Lung microbiome: new insights into bronchiectasis' outcome.

The present treatments for bronchiectasis, which is defined by pathological dilatation of the airways, are confined to symptom relief and minimizing exacerbations. The condition is becoming more common worldwide. Since the disease's pathophysiology is not entirely well understood, developing novel treatments is critically important. The interplay of chronic infection, inflammation, and compromised mucociliary clearance, which results in structural alterations and the emergence of new infection, is most likely responsible for the progression of bronchiectasis. Other than treating bronchiectasis caused by cystic fibrosis, there are no approved treatments. Understanding the involvement of the microbiome in this disease is crucial, the microbiome is defined as the collective genetic material of all bacteria in an environment. In clinical practice, bacteria in the lungs have been studied using cultures; however, in recent years, researchers use next-generation sequencing methods, such as 16S rRNA sequencing. Although the microbiome in bronchiectasis has not been entirely investigated, what is known about it suggests that Haemophilus, Pseudomonas and Streptococcus dominate the lung bacterial ecosystems, they present significant intraindividual stability and interindividual heterogeneity. Pseudomonas and Haemophilus-dominated microbiomes have been linked to more severe diseases and frequent exacerbations, however additional research is required to fully comprehend the role of microbiome in the evolution of bronchiectasis. This review discusses recent findings on the lung microbiota and its association with bronchiectasis.

Advances in Understanding the Human Gut Microbiota and Its Implication in Pediatric Celiac Disease-A Narrative Review.

Celiac disease (CD) is a multifactorial disorder, defined by a complex interplay of genetic and environmental factors. Both genetic predisposition and dietary exposure to gluten are essential factors in triggering CD. However, there is proof that their presence is necessary, but not sufficient, for disease development. Through gut microbiota modulation, several additional environmental factors have shown their potential role as co-factors in CD pathogenesis. The aim of this review is to illustrate the possible mechanisms that stand behind the gut microbiota's involvement in CD pathogenesis. Furthermore, we discuss microbiota manipulation's potential role as both a preventative and therapeutic option. The available literature provides evidence that even before CD onset, factors including cesarean birth and formula feeding, as well as intestinal infection exposure, amplify the risk of CD in genetically predisposed individuals, due to their influence on the intestinal microbiome composition. Active CD was associated with elevated levels of several Gram-negative bacterial genera, including Bacteroides, Escherichia, and Prevotella, while beneficial bacteria such as lactobacilli and bifidobacteria were less abundant. Viral and fungal dysbiosis has also been described in CD, evidencing specific taxa alteration. A gluten-free diet (GFD) may improve the clinical symptoms and duodenal histopathology, but the persistence of intestinal dysbiosis in CD children under a GFD urges the need for additional therapy. Probiotics, prebiotics, and fecal microbial transplant have demonstrated their efficacy in restoring gut microbiota eubiosis in adult CD patients; however, their efficacy and safety as adjunctive therapies to a GFD in pediatric patients needs further investigation.

Connection between Celiac Disease and Systemic Lupus Erythematosus in Children-A Development Model of Autoimmune Diseases Starting from What We Inherit to What We Eat.

Celiac disease (CD) and systemic lupus erythematosus (SLE) are two diseases intensively studied in all age groups, with an increasing incidence at the global level, possibly due to the increased awareness of the diseases and their accurate diagnosis and as a consequence of the new research and innovation technologies that have appeared in medicine. The first is a controllable condition found in approximately 1% of the entire population in the form of a reaction to environmental stimuli affecting individuals with genetic susceptibility, causing gluten intolerance, gastrointestinal and extradigestive symptoms, starting from subclinical stages and culminating in severe malabsorption. On the other hand, lupus is an autoimmune disease with chameleon-like symptoms and found mainly in the female sex, which leaves its clinical mark on most organs, from the skin, eyes, and kidneys to the cardiovascular, pulmonary, neurological, osteoarticular, and hematological systems. Current studies focus on the correlation between celiac disease and other autoimmune pathologies such as autoimmune thyroiditis (Hashimoto and Graves-Basedow), type I diabetes, and systemic lupus erythematosus. The current review aims to present a summary of the data from the specialized literature regarding the intercurrents between celiac disease and lupus by analyzing the most recent studies published on PubMed.

Amiodarone induced lung disease.

Amiodarone, a primarily class III antiarrhythmic drug is one of the most commonly used drug in atrial fibrillation. A possible rare side effect of amiodarone treatment is to develop a diffuse parenchymal lung disorder - amiodarone pulmonary toxicity (APT). There is no pathognomonic findings to diagnose APT. A 64-year-old patient with multiple comorbidities presented in our hospital with worsening a five-month history of grade 3 mMRC dyspnea, wheezing, frequent nonproductive cough, fatigue. She has a medical history of atrial fibrillation in treatment with amiodarone 400mg/day for 2 years. Her oxygen saturation was 90% on room air, chest radiography showed disseminated lung irregular opacities with a tendency to confluence in right and left lung and chest computed tomography scan showed asymmetric centrilobular nodules and asymmetrical areas of dense ground glass opacity with few consolidation. Amiodarone pulmonary toxicity was suspected, the drug was stopped and treatment with methylprednisolone started. Worsening and progression of the disease can still be noted despite stopping amiodarone because of the long persistence and elimination of the drug, with the tendency to concentrate in tissues, such as lung. In our patient case the evolution and prognosis were good even the case illustrates neglected effects of amiodarone, potential severe one.

Surgical and Anatomical Particularities and Difficulties in Histopathological Sampling for Superior Vena Cava Syndrome.

The superior vena cava syndrome is due to the increased venous pressure in the upper torso, neck and head, caused by the obstruction of the superior vena cava. Both external and internal factors cause obstruction (95% are malign causes), and the most severe manifestation is represented by cerebral edema that can even lead to coma. The diagnostic algorithm for the superior vena cava syndrome is widely known. There are many controversies and discussions about the safety of histopathological sampling. The purpose of this paper is to assess such risks, the complication rate and the diagnostic yield of surgical sampling, by analyzing the 26 interventions performed in our clinic. Although the complication rate was higher than that observed in the absence of the superior vena cava syndrome, surgery remains mandatory for a rapid histopathological diagnosis, therefore demanding a protocol that must include a mandatory extemporaneous exam of the biopsy.