Helicobacter pylori Infection in Pediatric Patients: Update on Diagnosis and Eradication Strategies.

Helicobacter pylori infection is acquired mainly in childhood and remains an essential cause of peptic ulcer disease and gastric cancer. This article provides commentary on the last ESPGHAN/NASPGHAN guidelines and on publications made after the consensus conference of 2015. The majority of infected children are asymptomatic and pediatric studies do not support a role for H. pylori in functional disorders such as recurrent abdominal pain. The role of H. pylori infection in failure to thrive, children's growth, type I diabetes mellitus (T1DM), and celiac disease remains controversial. The diagnosis of infection should be based on upper-digestive endoscopy with biopsy-based methods. Eradication control after treatment should be based on validated non-invasive tests. Nodular gastritis is the main endoscopic finding of childhood H. pylori infection, but gastroduodenal erosions/ulcers are seen in some children, especially after 10 years of age. When indicated, eradication treatment should be given when good compliance is expected and based on the antimicrobial susceptibility profile.SCOPUS: re.jinfo:eu-repo/semantics/publishe

Molecular Structure, Biosynthesis, and Distribution of Coenzyme Q

Coenzyme Q is a very old molecule in evolutionary terms that has accumulated numerous functions in the cellular metabolism beyond its primordial function, the electron transport. In all organisms, coenzyme Q maintains a highly conserved structure allowing a localization inside cell membranes in a hydrophobic environment thanks to having an isoprenoid tail, and at the same time allows the polar ring benzene to interact with acceptors and electron donors. Coenzyme Q deficiency constitutes a group of mitochondrial diseases. Affected patients suffer mainly a decrease in energy production that induces dysfunctions in most organs and body systems. Current therapeutic alternatives are based on increasing coenzyme Q levels either through induction of endogenous mechanisms or exogenous supplementation. This chapter includes both aspects, the mechanisms associated with the coenzyme Q supplementation and the regulatory mechanisms of coenzyme Q biosynthesis. In terms of synthesis, the structure of coenzyme Q is complicated since it requires the participation of two well-differentiated pathways that must be carefully regulated. The synthesis is carried out through the participation of a multienzyme complex located in the inner mitochondrial membrane and controlled by different levels of regulation that at this time are not well-known