Ospedale di Cattinara

RATIONALE: This initiative is focused on building a global consensus around core diagnostic criteria for malnutrition in adults in clinical settings. METHODS: In January 2016, the Global Leadership Initiative on Malnutrition (GLIM) was convened by several of the major global clinical nutrition societies. GLIM appointed a core leadership committee and a supporting working group with representatives bringing additional global diversity and expertise. Empirical consensus was reached through a series of face-to-face meetings, telephone conferences, and e-mail communications. RESULTS: A two-step approach for the malnutrition diagnosis was selected, i.e., first screening to identify "at risk" status by the use of any validated screening tool, and second, assessment for diagnosis and grading the severity of malnutrition. The malnutrition criteria for consideration were retrieved from existing approaches for screening and assessment. Potential criteria were subjected to a ballot among the GLIM core and supporting working group members. The top five ranked criteria included three phenotypic criteria (weight loss, low body mass index, and reduced muscle mass) and two etiologic criteria (reduced food intake or assimilation, and inflammation or disease burden). To diagnose malnutrition at least one phenotypic criterion and one etiologic criterion should be present. Phenotypic metrics for grading severity as Stage 1 (moderate) and Stage 2 (severe) malnutrition are proposed. It is recommended that the etiologic criteria be used to guide intervention and anticipated outcomes. The recommended approach supports classification of malnutrition into four etiology-related diagnosis categories. CONCLUSION: A consensus scheme for diagnosing malnutrition in adults in clinical settings on a global scale is proposed. Next steps are to secure further collaboration and endorsements from leading nutrition professional societies, to identify overlaps with syndromes like cachexia and sarcopenia, and to promote dissemination, validation studies, and feedback. The diagnostic construct should be re-considered every 3-5 years.

BACKGROUND: This initiative aims to build a global consensus around core diagnostic criteria for malnutrition in adults in clinical settings. METHODS: The Global Leadership Initiative on Malnutrition (GLIM) was convened by several of the major global clinical nutrition societies. Empirical consensus was reached through a series of face-to-face meetings, telephone conferences, and e-mail communications. RESULTS: A 2-step approach for the malnutrition diagnosis was selected, that is, first screening to identify at risk status by the use of any validated screening tool, and second, assessment for diagnosis and grading the severity of malnutrition. The malnutrition criteria for consideration were retrieved from existing approaches for screening and assessment. Potential criteria were subjected to a ballot among GLIM participants that selected 3 phenotypic criteria (non-volitional weight loss, low body mass index, and reduced muscle mass) and 2 etiologic criteria (reduced food intake or assimilation, and inflammation or disease burden). To diagnose malnutrition at least 1 phenotypic criterion and 1 etiologic criterion should be present. Phenotypic metrics for grading severity are proposed. It is recommended that the etiologic criteria be used to guide intervention and anticipated outcomes. The recommended approach supports classification of malnutrition into four etiology-related diagnosis categories. CONCLUSIONS: A consensus scheme for diagnosing malnutrition in adults in clinical settings on a global scale is proposed. Next steps are to secure endorsements from leading nutrition professional societies, to identify overlaps with syndromes like cachexia and sarcopenia, and to promote dissemination, validation studies, and feedback. The construct should be re-considered every 3-5 years.

PURPOSE: To assess whether characterization of solid focal liver lesions could be improved by using ultrasonographic (US) contrast-specific modes after sulfur hexafluoride-filled microbubble contrast agent injection, as compared with lesion characterization achieved with preliminary baseline US. MATERIALS AND METHODS: Four hundred fifty-two solid focal hepatic lesions that were considered indeterminate at baseline gray-scale and color Doppler US were examined after microbubble contrast agent injection performed by using low-acoustic-power contrast-specific modes during the arterial (10-40 seconds after injection), portal venous (50-90 seconds after injection), and late (100-300 seconds after injection) phases. Two readers independently and retrospectively reviewed baseline and contrast material-enhanced US scans and classified each depicted lesion as malignant or benign according to standard diagnostic criteria. Sensitivity, specificity, accuracy, and positive and negative predictive values and areas under the receiver operating characteristic curve (Az) were calculated by considering histologic analysis (317 patients) or contrast-enhanced helical computed tomography followed by serial US 3-6 months apart (135 patients) as the reference standards. RESULTS: Different contrast enhancement patterns were observed according to lesion characteristics. During the late phase, benign lesions were predominantly hyper- or isoechoic relative to the adjacent liver parenchyma, whereas malignant lesions were predominantly hypoechoic. Review of the contrast-enhanced US scans after baseline image review yielded significantly improved diagnostic performance (P <.05). Overall diagnostic accuracy was 49% before versus 85% after review of the contrast-enhanced scan for reader 1 and 51% before versus 88% after review of the contrast-enhanced scan for reader 2. Diagnostic confidence-that is, the Az-was 0.820 before versus 0.968 after review of the contrast-enhanced scan for reader 1 and 0.831 before versus 0.978 after review of the contrast-enhanced scan for reader 2. CONCLUSION: The use of contrast-specific modes with a sulfur hexafluoride contrast agent led to improved characterization of solid focal liver lesions.

Abstract The COVID‐19 pandemic is an unprecedented health crisis as entire populations have been asked to self‐isolate and live in home‐confinement for several weeks to months, which in itself represents a physiological challenge with significant health risks. This paper describes the impact of sedentarism on the human body at the level of the muscular, cardiovascular, metabolic, endocrine and nervous systems and is based on evidence from several models of inactivity, including bed rest, unilateral limb suspension, and step‐reduction. Data form these studies show that muscle wasting occurs rapidly, being detectable within two days of inactivity. This loss of muscle mass is associated with fibre denervation, neuromuscular junction damage and upregulation of protein breakdown, but is mostly explained by the suppression of muscle protein synthesis. Inactivity also affects glucose homeostasis as just few days of step reduction or bed rest, reduce insulin sensitivity, principally in muscle. Additionally, aerobic capacity is impaired at all levels of the O 2 cascade, from the cardiovascular system, including peripheral circulation, to skeletal muscle oxidative function. Positive energy balance during physical inactivity is associated with fat deposition, associated with systemic inflammation and activation of antioxidant defences, exacerbating muscle loss. Importantly, these deleterious effects of inactivity can be diminished by routine exercise practice, but the exercise dose–response relationship is currently unknown. Nevertheless, low to medium‐intensity high volume resistive exercise, easily implementable in home‐settings, will have positive effects, particularly if combined with a 15–25% reduction in daily energy intake. This combined regimen seems ideal for preserving neuromuscular, metabolic and cardiovascular health.

Knowing the likelihood of failure of noninvasive positive pressure ventilation (NPPV) in patients with exacerbation of chronic obstructive pulmonary disease (COPD) could indicate the best choice between NPPV and endotracheal intubation instituted earlier. For this purpose, two risk charts were designed (at admission and after 2 h of NPPV) that included all relevant measurable clinical prognostic indicators derived from a population representing the patients seen routinely in clinical practice. Risk stratification of NPPV failure was assessed in 1,033 consecutive patients admitted to experienced hospital units, including two intensive care units, six respiratory intermediate care units, and five general wards. NPPV was successful in 797 patients. Patients with a Glasgow Coma Score <11, acute physiology and chronic health evaluation (APACHE) II > or =29, respiratory rate > or =30 breaths x min(-1) and pH at admission <7.25 have a predicted risk of failure >70%. A pH <7.25 after 2 h greatly increases the risk (>90%). The risk charts were validated on an independent group of 145 consecutive COPD patients treated with NPPV due to an acute ventilatory failure episode. To identify patients with a probability of failure >50%, the sensitivity and specificity were 33% and 96.7% on admission and 52.9% and 94.1% after 2 h of NPPV, respectively. The prediction chart, based on data from the current study, can function as a simple tool to predict the risk of failure of noninvasive positive pressure ventilation and thus improve clinical management of patients tailoring medical intervention.

Primary biliary cirrhosis (PBC) is a classical autoimmune liver disease for which effective immunomodulatory therapy is lacking. Here we perform meta-analyses of discovery data sets from genome-wide association studies of European subjects (n=2,764 cases and 10,475 controls) followed by validation genotyping in an independent cohort (n=3,716 cases and 4,261 controls). We discover and validate six previously unknown risk loci for PBC (Pcombined<5 × 10(-8)) and used pathway analysis to identify JAK-STAT/IL12/IL27 signalling and cytokine-cytokine pathways, for which relevant therapies exist.

Alveolar type II (ATII) cells are a key structure of the distal lung epithelium, where they exert their innate immune response and serve as progenitors of alveolar type I (ATI) cells, contributing to alveolar epithelial repair and regeneration. In the healthy lung, ATII cells coordinate the host defense mechanisms, not only generating a restrictive alveolar epithelial barrier, but also orchestrating host defense mechanisms and secreting surfactant proteins, which are important in lung protection against pathogen exposure. Moreover, surfactant proteins help to maintain homeostasis in the distal lung and reduce surface tension at the pulmonary air-liquid interface, thereby preventing atelectasis and reducing the work of breathing. ATII cells may also contribute to the fibroproliferative reaction by secreting growth factors and proinflammatory molecules after damage. Indeed, various acute and chronic diseases are associated with intensive inflammation. These include oedema, acute respiratory distress syndrome, fibrosis and numerous interstitial lung diseases, and are characterized by hyperplastic ATII cells which are considered an essential part of the epithelialization process and, consequently, wound healing. The aim of this review is that of revising the physiologic and pathologic role ATII cells play in pulmonary diseases, as, despite what has been learnt in the last few decades of research, the origin, phenotypic regulation and crosstalk of these cells still remain, in part, a mystery.

Idiopathic pulmonary fibrosis (IPF) is a serious disease of the lung, which leads to extensive parenchymal scarring and death from respiratory failure. The most accepted hypothesis for IPF pathogenesis relies on the inability of the alveolar epithelium to regenerate after injury. Alveolar epithelial cells become apoptotic and rare, fibroblasts/myofibroblasts accumulate and extracellular matrix (ECM) is deposited in response to the aberrant activation of several pathways that are physiologically implicated in alveologenesis and repair but also favor the creation of excessive fibrosis via different mechanisms, including epithelial⁻mesenchymal transition (EMT). EMT is a pathophysiological process in which epithelial cells lose part of their characteristics and markers, while gaining mesenchymal ones. A role for EMT in the pathogenesis of IPF has been widely hypothesized and indirectly demonstrated; however, precise definition of its mechanisms and relevance has been hindered by the lack of a reliable animal model and needs further studies. The overall available evidence conceptualizes EMT as an alternative cell and tissue normal regeneration, which could open the way to novel diagnostic and prognostic biomarkers, as well as to more effective treatment options.

The severe acute respiratory syndrome coronavirus 2 and the disease it causes, coronavirus disease 2019 (COVID-19) is generating a rapid and tragic health emergency in Italy due to the need to provide assistance to an overwhelming number of infected patients and, at the same time, treat all the non-deferrable oncological and benign conditions. A panel of Italian urologists has agreed on possible strategies for the reorganization of urological routine practice and on a set of recommendations that should facilitate the process of rescheduling both surgical and outpatient activities during the COVID-19 pandemic and in the subsequent phases. This document could be a valid tool to be used in routine clinical practice and, possibly, a cornerstone for further discussion on the topic also considering the further evolution of the COVID-19 pandemic. It also may provide useful recommendations for national and international urological societies in a condition of emergency.

Sexual dysfunction is a very important but often overlooked symptom of multiple sclerosis. To investigate the type and frequency of symptoms of sexual dysfunction in patients suffering from multiple sclerosis, we performed a case-control study comparing 108 unselected patients with definite multiple sclerosis, 97 patients with chronic disease and 110 healthy individuals with regard to sexual function, sphincteric function, physical disorders impeding sexual activity and the impact of sexual dysfunction on social life. Information has been collected from a face-to-face structured interview performed by a doctor of the same gender as the patient. The disability, the cognitive performances, the psychiatric conditions and the psychological profile of patients and controls have been assessed. Sexual dysfunction was present in 73.1% of cases, in 39.2% of chronic disease controls and in 12.7% of healthy controls (P<0.0001). Male cases reported symptoms of sexual dysfunction more frequently than female cases (P<0.002). Symptoms of sexual dysfunction more commonly reported in patients with multiple sclerosis were anorgasmia or hyporgasmia (37.1%), decreased vaginal lubrication (35.7%) and reduced libido (31.4%) in women, and impotence or erectile dysfunction (63.2%), ejaculatory dysfunction and/or orgasmic dysfunction (50%) and reduced libido (39.5%) in men. Seventy-five per cent of cases, 51.5% of chronic disease controls and 28.2% of healthy controls (P<0.0001) experienced symptoms of sphincteric dysfunction. In conclusion, a substantial part of our sample of patients with multiple sclerosis reported symptoms of sexual and sphincteric dysfunction. Both sexual and sphincteric dysfunction were significantly more common in patients with multiple sclerosis than in either control group. Our findings suggest that a peculiar damage of the structures involved in sexual function is responsible for the dysfunction in patients with multiple sclerosis, but the highly significant lower frequency of symptoms of depression and anxiety in healthy controls may also imply a possible causative role of psychological factors.

A high prevalence of chronic hepatitis C virus (HCV) infection has recently been shown in a subset of B-cell non-Hodgkin's lymphomas, most of which belong to the lymphoplasmacytoid lymphoma/immunocytoma subtype and are characterized by the production of a monoclonal IgM cryoglobulin with rheumatoid factor activity. To better define the stage of differentiation of the malignant B cell and to investigate the role of chronic antigen stimulation in the pathogenesis of the HCV-associated immunocytomas, we analyzed the variable (V) region gene repertoire in 16 cases with this type of tumor. The lymphoma-derived V gene sequences were successfully determined in 8 cases; 5 of them expressed the 51p1 VH gene in combination with the kv325 VL gene. Moreover, a monoclonal 51p1-expressing B-cell population was detected in 4 of the remaining immunocytomas by an allele-specific Ig gene fingerprinting assay, indicating that HCV-associated immunocytomas represent clonal proliferations of a highly selected B-cell population. Somatic mutations and intraclonal diversity were observed in all of the lymphoma V genes, and clonally related IgM and IgG VH transcripts indicative of isotype switching were present in one case. These findings are consistent with an antigen-driven process and support a role for chronic antigen stimulation in the growth and clonal evolution of HCV-associated immunocytomas.

BACKGROUND: The EURObservational Research Programme-Atrial Fibrillation General Registry Pilot Phase (EORP-AF Pilot) provides systematic collection of contemporary data regarding the management and treatment of 3119 subjects with AF from 9 member European Society of Cardiology (ESC) countries. In this analysis, we report the development of symptoms, use of antithrombotic therapy and rate vs. rhythm strategies, as well as determinants of mortality and/or stroke/transient ischaemic attack (TIA)/peripheral embolism during 1-year follow-up in this contemporary European registry of AF patients. METHODS: The registry population comprised consecutive in- and out-patients with AF presenting to cardiologists in participating ESC countries. Consecutive patients with AF documented by ECG were enrolled. Follow-up was performed by the local investigator, initially at 1 year, as part of a long-term cohort study. RESULTS: At the follow-up, patients were frequently asymptomatic (76.8%), but symptoms are nevertheless common among paroxysmal and persistent AF patients, especially palpitations, fatigue, and shortness of breath. Oral anticoagulant (OAC) use remains high, ∼78% overall at follow-up, and of those on vitamin K antagonist (VKA), 84% remained on VKA during the follow-up, while of those on non-VKA oral anticoagulant (NOAC) at baseline, 86% remained on NOAC, and 11.8% had changed to a VKA and 1.1% to antiplatelet therapy. Digitalis was commonly used in paroxysmal AF patients. Of rhythm control interventions, electrical cardioversion was performed in 9.7%, pharmacological cardioversion in 5.1%, and catheter ablation in 4.4%. Despite good adherence to anticoagulation, 1-year mortality was high (5.7%), with most deaths were cardiovascular (70%). Hospital readmissions were common, especially for atrial tachyarrhythmias and heart failure. On multivariate analysis, independent baseline predictors for mortality and/or stroke/TIA/peripheral embolism were age, AF as primary presentation, previous TIA, chronic kidney disease, chronic heart failure, malignancy, and minor bleeding. Independent predictors of mortality were age, chronic kidney disease, AF as primary presentation, prior TIA, chronic obstructive pulmonary disease, malignancy, minor bleeding, and diuretic use. Statin use was predictive of lower mortality. CONCLUSION: In this 1-year follow-up analysis of the EORP-AF pilot general registry, we provide data on the first contemporary registry focused on management practices among European cardiologists, conducted since the publication of the new ESC guidelines. Overall OAC use remains high, although persistence with therapy may be problematic. Nonetheless, continued OAC use was more common than in prior reports. Despite the high prescription of OAC, 1-year mortality and morbidity remain high in AF patients, particularly from heart failure and hospitalizations.

RATIONALE: Angiotensin-converting enzyme (ACE)2 opposes the actions of angiotensin (Ang) II by degrading it to Ang 1-7. OBJECTIVE: Given the important role of Ang II/Ang 1-7 in atherogenesis, we investigated the impact of ACE2 deficiency on the development of atherosclerosis. METHODS AND RESULTS: C57Bl6, Ace2 knockout (KO), apolipoprotein E (ApoE) KO and ApoE/Ace2 double KO mice were followed until 30 weeks of age. Plaque accumulation was increased in ApoE/Ace2 double KO mice when compared to ApoE KO mice. This was associated with increased expression of adhesion molecules and inflammatory cytokines, including interleukin-6, monocyte chemoattractant protein-1, and vascular cell adhesion molecule-1, and an early increase in white cell adhesion across the whole aortae on dynamic flow assay. In the absence of a proatherosclerotic (ApoE KO) genotype, ACE2 deficiency was also associated with increased expression of these markers, suggesting that these differences were not an epiphenomenon. ACE inhibition prevented increases of these markers and atherogenesis in ApoE/ACE2 double KO mice. Bone marrow macrophages isolated from Ace2 KO mice showed increased proinflammatory responsiveness to lipopolysaccharide and Ang II when compared to macrophages isolated from C57Bl6 mice. Endothelial cells isolated from Ace2 KO mice also showed increased basal activation and elevated inflammatory responsiveness to TNF-α. Similarly, selective inhibition of ACE2 with MLN-4760 also resulted in a proinflammatory phenotype with a physiological response similar to that observed with exogenous Ang II (10(-7) mol/L). CONCLUSIONS: Genetic Ace2 deficiency is associated with upregulation of putative mediators of atherogenesis and enhances responsiveness to proinflammatory stimuli. In atherosclerosis-prone ApoE KO mice, these changes potentially contribute to increased plaque accumulation. These findings emphasize the potential utility of ACE2 repletion as a strategy to reduce atherosclerosis.

AIMS: Anaemia is a common comorbidity in chronic heart failure (CHF). The predictors of new onset anaemia (NOA) and its long-term prognostic value, particularly in patients treated with beta-blockers, are not known. METHODS AND RESULTS: In COMET, 3029 patients with CHF in NYHA II-IV and EF <35% were randomized to carvedilol or metoprolol tartrate and were followed for an average of 58 months. Plasma haemoglobin (Hb) concentrations were measured at a central laboratory at randomization, at four monthly intervals for the first year and annually thereafter. According to WHO criteria, anaemia was defined when Hb measured <13 g/dL for men and <12 g/dL for women. We considered anaemia to be severe when Hb <11.5 g/dL for men and <10.5 g/dL for women. The baseline mean Hb was 14.2 +/- 1.5 g/dL (n = 2996) and 15.9% of patients had anaemia (males, 16.0%; females, 15.2%). At baseline, severe anaemia was found in 3.3% of patients (males, 3.6%; females, 2.0%). During the study, all-cause mortality (RR 1.47) death or hospitalization (RR 1.28), and heart failure hospitalization (RR 1.43, all P < 0.0001) were higher in anaemic when compared with non-anaemic patients. In patients without anaemia at baseline, at the end of the study, the cumulative frequency of NOA was 28.1% in males and 27.0% in females. NOA increased over time from 14.2% at year 1 to 27.5% at year 5. Predictors of NOA were: higher age, diuretic dose, creatinine (all P < 0.0001), higher serum potassium, lower serum sodium, body mass index, and use of aldosterone antagonists, carvedilol, and digitalis (all P < 0.03). Treatment with carvedilol (vs. metoprolol tartrate) was associated with a 24% increased risk to develop NOA (P = 0.0047), but not severe anaemia (P = 0.18). Patients with a Hb decrease of >3 g/dL (RR 3.37, P < 0.0001) or of 2.0-3.0 g/dL (RR 1.47, P = 0.011) from baseline had an increased subsequent mortality when compared with patients having Hb increases of 0-1.0 g/dL. CONCLUSION: In stable ambulatory CHF patients, development of NOA is frequent and can be predicted by a set of clinical variables. Decreases in Hb over time relate to future increased morbidity and mortality.

An important issue in contemporary cognitive neuroscience concerns the role of motor production processes in perceptual and conceptual analysis. To address this issue, we studied the performance of a large group of unilateral stroke patients across a range of tasks using the same set of common manipulable objects. All patients (n = 37) were tested for their ability to demonstrate the use of the objects, recognize the objects, recognize the corresponding object-associated pantomimes, and imitate those same pantomimes. At the group level we observed reliable correlations between object use and pantomime recognition, object use and object recognition, and pantomime imitation and pantomime recognition. At the single-case level, we document that the ability to recognize actions and objects dissociates from the ability to use those same objects. These data are problematic for the hypothesis that motor processes are constitutively involved in the recognition of actions and objects and frame new questions about the inferences that are merited by recent findings in cognitive neuroscience.

OBJECTIVE. The objective of our study was to evaluate contrast-enhanced sonography

OBJECTIVES: It is important to recognize osteonecrosis of the jaws in patients treated with bisphosphonates because an early diagnosis can make a significant difference to the outcome of the disease. The aim of this study is to describe the radiological features of bisphosphonate osteonecrosis (BON) in order to aid its prompt recognition. METHODS: A conventional radiograph, a computed tomograph (CT), a magnetic resonance image (MRI) and a 99Tc(m)-MDP 3-phase bone scan were carried out for 11 patients with BON. The main imaging findings of osteonecrosis are described. RESULTS: Conventional radiography and CT displayed osteolytic lesions with the involvement of cortical bone. MRI demonstrated the characteristic features of osteonecrosis and the oedema of soft tissues. Both CT and MRI were very useful in defining the extent of the lesions. 99Tc(m)-MDP three-phase bone scan was the most sensitive tool to detect the osteonecrosis at an early stage. CONCLUSIONS: 99Tc(m)-MDP three-phase bone scans who could be used as a screening test to detect subclinical osteonecrosis in patients who have received bisphosphonates. CT scans and MRI are useful in defining the features and extent of osteolytic lesions.

Since its first description, the acute respiratory distress syndrome (ARDS) has been acknowledged to be a major clinical problem in respiratory medicine. From July 2015 to July 2016 almost 300 indexed articles were published on ARDS. This review summarises only eight of them as an arbitrary overview of clinical relevance: definition and epidemiology, risk factors, prevention and treatment. A strict application of definition criteria is crucial, but the diverse resource-setting scenarios foster geographic variability and contrasting outcome data. A large international multicentre prospective cohort study including 50 countries across five continents reported that ARDS is underdiagnosed, and there is potential for improvement in its management. Furthermore, epidemiological data from low-income countries suggest that a revision of the current definition of ARDS is needed in order to improve its recognition and global clinical outcome. In addition to the well-known risk-factors for ARDS, exposure to high ozone levels and low vitamin D plasma concentrations were found to be predisposing circumstances. Drug-based preventive strategies remain a major challenge, since two recent trials on aspirin and statins failed to reduce the incidence in at-risk patients. A new disease-modifying therapy is awaited: some recent studies promised to improve the prognosis of ARDS, but mortality and disabling complications are still high in survivors in intensive care.

Importance: An altered sense of smell and taste has been reported to be associated with coronavirus disease 2019 (COVID-19). To understand the evolution of these symptoms during the course of the disease is important to identify patients with persistent loss of smell or taste and estimate the impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on the burden of olfactory and gustative dysfunctions. Objective: To evaluate the evolution of the loss of sense of smell and taste in a case series of mildly symptomatic patients with SARS-CoV-2 infection. Design, Setting, and Participants: This cross-sectional survey-based study included 202 mildly symptomatic adults (≥18 years) consecutively assessed at Treviso Regional Hospital, Italy, between March 19 and March 22, 2020, who tested positive for SARS-CoV-2 RNA by polymerase chain reaction on nasopharyngeal and throat swabs. Main Outcomes and Measures: Prevalence of altered sense of smell and taste at follow-up and their variation from baseline. Results: Of 202 patients completing the survey at baseline, 187 (92.6%) also completed the follow-up survey (103 [55.1%] women; median age, 56 years). The evaluation of the evolution of altered sense of smell or taste in the 113 patients reporting sudden onset of these symptoms at baseline showed that 55 patients (48.7%; 95% CI, 39.2-58.3) reported complete resolution of smell or taste impairment, 46 (40.7%; 95% CI, 31.6-50.4) reported an improvement in the severity, and only 12 (10.6%; 95% CI, 5.6-17.8) reported the symptom was unchanged or worse. Persistent loss of smell or taste was not associated with persistent SARS-CoV-2 infection. Conclusions and Relevance: At 4 weeks from the onset, 89% of the SARS-CoV-2-positive mildly symptomatic patients who had had a sudden onset of altered sense of smell or taste experienced a complete resolution or improvement of these symptoms. Persistent loss of smell or taste was not associated with persistent SARS-CoV-2 infection.

The purpose of this study was to evaluate the capability and the reliability of diffusion-weighted MRI in the evaluation of normal kidney and different renal lesions. 39 patients (10 normal volunteers and 29 patients with known renal lesions) underwent MRI of the kidneys by using a 1.5 T superconducting magnet. Axial fat suppressed turbo spin echo (TSE) T(2) and coronal fast field echo (FFE) T(1) or TSE T(1) weighted images were acquired for each patient. Diffusion-weighted (DW) images were obtained in the axial plane during breath-hold (17 s) with a spin-echo echo planar imaging (SE EPI) single shot sequence (repetition time (TR)=2883 ms, echo time (TE)=61 ms, flip angle=90 degrees ), with b value of 500 s mm(-2). 16 slices were produced with slice thickness of 7 mm and interslice gap of 1 mm. An apparent diffusion coefficient (ADC) map was obtained at each slice position. The ADC was measured in an approximately 1 cm region of interest (ROI) within the normal renal parenchyma, the detected renal lesions and the collecting system if dilated. ADC values in normal renal parenchyma ranged from 1.72 x 10(-3) mm(2) s(-1) to 2.65 x 10(-3) mm(2) s(-1), while ADC values in simple cysts (n=13) were higher (2.87 x 10(-3) mm(2) s(-1) to 4.00 x 10(-3) mm(2) s(-1)). In hydronephrotic kidneys (n=6) the ADC values of renal pelvis ranged from 3.39 x 10(-3) mm(2) s(-1) to 4.00 x 10(-3) mm(2) s(-1). In cases of pyonephrosis (n=3) ADC values of the renal pelvis were found to be lower than those of renal pelvis of hydronephrotic kidneys (0.77 x 10(-3) mm(2) s(-1) to 1.07 x 10(-3) mm(2) s(-1)). Solid benign and malignant renal tumours (n=7) showed ADC values ranging between 1.28 x 10(-3) mm(2) s(-1) and 1.83 x 10(-3) mm(2) s(-1). In conclusion diffusion-weighted MR imaging of the kidney seems to be a reliable way to differentiate normal renal parenchyma and different renal diseases. Clinical experience with this method is still preliminary and further studies are required.