Celiac Disease and Gallbladder: Pathophysiological Aspects and Clinical Issues.

Background: Celiac Disease (CD) is an immune-mediated disorder which primarily affects the small intestine; however, extra-intestinal organs are often affected by the pathological process, too. As regards the digestive system, liver alterations in CD patients have been widely described, which can also extend to the biliary tract. Notably, gallbladder function can be altered in CD patients. In this review, we specifically analyze and summarize the main pathophysiological aspects and clinical evidence of gallbladder dysfunction in CD patients, in order to discuss the potential medical complications and clinical research gaps. In addition to some perturbations of bile composition, CD patients can develop gallbladder dysmotility, which mainly expresses with an impaired emptying during the digestive phase. The main pathophysiological determinant is a perturbation of cholecystokinin secretion by the specific duodenal enteroendocrine cells in response to the appropriate nutrient stimulation in CD patients. This situation appears to be reversible with a gluten-free diet in most cases. Despite this gallbladder impairment, CD patients do not seem to be more predisposed to gallbladder complications, such as calculous and acalculous cholecystitis. However, very few clinical studies have actively investigated these clinical aspects, which may not be completely evidenced so far; alternatively, the substantial improvements in the last two decades regarding CD diagnosis, which have reduced the diagnostic delay (and related dietary treatment), may have lessened the potential clinical consequences of CD-related gallbladder dysfunction. Specific clinical studies focused on these aspects are needed for a better understanding of the clinical implications of gallbladder alterations in CD patients.

Mycoplasma pneumoniae Seroprevalence and Total IgE Levels in Patients with Juvenile Idiopathic Arthritis.

BACKGROUND: Mycoplasma pneumoniae (M. pneumoniae) is implicated in several immune-mediated extrapulmonary manifestations, including reactive arthritis. Recently, increased total serum IgE were reported in children developing M. pneumoniae-related extrapulmonary diseases (MpEPDs). Here, we aimed at analyzing these aspects in children affected with rheumatic disorders and, in detail, Juvenile Idiopathic Arthritis (JIA). METHODS: M. pneumoniae serology (IgG and IgM) and total serum IgE were concomitantly analyzed in 139 pediatric patients diagnosed with: JIA (Group 1, n = 85), or any rheumatic disease other than JIA (Group 2, n = 27), or non-inflammatory endocrinological disorders (Group 3, n = 27). RESULTS: Overall, 19.4% M. pneumoniae seroprevalence was observed in this hospitalized pediatric population, without signicant differences among the three groups. No significant differences in total serum IgE levels were noted among these groups; however, a second analysis excluding children with very high (and clearly abnormal) IgE levels suggested that JIA patients and, in detail, those with oligopolyarticular forms may have higher serum IgE concentrations. This relative difference among groups in serum IgE level seems to be more pronounced in M. pneumoniae seropositive children. CONCLUSIONS: M. pneumoniae infection should be actively sought in children developing immune-mediated diseases, including patients affected with JIA and, especially, in oligopolyarticular forms. There is some evidence that total serum IgE levels may tend to be increased in patients with oligopolyarticular JIA subtype and especially in those resulting as M. pneumoniae seropositive. However, further and focused research is needed to confirm these preliminary results and to clarify the relation between M. pneumoniae infection, atopic status, and immune-mediated arthritis.