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Chronic abdominal pain is the primary symptom of chronic pancreatitis, but unfortunately it is difficult to treat. Vagal nerve stimulation studies have provided evidence of anti-nociceptive effect in several chronic pain conditions. We investigated the pain-relieving effects of transcutaneous vagal nerve stimulation in comparison to sham treatment in chronic pancreatitis patients. We conducted a randomised double-blinded, sham-controlled, crossover trial in patients with chronic pancreatitis. Patients were randomly assigned to receive a two-week period of cervical transcutaneous vagal nerve stimulation using the gammaCore device followed by a two-week sham stimulation, or vice versa. We measured clinical and experimental endpoints before and after each treatment. The primary clinical endpoint was pain relief, documented in a pain diary using a visual analogue scale. Secondary clinical endpoints included Patients' Global Impression of Change score, quality of life and Brief Pain Inventory questionnaire. Secondary experimental endpoints included cardiac vagal tone and heart rate. No differences in pain scores were seen in response to two weeks transcutaneous vagal nerve stimulation as compared to sham treatment (difference in average pain score (visual analogue scale): 0.17, 95%CI (-0.86;1.20), P = 0.7). Similarly, no differences were seen for secondary clinical endpoints, except from an increase in the appetite loss score (13.9, 95%CI (0.5:27.3), P = 0.04). However, improvements in maximum pain scores were seen for transcutaneous vagal nerve stimulation and sham treatments as compared to their respective baselines: vagal nerve stimulation (-1.3±1.7, 95%CI (-2.21:-0.42), P = 0.007), sham (-1.3±1.9, 95%CI (-2.28:-0.25), P = 0.018). Finally, heart rate was decreased after two weeks transcutaneous vagal nerve stimulation in comparison to sham treatment (-3.7 beats/min, 95%CI (-6.7:-0.6), P = 0.02). In this sham-controlled crossover study, we found no evidence that two weeks transcutaneous vagal nerve stimulation induces pain relief in patients with chronic pancreatitis. The study is registered at NCT03357029; www.clinicaltrials.gov.

The need for early non-invasive diagnostic tools for chronic liver fibrosis is growing, particularly in individuals with obesity, non-alcoholic fatty liver disease (NAFLD), and the metabolic syndrome (MetS) since prevalence of these conditions is increasing. This case-control study compared non-invasive liver fibrosis markers in obesity with NAFLD and MetS (NAFLD-MetS, n  = 33), in obese ( n  = 28) and lean ( n  = 27) control groups. We used MRI (T1 relaxation times (T1) and liver stiffness), circulating biomarkers (CK18, PIIINP, and TIMP1), and algorithms (FIB-4 index, Forns score, FNI, and MACK3 score) to assess their potential in predicting liver fibrosis risk. We found that T1 (892 ± 81 ms vs. 818 ± 64 ms, p  < 0.001), FNI (15 ± 12% vs. 9 ± 7%, p  = 0.018), CK18 (166 ± 110 U/L vs. 113 ± 41 U/L, p  = 0.019), and MACK3 (0.18 ± 0.15 vs. 0.05 ± 0.04, p  < 0.001) were higher in the NAFLD-MetS group compared with the obese control group. Moreover, correlations were found between CK18 and FNI ( r  = 0.69, p  < 0.001), CK18 and T1 ( r  = 0.41, p  < 0.001), FNI and T1 ( r  = 0.33, p  = 0.006), MACK3 and FNI ( r  = 0.79, p  < 0.001), and MACK3 and T1 ( r  = 0.50, p  < 0.001). We show that liver fibrosis markers are increased in obese individuals with NAFLD and MetS without clinical signs of liver fibrosis. More studies are needed to validate the use of these non-invasive biomarkers for early identification of liver fibrosis risk.

Background and Objectives: Both chronic pancreatitis (CP) and pancreatic ductal adenocarcinoma (PDAC) may lead to cachexia, sarcopenia, and osteoporosis due to different mechanisms. Neither patient gender, age, nor body weight are good predictors of these metabolic changes having a significant negative impact on the quality of life (QOL) and treatment outcomes. The aim of this study was to evaluate radiological changes in body composition and to compare them with manifestations of exocrine and endocrine pancreatic insufficiency, body mass, and QOL among patients with CP and PDAC. Materials and Methods: Prospectively collected data of 100 patients with diagnosed CP or PDAC were used for analysis. All patients underwent dual-energy X-ray absorptiometry (DXA), computed tomography (CT), and magnetic resonance imaging (MRI). The European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-C30 (EORTC QLQ-C30) was used to assess QOL. Diabetes and changes in fecal elastase-1 were also assessed. Results: There was no significant difference in skeletal muscle mass (SMM) among patients with CP and PDAC (p = 0.85). Significantly more underweight patients had low SMM (p = 0.002). Patients with CP had more pronounced pancreatic fibrosis (PF) (p < 0.001). Data showed a significant relationship between a high degree of PF and occurrence of diabetes (p = 0.006) and low fecal elastase-1 levels (p = 0.013). A statistically significant lower QOL was determined in patients with PF ≥ 50% and in the CP group. Conclusions: Sarcopenia and osteoporosis/osteopenia are highly prevalent among patients with chronic pancreatitis and pancreatic cancer, and CT- and MRI-based assessment of body composition and pancreatic fibrosis could be a potentially useful tool for routine detection of these significant metabolic changes.

Emerging evidence shows, that distal symmetric peripheral neuropathy (DSPN) also involves alterations in the central nervous system. Hence, the aims were to investigate brain metabolites in white matter of adults with diabetes and DSPN, and to compare any cerebral disparities with peripheral nerve characteristics. In type 1 diabetes, brain metabolites of 47 adults with confirmed DSPN were compared with 28 matched healthy controls using proton magnetic resonance spectroscopy (H-MRS) in the parietal region including the sensorimotor fiber tracts. Adults with diabetes had 9.3% lower ratio of N-acetylaspartate/creatine (NAA/cre) in comparison to healthy (p < 0.001). Lower NAA/cre was associated with lower sural (p = 0.01) and tibial (p = 0.04) nerve amplitudes, longer diabetes duration (p = 0.03) and higher age (p = 0.03). In addition, NAA/cre was significantly lower in the subgroup with proliferative retinopathy as compared to the subgroup with non-proliferative retinopathy (p = 0.02). The association to peripheral nerve dysfunction, indicates concomitant presence of DSPN and central neuropathies, supporting the increasing recognition of diabetic neuropathy being, at least partly, a disease leading to polyneuropathy. Decreased NAA, is a potential promising biomarker of central neuronal dysfunction or loss, and thus may be useful to measure progression of neuropathy in diabetes or other neurodegenerative diseases.

Patients with schizophrenia have excess cardiovascular risk, contributing to a reduced life expectancy of 15–20 years compared with the general population. To improve the understanding of the development and clinical trajectory of cardiovascular disease in patients with schizophrenia, we are conducting a prospective cohort study with comprehensive cardiovascular and psychiatric follow-up examinations every third year from baseline. In the present study, we aimed to describe and analyze the baseline results of this prospective cohort. The prospective cohort study enrolled participants with recent-onset schizophrenia (planned: n = 100), chronic schizophrenia (planned: n = 200), and controls for recent-onset patients (planned: n = 100) in the North Denmark Region from 2015–2019. We included 70 patients with recent-onset schizophrenia (mean age, 24.5 years; males, 54%; mean illness duration, 1 year), 165 patients with chronic schizophrenia (mean age, 49.5 years; males, 57%; mean illness duration, 21.1 years), and 85 controls for recent-onset patients (mean age, 24.4 years; males, 53%). At baseline, cardiovascular risk factors were highly prevalent in patients with schizophrenia (metabolic syndrome: 60%, hypercholesterolemia: 13%, diabetes: 13%, hypertension: 4%). Conversely, the prevalence of manifest cardiac disease, including heart failure, coronary artery disease, and atrial fibrillation/flutter was overall low (~1%). In conclusion, point-prevalences of cardiovascular risk factors were relatively high in patients with schizophrenia, while severe cardiac disease was less pronounced at baseline. Further prospective assessment is planned to determine and understand cardiovascular disease progression, and whether there are differences in the clinical trajectory between patients with recent-onset/chronic schizophrenia and controls over time.

ObjectiveIn patients with painful chronic pancreatitis (CP) there is increasing evidence of abnormal pain processing in the central nervous system. Using magnetic resonance (MR) diffusion tensor imaging, brain microstructure in areas involved in processing of visceral pain was characterised and these findings were correlated to clinical pain scores.Methods23 patients with CP pain and 14 controls were studied in a 3T MR scanner. Apparent diffusion coefficient (ADC) (ie, diffusivity of water) and fractional anisotropy (FA) (ie, organisation of fibres) values were assessed in the amygdala, cingulate cortex, insula, prefrontal cortex and secondary sensory cortex. Daily pain scores and the Brief Pain Inventory Short Form were collected 1 week before the investigation.ResultsIn grey matter, patients had increased ADC values in amygdala, cingulate cortex, insula and prefrontal cortex, as well as decreased FA values in cingulate cortex and secondary sensory cortex. In white matter, patients had increased ADC values in insula and prefrontal cortex, and decreased FA values in insula and prefrontal cortex (all p values <0.05). An effect modification from the pain pattern (attacks vs continuous pain) was seen in the insula and secondary sensory cortex (p values <0.05), but no effect modifications from diabetes, alcoholic aetiology and opioid treatment were seen (all p values >0.05). Microstructural changes in cingulate and prefrontal cortices were correlated to patients' clinical pain scores.ConclusionThe findings suggest that microstructural changes of the brain accompany pain in CP. The changes are likely to be a consequence of ongoing pain and structural reorganisation of the neuromatrix as also seen in other diseases characterised by chronic pain.

Magnetic resonance elastography (MRE) is a non-invasive technique suitable for assessing mechanical properties of tissues, i.e., stiffness. MRE of the pancreas is relatively new, but recently an increasing number of studies have successfully assessed pancreas diseases with MRE aiming to differentiate healthy from pathological pancreatic tissue with or without fibrosis. This review will systematically describe the practical and clinical applications of pancreatic MRE. We conducted a systematic literature search with a pre-specified search strategy using PubMed and Embase according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. English peer-reviewed articles applying MRE of the pancreas were included. Two independent reviewers assessed the studies. The literature search yielded 14 studies. The pancreatic stiffness for healthy volunteers ranged from 1.11. to 1.21 kPa at a driver frequency of 40 Hz. In benign tumors, the stiffness values were slightly higher or sometimes even lower (range 0.78 to 2.00 kPa), compared to the healthy pancreas parenchyma whereas, in malignant tumors, the stiffness values tended to be higher (1.42 to 6.06 kPa). The pancreatic stiffness was increased in both acute (median: 1.99 kPa) and chronic pancreatitis (> 1.50 kPa). MRE is a promising technique for detecting and quantifying pancreatic stiffness. It is related to fibrosis and seems to be useful in assessing treatment response and clinical follow-up of pancreatic diseases. However, most of the described practical settings were characterized by a lack of uniformity and inconsistency in reporting standards across studies. Harmonization between centers is necessary to achieve more consensus and optimization of pancreatic MRE protocols.

ObjectivesThe aim was to describe the pancreatic volume (PV) in a cohort of subjects with no prior history of pancreatic disease, and to explore the relationship between PV and conventional two-point measurements of the pancreas. Associations between PV, gender, age, abdominal body composition, and human height were explored as well.MethodsCT scans from 204 trauma patients (20–80 years, 100 males) were evaluated. PV was measured with semi-automatic segmentation. Standardized two-point measurements of the pancreas were obtained together with L1 vertebral body size (a proxy for human height) and abdominal body composition. Associations between PV and the other parameters were explored using uni- and multivariate linear regression.ResultsThe mean PV was 77.9 ± 21.7(SD) cm3 with an interindividual variability from 18.8 to 139.8 cm3. The transversal diameter of the pancreatic head showed the strongest correlation to PV (r = 0.500, p < 0.001). Age, width of the L1 vertebral body, and visceral fat cross-sectional area were all independently associated with PV (all p < 0.001), while no independent association was seen for gender (p = 0.441).ConclusionsThe pancreatic volume is subject to a large interindividual variability and is associated with age, human height and body composition, while gender had no independent influence on the pancreatic volume. Thus, future studies using PV as an outcome parameter should be evaluated in the context of anthropometric profiles.

Understanding ethnic variations in body composition is crucial for assessing health risks. Universal models may not suit all ethnicities, and there is limited data on the Inuit population. This study aimed to compare body composition between Inuit and European adults using computed tomography (CT) scans and to investigate the influence of demographics on these measurements. A retrospective analysis was conducted on 50 adults (29 Inuit and 21 European) who underwent standard trauma CT scans. Measurements focused on skeletal muscle index (SMI), various fat indices, and densities at the third lumbar vertebra level, analyzed using the Wilcoxon-Mann-Whitney test and multiple linear regression. Inuit women showed larger fat tissue indices and lower muscle and fat densities than European women. Differences in men were less pronouncehd, with only Intramuscular fat density being lower among Inuit men. Regression indicated that SMI was higher among men, and skeletal muscle density decreased with Inuit ethnicity and age, while visceral fat index was positively associated with age. This study suggests ethnic differences in body composition measures particularly among women, and indicates the need for Inuit-specific body composition models. It higlights the importance of further research into Inuit-specific body composition measurements for better health risk assessment.

Arterial calcification is associated with cardiovascular mortality in dialysis patients. Active matrix Gla protein (MGP) is a vitamin K-dependent inhibitor of arterial calcification. Elevated plasma concentrations of inactive MGP, i.e. dephosphorylated-uncarboxylated MGP (dp-ucMGP), are prevalent in dialysis patients. MGP inactivity might contribute to arterial calcification. We investigated whether vitamin K supplementation had an effect on arterial calcification in chronic dialysis patients. In a 2-year, double-blind, placebo-controlled intervention trial, 48 dialysis patients were randomized to vitamin K [menaquinone-7 (MK-7), 360 µg daily] or placebo. MK-7 in serum and dp-ucMGP in plasma were used to assess vitamin K status. Carotid-femoral pulse wave velocity (cfPWV) and scores of coronary arterial calcification (CAC) and abdominal aortic calcification (AAC) were used to assess arterial calcification. Thirty-seven participants completed Year 1, and 21 completed Year 2. At Year 2, serum MK-7 was 40-fold higher, and plasma dp-ucMGP 40% lower after vitamin K supplementation compared with placebo {mean dp-ucMGP difference: -1380 pmol/L [95% confidence interval (CI) -2029 to -730]}. There was no significant effect of vitamin K supplementation on cfPWV [mean difference at Year 2: 1.2 m/s (95% CI -0.1 to 2.4)]. CAC Agatston score increased significantly in vitamin K supplemented participants, but was not significantly different from placebo [mean difference at Year 2: 664 (95% CI -554 to 1881)]. AAC scores increased in both groups, significantly so within the placebo group at Year 1, but with no significant between-group differences. Vitamin K supplementation improved vitamin K status, but did not hinder or modify the progression of arterial calcification in dialysis patients.