The most common inherited condition that results in death, particularly in those of Caucasian heritage, is cystic fibrosis (CF). Of all the young adults diagnosed with cystic fibrosis, 20% will develop hyperglycemia as a complication, later classified as a disease associated with cystic fibrosis. Impaired insulin secretion and glucose intolerance represent the primary mechanisms associated with diabetes (type 1 or type 2) and cystic fibrosis. Oxidative stress represents the imbalance between oxygen-reactive species and antioxidant defense mechanisms. This pathogenic mechanism is vital in triggering other chronic diseases, including cystic fibrosis-related diabetes. It is essential to understand oxidative stress and the significant impact it has on CFRD. This way, therapies can be individually adjusted and tailored to each patient’s needs. This review aims to understand the connection between CFRD and oxidative stress. As a subsidiary element, we analyzed the effects of glycemic balance on complications and their evolution over time, providing insights into their potential benefits in mitigating oxidative stress-associated complications.

Background and Objectives: The role of adenosine deaminase (ADA) in pulmonary tuberculosis (PTB) remains insufficiently defined in advanced forms of disease. Likewise, the systemic immune inflammatory index (SII) has not been validated in severe PTB. This 6-year prospective observational study aims to evaluate biomarker signatures of serum ADA and SII. Materials and Methods: According to the PTB case definition, 232 adult patients were divided into group 1, with a positive bacteriologic exam (n = 168), and group 2, without bacteriological confirmation (n = 64). ADA serum levels were compared by age, gender, nutritional status, morphologic and bacteriological pattern of PTB lesions, survival status, along with serum levels of other inflammatory biomarkers. All patients with comorbidities, interfering with the level of ADA, were excluded to avoid bias. Results: A total cohort of 208 PTB adults, aged 54.37 ± 14.365 years, included 156 males. The overall mortality was 11.53%. Death occurred after a mean interval of 1.63 ± 3.228 months after PTB diagnosis. ADA serum mean levels were 32.94 ± 9.146 IU/L, significantly higher in G1 (p = 0.002), in patients with delayed diagnosis of PTB (p = 0.000), with lung cavitation (p = 0.003), and death as a poor outcome (p ˂ 0.02). SII had a mean value of 1752.226 ± 2704.150, significantly increased in bacteriologically confirmed PTB cases (p = 0.018), delayed diagnosis (p = 0.002), cavitary advanced pulmonary tuberculosis (APT) (p = 0.002), and deceased (p = 0.003). Both an ADA cut-off elevated risk value of over 30 IU/L and SII of over 902 were fulfilled by 73 patients, with 2.10 higher risk of advanced PTB (p = 0.006) and 4.49 higher risk of mortality (p = 0.000). Conclusions: Serum ADA and SII are recommended as predictors of advanced and severe pulmonary TB. These findings indicate that ADA and SII, when elevated together, delineate a high-risk PTB phenotype with greater disease severity and early mortality. The combination offers a pragmatic, biomarker-based approach to risk stratification in PTB.

Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease in humans. It is a multisystemic disorder characterized by progressive cystic dilatation of both kidneys, with variable extrarenal manifestations in the gastrointestinal tract (hepatic cysts), cardiovascular system, reproductive organs and brain. An important issue of patients with hepatorenal cystic disease is the fact that complications can arise due to the growing of the cysts: local kidney complications (intracystic infection, intracystic hemorrhage) and local liver complications (portal hypertension as a result of portal vein compression by cysts, bile duct compression, ruptures and bleedings of the cysts, obstruction of the liver veins). Objective: The main purpose of our case presentation is to emphasize the fact that ADPKD can be an aggressive disease with multiple complications, which requires an early diagnosis in order to properly avoid possible complications. Material and Method: We present the case of a 61 years old male, known with polycystic hepatorenal disease, chronic kidney disease (CKD) in chronic hemodialysis since 2010, renal hypertension, hypertensive cardiomyopathy, renal anemia and stage 1 chronic lymphatic leukemia. The patient was diagnosed with hepatorenal polycystic disease 20 years ago and 9 years ago he started undergoing renal replacement therapy by hemodialysis. Three months ago, the patient presented a suddenly installed ascitic syndrome for which an MRI was performed. The imagistic investigation revealed multiple kidney and liver cysts, with secondary compression of the portal vein and a tumoral mass that may suggest an adenocarcinoma. Results: The investigations performed confirm the diagnosis of portal hypertension secondary to compression due to cystic formations. Conclusions: Hepatorenal polycystic disease has numerous clinical variations, so it needs to be followed in a multidisciplinary way with rapid therapeutic measures to prevent complications. Further investigations are needed when dealing with suspicious cystic formations with an uncertain substrate.