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Background: The literature has shown a significant association between traumatic experiences and eating psychopathology, showing a greater symptomatology in patients with trauma history. Less is known about the associations between trauma and cognitive schemas, and personality traits and the differences between childhood and adulthood trauma experiences. Thus, this paper aims to assess the clinical and psychological characteristics of eating disorder (ED) patients, looking for differences between patients without a history of trauma and patients with trauma experiences, as well as at possible differences between exposure in childhood, adulthood, or repeated events. Another aim of the paper is to evaluate the possible mediation role of cognitive schemas and personality traits in the relationship between early trauma and eating psychopathology.Methods: From January to November 2020, 115 consecutive inpatients admitted for a specific multidisciplinary ED treatment in a dedicated Unit were evaluated for trauma, differentiating between trauma occurring in childhood and adulthood. The subjects were evaluated for early maladaptive schemas (EMS), personality traits, trauma symptomatology, quality of life, and specific psychopathologies linked to EDs. Mediation analyses between childhood and adulthood trauma and eating psychopathology were performed, with EMS and personality traits as mediators.Results: Patients with a history of trauma showed higher physical and psychological symptomatology scores, with a more impaired clinical profile in patients with both childhood and adulthood trauma exposure. The mediation analysis showed a specific mediator role for the “disconnection and rejection (DR)” EMS factor in the relationship between childhood trauma (cT) and eating psychopathology.Conclusion: Trauma experiences are associated with more severe clinical symptomatology in EDs and may need a specific assessment in patients with failed outpatient standard treatments. Specific cognitive schemas linked to DR domain should be evaluated in treatments for ED patients with history of trauma due to the mediation role between trauma and eating psychopathology. The need for outcome studies about treatment approaches for ED patients with history of trauma is discussed.

Background:Cortical lesions (CLs) are typical of multiple sclerosis (MS) and have been recently incorporated in MS diagnostic criteria. Thus, the ‘no evidence of disease activity’ (NEDA) definition should now include CLs. The aim of this study was to evaluate the NEDA3 + CL status in natalizumab- or fingolimod-treated relapsing remitting MS (RMS) patients.Methods:Natalizumab- or fingolimod-treated RMS patients were enrolled in a 2-year longitudinal study based on clinical and magnetic resonance imaging (MRI) evaluations performed respectively biannually and annually. CLs were detected by double inversion recovery. The NEDA3 + CL condition was evaluated at baseline (T0) and at the end of the first (T1) and second (T2) year.Results:Of the 137 RMS patients included in the study, 86 were propensity-matched. At T2, the annualized relapse rate was lower on natalizumab (p = 0.021), but the effect on white matter lesions (p = 0.29) and the proportion of NEDA-3 patients (p = 0.14) were similar in the two treatment arms. At T2, 11.6% natalizumab- and 62.8% fingolimod-treated patients had new CLs (p < 0.001) and a higher proportion of natalizumab-treated patients (55.8% versus 11.6%, p < 0.001) achieved the NEDA3 + CL status (hazard ratio 5.2, p < 0.001).Conclusion:The incorporation of CLs in the NEDA-3 definition highlighted the higher efficacy of natalizumab versus fingolimod in suppressing disease activity in RMS patients.

BackgroundThe cause and clinical significance of the transient decrease in platelet (PLT) count observed in relapsing remitting multiple sclerosis (RRMS) during alemtuzumab administration remain undefined. The aim of this study was to analyse the kinetics and clinical relevance of early onset thrombocytopaenia in alemtuzumab-treated RRMS.MethodsA total of 26 patients with RRMS were included in a longitudinal study. Blood samples were collected immediately before the first alemtuzumab infusion (D0), and after 3 days (D3), 28 days (D28) and 49 days (D49). PLT, red blood cell (RC), leucocyte and lymphocyte counts, haemoglobin (Hb) concentration and haematocrit (Htc) were measured. Patients with MS were clinically evaluated every day of drug infusion and then at D28 and D49 to verify the presence of signs or symptoms suggestive of thrombocytopaenia.ResultsPLT number significantly decreased at D3 (p < 0.005) and was associated with a decrease in RC count (r: 0.53, p < 0.01), Hb (r: 0.42, p = 0.05) and Htc (r: 0.53, p < 0.01). A progressive reversion of PLT number to normal values was observed at D28 and D49. A mild thrombocytopaenia was observed in 12 patients (46.2%), 8 of which (66.6%) had PLT nadir values at D3, and 4 (33.3%) at D28. No sign or symptom suggestive of thrombocytopaenia was observed. A strong correlation between pretreatment and nadir PTL counts (r: 0.59, p < 0.005) was observed; indeed, mild thrombocytopaenia was observed more frequently in these patients with a baseline PTL count lower than 230 × 109/L (83.3% versus 42.9%, p < 0.05).ConclusionsThe early PLT decrease in alemtuzumab-treated patients is transient, mild, not associated with clinically relevant events and is probably related to the cytokine-released syndrome. Notwithstanding this, our findings suggest the opportunity for PLT monitoring during infusion and in the following 2 months, since a decrease in PLT count may occur.

Background: Apart from IgG oligoclonal bands, no other biomarker has, to date, been validated for diagnostic and/or prognostic purposes in multiple sclerosis (MS). Aim: To investigate a wide panel of cytokines and chemokines in the cerebrospinal fluid (CSF) of relapsing-remitting MS (RRMS) patients and evaluate their association with clinical and magnetic resonance imaging (MRI) parameters, as well as their predictive clinical value. Methods: Fifty-one RRMS at clinical onset and 17 other not inflammatory neurological disorders (ONINDs) underwent brain MRI (including 3D-T1, 3D-FLAIR, and 3-DIR sequences) and CSF examination. Eighty-seven cytokines and chemokines were analyzed in CSF by Multiplex technology. Results: Compared to ONIND, CXCL-10, CXCL-11, CXCL-13, CCL-1, CCL-2, CCL-3, CCL-22, IL-16, and BAFF were significantly (p < 0.05) increased in RRMS CSF. However, only CCL-3 was associated with both MS diagnosis and IgGOB detection. Based on a 95%CI in ONIND (cut-off value: 0.798 pg/ml) and ROC analysis (cut-off value: 0.495 pg/ml), RRMS patients were stratified in CCL-3 high (>0.736 pg/mL), CCL-3 medium , and CCL-3 low (<0.495 pg/ml). Survival analysis disclosed a strong association between high CCL-3 values and disease reactivation (OR = 4.9, 95%CI: 1.8-13.3, p < 0.005) in the following 2 years. Conclusions: CCL-3 deserves further investigation as a candidate prognostic biomarker for RRMS.