Vitamin D and inflammatory bowel disease: what do we know so far?

In the last years,several studies have focused on the involement of vitamin D in different physiological and pathological processes. One of the most interesting actions occurs in the Inflammatory bowel disease, where a higher prevalence of vitamin D deficiency has been observed. This study aimed to review the literature in order to explain its relationship with the disease, the risk factors, measuring the importance of sun exposure, describing how treatments are affected or observing the effect of vitamin supplementation in this type of patients.

Posterolateral Bochdalek diaphragmatic hernia in adults.

Bochdalek hernias (BHs) are produced in the posterolateral area of the diaphragm. They are generally congenital, appearing in childhood, but are also detected in asymptomatic adult patients seeking medical attention for other reasons. Computed tomography (CT) or magnetic resonance imaging (MRI) is used for the correct diagnosis of the hernia type and for its localization, facilitating its management and the choice of treatment. We describe three cases of Bochdalek hernia, two on the right side and one bilateral, which was larger on the right than left side. All of these hernias contained only omental fat. In one patient, the right kidney was adjacent to the diaphragmatic defect but remained within the abdomen. The patients showed no symptoms and were not surgically treated. Examination by multislice CT with the possibility of coronal and sagittal reconstruction should be considered the standard method for diagnosing this entity. MRI in T1 is highly valuable to evaluate fat-containing chest lesions. The incidental finding of BH in asymptomatic adults is increasing, thanks to the wider application of new imaging techniques.

Preventive effect of zaprinast and 3-isobutyl, 1-methylxanthine (phosphodiesterase inhibitors) on gastric injury induced by nonsteroidal antiinflammatory drugs in rats.

Cyclic GMP plays an important role in maintaining homeostasis in the gastric mucosa. NSAIDs damage the mucosa by mechanisms that may be mediated by alterations in the intragastric concentration of cyclic GMP. To test this hypothesis we studied the effects of the oral administration of acetylsalicylic acid (100, 300, and 500 mg/kg), piroxicam (5, 10, and 20 mg/kg) and sodium diclofenac (10, 25, 50, and 100 mg/kg), and of their interaction with zaprinast (5 mg/kg) and IBMX (10 mg/kg), on intragastric concentrations of cyclic GMP and the gastric erosive index in rats. All determinations were done 3 hr after the NSAID was given. All NSAIDs induced dose-dependent decreases in mucosal concentrations of cyclic GMP, which correlated inversely with the surface area showing mucosal injury. In contrast, cyclic GMP concentrations remained normal, and no intragastric damage was seen in rats given zaprinast (cyclic GMP-specific phosphodiesterase inhibitor) or IBMX (non-specific phosphodiesterase inhibitor) or in combination with NSAIDs. These findings are in line with the hypothesis that cyclic GMP is involved in the biochemical mechanisms of NSAID-induced gastric injury.