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Background Functional chest pain (FCP) is characterized by the presence of chest pain of presumed esophageal origin, but with a negative workup on routine investigations, including ruling out gastroesophageal reflux disease (GERD). Antidepressants are frequently prescribed to treat FCP and are presumed to act as neuromodulators of visceral hypersensitivity. However, there is little evidence of their efficacy in patients with FCP. We retrospectively assessed the efficacy of citalopram or amitriptyline vs. no treatment in patients with FCP. Methods Esophageal diseases, including GERD, eosinophilic esophagitis and major esophageal motility disorders, were excluded. Thus, patients with established FCP according to Rome IV criteria were included in the study. Then, patients treated for at least 3 months with citalopram 20 mg, amitriptyline 50 mg, or observation were selected. The primary endpoint was complete disappearance or significant amelioration of symptoms at the end of treatment. Results Over a 5-year period, 102 patients (74 female; mean age 49±10 years) were diagnosed with FCP and were recognized to have received once daily citalopram (n=32), amitriptyline (n=34), or no treatment (n=36). After a 3-month follow up, improvement in chest pain was reported by 16 (47.1%) patients treated with citalopram, 18 (56.3%) patients treated with amitriptyline, and 4 (11.1%) patients without treatment (P=0.02 and 0.01 for no treatment vs. citalopram and amitriptyline therapy, respectively). Conclusion Both citalopram and amitriptyline are effective pharmacological options in the symptomatic relief of almost 50% patients with well characterized FCP. [ABSTRACT FROM AUTHOR]

The development of biological agents against tumor necrosis factor (TNF) has revolutionized the management of inflammatory bowel disease(IBD), frequently achieving induction and maintenance of remission in both ulcerative colitis and Crohn’s disease. However, a loss of response due to the development of anti-drug antibodies (ADA) is seen annually in approximately 20% of IBD patients receiving anti-TNF therapy. Current evidence suggests that the use of immunomodulators (IMM), such as thiopurines (azathioprine and 6-mercaptopurine) or methotrexate, may prevent or suppress ADA formation. In this article, we present a comprehensive review of the available literature regarding the efficacy of IMM in the prevention and suppression of ADA development to anti-TNF therapy in patients with IBD. [ABSTRACT FROM AUTHOR]

Background Galectin-3 (gal-3) has been proposed as a marker of established renal impairment, with predictive value in stable decompensated cirrhosis. Methods 150 stable decompensated patients were assessed in 2 transplant centers. Patients' renal function was assessed using 51Chromium-EDTA ("true" glomerular filtration rate). We measured basic laboratory variables and gal-3 in serum samples. Factors associated with patients' outcomes were determined. Results Our patients were followed up for 12 months (range 1-48, interquartile range [IQR] 6, 95% confidence interval [CI] 10-13.5) and their mean prognostic scores were Child-Turcotte-Pugh (CTP) 7±2 and model for end-stage liver disease and sodium (MELD-Na) 15±6. Median gal-3 levels were 22 ng/mL. In a multivariate analysis of 94 patients (training group), gal-3 (hazard ratio [HR] 1.026, 95% confidence interval [CI] 1.011-1.041; P=0.003) and serum sodium (HR 1.032, 95%CI 1.006-1.062; P=0.05) were the only factors independently associated with patients' outcomes. Kaplan-Meier analysis using the median gal-3 values revealed different times of survival (log-rank P=0.006). We derived a new prognostic score, (0.026) × serum gal-3+ (-0.079) × serum sodium, with very good discriminative accuracy for the outcome (area under the curve [AUC] 0.71, 95%CI 0.63-0.88), similar to that of the MELD-Na score (AUC 0.69, 95%CI 0.67-0.89; P=0.73), while its diagnostic accuracy was validated in the remaining 56 decompensated patients (AUC 0.81, 95%CI 0.65-0.97). Conclusions Gal-3 proved to be an accurate and plausible biomarker of renal dysfunction in patients with decompensated cirrhosis. A new prognostic model incorporating gal-3 and sodium was derived, with very good discriminative accuracy for the outcome. [ABSTRACT FROM AUTHOR]