertensive crisis after administration of intravenous LOCM.

Added value of contrast-enhanced CISS imaging in relation to conventional MR images for the evaluation of intracavernous cranial nerve lesions.

INTRODUCTION: The normal cranial nerves (CNs) of the cavernous sinus can be clearly demonstrated using contrast-enhanced constructive interference in steady-state (CISS) magnetic resonance imaging (MRI). This study used the method to evaluate pathological CNs III, IV, V(1), V(2), and VI in cavernous sinuses affected by inflammatory and neoplastic diseases. METHODS: MR images from 17 patients with diseases involving the cavernous sinuses and/or causing neuropathy in CNs III-VI were retrospectively evaluated. The patients were divided into inflammatory (n=11) and neoplastic (n=6) groups. We defined CNs as abnormal when they exhibited enlargement or enhancement. CNs were evaluated using both contrast-enhanced CISS and T1-weighted MRI. RESULTS: In the inflammatory group, abnormal CNs were identified by contrast-enhanced CISS MRI in 13 of 25 symptomatic CNs (52%) in eight patients, but in only two CNs (8%) in two patients by contrast-enhanced T1-weighted MRI. In the neoplastic group, both sequences of contrast-enhanced CISS and T1-weighted MRI detected abnormalities in the same three of eight symptomatic CNs (37.5%), i.e., the three CNs were all in the same patient with adenoid cystic carcinoma. CONCLUSION: Contrast-enhanced CISS MRI is useful for detecting CN abnormalities in inflammatory pathological conditions of the cavernous sinuses.

Clinical and imaging characteristics of localized megalencephaly: a retrospective comparison of diffuse hemimegalencephaly and multilobar cortical dysplasia.

INTRODUCTION: Hemimegalencephaly is a well-known congenital malformation. However, localized megalencephaly, which may be one of the subtypes of hemimegalencephaly, has not been separately investigated. In the present study, we attempted to characterize the clinical and magnetic resonance (MR) imaging features of localized megalencephaly in comparison with ordinary diffuse hemimegalencephaly and multilobar cortical dysplasia. METHODS: MR findings for 43 patients with hemimegalencephaly and ten with multilobar cortical dysplasia, which is the differential diagnosis of localized megalencephaly, were retrospectively reviewed. Clinical findings such as the onset and severity of seizures and imaging findings including the affected area of the brain, structures outside of the hemisphere, and interval morphological changes were examined. RESULTS: Of the 43 patients, 11 showed signs of localized megalencephaly (25.6%). Localized megalencephaly was predominantly seen on the left side (72.7%) and had a tendency toward severe-grade seizures compared to multilobar cortical dysplasia. The frequencies of the extracerebral abnormalities in the diffuse hemimegalencephaly, localized megalencephaly, and multilobar cortical dysplasia groups were 84.4%, 36.4%, and 0.0%, respectively. There were three localized megalencephaly patients whose affected areas shrank and whose images were similar to those of multilobar cortical dysplasia. CONCLUSION: Localized megalencephaly accounts for one quarter of all hemimegalencephaly cases in this study. The incidence of extracerebral abnormalities in patients with localized hemimegalencephaly was almost half that of patients with diffuse hemimegalencephaly. Extracerebral abnormalities were absent in patients with multilobar cortical dysplasia. Associated extracerebral abnormalities may be a clue to differentiating localized megalencephaly from multilobar cortical dysplasia.

Quantification of hepatic arterial and portal perfusion with dynamic computed tomography: comparison of maximum-slope and dual-input one-compartment model methods.

PURPOSE: The aim of this study was to compare the maximum-slope (MS) and dual-input one-compartment model (DOCM) methods in hepatic perfusion computed tomography (CT). MATERIALS AND METHODS: A total of 37 patients with known or suspected liver disease underwent single-location dynamic CT after arterial or venous bolus injection of contrast material. Perfusion CT images were created by the MS (dividing the peak gradient of the time-attenuation curve by the peak vessel CT number) and DOCM-calculating from the equation dC ( L )(t)/dt = k ( a ) C ( a )(t - tau( a )) + k ( p ) C ( p )(t - tau( p )) - k ( v ) C ( L )(t)-methods. The perfusion parameters hepatic arterial perfusion (HAP), portal venous perfusion (PVP), and hepatic perfusion index (HPI) were determined. RESULTS: The PVP of the tumor-free hepatic parenchyma determined by the MS method was lower than that obtained by the DOCM method (P < 0.001) with both injections. HAP determined by the MS method was lower than that obtained by the DOCM method with venous injection (P = 0.001), although there was no difference between the methods for HAP with arterial injection (P = 0.154). Most of the perfusion parameters showed linear correlations between the two analytical methods. CONCLUSION: Except for HAP with arterial injection, the perfusion parameters obtained with the MS method were lower than those obtained with the DOCM method.

Detection of metastatic lesions from malignant pheochromocytoma and paraganglioma with diffusion-weighted magnetic resonance imaging: comparison with 18F-FDG positron emission tomography and 123I-MIBG scintigraphy.

OBJECTIVE: To investigate the diagnostic features of whole-body diffusion-weighted magnetic resonance imaging (DWI) as compared with 2-[(18)F]-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) and (123)I-meta-iodo-benzyl guanidine scintigraphy (MIBG) on metastatic lesions of patients with malignant pheochromocytoma or paraganglioma. METHODS: We prospectively studied 11 patients with histologically confirmed pheochromocytoma/paraganglioma and possible metastatic lesions. FDG-PET, MIBG, and DWI examinations were performed within 1 week, and the images were visually interpreted. Abnormal positive uptake either on MIBG or on FDG-PET was considered as metastases. Abnormal high signal intensities on DWI were considered as metastases using conventional T1-and T2-weighted images as reference. RESULTS: FDG-PET and DWI demonstrated metastatic lesions in all 11 patients, but MIBG showed no metastatic lesions in two patients. The numbers of lymph node metastases depicted on FDG-PET, MIBG, and DWI were 19, 6, and 39; bone metastases were 50, 49, and 60; liver metastases were 9, 9, and 15; lung metastases were 5, 7, and 5, respectively. MIBG failed to demonstrate many metastatic lesions, which were demonstrated on FDG-PET or DWI, although two mediastinal lymph node metastases, three lung metastases, and six bone metastases, which were not seen on DWI, were clearly demonstrated on MIBG. DWI showed 15 liver metastases, but 6 of them were not seen on FDG-PET or MIBG. CONCLUSIONS: DWI may be particularly advantageous in depicting lymph node and liver metastases and may have a higher rate of detecting metastatic lesions when compared with MIBG or FDG-PET. The limitations of DWI were possible false-positive finding, and probable lower detectability of mediastinal lymph node and lung metastasis.

Air embolism detected during computed tomography fluoroscopically guided transthoracic needle biopsy.

Air embolism is a rare but potentially fatal complication of percutaneous needle biopsy of the lung. We report a case of cerebral air embolism which occurred during computed tomography (CT)-guided needle biopsy. Air entering the aorta is depicted on CT-fluoroscopy images of the procedure.