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Noncontrast Chest Computed Tomographic Imaging of Obesity and the Metabolic Syndrome: Part II Noncardiovascular Findings.
Nattenmüller, J, Schlett, CL, Tsuchiya, N, Reeder, SB, Pickhardt, PJ, Kramer, H, Kauczor, HU, Wielpütz, MO, Seo, JB, Hatabu, H, et al
Journal of thoracic imaging. 2019;(2):126-135
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Abstract
The purpose of this review article is to acquaint the reader with the current state of the art for the noncardiovascular imaging biomarkers of metabolic syndrome found on noncontrast computed tomography (NCCT) of the chest and their prognostic significance. Routine chest NCCT includes quantitative information with regard to tissue density and organ volumes in the neck, chest, and upper abdomen. The specific imaging biomarkers that may be seen in association with metabolic syndrome include low thyroid iodine organification, hepatic steatosis, sarcopenia (muscle volume and density), demineralization of the thoracic and upper lumbar vertebral bodies, loss of axial skeletal muscle mass, premature lung inflammation, and an increased deposition of subcutaneous and visceral fat. These easily identified imaging biomarkers can have prognostic implications, which include nonalcoholic steatohepatitis, cirrhosis, hypothyroidism, early lung fibrosis with interstitial abnormalities, sarcopenia, and osteoporotic thoracic and lumbar spine vertebral body compression fractures. NCCT examinations of the chest have the opportunity to become an important imaging tool for outcomes research.
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Imaging appearances of toxic and acquired metabolic encephalopathic disorders.
Vamadevan, T, Howlett, D, Filyridou, M
British journal of hospital medicine (London, England : 2005). 2019;(7):372-376
Abstract
Most imaging findings relating to toxic and acquired metabolic disorders follow a certain pattern with affinity to a specific topographic area, which can help narrow the differential diagnosis. This is especially useful when the clinical presentation can be variable and there is diagnostic uncertainty. Usually, there is bilateral symmetrical abnormality within the deep grey matter structures and the cerebral cortex because of the high metabolic activity and raised oxygen requirements in these areas. Magnetic resonance imaging, particularly diffusion weighted imaging and fluid-attenuated inversion recovery sequences, is very important in differentiating between various aetiologies in this group. Magnetic resonance imaging can be useful in demonstrating both acute and chronic damage, in evaluating treatment response and in disease prognostication. This pictorial review discusses the computed tomography and magnetic resonance imaging appearances of a spectrum of toxic and metabolic disorders observed in a district general hospital with reference to clinical presentation and imaging features that may allow diagnosis. This includes carbon monoxide poisoning, hypoglycaemia, non-ketotic hyperglycaemia, osmotic demyelination syndrome, posterior reversible encephalopathy syndrome, hypoxic ischaemic encephalopathy, the syndrome of delayed post-hypoxic leukoencephalopathy, hepatic encephalopathy and cocaine toxicity.
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Psoas muscle fluorine-18-labelled fluoro-2-deoxy-d-glucose uptake associated with the incidence of existing and incipient metabolic derangement.
Kim, JY, Jun, DW, Choi, J, Nam, E, Son, D, Choi, YY
Journal of cachexia, sarcopenia and muscle. 2019;(4):894-902
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Abstract
BACKGROUND Skeletal muscle glucose utilization is an important component of whole-body glucose consumption in normal humans. Fluorine-18-labelled fluoro-2-deoxy-d-glucose (18 F-FDG) is a non-invasive molecular imaging probe for evaluating tissue glucose utilization. It remains unclear whether or not 18 F-FDG uptake by skeletal muscle has utility as a biomarker for metabolic derangement. We investigated the utility of measurement of muscle 18 F-FDG positron emission tomography/computed tomography uptake as a surrogate marker for existing and incipient metabolic abnormalities. METHODS Fluorine-18-labelled fluoro-2-deoxy-d-glucose (18 F-FDG) uptakes of insulin-sensitive organs (liver, pancreas, mesenteric visceral fat, psoas muscle, and abdominal subcutaneous fat) and their association with metabolic abnormalities were evaluated in an experimental group comprising 91 men and 66 women (mean age 49.9 ± 11.1 years). In this cross-sectional cohort, we assessed the predictive power of the optimal cut-off 18 F-FDG uptake [maximum standardized uptake value (SUVmax )]. We confirmed its feasibility and reliability for diagnosis of existing and incipient metabolic derangement in the validation group (longitudinal cohort comprising 91 men and 67 women; mean age 52.6 ± 7.9 years). RESULTS Fluorine-18-labelled fluoro-2-deoxy-d-glucose (18 F-FDG) uptake (SUVmax ) of psoas muscle was strongly correlated with clinical metabolic parameters in the experimental group. It was positively correlated with waist circumference, body mass index, fasting glucose, triglyceride, systolic and diastolic pressure, and negatively correlated with high-density lipoprotein cholesterol levels (for all, P < 0.05). SUVmax of the psoas muscle also showed the best area under the curve value (0.779) as a predictor of metabolic syndrome (MetS) in the experimental group. Using the optimal cut-off SUVmax of 1.34, the sensitivity, specificity, accuracy, positive, and negative predictive value for predicting existing MetS in the experimental group were 70.0%, 84.6%, 80.9%, 60.9%, and 89.2%, respectively. In the validation group, corresponding values were 47.6%, 92.3%, 86.1%, 50.0%, and 91.6%, respectively. Existing and incipient MetS were significantly higher in subjects with high 18 F-FDG uptake by the psoas muscle (SUVmax > 1.34). Subjects with higher psoas muscle SUVmax had a 3.3-fold increased risk of developing MetS (P = 0.017). CONCLUSIONS Fluorine-18-labelled fluoro-2-deoxy-d-glucose (18 F-FDG) uptake of psoas muscle is a promising surrogate marker for existing and incipient metabolic derangement.
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Systemic vascular inflammation in abdominal aortic aneurysm patients: a contrast-enhanced PET/CT study.
Morbelli, S, Ghigliotti, G, Spinella, G, Marini, C, Bossert, I, Cimmino, M, Pane, B, Rousas, N, Cittadini, G, Massollo, M, et al
The quarterly journal of nuclear medicine and molecular imaging : official publication of the Italian Association of Nuclear Medicine (AIMN) [and] the International Association of Radiopharmacology (IAR), [and] Section of the Society of.... 2014;(3):299-309
Abstract
AIM: The aim of this paper was to investigate the presence of systemic vascular inflammation and its relationship with risk factors and biomarkers of systemic inflammation related to atherosclerosis in asymptomatic abdominal aortic aneurysm (AAA) patients. METHODS Thirty AAA patients and 30 age-matched controls underwent contrast-enhanced 2-deoxy-2-[18F]fluoro-D-glucose (FDG) PET/CT. C-reactive protein, erythrocyte sedimentation rate, white blood cell count and differential, serum fibrinogen, D-dimer and full lipid panel were also evaluated. Region of interest analyses were performed to obtain target-to-background (TBR) metabolism of aorta, subclavian, carotid, iliac arteries and AAA. CT-based arterial calcium load (CL) was evaluated. Arterial Metabolism and CL intergroup differences were tested (unpaired t-test). Linear regression analysis was performed only between blood biomarkers on one side and both TBR and ACL of the arterial districts that resulted significantly different between patients and controls on the other. In all the analyses P values <0.05 were considered significant. RESULT FDG-uptake was higher with respect to controls in aorta, carotid and iliac arteries (P<0.01, P<0.007, P<0.04 respectively). AAA and aorta metabolism showed an inverse correlation with HDL-chol (P<0.02 and P<0.01, respectively) while only aorta showed a direct correlation with lymphocytes' count (P<0.02). Carotid metabolism was directly correlated with monocytes' count and C-reactive protein concentration (P<0.02 and P<0.004, respectively). CONCLUSION The present findings support the relevance of systemic vascular inflammation in all phases of atherosclerosis-related disorders. Moreover they confirm the concept that acute ischemic syndromes might represent the local result of a systemic inflammation rather than the focal involvement of a single arterial lesion.
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PET/CT imaging in inflammatory myopathies.
Al-Nahhas, A, Jawad, AS
Annals of the New York Academy of Sciences. 2011;:39-45
Abstract
Inflammatory muscle diseases are a group of muscle disorders characterized by muscle weakness, fatigue, and an association with malignancy and paraneoplastic syndrome. A diagnosis of idiopathic inflammatory myopathy is suggested by abnormal myometry and rising creatine kinase, but tissue diagnosis is also needed. Magnetic resonance imaging (MRI) helps localize the appropriate site of biopsy, demonstrate the extent of muscle involvement, and monitor the response to therapy. However, the sensitivity of magnetic resonance (MR) is limited, and whole-body imaging is still far from routine. [(18) F]Fluoro-desoxy-glucose (FDG) positron emission tomography (PET)/computed tomography (CT) is currently the ultimate metabolic imaging technique for the management of cancer. It has also been shown to detect inflammatory conditions and to monitor their response to treatment. The use of FDG PET in screening for underlying malignancies is widely reported and recommended in patients with paraneoplastic syndrome. Unfortunately, only a few reports have been published to show the value of FDG PET in inflammatory muscle diseases, which as we show herein, deserve further pursuit.
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Recent advances in cytogenetics and molecular biology of adult hepatocellular tumors: implications for imaging and management.
Shanbhogue, AK, Prasad, SR, Takahashi, N, Vikram, R, Sahani, DV
Radiology. 2011;(3):673-93
Abstract
Focal nodular hyperplasia (FNH), hepatocellular adenoma (HCA), and hepatocellular carcinoma (HCC) compose hepatocellular neoplasms that occur in adults. These tumors demonstrate characteristic epidemiologic and histopathologic features and clinical and imaging manifestations. HCAs are monoclonal neoplasms characterized by increased predilection to hemorrhage or rupture and occasional transformation to HCC. On the other hand, FNH is a polyclonal tumorlike lesion that occurs in response to increased perfusion and has an indolent clinical course. Up to 90% of HCCs occur in the setting of cirrhosis. Chronic viral hepatitis (hepatitis B and hepatitis C) infection and metabolic syndrome are major risk factors that can induce HCCs in nonfibrotic liver. Recent advances in pathology and genetics have led to better understanding of the histogenesis, natural history, and molecular events that determine specific oncologic pathways used by these neoplasms. HCAs are now believed to result from specific genetic mutations involving TCF1 (transcription factor 1 gene), IL6ST (interleukin 6 signal transducer gene), and CTNNB1 (β catenin-1 gene); FNHs are characterized by an "imbalance" of angiopoietin. While the β catenin signaling pathway is associated with well- and moderately differentiated HCCs, mutations involving p53 (tumor protein 53 gene), MMP14 (matrix metalloproteinase 14 gene), and RhoC (Ras homolog gene family, member C) are associated with larger tumor size, higher tumor grade with resultant shortened tumor-free survival, and poor prognosis. Fibrolamellar carcinoma (FLC), a unique HCC subtype, exhibits genomic homogeneity that partly explains its better overall prognosis. On the basis of recent study results involving cytogenetics and oncologic pathways of HCCs, novel drugs that act against molecular targets are being developed. Indeed, sorafenib (a multikinase inhibitor) is currently being used in the successful treatment of patients with advanced HCC. Characterization of genetic abnormalities and genotype-phenotype correlations in adult hepatocellular tumors provides better understanding of tumor pathology and biology, imaging findings, prognosis, and response to molecular therapeutics.