MDCT of the liver in obese patients: evaluation of a different method to optimize iodine dose.

PURPOSE: To prospectively compare two different approaches for estimating the amount of intravenous contrast media (CM) needed for multiphasic MDCT of the liver in obese patients. MATERIALS AND METHODS: This single-center, HIPAA-compliant prospective study was approved by our Institutional Review Board. Ninety-six patients (55 men, 41 women), with a total of 42 hypovascular liver lesions, underwent MDCT of the liver. The amount of contrast medium injected was computed according to the patient's lean body weight which was estimated using either a bioimpedance device (Group A) or the James formula (Group B). The following variables were compared between the two groups: the amount of contrast medium injected (in grams of Iodine, gI), the contrast enhancement index (CEI) and the lesion-to-liver contrast-to-noise ratio. RESULTS: Protocols A and B yielded significant differences in the amount of CM injected (mean values 41.9 ± 4.41 gI in Group A vs. 35.9 ± 5.75 gI in Group B; P = 0.021). The mean CEI value and lesion-to-liver contrast-to-noise ratio measured on the portal phase were significantly higher with protocol A than with protocol B (P < 0.05). CONCLUSIONS: Our study shows that the adoption of a bioimpedance device in obese patients improves liver parenchymal enhancement and lesion conspicuity.

Interleukin-18 modulation in autism spectrum disorders.

BACKGROUND: Autism spectrum disorder (ASD) is a neurodevelopmental disease which affects 1 in 88 children. Its etiology remains basically unknown, but it is apparent that neuroinflammation is involved in disease development. Great attention has been focused on pro-inflammatory cytokines, and several studies have reported their dysfunction unbalance in serum as well as in the brain. The present work aimed at evaluating putative dysregulation of interleukin-18 (IL-18), a pro-inflammatory cytokine of the IL-1 family in the sera of patients with ASD of different grades, compared to healthy controls, as well as in postmortem brain samples obtained from patients with tuberous sclerosis as well as acute inflammatory diseases. Moreover, quantitative analysis of IL-18 was performed in the sera and brain obtained from Reeler mice, an experimental model of autism. METHODS: Serum IL-18 levels were measured by ELISA. IL-18 was localized by immunohistochemical analysis in brain sections obtained from tuberous sclerosis and encephalitis patients, as well as from gender- and age-matched controls, and in the brain sections of both Reeler and wild-type mice. IL-18 was also quantified by Western blots in homogenates of Reeler and wild-type mice brains. IL-18 binding protein (IL-18BP) was evaluated in Reeler and wild-type mice plasma as well as in their brains (sections and homogenates). RESULTS: IL-18 content decreased in the sera of patients with autism compared to healthy subjects and in Reeler sera compared to wild-type controls. IL-18 was detected within glial cells and neurons in the brain of subjects affected by tuberous sclerosis and encephalitis whereas in healthy subjects, only a weak IL-18 positivity was detected at the level of glial cells. Western blot identified higher amounts of IL-18 in Reeler brain homogenates compared to wild-type littermates. IL-18BP was expressed in higher amounts in Reeler brain compared to the brain of wild-type mice, whereas no significant difference was detected comparing IL-18BP plasma levels. CONCLUSIONS: IL-18 is dysregulated in ASD patients. Further studies seemed necessary to clarify the molecular details behind IL-18 increase in the brain and IL-18 decrease in the sera of patients. An increase in the size of the patient cohort seems necessary to ascertain whether decreased IL-18 content in the sera can become a predictive biomarker of ASD and whether its measure, in combination with other markers (e.g., increased levels of brain-derived neurotrophic factor (BDNF)), may be included in a diagnostic panel.