Post-cardiac injury syndrome and pericardial effusion recurrence after pericardial effusion drainage in chronic idiopathic pericardial effusion.

INTRODUCTION: The management of even large pericardial effusions in asymptomatic patients is still a matter of debate. Aim of the present study is to explore, in a multicenter setting, the rate of post-cardiac injury syndromes (PCIS) and pericardial effusion recurrence after pericardial effusion drainage procedure. MATERIAL AND METHODS: This is a multicenter international retrospective study including a consecutive cohort of patients diagnosed with large, chronic and idiopathic pericardial effusions, prospectively evaluated from January 2003 to December 2021 who underwent a clinically indicated pericardial drainage procedure. Two separate end-points were recorded: 1) recurrence of pericardial effusion after drainage without any sign of pericardial inflammation 2) occurrence of PCIS, defined as the new onset of pericarditis 1 to 6 weeks after pericardial intervention. RESULTS: 124 patients were enrolled (50 % female, mean age 64 years old). A mean follow-up of 29.6 ± 25.6 months was obtained in 110 patients (88 %). 110 patients were treated with pericardiocentesis (89 %), 25 with pleuro-pericardial windows (20 %), and 1 with pericardiectomy (1 %). PCIS occurred in 21 out of 124 patients followed for at least 6 weeks (16.9%). Recurrence of pericardial effusion after drainage without any sign of pericardial inflammation occurred in 68 out of 110 patients at a longer follow-up (61.8 %). At multivariate analysis only inflammatory cells in pericardial fluid was associated with PCIS and pericardiocentesis with pericardial effusion recurrency. CONCLUSION: Our data support the need of caution with the use of pericardiocentesis in asymptomatic patients with large pericardial effusion as it is often associated with pericardial effusion recurrence. Of interest the presence of inflammatory cells in the pericardial fluid is associated with PCIS after pericardial drainage procedures.

Acute myocarditis as first presentation of severe ulcerative colitis in a young man. Multidisciplinary management and long-term follow-up.

Myocarditis is a rare extra-intestinal complication of inflammatory bowel disease (IBD), in particular, ulcerative colitis.We report a case of acute myocarditis as first manifestation of severe ulcerative colitis. A 22-year-old man was admitted with fever, bloody diarrhea, and fatigue. He had suffered from frequent bloody diarrhea, abdominal pain, fatigue, and weight loss for one month. A 12-lead-electrocardiogram showed sinus rhythm with QRS fragmentation and T waves inversion. High sensitivity troponin-I was elevated and the echocardiogram showed a mild pericardial effusion and inferior hypokinesia with normal ejection fraction. Cardiac magnetic resonance disclosed late enhancement in the inferior wall, corroborating the hypothesis of myocarditis. One week later, a colonoscopy revealed severe ulcerative extensive colitis (Mayo subscore 3). 5-aminosalicylic acid (mesalazine) and systemic steroid were started with good clinical and biochemical response. The following days the patient developed mesalazine hepatic and pancreatic induced toxicity requiring drug discontinuation and strict multi-disciplinary follow-up. At 7 months follow-up intestinal symptoms were well controlled with complete normalization of liver and pancreatic enzymes. Transthoracic echocardiography showed normal biventricular function and pericardial effusion resolution.This case underscores the importance of a high suspicion for extra intestinal involvement in patients with IBD. These complications may be multifactorial and need multidisciplinary management. Learning objective: •When a patient was first-time diagnosed with a severe form of inflammatory bowel disease or has a disease relapse, bear in mind myocarditis as possible extra intestinal manifestation.•Multidisciplinary management is crucial to ensure the best level of care and follow-up in a such challenging and insidious clinical picture.

Clinical risk scores for the early prediction of severe outcomes in patients hospitalized for COVID-19.

Coronavirus disease of 2019 (COVID-19) is associated with severe acute respiratory failure. Early identification of high-risk COVID-19 patients is crucial. We aimed to derive and validate a simple score for the prediction of severe outcomes. A retrospective cohort study of patients hospitalized for COVID-19 was carried out by the Italian Society of Internal Medicine. Epidemiological, clinical, laboratory, and treatment variables were collected at hospital admission at five hospitals. Three algorithm selection models were used to construct a predictive risk score: backward Selection, Least Absolute Shrinkage and Selection Operator (LASSO), and Random Forest. Severe outcome was defined as the composite of need for non-invasive ventilation, need for orotracheal intubation, or death. A total of 610 patients were included in the analysis, 313 had a severe outcome. The subset for the derivation analysis included 335 patients, the subset for the validation analysis 275 patients. The LASSO selection identified 6 variables (age, history of coronary heart disease, CRP, AST, D-dimer, and neutrophil/lymphocyte ratio) and resulted in the best performing score with an area under the curve of 0.79 in the derivation cohort and 0.80 in the validation cohort. Using a cut-off of 7 out of 13 points, sensitivity was 0.93, specificity 0.34, positive predictive value 0.59, and negative predictive value 0.82. The proposed score can identify patients at low risk for severe outcome who can be safely managed in a low-intensity setting after hospital admission for COVID-19.

Liver alterations in anorexia nervosa are not caused by insulin resistance.

BACKGROUND: Liver dysfunction has been widely reported in connection with anorexia nervosa (AN) but the pathogenesis of these alterations has never been fully understood despite reported theories about the presence of insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD). The aim of this study is to investigate if hypertransaminasemia in AN is linked to IR and NAFLD. METHODS: Anthropometric data and laboratory exams of 34 patients and 34 controls were analyzed, including alanine-aminotransferase, aspartate-aminotransferase and homeostatic model assessment of insulin resistance (HOMA-IR) index. All subjects also underwent magnetic resonance imaging (MRI), ultrasonography (US), and transient elastography (TE). RESULTS: Evidence of increased alanine aminotransferase in AN patients was confirmed in our sample together with a lower HOMA-IR index compared to controls. Positive results in US appeared in 16 patients vs none in controls (p = 0.0007); patients with liver parenchyma abnormalities in US were not different than normal-US patients in any of the studied variables. Only one patient showed non-alcoholic fatty liver disease in MRI while abnormal TE was found in four patients and never in controls. CONCLUSIONS: Liver damage suggested by increased serum liver enzymes cannot be due to liver steatosis but potentially to a different liver disease (not identified by MRI) or to an early liver fibrosis not associated with an insulin-resistant status.

Transcranial direct current stimulation modulates implicit attitudes towards food in eating disorders.

OBJECTIVE: Neuromodulation of regions involved in food processing is increasingly used in studies on eating behaviors, but results are controversial. We assessed the effects of anodal transcranial direct current stimulation (a-tDCS) on food and body implicit preferences in patients with eating disorders (EDs). METHOD: Thirty-six ED patients and 36 healthy females completed three sessions with a-tDCS applied to the medial-prefrontal cortex (mPFC), the right extrastriate body area (rEBA) or in sham mode. Each participant then completed three Implicit Association Tests (IATs) on tasty/tasteless food, underweight/overweight body images, flowers versus insects as control. Differences in latency between incongruent and congruent blocks were calculated (D score). RESULTS: The tDCS by group interaction was significant for the IAT-food D score, with patients showing weaker preference for tasty food than controls in sham, but not a-tDCS sessions. In particular, rEBA stimulation significantly increased patients' D score compared to sham. Moreover, a-tDCS over mPFC and rEBA selectively increased patients' reaction times in the incongruent blocks of the IAT-food. DISCUSSION: A-tDCS on frontal and occipito-temporal cortices modulated food preferences in ED patients. The effect was specific for food images and selective in patients, but not in healthy participants. These findings suggest that neuromodulation of these regions could affect implicit food attitudes.

Microbiota in anorexia nervosa: The triangle between bacterial species, metabolites and psychological tests.

Anorexia nervosa (AN) is a psychiatric disease with devastating physical consequences, with a pathophysiological mechanism still to be elucidated. Metagenomic studies on anorexia nervosa have revealed profound gut microbiome perturbations as a possible environmental factor involved in the disease. In this study we performed a comprehensive analysis integrating data on gut microbiota with clinical, anthropometric and psychological traits to gain new insight in the pathophysiology of AN. Fifteen AN women were compared with fifteen age-, sex- and ethnicity-matched healthy controls. AN diet was characterized by a significant lower energy intake, but macronutrient analysis highlighted a restriction only in fats and carbohydrates consumption. Next generation sequencing showed that AN intestinal microbiota was significantly affected at every taxonomic level, showing a significant increase of Enterobacteriaceae, and of the archeon Methanobrevibacter smithii compared with healthy controls. On the contrary, the genera Roseburia, Ruminococcus and Clostridium, were depleted, in line with the observed reduction in AN of total short chain fatty acids, butyrate, and propionate. Butyrate concentrations inversely correlated with anxiety levels, whereas propionate directly correlated with insulin levels and with the relative abundance of Roseburia inulinivorans, a known propionate producer. BMI represented the best predictive value for gut dysbiosis and metabolic alterations, showing a negative correlation with Bacteroides uniformis (microbiota), with alanine aminotransferase (liver function), and with psychopathological scores (obsession-compulsion, anxiety, and depression), and a positive correlation with white blood cells count. In conclusion, our findings corroborate the hypothesis that the gut dysbiosis could take part in the AN neurobiology, in particular in sustaining the persistence of alterations that eventually result in relapses after renourishment and psychological therapy, but causality still needs to be proven.

Liver steatosis (LS) evaluated through chemical-shift magnetic resonance imaging liver enzymes in morbid obesity; effect of weight loss obtained with intragastric balloon gastric banding.

The aim of this study was to evaluate in morbid obesity clinical and metabolic effects related to weight loss on liver steatosis (LS), measured through chemical-shift magnetic resonance imaging (MRI) and liver enzymes. Forty obese subjects (8 M/32 W; BMI 42.8 ± 7.12 kg/m(2), mean ± SD) were evaluated for LS through ultrasound (US-LS), chemical-shift MRI (MRI-LS), liver enzymes [aspartate aminotransferase (AST), alanine aminotransferase (ALT), γ-glutamyltransferase (GGT), alkaline phosphatase (ALP)], anthropometric parameters [weight, BMI, waist circumference (WC)], lipids, insulin, insulin resistance (HOMA-IR), glycated hemoglobin (HbA1c), oral glucose tolerance test, and body composition [fat mass (FM) and fat-free mass (FFM) at bio-impedance analysis (BIA)]. Anthropometric measures, MRI-LS, BIA, and biochemical parameters were reevaluated 6 months later in 18 subjects undergoing restrictive bariatric approach, i.e., intragastric balloon (BIB, n = 13) or gastric banding (LAGB, n = 5), and in 13 subjects receiving hypocaloric diet. At baseline, US-LS correlates only with MRI-LS, and the latter correlates with ALT, AST, and GGT. After 6 months, subjects undergoing BIB or LAGB had significant changes of BMI, weight, WC, ALT, AST, GGT, ALP, HbA1c, insulin, HOMA-IR, FM, FFM, and MRI-LS. Diet-treated obese subjects had no significant change of any parameter under study; change of BMI, fat mass, and fat-free mass was significantly greater in LAGB/BIB subjects than in diet-treated subjects. Change of MRI-LS showed a significant correlation with changes in weight, BMI, WC, GGT, ALP, and basal MRI-LS. Significant weight loss after BIB or LAGB is associated with decrease in chemical-shift MRI-LS and with reduction in liver enzymes; chemical-shift MRI and liver enzymes allow monitoring of LS in follow-up studies.

Cholesterol metabolism after bariatric surgery in grade 3 obesity: differences between malabsorptive and restrictive procedures.

OBJECTIVE: Malabsorptive bariatric surgery (biliopancreatic diversion and biliointestinal bypass [BIBP]) reduces serum cholesterol levels more than restrictive surgery (adjustable gastric banding [AGB]), and this is thought to be due to greater weight loss. Our aim was to evaluate the changes of cholesterol metabolism induced by malabsorptive and restrictive surgery independent of weight loss. RESEARCH DESIGN AND METHODS: In a nonrandomized, self-selected, unblinded, active-comparator, bicenter, 6-month study, glucose metabolism (blood glucose and serum insulin levels and homeostasis model assessment of insulin resistance [HOMA-IR] index) and cholesterol metabolism (absorption: serum campesterol and sitosterol levels; synthesis: serum lathosterol levels; catabolism: rate of appearance and serum concentrations of serum 7-α- and serum 27-OH-cholesterol after infusions of deuterated 7-α- and 27-OH-cholesterol in sequence) were assessed in grade 3 obesity subjects undergoing BIBP (n = 10) and AGB (n = 10). Evaluations were performed before and 6 months after surgery. RESULTS: Subjects had similar values at baseline. Weight loss was similar in the two groups of subjects, and blood glucose, insulin levels, HOMA-IR, and triglycerides decreased in a similar way. In contrast, serum cholesterol, LDL cholesterol, non-HDL cholesterol, serum sitosterol, and campesterol levels decreased and lathosterol levels increased only in BIBP subjects, not in AGB subjects. A significant increase in 7-α-OH-cholesterol occurred only with BIBP; serum 27-OH-cholesterol decreased in both groups. CONCLUSIONS: Malabsorptive surgery specifically affects cholesterol levels, independent of weight loss and independent of glucose metabolism and insulin resistance. Decreased sterol absorption leads to decreased cholesterol and LDL cholesterol levels, accompanied by enhanced cholesterol synthesis and enhanced cholesterol catabolism. Compared with AGB, BIBP provides greater cholesterol lowering.

Treatment with PEG-interferon and ribavirin for chronic hepatitis C increases neutrophil and monocyte chemotaxis.

The incidence of infections increases during treatment with pegylated interferon (PEG-IFN) and ribavirin (RBV) for chronic hepatitis C (CHC). Despite a reduction in neutrophil count, there is no clear relationship between infection occurrence and neutropenia. In the present study we investigated whether HCV treatment alters leukocyte function. We studied cell chemotaxis, reactive oxygen species, neutrophil phagocytosis, CR3 expression, and plasma colony stimulating factors (CSF) in 20 healthy subjects and 20 patients with CHC (10 with cirrhosis) at baseline, during antiviral treatment (at 4, 12, 24 weeks), and 12 weeks after discontinuation. Our results demonstrate that neutrophil chemotaxis and oxidative burst significantly increased during treatment and returned to baseline at the end of therapy. CR3 neutrophil expression was enhanced in baseline CHC compared to controls but did not change during antiviral treatment. Chemotaxis, oxidative burst, phagocytosis, and CSF levels did not differ significantly between patients before treatment and control subjects or among CHC cases according to the presence of cirrhosis in either cell subpopulation. In conclusion, the innate immune cell activity is enhanced in patients with CHC during antiviral treatment and returns to normal after its discontinuation thus possibly playing a role in their susceptibility to infections.

Primary biliary cirrhosis is not an additional risk factor for bone loss in women receiving regular calcium and vitamin D supplementation: a controlled longitudinal study.

BACKGROUND AND GOALS: Alterations in bone metabolism in primary biliary cirrhosis (PBC) are generally considered to be highly prevalent and severe, but no data are available from prospective studies with adequate control groups. The aims of this study were: (1) to measure changes in bone mineral density (BMD) over time; (2) to correlate the degree of bone loss with the severity of liver disease; and (3) to characterize bone disease in PBC patients receiving regular calcium and vitamin D supplementation. STUDY: We enrolled 118 women with PBC (mean age+/-SD: 56+/-11 y; 72% postmenopausal; 43% with cirrhosis), and measured BMD (lumbar spine, DXA-Hologic) at entry and serially over the following 5 years. The controls were 472 healthy women selected from a large observational group matched for age and menopausal status (mean age+/-SD: 55+/-10 y; 73% postmenopausal). RESULTS: Mean BMD was 0.851+/-0.142 g/cm2 in the PBC group and 0.857+/-0.158 g/cm2 in the control group; the prevalence of osteoporosis was 28% and 29%, respectively. BMD significantly correlated with age and postmenopausal status, but not with liver cirrhosis or serum bilirubin levels. The biochemical markers of bone turnover were high in about 50% of the patients. The yearly bone loss in the PBC group was 0.008 g/cm2 (95% confidence interval: 0.014-0.003) similar to that calculated in the control group. CONCLUSIONS: Among patients with PBC, the prevalence of osteoporosis and the yearly rate of BMD loss are similar to those observed in the general population, and are not associated with the severity of liver disease.

Decrease and dysfunction of dendritic cells correlate with impaired hepatitis C virus-specific CD4+ T-cell proliferation in patients with hepatitis C virus infection.

Through the production of stimulatory and suppressive cytokines, dendritic cells (DCs) regulate virus-specific immune responses that are crucial to virus eradication. To explore a possible role of DCs in the persistence of hepatitis C virus (HCV) infection, in this study we analysed peripheral blood DCs (PBDCs) in patients with chronic hepatitis C (CHC) compared with those in both healthy seronegative (HSN) controls and a group of subjects who had spontaneously resolved infection, defined as healthy HCV-seropositive (HSP), and we evaluated the relationships between PBDCs and HCV-specific CD4(+) T-cell reactivity. The number of PBDCs, their immunophenotype and expression of regulatory cytokines were evaluated by flow cytometry on whole-blood samples. HCV-specific CD4(+) T-cell activation, proliferation and cytokine production were evaluated in cultures of peripheral blood mononuclear cells (PBMCs) stimulated in vitro with HCV peptides. We found that PBDCs from CHC subjects were numerically reduced and showed lower interleukin-12 (IL-12) and higher IL-10 expression than those from HSN controls. PBDCs from HSP subjects were similar to those from HSN controls. HCV-specific CD4(+) T-cell proliferation was less frequent and vigorous in CHC than in HSP patients and was directly related to the number of PBDCs and their IL-12 production but inversely related to their IL-10 production. Taken together, these results seem to suggest that cytokines of DC origin contribute to the regulation of HCV-specific immunity in CHC patients and indicate that PBDCs may represent a novel non-invasive tool for immune monitoring of these patients.