Type 2 diabetes mellitus (T2DM) remains one of the most problematic and economic consumer disorders worldwide, with growing prevalence and incidence. Over the last years, substantial research has highlighted the intricate relationship among gut microbiota, dysbiosis and metabolic syndromes development. Changes in the gut microbiome composition lead to an imbalanced gastrointestinal habitat which promotes abnormal production of metabolites, inflammatory status, glucose metabolism alteration and even insulin resistance (IR). Short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO), lipopolysaccharide, aromatic amino acids and their affiliated metabolites, contribute to T2DM via different metabolic and immunologic pathways. In this narrative review, we discuss the immunopathogenic mechanism behind gut dysbiosis, T2DM development and the major known diabetic microvascular complications (retinopathy, neuropathy and nephropathy), the beneficial use of pre- and pro-biotics and fecal microbiota transplantation in T2DM management and new findings and future perspectives in this field.
Nonalcoholic fatty liver disease (NAFLD) is an emerging worldwide problem and its association with other metabolic pathologies has been one of the main research topics in the last decade. The aim of this review article is to provide an up-to-date correlation between hypothyroidism and NAFLD. We followed evidence regarding epidemiological impact, immunopathogenesis, thyroid hormone-liver axis, lipid and cholesterol metabolism, insulin resistance, oxidative stress, and inflammation. After evaluating the influence of thyroid hormone imbalance on liver structure and function, the latest studies have focused on developing new therapeutic strategies. Thyroid hormones (THs) along with their metabolites and thyroid hormone receptor β (THR-β) agonist are the main therapeutic targets. Other liver specific analogs and alternative treatments have been tested in the last few years as potential NAFLD therapy. Finally, we concluded that further research is necessary as well as the need for an extensive evaluation of thyroid function in NAFLD/NASH patients, aiming for better management and outcome.
Oral microbiota formation begins from birth, and everything from genetic components to the environment, alongside the host’s behavior (such as diet, smoking, oral hygiene, and even physical activity), contributes to oral microbiota structure. Even though recent studies have focused on the gut microbiota’s role in systemic diseases, the oral microbiome represents the second largest community of microorganisms, making it a new promising therapeutic target. Periodontitis and dental caries are considered the two main consequences of oral bacterial imbalance. Studies have shown that oral dysbiosis effects are not limited locally. Due to technological advancement, research identified oral bacterial species in heart valves. This evidence links oral dysbiosis with the development of valvular heart disease (VHD). This review focuses on describing the mechanism behind prolonged local inflammation and dysbiosis, that can induce bacteriemia by direct or immune-mediated mechanisms and finally VHD. Additionally, we highlight emerging therapies based on controlling oral dysbiosis, periodontal disease, and inflammation with immunological and systemic effects, that exert beneficial effects in VHD management.
Early identification of acute pancreatitis etiology is essential for choosing the best therapeutic management. The main causes are cholelithiasis and alcohol consumption. Tumors that obstruct the main pancreatic duct are uncommon causes of acute pancreatitis. Duodenal neuroendocrine tumors are rare entities and may be exceptional causes of acute pancreatitis. A 57-year-old male, with associated severe cardiovascular pathology, was admitted with clinical and biological picture of acute pancreatitis. Biliary and alcoholic causes were excluded. Abdominal contrast-enhanced computed tomography scan identified circumferential wall thickening of the second segment of the duodenum with peri-ampullary and papillary nodular non-homogenous contrast enhancement aspect. Upper gastrointestinal endoscopy described irregular hypertrophic duodenal mucosal folds and biopsies were performed. The histopathological diagnosis after immunohistochemistry tests was duodenal large-cell neuroendocrine carcinoma. The patient was referred to the oncology clinic and palliative treatment was initiated. The evolution was marked by additional complications due to the tumor evolutionupper gastrointestinal bleeding and obstructive jaundice, conservatory treated and, respectively, by interventional radiology technique. This case illustrates that, although often obvious, etiological diagnosis approach of acute pancreatitis can be sometimes challenging. Tumor cause is infrequent and requires thorough work-up, as the treatment is different. Although extremely rare and sometimes with mild clinical presentation, duodenal neuroendocrine carcinomas may have dramatic onset and evolution, involving extensive therapeutic resources.
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