Magnesium—A Potential Key Player in Inflammatory Bowel Diseases?

The altered magnesium status in inflammatory bowel disease (IBD) patients may have a significant clinical imprint considering its role in cell signaling and genomic stability, as well as its involvement in IBD patients’ fatigue. Our study pioneers the investigation of magnesium hair concentration patterns in an adult population of IBD patients. The hair magnesium concentration in IBD patients is compared to healthy controls in order to identify correlations between the magnesium status and relevant parameters related to disease activity, psychological status, and sleep quality. We report a significantly lower hair magnesium concentration within the IBD group compared to healthy controls (95%CI: 0.006–0.062; p = 0.017) and lower levels in CD compared to UC (95%CI: −0.061–−0.002; p = 0.038). We identified a borderline statistical significance between the hair magnesium concentration and UC disease activity (95%CI; −0.679–0.008; p = 0.055) and a significantly lower magnesium concentration in patients who reported increased sleep latency (95%CI −0.65–−0.102; p = 0.011) or decreased sleep duration (95%CI −0.613–−0.041; p = 0.028). Our results advance several hypotheses with substantial clinical impact to be confirmed in future studies. Magnesium levels appear to be modified in IBD patients, which suggests it either plays a primary role in disease pathophysiology or a is result of the disease’s evolution. Magnesium could be used in predictive models for clinical/subclinical disease activity. Moreover, magnesium supplementation may improve IBD evolution and sleep quality for patients with a deficit of this mineral. However, confirmatory evidence-based studies are needed to generate specific dosing, time of supplementation, and optimum monitoring of magnesium status in IBD patients.     

Arthritis associated with Mycoplasma pneumoniae in a pediatric patient: A case report

Introduction:Mycoplasma pneumoniae (MP) infection in infants is usually overlooked and it might result in important complications if left untreated. MP-induced arthritis is probably the least common extrapulmonary manifestation and frequently leads to delays in the diagnosis.Patient concerns:We report the case of a 2-year-old female child admitted in our clinic for prolonged fever (onset 2 weeks before the admission), for which the general practitioner established the diagnosis of acute pharyngitis and recommended antibiotics. But the fever persisted and the patient was referred to a pediatrician.Diagnosis:The laboratory tests revealed leukocytosis with neutrophilia, elevated C-reactive protein and liver cytolysis. The blood and urine cultures, as well as the serological hepatitis B and C, toxoplasmosis, Epstein Barr virus, Rubella, Herpes virus, and cytomegalovirus were negative. The chest X-ray established the diagnosis of pneumonia. The fever persisted for approximately 2 weeks after admission. On the 2nd week of admission, the patient began to experience gait difficulties complaining of pain in the right hip and ankle. The cardiology and pneumology consults revealed no pathological findings. The evolution was favorable after the initiation of Levofloxacin and MP infection was detected as we suspected. Moreover, the ultrasound of the hip revealed a mild joint effusion, while the ankle joint appeared to be normal at ultrasound. Thus, we established the diagnosis of hip and ankle arthritis based on the clinical and ultrasound findings.Interventions:Levofloxacin by vein was continued for 5 days, replaced afterwards with clarithromycin orally for 2 weeks.Outcomes:The gait difficulties persisted for approximately 5 months from the initial diagnosis, and improved once the titer of immunoglobulin M anti-MP antibodies lowered considerably. After more than 8 months, the patient was completely asymptomatic and the immunoglobulin M anti-MP was close to the normal range.Conclusion:The awareness of MP-induced arthritis in children represents the cornerstone in preventing diagnostic delays and initiating the proper treatment.     

Stenting for cervical tracheo-esophageal malignant fistula: a case report

Esophago-respiratory neoplastic fistulas present serious problems of management, mostly because of the severe status of the patient. The authors present the case of a 49-year-old patient with a malignant eso-tracheal fistula manifesting as mild dysphagia and dyspnoea. An endoscopic palliative treatment of the fistula was performed introducing a metallic coated stent into the esophagus. The multiple stent displacement required a definitive, very high positioning of the stent in the lower pharynx, with significant discomfort. Severe respiratory conditions regressed and the patient survived 6 months after the initial placement. The authors suggest endoscopic palliation with esophageal prosthesis as the therapeutic choice in those cases not amenable to surgery.     

Late life metabolic syndrome, early growth, and common polymorphism in the growth hormone and placental lactogen gene cluster

Low rates of fetal and infant growth are associated with the metabolic syndrome and cardiovascular disease in later life. We investigated common genetic variation in the GH-CSH gene cluster on chromosome 17q23 encoding GH, placental lactogens [chorionic somatomammotropins (CSH)], and placental GH variant in relation to fetal and infant growth and phenotypic features of the metabolic syndrome in subjects aged 59-72 yr from Hertfordshire, UK. Allele groups T, D1, and D2 of a locus herein designated CSH1.01 were examined in relation to GH-CSH single nucleotide polymorphisms and to specific phenotypes. Average birth weights were similar for all genotype groups. Men with T alleles were significantly lighter at 1 yr of age, shorter as adults, and had higher blood pressures, fasting insulin (T/T 66% higher than D2/D2) and triglyceride concentrations, and insulin and glucose concentrations during a glucose tolerance test. Birth weight and 1-yr weight associations with metabolic syndrome traits were independent of the CSH1.01 effects. Common diversity in GH-CSH correlates with low 1-yr weight and with features of the metabolic syndrome in later life. GH-CSH genotype adds substantially to, but does not account for, the associations between low body weight, at birth and in infancy, and the metabolic syndrome.     

Characterization of the anti‐HBV activity of HLP1–23, a human lactoferrin‐derived peptide

Lactoferrin (Lf) was shown to exhibit its antiviral activity at an early phase of viral infection and a mechanism whereby the protein interacts with host cell surface molecules has been suggested. In this study, human Lf (HLf) and seven HLf‐derived synthetic peptides (HLP) corresponding to the N‐terminal domain of the native protein (1–47 amino acids sequence) were assayed for their capacity to prevent hepatitis B virus (HBV) infection and replication using the HepaRG and HepG2.2.2.15 cell lines. Of the series tested, four peptides showed 40–75% inhibition of HBV infection in HepaRG cells, HLP_1–23, containing the GRRRR cationic cluster, being the most potent. Interestingly, this cluster is one of the two glycosaminoglycan binding sites of the native HLf involved in its antiviral activity; however, the mechanism of the HLP_1–23 action was different from that of the full‐length protein, the peptide inhibiting HBV infection when pre‐incubated with the virus, while no effect was observed on the target cells. It is suggested that the cationic cluster is sufficient for the peptide to interact stably with negatively charged residues on the virion envelope, while the absence of the second glycosaminoglycan binding site prevents its efficient attachment to the cells. In conclusion, this peptide may constitute a non‐toxic approach for potential clinical applications in inhibiting HBV entry by neutralizing the viral particles. J. Med. Virol. 85:780–788, 2013. © 2013 Wiley Periodicals, Inc.     

Platelet-derived growth factors induced lymphangiogenesis: evidence,unanswered questions and upcoming challenges

Crosstalk between angiogenesis and lymphangiogenesis in embryonic development continues during postnatal life and has specific mechanisms involving factors that initiate activation of the intracellular cascade for their specific receptors. Platelet-derived growth factors (PDGFs) and their corresponding receptors (PDGFRs) are known as important regulators of blood vessel development in both normal and pathologic angiogenesis. Despite some recent papers which reported a potential role of the PDGF/PDGFR axis in lymphatic spread of tumor cells, a few papers have suggested the potential role of PDGFs in tumor lymphangiogenesis development. The present paper summarizes the potential lymphangiogenic role of the PDGF/PDGFR axis, underlying upcoming challenges in the field.