The etiology of metabolic disorders, such as obesity, has been predominantly associated with the gut microbiota, which is acknowledged as an endocrine organ that plays a crucial role in modulating energy homeostasis and host immune responses. The presence of dysbiosis has the potential to impact the functioning of the intestinal barrier and the gut-associated lymphoid tissues by allowing the transit of bacterial structural components, such as lipopolysaccharides. This, in turn, may trigger inflammatory pathways and potentially lead to the onset of insulin resistance. Moreover, intestinal dysbiosis has the potential to modify the production of gastrointestinal peptides that are linked to the feeling of fullness, hence potentially leading to an increase in food consumption. In this literature review, we discuss current developments, such as the impact of the microbiota on lipid metabolism as well as the processes by which its changes led to the development of metabolic disorders. Several methods have been developed that could be used to modify the gut microbiota and undo metabolic abnormalities. Methods: After researching different databases, we examined the PubMed collection of articles and conducted a literature review. Results: After applying our exclusion and inclusion criteria, the initial search yielded 1345 articles. We further used various filters to narrow down our titles analysis and, to be specific to our study, selected the final ten studies, the results of which are included in the Results section. Conclusions: Through gut barrier integrity, insulin resistance, and other influencing factors, the gut microbiota impacts the host’s metabolism and obesity. Although the area of the gut microbiota and its relationship to obesity is still in its initial stages of research, it offers great promise for developing new therapeutic targets that may help prevent and cure obesity by restoring the gut microbiota to a healthy condition.

Lesions commonly associated with HIV infection include oral candidiasis, herpes simplex infection, oral Kaposi’s sarcoma, hairy leukoplakia, periodontal diseases (linear gingival erythema and necrotizing ulcerative periodontitis), xerostomia, human papillomavirus-associated warts, aphthous ulcers, non-Hodgkin’s lymphoma, histoplasmosis, carcinoma, exfoliative cheilitis, and HIV salivary gland disease. Non-Hodgkin’s lymphoma (NHL) is the most common cancer in people living with HIV (PLWH), and the incidence is increased for aggressive B-cell NHL. Plasmablastic lymphoma (PbL) is a rare and aggressive B-cell malignancy that is often unresponsive to chemotherapy and usually has a poor prognosis. We hereby present the case of a patient with a recent history of COVID-19 infection who was diagnosed with HIV and NHL, with manifestations in the oral cavity and a favorable evolution after the introduction of antiviral therapy, specific chemotherapy, and radiotherapy. Dental expertise is necessary for the appropriate management of oral manifestations of HIV infection or AIDS, and lymphoma should be included in the differential diagnosis of any oral lesions.

Background and Objectives: Psoriasis is a chronic immune-mediated inflammatory disease requiring reliable diagnostic and monitoring tools. Salivary interleukins have emerged as promising non-invasive biomarkers, reflecting systemic inflammation and offering practical advantages such as ease of collection and improved patient compliance. Materials and Methods: This review synthesizes the current evidence on key salivary cytokines—IL-1β, IL-6, TNF-α, and IL-17—in relation to psoriasis pathogenesis, diagnosis, and treatment monitoring. It also compares saliva to blood-based diagnostics, emphasizing benefits like cost-effectiveness and suitability for repeated sampling. Methodological challenges, including heterogeneity in collection protocols and limited longitudinal data, are critically examined. Results: Advances in biologic therapies have deepened the understanding of psoriasis immunopathogenesis, highlighting interleukins as central biomarkers. Recent findings identify IL-37 and IL-38 as novel regulatory cytokines with anti-inflammatory roles. While elevated serum TNF-α levels in psoriatic patients are well documented, some inconsistencies persist. Notably, saliva has proven to be a viable alternative diagnostic fluid, supporting large-scale screening and routine clinical monitoring. Conclusions: Salivary interleukins—particularly IL-1β, IL-6, TNF-α, and IL-17—represent valuable, non-invasive biomarkers for early detection, disease severity assessment, and therapeutic response monitoring in psoriasis. Standardizing saliva-based methods and conducting large-scale studies are essential next steps to support their integration into personalized clinical practice.

Background and Objectives: Hematological disorders, especially chronic anemia and coagulation disorders, are common in patients with chronic kidney disease (CKD). Severe anemia is associated with increased cardiovascular morbidity and mortality in this special group of patients and is also responsible for decreased hope and quality of life. Despite the use of appropriate iron therapy and erythropoietin-stimulating agents, red blood cell transfusion is occasionally required, usually in the setting of acute bleeding or for correction of perioperative anemia. The COVID-19 pandemic has accelerated the progression of chronic diseases and worsened the outcomes for patients with nephrological conditions. As a precautionary measure against infections, patients’ access to hospitalization for their procedures has been reduced and their chronic complications, including hematological abnormalities, have gotten out of control. Materials and Methods: Our retrospective observational study was designed to evaluate the impact of the COVID-19 pandemic on blood transfusion for the patients with chronic kidney disease hospitalized in our emergency county medical unit, over a period of four years (2019–2022) who were admitted or at least referred for evaluation to the Nephrology department. We also followed the measures adopted to ensure the necessary blood products during this time. Results: Between 2190–2022, a total of 24,096 hospitalized patients were transfused at the Emergency County Clinical Hospital in Constanta, Romania. Meanwhile, in the nephrology and other medical or surgical wards of our medical unit, 1590 CKD patients were transfused with different blood derivatives. During the pandemic years, as expected, the number of transfused patients and transfused blood units decreased by 4% and 7%, respectively, in comparison with the pre-pandemic year, 2019. Unlike the general trend of transfusion activity, more patients with CKD transfused in 2022 (580) than before the pandemic (414 in 2019), and the number of blood units was higher in 2022 than in 2019 for red blood products and plasma. Between 2020–2022, from the total number of transfused patients in our study, 254 with CKD patients (16%) and 798 non-CKD (4%) died in-hospital. Conclusions: The adaptive strategies implemented to ensure the necessary blood products in the hospital during the COVID-19 pandemic mainly included restrictive transfusion and limitation of elective surgical procedures. The subject matter of the article is important as blood shortages are a problem that healthcare workers may encounter in future pandemics.

There have been relatively few studies revealing a decreased platelet count in chronic kidney disease (CKD). Although this hematological abnormality is not as well documented as renal anemia, platelet functions are altered in the uremic environment and there is an increased risk of bleeding. The aim of this study was to assess the effectiveness of the administration of platelet concentrate in CKD based on how patient prognosis was influenced by platelet transfusion therapy. The study monitored 104 patients with CKD and thrombocytopenia who received platelet transfusion during their hospitalization in the period from 2015 to 2021. The complete blood cell count, serum urea and creatinine, and inflammatory status were tested upon admission. The number of transfused platelet units were considered for each patient. A Kruskal–Wallis H test showed that for one transfused platelet unit, the distribution of the number of platelets (×10³/µL) was the same across the categories of associated diagnoses, which was seen as possible risk factors for thrombocytopenia, including liver cirrhosis and urosepsis. With a single exception, all patients exceeded the critical threshold of 20 × 10³/µL and 14 patients remained under 50 × 10³/µL. Even though our patients exceeded the critical threshold of platelet numbers, in patients with multiple comorbidities, severe, uncontrolled hemorrhages could not be prevented in 4.83% of cases.

Background: Myocardial ischemia remains a major cause of morbidity and mortality worldwide. Although traditional risk factors are well-established, genetic predisposition—particularly involving MTHFR polymorphisms—has garnered increasing attention. This study investigates the association between MTHFR C677T and A1298C polymorphisms and first-episode myocardial ischemia in a Romanian population. Methods: This study included 69 adult patients with first-episode myocardial ischemia and 55 healthy controls, matched by age and sex. Participants were recruited from southeastern Romania between 2023 and 2025. Clinical data—such as blood pressure, body mass index, smoking, and alcohol consumption—were recorded. Genotyping for MTHFR C677T and A1298C polymorphisms was performed using a real-time PCR-based assay (Bosphore^® MTHFR 677-1298 Detection Kit v2), following the manufacturer’s protocol. Results: A significantly higher frequency of homozygous mutant genotypes was observed in patients with myocardial ischemia. The TT genotype of MTHFR C677T was present in 71% of patients, compared to only 7.3% of controls. Similarly, the CC genotype of A1298C was detected in 59.4% of patients, versus 7.3% in controls. These genotypic patterns suggest a strong genetic predisposition among affected individuals. The association between MTHFR polymorphisms and myocardial ischemia was particularly evident in participants over 50 years of age, indicating a possible interaction between genetic vulnerability and age-related cardiovascular risk. Conclusions: Our findings indicate a strong association between MTHFR C677T and A1298C homozygous mutant genotypes and the risk of first-episode myocardial ischemia, particularly in older adults. These results underscore the potential role of genetic screening in early cardiovascular risk stratification.