[11C]Choline PET/CT in a Patient with Prostate Cancer Biochemical Recurrence Showing Two Suspicious Findings in the Breast and Liver.

A 79-year-old man with prostate cancer (PCa) was referred to our center to perform a [11C]Choline PET/CT for biochemical recurrence. Positron emission tomography/computed tomography (PET/CT) scan detected PCa recurrence in the prostate gland and several pelvic and abdominal lymph nodes. Two abnormal uptakes were also identified in the right breast and in the liver, respectively. Breast histological findings turned out to be gynecomastia, while the liver lesion resulted in a benign perfusion anomaly at follow-up magnetic resonance imaging (MRI). Although incidental findings were benign in this case, it is important to always investigate abnormal uptakes of [11C]Choline, as it could be an expression of further metastases or synchronous malignancies such as breast cancer and hepatocellular carcinoma.

Single-cell transcriptome analysis reveals tumoral microenvironment heterogenicity and hypervascularization in human carotid body tumor.

Carotid body tumor (CBT) is a rare neck tumor located at the adventitia of the common carotid artery bifurcation. The prominent pathological features of CBT are high vascularization and abnormal proliferation. However, single-cell transcriptome analysis of the microenvironment composition and molecular complexity in CBT has yet to be performed. In this study, we performed single-cell RNA sequencing (scRNA-seq) analysis on human CBT to define the cells that contribute to hypervascularization and chronic hyperplasia. Unbiased clustering analysis of transcriptional profiles identified 16 distinct cell populations including endothelial cells (ECs), smooth muscle cells (SMCs), neuron cells, macrophage cells, neutrophil cells, and T cells. Within the ECs population, we defined subsets with angiogenic capacity plus clear signs of later endothelial progenitor cells (EPCs) to normal ECs. Two populations of macrophages were detectable in CBT, macrophage1 showed enrichment in hypoxia-inducible factor-1 (HIF-1) and as well as an early EPCs cell-like population expressing CD14 and vascular endothelial growth factor. In addition to HIF-1-related transcriptional protein expression, macrophages1 also display a neovasculogenesis-promoting phenotype. SMCs included three populations showing platelet-derived growth factor receptor beta and vimentin expression, indicative of a cancer-associated fibroblast phenotype. Finally, we identified three types of neuronal cells, including chief cells and sustentacular cells, and elucidated their distinct roles in the pathogenesis of CBT and abnormal proliferation of tumors. Overall, our study provided the first comprehensive characterization of the transcriptional landscape of CBT at scRNA-seq profiles, providing novel insights into the mechanisms underlying its formation.

Glioblastoma simulating an arteriovenous malformation: a case report.

Glioblastoma is the most common primary malignant brain tumor in adults. It is enhanced by the abnormal proliferation of central nervous system cells called astrocytes. Microvascular endothelial proliferation is one of the criteria for a histological diagnosis. Hypervascular glioblastoma simulating an arteriovenous malformation is an involuntary manifestation and constitutes a rare entity. Case presentation: The authors report a case of a 44-year-old patient with no history followed. Symptoms began 6 months ago with the gradual onset of headaches without vomiting or seizures associated with a drop in normal visual acuity without neurological deficit. Cerebral imaging including cerebral angiography concluding with a right parieto-occipital cerebral process probably associated with an arteriovenous malformation. Clinical discussion: The management was surgical by biopsy after a right parieto-occipital bone flap concluding in glioblastoma. The patient needs chemotherapy and radiotherapy sessions with good clinical evolution. Conclusion: The coexistence of an arteriovenous malformation and glioblastoma remains an association whose pathophysiology still remains to be explored.

Hypertrophic osteoarthropathy associated with lung cancer: Possible links among hypoxia-inducible factor-1α, vascular endothelial growth factor, and hypervascularization.

Hypertrophic osteoarthropathy (HOA) is a paraneoplastic syndrome, the exact pathogenesis of which remains to be elucidated. The case of a 69-year-old man who developed intractably painful HOA secondary to lung cancer is presented. Contrast-enhanced computed tomography of the chest showed an 80-mm solid nodule with a large low-density area. The patient was diagnosed as having stage IIIA undifferentiated non-small cell lung cancer. The combination of carboplatin and paclitaxel with bevacizumab reduced tumor size and plasma vascular endothelial growth factor (VEGF) levels, relieving his leg pain. On immunohistochemical examination, lung cancer cells were positive for VEGF. A hypoxic tumor microenvironment may have caused some lung cancer cells to express hypoxia-inducible factor-1α, which contributed, at least in part, to the production of VEGF. The deep dermis vessels showed proliferation in the shin, with their thickened walls positive for VEGF. These findings may encourage investigators to explore novel management strategies for painful HOA.

The pathophysiology of chronic subdural hematoma revisited: emphasis on aging processes as key factor.

Chronic subdural hematoma (CSH) affects mostly elderly subjects. Previously, pathophysiological concepts suggested that CSH is secondary to degradation of subdural collections of blood and its products exerting merely a mass effect on the underlying brain. During the last decades, however, new insights into the pathogenetic mechanisms urge us to reconsider such a simplistic view. Here, we critically review novel pathophysiological, imaging, interventional, and medical treatment aspects and establish an integrative concept of the pathogenesis of CSH stressing the role of age as key factor. Trauma is considered a trigger event that unleashes a cascade of immunological and angiogenic age-dependent responses. These are associated with hypervascularization of the outer hematoma membrane, rebleeding, and exsudation which are crucial determinants for further development and propagation of CSH. Neurosurgical evacuation of the hematoma has long been thought the only viable treatment option, and it is still the method of choice in the majority of cases. Only more recently, embolization of the middle meningeal artery has been introduced as an alternative to surgery, and pharmacological treatment options are being investigated. Persons with advanced age trauma and other trigger events encounter a repair system with characteristics of senescence. This repair system implies a dysfunctional secretory phenotype of senescent cells and results in an insufficient repair process including chronic inflammation and fibrosis. Increased knowledge about the pathomechanisms of CSH will inform future studies and open new perspectives for its treatment and possibly also for its prevention.

Risk Factors for Hypervascularization in Hepatobiliary Phase Hypointense Nodules without Arterial Phase Hyperenhancement: A Systematic Review and Meta-analysis.

RATIONALE AND OBJECTIVES: To perform a systematic review and meta-analysis to determine risk factors for hypervascularization in hepatobiliary phase (HBP) hypointense nodules without arterial phase hyperenhancement (APHE) in patients with hepatocellular carcinoma (HCC). MATERIALS AND METHODS: Pubmed and EMBASE databases were searched up to May 7, 2020. Studies which evaluated radiologic and clinical risk factors for hypervascularization in HBP hypointense nodules without APHE were included. Hazard ratios were meta-analytically pooled using random-effects model. Methodological quality of included studies was assessed using Quality in Prognostic Studies (QUIPS) tool. RESULTS: Sixteen studies with 934 patients were included. HBP hypointense nodules without APHE with baseline size greater than 10 mm, T2 hyperintensity, and restricted diffusion showed risk for hypervascularization with pooled HRs of 2.95 (95% confidence interval [CI], 1.94-4.20), 4.21 (95% CI, 1.15-15.40), 5.83 (95% CI, 1.42-23.95), respectively. Previous HCC history contributed to hypervascularization of the nodules with hazard ratio of 2.06 (95% CI, 1.23-3.44). T1 hyperintensity, intralesional fat, Child-Pugh Class B, sex, alfa-fetoprotein, hepatitis B or C infection were not significant risk factors for hypervascularization (p ≥0.05). Study quality was generally moderate. CONCLUSION: HBP hypointense nodules without APHE on gadoxetic acid-enhanced MRI with baseline size greater than 10 mm, T2 hyperintensity, restricted diffusion and previous hepatocellular carcinoma history pose higher risk for hypervascularization. Proper patient management in patients with HBP hypointense nodules without APHE on gadoxetic acid-enhanced MRI may need to be tailored according to these risk factors.

A large adrenocortical adenoma surrounded with a renal arteriovenous malformation.

INTRODUCTION: Large adrenal adenomas are clinically rare. We report a case of a large adrenal adenoma with a renal arteriovenous malformation, mimicking a malignant adrenal tumor in preoperative imaging. CASE PRESENTATION: A 66-year-old woman presented to a local hospital with abdominal pain. A right adrenal tumor was detected, 66 mm in diameter and surrounded by thick and tortuous vessels. Based on the imaging findings, pheochromocytoma was suspected. However, clinical symptoms and endocrine abnormalities were absent, and radionuclide accumulation in scintigraphy was negative. Laparoscopic right adrenalectomy was performed. Intraoperatively, a notable growth of vessels forming a nidus surrounding the tumor was observed. Pathologically, this was diagnosed as an adrenocortical adenoma in conjunction with a renal arteriovenous malformation. CONCLUSION: We report a case of a large adrenal tumor surrounded with an arteriovenous malformation. To the best of our knowledge, this is the first reported case of this combination.

Effect of Force, Posture, and Repetitive Wrist Motion on Intraneural Blood Flow in the Median Nerve.

OBJECTIVES: Pinching, deviated wrist postures, and repetitive motion are risk factors for carpal tunnel syndrome. Hypervascularization of the median nerve and increased intraneural blood flow proximal to the carpal tunnel result in finger force and deviated wrist postures. The purpose of this study was to determine the effects of pinching with and without force, wrist posture, and repetitive wrist motion on intraneural blood flow in the median nerve. METHODS: Eleven healthy and 11 carpal tunnel syndrome-symptomatic individuals completed 3 sections of this study: 15 pinch posture force trials, 3 repetitive wrist motion trials, and 3 static wrist posture trials. Intraneural blood flow (centimeters per second) was measured with pulsed wave Doppler ultrasound during each trial. Transverse B-mode images obtained from static trials were used to calculate the median nerve cross-sectional area and circumference. RESULTS: An analysis of variance statistical analysis revealed significant main effects of pinch posture force (F4,80 = 21.397; P < .001) and wrist posture (F2,40 = 14.545; P < .001). Intraneural blood flow velocities were significantly greater when 6 N of force was applied by the thumb, finger, or pinch compared to no applied force in the same postures. Intraneural blood flow velocities were higher at 30° wrist flexion (mean ± SD, 2.24 ± 0.42 cm/s) than neutral (2.06 ± 0.45 cm/s) and 30° wrist extension (1.97 ± 0.46 cm/s). No changes were found in response to repetitive wrist motion. CONCLUSIONS: Flexed wrists as well as applied finger and thumb forces increase median nerve blood flow at the entry to the carpal tunnel, which may negatively affect the median nerve.

Hypervascularization in mTOR-dependent focal and global cortical malformations displays differential rapamycin sensitivity.

OBJECTIVES: Patients with mammalian target of rapamycin (mTOR)-dependent malformations of cortical development (MCDs) associated with seizures display hyperperfusion and increased vessel density of the dysmorphic cortical tissue. Some studies have suggested that the vascular defect occurred independently of seizures. Here, we further examined whether hypervascularization occurs in animal models of global and focal MCD with and without seizures, and whether it is sensitive to the mTOR blocker, rapamycin, that is approved for epilepsy treatment in tuberous sclerosis complex. METHODS: We used two experimental models of mTOR-dependent MCD consisting of conditional transgenic mice containing Tsc1null cells in the forebrain generating a global malformation associated with seizures and of wild-type mice containing a focal malformation in the somatosensory cortex generated by in utero electroporation (IUE) that does not lead to seizures. Alterations in blood vessels and the effects of a 2-week-long rapamycin treatment on these phenotypes were assessed in juvenile mice. RESULTS: Blood vessels in both the focal and global MCDs of postnatal day 14 mice displayed significant increase in vessel density, branching index, total vessel length, and decreased tissue lacunarity. In addition, rapamycin treatment (0.5 mg/kg, every 2 days) partially rescued vessel abnormalities in the focal MCD model, but it did not ameliorate the vessel abnormalities in the global MCD model that required higher rapamycin dosage for a partial rescue. SIGNIFICANCE: Here, we identified hypervascularization in mTOR-dependent MCD in the absence of seizures in young mice, suggesting that increased angiogenesis occurs during development in parallel to alterations in corticogenesis. In addition, a predictive functional outcome is that dysplastic neurons forming MCD will have better access to oxygen and metabolic supplies via their closer proximity to blood vessels. Finally, the difference in rapamycin sensitivity between a focal and global MCD suggest that rapamycin treatment will need to be titrated to match the type of MCD.

Chemoresistance and the Self-Maintaining Tumor Microenvironment.

The progression of cancer is associated with alterations in the tumor microenvironment, including changes in extracellular matrix (ECM) composition, matrix rigidity, hypervascularization, hypoxia, and paracrine factors. One key malignant phenotype of cancer cells is their ability to resist chemotherapeutics, and elements of the ECM can promote chemoresistance in cancer cells through a variety of signaling pathways, inducing changes in gene expression and protein activity that allow resistance. Furthermore, the ECM is maintained as an environment that facilitates chemoresistance, since its constitution modulates the phenotype of cancer-associated cells, which themselves affect the microenvironment. In this review, we discuss how the properties of the tumor microenvironment promote chemoresistance in cancer cells, and the interplay between these external stimuli. We focus on both the response of cancer cells to the external environment, as well as the maintenance of the external environment, and how a chemoresistant phenotype emerges from the complex signaling network present.

Superparamagnetic iron oxide-enhanced magnetic resonance imaging is useful in predicting malignant potential of vascular transformation of hypointense hypovascular nodules on gadoxetic acid-enhanced magnetic resonance imaging.

AIM: To examine whether superparamagnetic iron oxide (SPIO)-enhanced magnetic resonance imaging (MRI) can be used to assess the malignant potential of hepatic hypovascular nodules showing hypointensity during the hepatobiliary phase (HBP) on gadoxetic acid (Gd-EOB-DTPA)-enhanced MRI. METHODS: The study included 42 patients with chronic liver disease who had small hypovascular nodules (5-15 mm) showing hypointensity during the HBP on Gd-EOB-DTPA-enhanced MRI. The SPIO-enhanced T2-weighted MRI analyzed whether the signal intensity of each nodule was high. Nodules were prospectively followed up until hypervascularization by periodic Gd-EOB-DTPA-enhanced MRI. Initial MRI findings and clinical variables were used to analyze predictive factors for hypervascularization. RESULTS: We analyzed 77 nodules, of which 19 (25%) showed hypervascularization during the observation period. The cumulative rates for hypervascularization were 11% and 22% at 1 and 2 years, respectively. Hyperintensity was observed in 12 nodules (16%) on SPIO-enhanced T2-weighted MRI; among these, 7 (58%) showed hypervascularization, whereas 12 (18%) of the remaining 65 nodules without hyperintensity showed hypervascularization (P = 0.007). A Cox model revealed that independent predictors of hypervascularization included hyperintense nodules on SPIO-enhanced MRI (P < 0.001). The cumulative rates for hypervascularization in hyperintense nodules on SPIO-enhanced MRI were 52% at 1 year, whereas these rates were 3% for non-hyperintense nodules. CONCLUSION: Superparamagnetic iron oxide-enhanced MRI is useful for predicting the malignant potential of vascular transformation of hypovascular nodules with hypointensity observed in the HBP on Gd-EOB-DTPA-enhanced MRI.

Outcome of hypovascular hepatic nodules with positive uptake of gadoxetic acid in patients with cirrhosis.

OBJECTIVES: To evaluate the longitudinal risk to patients with cirrhosis of hypervascular hepatocellular carcinoma (HCC) developing from hypovascular hepatic nodules that show positive uptake of gadoxetic acid (hyperintensity) on hepatocyte phase images. METHODS: In 69 patients, we evaluated findings from serial follow-up examinations of 633 hepatic nodules that appeared hypovascular and hyperintense on initial gadoxetic acid-enhanced magnetic resonance imaging (EOB-MRI) until the nodules demonstrated hypervascularity and were diagnosed as hypervascular HCC. Cox analyses were performed to identify risk factors for the development of hypervascular HCCs from the nodules. RESULTS: The median follow-up was 663 days (range, 110 to 1215 days). Hypervascular HCCs developed in six of the 633 nodules (0.9 %) in five of the 69 patients. The only independent risk factor, the nodule's initial maximum diameter of 10 mm or larger, demonstrated a hazard ratio of 1.25. The one-year risk of hypervascular HCC developing from a nodule was 0.44 %. The risk was significantly higher for nodules of larger diameter (1.31 %) than those smaller than 10 mm (0.10 %, p < 0.01). CONCLUSIONS: Hypervascular HCC rarely develops from hypovascular, hyperintense hepatic nodules. We observed low risk even for nodules of 10 mm and larger diameter at initial examination. KEY POINTS: • Hypervascularization was rare on follow-up examination of hypovascular, hyperintense nodules • The risk of hypervascularization in a nodule increased with large size • Hypovascular, hyperintense nodules require neither treatment nor more intense follow-up.

Presence of non-hypervascular hypointense nodules on Gadolinium-ethoxybenzyl-diethylenetriamine pentaacetic acid-enhanced magnetic resonance imaging in patients with hepatocellular carcinoma.

BACKGROUND AND AIMS: Gadolinium-ethoxybenzyl-diethylenetriamine pentaacetic acid (Gd-EOB-DTPA)-enhanced magnetic resonance imaging (MRI) performed before curative therapy for hepatocellular carcinoma (HCC) can distinguish between intrahepatic distant recurrence and hypervascularization. This study aimed to retrospectively evaluate the presence of non-hypervascular hypointense nodules on hepatobiliary phase images from Gd-EOB-DTPA-enhanced MRI as a risk factor of the intrahepatic distant recurrence of early stage HCC following radiofrequency ablation (RFA). METHODS: A total of 132 patients who underwent preprocedural Gd-EOB-DTPA-enhanced MRI followed by initial RFA were retrospectively analyzed. Post-RFA intrahepatic distant recurrence, which excluded the hypervascularization of non-hypervascular hypointense nodules detected by preprocedural Gd-EOB-DTPA-enhanced MRI, was evaluated according to the presence of non-hypervascular hypointense nodules on preprocedural Gd-EOB-DTPA-enhanced MRI. RESULTS: Intrahepatic distant recurrence rates following RFA were higher in patients with non-hypervascular hypointense nodules (1-year: 22.5%, 2-year: 52.1%, 5-year: 89.1%) compared with in patients without non-hypervascular hypointense nodules (1-year: 7.0%, 2-year: 28.8%, 5-year: 48.7%). The presence of non-hypervascular hypointense nodules was associated with markedly increased cumulative recurrence rates of both identical and different subsegment intrahepatic distant recurrence, being an independent risk factor for post-RFA identical and different subsegment intrahepatic distant recurrence (identical: HR = 2.365, P = 0.027; different: HR = 3.276, P < 0.001). CONCLUSION: The presence of non-hypervascular hypointense nodules on hepatobiliary phase images from Gd-EOB-DTPA-enhanced MRI obtained prior to RFA is an important predictive factor of intrahepatic distant recurrence following RFA of HCC.

Assessment of clinical and magnetic resonance imaging features of de novo hypervascular hepatocellular carcinoma using gadoxetic acid-enhanced magnetic resonance imaging.

AIM: To clarify the clinical and magnetic resonance imaging (MRI) features of de novo hypervascular hepatocellular carcinoma (HCC) using serial gadoxetic acid-enhanced MRI. METHODS: The institutional review board approved this retrospective study. After review of 1007 MRI examinations in 240 patients with chronic liver disease, 17 newly developed hypervascular HCCs in 16 patients detected by follow-up from initial MRI examination without hepatocellular nodules were evaluated. The clinical and MRI findings such as previous treatment history for HCC, period to hypervascular HCC onset, presence or absence of hypovascular hypointense nodules on hepatobiliary phase before hypervascularization, and intralesional fat component were recorded or evaluated. Statistical evaluations included Fisher's exact test, χ2 -test, and Mann-Whitney U-test. RESULTS: In 17 HCCs, 12 (71%) were de novo hypervascular HCC without showing hypovascular hypointense nodule on hepatobiliary phase before hypervascularization (de novo group) and 5 (29%) were hypervascularized HCC developed during multistep hepatocarcinogenesis (multistep group). The incidence of previous treatment history for HCC in the de novo group (91%) was significantly higher than that in the multistep group (20%) (P = 0.013). The duration to hypervascular HCC onset from initial examination was shorter in the de novo group (mean, 291 days) than in the multistep group (mean, 509 days) (P = 0.035). The incidence of fat-containing lesion in the de novo group (0%) was lower than that in the multistep group (40%) (P = 0.074). CONCLUSION: De novo hypervascular HCC is characterized by rapid growth, patients with previous treatment history for HCC, and lack of intralesional fat, compared to hypervascular HCC with multistep progression.

A case of massive hemoptysis related to a smoking-history: an acquired form of the Dieulafoy's disease?

The hypervascularization of the bronquial wall, secondary to chronic bronchopulmonary inflammation is a bleeding etiology in smokers, but insufficient to explain certain massive recurrent cases. We report a case of a woman with a smoking history who presented a recurrent and massive hemoptysis. A diagnostic study with laboratory tests, bronchoscopy, computed tomography and echocardiogram did not identify the etiological cause. However, bronchial arteriography showed right and left bronchial tortuous and dilated arteries and demonstrated that a bronchovascular fistula was the origin of the hemoptysis. An acquired form of the Dieulafoy's disease in this context of a smoking history might justify such findings. Bronchial arteriography as a diagnostic method should be the preferred choice rather than bronchoscopy in these cases.

Distinguishing gouty arthritis from calcium pyrophosphate disease and other arthritides.

OBJECTIVE: Differentiating gout, calcium pyrophosphate deposition disease (CPPD), and non-crystal-related inflammatory arthropathies (non-CRA) is essential but often clinically impossible. The sonographic double contour (DC) sign may have good specificity for gout in highly specialized centers, but it can be challenging to use it to distinguish gout from cartilage hyperenhancements in CPPD. We evaluated the diagnostic value of the DC sign alone and in combination with Doppler signals and uric acid (UA) levels in patients with acute arthritis. METHODS: We retrospectively investigated 225 acutely inflamed joints and documented the presence of DC, Doppler hypervascularization, and serum UA (SUA) levels. All patients underwent synovial fluid (SF) analysis. Sensitivity, specificity, and positive predictive values were calculated, and correlation analyses and a binary regression model were used to investigate their diagnostic values. RESULTS: The sensitivity of DC sign for crystalline arthritides was 85% and specificity 80%. Its specificity for gout was 64%, for CPPD 52%. In contrast to non-CRA hypervascularization, degree 2 and 3 Doppler signals were highly associated with gout and less with CPPD (p < 0.01). The combination of DC sign with hypervascularization and elevated UA levels increased specificity for gout to more than 90% and resulted in a 7-fold increase of the likelihood of diagnosis of gout (p < 0.01), but with a loss of sensitivity (42%). CONCLUSION: The DC sign alone is suitable for predicting crystal-related arthropathies, but it cannot reliably distinguish gout from CPPD in everyday clinical routine. Combining hypervascularization and SUA levels increases the diagnostic value, leading us to propose a diagnostic algorithm.

Clinical value of gadoxetic acid-enhanced magnetic resonance imaging in surgery for hepatocellular carcinoma - with a special emphasis on early hepatocellular carcinoma.

Gadoxetic acid- or gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid-enhanced magnetic resonance imaging (EOB-MRI) achieves excellent lesion detection and characterization for both hypervascular hepatocellular carcinoma (HCC) in arterial phase imaging and hypovascular early HCC (small well-differentiated HCC of the vaguely nodular type) in hepatobiliary phase imaging, and has become an indispensable imaging modality in the treatment of HCC. Early HCCs have been detected more frequently since the introduction of EOB-MRI into daily clinical practice. Early HCC is known to progress to conventional hypervascular HCC, and many risk factors have been identified for the hypervascularization of early HCC including the diameter of the tumor, presence of fat, and imaging findings of EOB-MRI. The rate of the development of hypervascular HCC was previously reported to be high in patients with chronic liver disease and early HCC. The presence of early HCC is regarded as a predictor for the recurrence of HCC following hepatic resection. On the other hand, although early HCC itself is currently not regarded as a target lesion for hepatic resection, early HCC at high risk of hypervascularity needs to be treated by local ablation therapy. If concomitant early HCC with progressed HCC is at high risk of hypervascularization and the functional liver reserve of a patient is sufficient, its simultaneous treatment at the time of hepatic resection for progressed HCC is recommended. Further studies on larger numbers of patients are needed before this strategy is adopted.

Early dynamic 18F-FDG PET to detect hyperperfusion in hepatocellular carcinoma liver lesions.

UNLABELLED: In addition to angiographic data on vascularity and vascular access, demonstration of hepatocellular carcinoma (HCC) liver nodule hypervascularization is a prerequisite for certain intrahepatic antitumor therapies. Early dynamic (ED) (18)F-FDG PET/CT could serve this purpose when the current standard method, contrast-enhanced (CE) CT, or other CE morphologic imaging modalities are unsuitable. A recent study showed ED (18)F-FDG PET/CT efficacy in this setting but applied a larger-than-standard (18)F-FDG activity and an elaborate protocol likely to hinder routine use. We developed a simplified protocol using standard activities and easily generated visual and descriptive or quantitative endpoints. This pilot study assessed the ability of these endpoints to detect HCC hyperperfusion and, thereby, evaluated the suitability in of the protocol everyday practice. METHODS: Twenty-seven patients with 34 HCCs (diameter ≥ 1.5 cm) with hypervascularization on 3-phase CE CT underwent liver ED (18)F-FDG PET for 240 s, starting with (18)F-FDG (250-MBq bolus injection). Four frames at 15-s intervals, followed by 3 frames at 60-s intervals were reconstructed. Endpoints included focal tracer accumulation in the first 4 frames (60 s), subsequent focal washout, and visual and quantitative differences between tumor and liver regions of interest in maximum and mean ED standardized uptake value (ED SUVmax and ED SUVmean, respectively) 240-s time-activity curves. RESULTS: All 34 lesions were identified by early focal (18)F-FDG accumulation and faster time-to-peak ED SUVmax or ED SUVmean than in nontumor tissue. Tumor peak ED SUVmax and ED SUVmean exceeded liver levels in 85% and 53%, respectively, of lesions. Nadir tumor signal showed no consistent pattern relative to nontumor signal. HCC had a significantly shorter time to peak and significantly faster rate to peak for both ED SUVmax and ED SUVmean curves and a significantly higher peak ED SUVmax but not peak ED SUVmean than the liver. CONCLUSION: This pilot study provided proof of principle that our simplified ED (18)F-FDG PET/CT protocol includes endpoints that effectively detect HCC hypervascularization; this finding suggests that the protocol can be used routinely.

Sinais de hipervascularização em imagens de ressonância magnética em metástases ósseas de carcinoma de células renais / Signs of hypervascularization at magnetic resonance imaging in bone metastases from renal cell carcinoma

OBJETIVO: Avaliar a frequência de hipervascularização pela visualização de vasos no interior ou ao redor de metástases ósseas de carcinoma de células renais. MATERIAIS E MÉTODOS: Foram avaliados, retrospectivamente, exames de ressonância magnética de 13 pacientes com diagnóstico de carcinoma de células renais, com 15 lesões ósseas metastáticas, que não haviam sido submetidos a nenhum tratamento. RESULTADOS: Foram encontrados sinais de hipervascularização em 12 das 15 lesões (80%), sendo 6 na coluna lombar, 3 na bacia, 1 na coluna torácica, 1 na ulna e 1 na tíbia. CONCLUSÃO: A alta frequência de hipervascularização em metástases ósseas de carcinoma de células renais encontrada neste trabalho pode sugerir a etiologia renal, tornando-se muito útil na apresentação clínica usual de lesão óssea única com neoplasia primária desconhecida.

OBJECTIVE: To evaluate the frequency of hypervascularization by visualizing vascular structures inside or around bone metastases from renal cell carcinoma. MATERIALS AND METHODS: Magnetic resonance imaging studies of 13 untreated patients with diagnosis of renal cell carcinoma and 15 metastatic bone lesions were retrospectively evaluated. RESULTS: Signs of hypervascularization were found in 12 of the 15 bone lesions (80%), 6 of them localized in the lumbar spine, 3 in the hip, 3 in the thoracic spine, 1 in the ulna and 1 in the tibia. CONCLUSION: The high frequency of hypervascularization of bone metastases from renal cell carcinoma found in the present study may suggest that the renal etiology is a useful parameter in the evaluation of a usual clinical presentation of a single bone lesion with unknown primary neoplasm.

A Case of Hypervascularization of the Glans after Epigastrico-dorsal Vein Anastomosis / 대한비뇨기과학회지

We recently experienced a case of hypervascularization of the glans after arterialization of the deep dorsal vein(Furlow`s method) in a 25-year-old man having vasculogenic impotence due to arterial insufficiency of the penis. The Hypervascularization of the glans was corrected by ligating the branches of the deep dorsal Vein at the corona of the penis.