MRI quantification techniques in fatty liver: the diagnostic performance of hepatic T1, T2, and stiffness measurements in relation to the proton density fat fraction

PURPOSENonalcoholic fatty liver disease (NAFLD) can progress to liver cirrhosis and is predicted to become the most frequent indication for liver transplantation in the near future. Noninvasive assessment of NAFLD is important for diagnosis and patient management. This study aims to prospectively determine the liver stiffness and T1 and T2 values in patients with NAFLD and to compare the diagnostic performance of magnetic resonance elastography (MRE) and mapping techniques in relation to the proton density fat fraction (PDFF).METHODSEighty-three patients with NAFLD and 26 participants with normal livers were imaged with a 1.5 T scanner. PDFF measurements obtained from the multiecho Dixon technique were used to quantify the liver fat. MRE, native T1 mapping (modified Look-Locker inversion recovery [MOLLI] schemes 5(3)3, 3(3)3(3)5, and 3(2)3(2)5 and the B1-corrected variable flip angle [VFA] method), and T2 mapping values were correlated with PDFF. The diagnostic performance of MRE and the mapping techniques were analyzed and compared.RESULTST1 values measured with the MOLLI schemes and the B1-corrected VFA (p < 0.001), and the stiffness values from MRE (p = 0.047) were significantly higher in the NAFLD group. No significant difference was found between the groups in terms of T2 values (p = 0.127). In differentiation of the NAFLD and control groups, the B1-corrected VFA technique had slightly higher accuracy and area under the curve (AUC) than the MOLLI schemes. In the NAFLD group, there was a good correlation between the PDFF, MOLLI 3(3)3(3)5 and 3(2)3(2)5, and VFA T1 measurements (r=0.732; r=0.735; r=0.716, p < 0.001, respectively).CONCLUSIONLiver T1 mapping techniques have the potential to distinguish steatotic from nonsteatotic livers, and T1 values seem to have a strong correlation with the liver fat content.

Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease, with an estimated worldwide prevalence of around 25% (1). It may range from simple steatosis, which is considered a benign condition, to nonalcoholic steatohepatitis (NASH), which can progress to fibrosis, cirrhosis, liver failure, and hepatocellular carcinoma. NAFLD is also known to be associated with metabolic syndrome, which is a risk factor for cardiovascular disease and type II diabetes mellitus (2–4).The gold standard method for diagnosing NAFLD and distinguishing its different patterns is a liver biopsy which has considerable limitations, including sampling errors, its invasive nature and associated complication risks, small sample size, and inter- and intraobserver variability (5, 6). These drawbacks constrain its utility for clinical monitoring and make it unsuitable as a screening method. Therefore, there is an urgent clinical need for an accurate noninvasive approach in the assessment of NAFLD. Accordingly, both the European Association for the Study of the Liver and the American Association for the Study of Liver Disease propose magnetic resonance imaging (MRI) as a noninvasive diagnostic tool for NAFLD (7, 8). Proton density fat fraction (PDFF)-based MRI and magnetic resonance spectroscopy (MRS) techniques are considered the most accurate noninvasive methods for the quantification of liver fat (9–12). The PDFF is accepted as a standardized biomarker of hepatic steatosis. Studies suggest that this biomarker is equivalent to the hepatic “signal fat fraction” (FF) after correcting all the confounding factors (13). However, PDFF measurement is not suitable for the assessment of any inflammation or fibrosis in NAFLD (13). On the other hand, recent studies have shown that other quantitative MRI techniques such as magnetic resonance elastography (MRE) and T1–T2 mapping can be useful in detecting hepatic inflammatory and fibrotic changes (14, 15–21). Thus, the application of a multiparametric MRI protocol might be helpful in liver tissue characterization and thereby in the risk stratification and therapeutic management of patients with NAFLD.In this prospective study, we aimed to determine liver stiffness and T1 and T2 values in patients with NAFLD and nonsteatotic subjects and compare the diagnostic performance of MRE and mapping techniques in relation to the FF.     

Minimally Invasive Treatment of Pilonidal Disease: Crystallized Phenol and Laser Depilation

Pilonidal disease has been treated surgically and by various other methods for many years. The most important problem associated with such treatment is recurrence, but cosmetic outcome is another important issue that cannot be ignored. Today, crystallized phenol is recognized as a treatment option associated with good medical and cosmetic outcomes. We hypothesized that the addition of laser depilation to crystallized phenol treatment of pilonidal disease might increase the rate of success, and this study aimed to determine if the hypothesis was true. Patients who were treated with crystallized phenol and 755-nm alexandrite laser depilation were retrospectively analyzed. In total, 42 (31 male and 11 female) patients were treated with crystallized phenol and alexandrite laser depilation and were followed up between January 2009 and January 2012. In all, 38 patients (90.5%) had chronic disease and 4 (9.5%) had recurrent disease. Among the patients, 26 (61.9%) recovered following 1 crystallized phenol treatment, and the remaining patients had complete remission following repeated treatment. Some patients needed multiple treatments, even up to 8 times. None of the patients had a recurrence during a mean 24 months (range, 6–30 months) of follow-up. Whatever method of treatment is used for pilonidal disease, hair cleaning positively affects treatment outcome. The present results support the hypothesis that the addition of laser depilation (which provides more permanent and effective depilation than other methods) to crystallized phenol treatment (a non-radical, minimally invasive method associated with very good cosmetic results) can increase the effectiveness of the treatment and also reduce the recurrence rate of the disease.     

A rare complication of mechanical aortic valve replacement: Separation in the region of the mitral‐aortic intervalvular fibrosa

A 28‐year‐old man was admitted to our emergency service with a shortness of breath and palpitation. On admission, his blood pressure was high and he was in hypertensive pulmonary edema. His physical examination showed rales in both lungs and pansystolic murmur at mitral focus. His medical history included aortic valve replacement (AVR) because of native aortic valve infective endocarditis. Transthoracic echocardiography (TTE) showed normal functional aortic valve. Color flow imaging demonstrated severe mitral regurgitation with posterior eccentric jet. To examine in detail, transesophageal echocardiography (TEE) and three‐dimensional (3D) echocardiography were performed. TEE disclosed a separation in the subaortic curtain leading to severe mitral regurgitation from the left ventricle to the left atrium. In addition to severe mitral regurgitation with posterior eccentric jet, 26‐mm‐long pouch was seen in mitral‐aortic intervalvular fibrosa (MAIVF) at 120° TEE view. This pouch was separated from the mitral anterior leaflet junction releasing the mitral anterior leaflet and causing prolapse and chorda rupture in the A2 scallop of the mitral anterior leaflet. The MAIVF connects the anterior mitral leaflet to the posterior portion of the aortic annulus. The separation of the MAIVF represents a complication of the aortic valve replacement.     

Targeted vessel reconstruction in non‐contrast‐enhanced steady‐state free precession angiography

Image quality in non‐contrast‐enhanced (NCE) angiograms is often limited by scan time constraints. An effective solution is to undersample angiographic acquisitions and to recover vessel images with penalized reconstructions. However, conventional methods leverage penalty terms with uniform spatial weighting, which typically yield insufficient suppression of aliasing interference and suboptimal blood/background contrast. Here we propose a two‐stage strategy where a tractographic segmentation is employed to auto‐extract vasculature maps from undersampled data. These maps are then used to incur spatially adaptive sparsity penalties on vascular and background regions. In vivo steady‐state free precession angiograms were acquired in the hand, lower leg and foot. Compared with regular non‐adaptive compressed sensing (CS) reconstructions (CS_low), the proposed strategy improves blood/background contrast by 71.3 ± 28.9% in the hand (mean ± s.d. across acceleration factors 1–8), 30.6 ± 11.3% in the lower leg and 28.1 ± 7.0% in the foot (signed‐rank test, P < 0.05 at each acceleration). The proposed targeted reconstruction can relax trade‐offs between image contrast, resolution and scan efficiency without compromising vessel depiction. Copyright © 2016 John Wiley & Sons, Ltd.     

Acute massıve pulmonary embolism assocıated wıth olanzapıne

Treatment with low-potency anti-psychotic agents is an important risk factor in the development of pulmonary embolism (PE). We report a case of 74 years old female patient receiving olanzapine for psychotic depression admitted to the emergency service with the complaints of chest pain and shortness of breath. She had tachypnea, hypotension and tachycardia. Arterial blood gas analysis showed hypoxemia-hypocapnia and D-dimer level was high. Computed tomographic pulmonary angiography (CTPA) demonstrated pulmonary embolism in both main pulmonary arteries, through lobar and segmental branches. Tissue plasminogen activator (t-PA) was administered in intensive care unit. As the only possible risk factor for PE was olanzapine, olanzapine treatment was terminated with pyschiatry consultation. During the 12-month follow-up of the patient; malignancy was not observed. Diagnosis and prevention of PE are the important goals to reduce morbidity and mortality in subjects receiving olanzapine.     

Differential Roles of GABAA Receptor Subtypes in Benzodiazepine-Induced Enhancement of Brain-Stimulation Reward

Benzodiazepines such as diazepam are widely prescribed as anxiolytics and sleep aids. Continued use of benzodiazepines, however, can lead to addiction in vulnerable individuals. Here, we investigate the neural mechanisms of the behavioral effects of benzodiazepines using the intracranial self-stimulation (ICSS) test, a procedure with which the reward-enhancing effects of these drugs can be measured. Benzodiazepines bind nonselectively to several different GABA_A receptor subtypes. To elucidate the α subunit(s) responsible for the reward-enhancing effects of benzodiazepines, we examined mice carrying a histidine-to-arginine point mutation in the α1, α2, or α3 subunit, which renders the targeted subunit nonresponsive to diazepam, other benzodiazepines and zolpidem. In wild-type and α1-point-mutated mice, diazepam caused a dose-dependent reduction in ICSS thresholds (reflecting a reward-enhancing effect) that is comparable to the reduction observed following cocaine administration. This effect was abolished in α2- and α3-point-mutant mice, suggesting that these subunits are necessary for the reward-enhancing action of diazepam. α2 Subunits appear to be particularly important, since diazepam increased ICSS thresholds (reflecting an aversive-like effect) in α2-point-mutant animals. Zolpidem, an α1-preferring benzodiazepine-site agonist, had no reward-enhancing effects in any genotype. Our findings implicate α2 and α3 subunit containing GABA_A receptors as key mediators of the reward-related effects of benzodiazepines. This finding has important implications for the development of new medications that retain the therapeutic effects of benzodiazepines but lack abuse liability.