SUMMARYLidocaine and related local anaesthetics have been shown to be effective in the treatment of ulcerative colitis (UC). However, the mechanisms underlying their therapeutic effect are poorly defined. Intestinal epithelial cells play an important role in the mucosal inflammatory response that leads to tissue damage in UC via the secretion of pro-inflammatory cytokines and chemokines. The aim of this study was to evaluate the direct immunoregulatory effect of lidocaine on pro-inflammatory cytokine and chemokine secretion from intestinal epithelial cells. HT-29 and Caco-2 cell lines were used as a model system and treated with lidocaine and related drugs. The expression of IL-8, IL-1b and the IL-1 receptor antagonist (RA) were assessed by ELISA and quantification of mRNA. In further experiments, the effect of lidocaine on the secretion of IL-8 from freshly isolated epithelial cells stimulated with TNFa was tested. Lidocaine, in therapeutic concentrations, inhibited the spontaneous and TNFa-stimulated secretion of IL-8 and IL-1b from HT-29 and Caco-2 cell lines in a dose-dependent manner. Similarly, suppression of IL-8 secretion was noted in the freshly isolated epithelial cells. Other local anaesthetics, bupivacaine and amethocaine, had comparable effects. Lidocaine stimulated the secretion of the anti-inflammatory molecule IL-1 RA. Both the inhibitory and the stimulatory effects of lidocaine involved regulation of transcription. The results imply that the therapeutic effect of lidocaine may be mediated, at least in part, by its direct effects on epithelial cells to inhibit the secretion of proinflammatory molecules on one hand while triggering the secretion of anti-inflammatory mediators on the other.

Renal function was assessed in 20 (11 female and 9 male, age 21-76 years, mean 53) renal patients with a creatinine clearance 25-145 ml/min, mean 95, to evaluate the effects of iohexol, a non-ionic low-osmolar contrast medium. Intravenous urography was performed in 16 patients and computed body tomography in 4, using a dose of iohexol ranged between 0.6-3.3 (mean 1.17) g/kg b.w. Different parameters of renal function were determined in the week preceding and 1, 3 and 5 days after the administration of iohexol. The principal renal effect of iohexol was an increase of urinary alanine aminopeptidase, gamma-glutamyltransferase, lactate dehydrogenase, alkaline phosphatase and N-acetyl-beta-D-glucosaminidase. The maximum increase of enzymuria was observed on day 1 after the administration of iohexol. In most cases enzymes returned to base-line values within 3 days. No relevant variation of renal hemodynamics (glomerular filtration rate and effective renal plasma flow) was observed after iohexol. In conclusion, iohexol can increase of urinary enzymes, but the effect is rapidly reversible and is not accompanied by a clinically significant impairment of renal hemodynamics.

Trousseau's syndrome was the unexpected manifestation of thrombotic events, often associated with the diagnosis of malignancies, since cancer has been recognized as a prothrombotic state. There is a wide experience using low molecular weight heparin or Fondaparinux, while the use of direct oral anticoagulants, as Rivaroxaban, had less extent.A 76-year-old woman was diagnosed by a Trousseau's syndrome, with multiple arterial and venous thrombotic events, representing the alarm signals of an advanced non-small cell lung cancer (NSCLC). The patient's burden of disease rapidly widespread, with unexpected and polidistrectual thrombotic events and an advanced NSCLC with pleural effusion carrying EGFR mutation.After the treatment with an inhibitor of activated Factor X, the thrombotic events did not stop. Starting new direct oral anticoagulant drug and the oral EGFR Tyrosine Kinase Inhibitor (TKI), according to the molecular features of lung cancer, she rapidly achieved good response on overall global burden of disease.The aim of this article was to report a case of Trousseau's syndrome anticipating lung cancer diagnosis that was successfully treated with a quick start of proper anticoagulant and targeted oncological treatments. The interruption of thromboembolic events represented the first sign of disease response to treatments.

Trousseau's syndrome was the unexpected manifestation of thrombotic events, often associated with the diagnosis of malignancies, since cancer has been recognized as a prothrombotic state. There is a wide experience using low molecular weight heparin or Fondaparinux, while the use of direct oral anticoagulants, as Rivaroxaban, had less extent.A 76-year-old woman was diagnosed by a Trousseau's syndrome, with multiple arterial and venous thrombotic events, representing the alarm signals of an advanced non-small cell lung cancer (NSCLC). The patient's burden of disease rapidly widespread, with unexpected and polidistrectual thrombotic events and an advanced NSCLC with pleural effusion carrying EGFR mutation.After the treatment with an inhibitor of activated Factor X, the thrombotic events did not stop. Starting new direct oral anticoagulant drug and the oral EGFR Tyrosine Kinase Inhibitor (TKI), according to the molecular features of lung cancer, she rapidly achieved good response on overall global burden of disease.The aim of this article was to report a case of Trousseau's syndrome anticipating lung cancer diagnosis that was successfully treated with a quick start of proper anticoagulant and targeted oncological treatments. The interruption of thromboembolic events represented the first sign of disease response to treatments.