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Heart failure (HF), which has a high morbidity and mortality rate, is nevertheless a common and crippling ailment, especially in older populations. The complicated pathophysiology of heart failure (HF), which includes oxidative stress, endothelial dysfunction, fibrosis, and inflammation, is frequently not sufficiently treated despite advances in medication. Inhibitors of the sodium-glucose co-transporter 2 (SGLT2) have become a key treatment for HF in patients with varying left ventricular ejection fractions (LVEF). SGLT2 inhibitors have been shown in recent clinical trials to considerably lower hospitalization rates for heart failure, cardiovascular mortality, and all-cause mortality. The mechanisms of SGLT2 inhibitors, such as better ventricular loading, increased heart metabolic efficiency, and decreased inflammation and necrosis, are covered in this review. Additionally, we provide an overview of four important clinical trials--DAPA-HF, EMPEROR-Reduced, EMPEROR-Preserved, and DELIVER--highlighting their effectiveness in lowering unfavorable cardiovascular outcomes for patients with heart failure who have preserved (HFpEF), slightly reduced (HFmrEF), or reduced (HFrEF). The results validate the need of SGLT2 inhibitors in allinclusive HF treatment plans by highlighting their adaptability and safety in a range of clinical contexts. [ABSTRACT FROM AUTHOR]

Introduction and purpose: Lactose, the primary carbohydrate in milk, requires the enzyme lactase for digestion. Deficiency in lactase activity leads to lactose intolerance, causing gastrointestinal symptoms. Understanding the genetic and environmental factors influencing lactase expression and activity is crucial. Moreover, accurate diagnostic methods and effective treatments are needed to manage lactose intolerance. This review aims to explore the current knowledge on lactase deficiency, lactose intolerance, diagnostic methods, and treatment options. State of knowledge: Lactase deficiency encompasses congenital, primary, and secondary forms, each with distinct etiologies. Although often used interchangeably, lactase deficiency and lactose intolerance differ. However, the association between lactase deficiency and lactose intolerance is complex, influenced by various factors including dietary habits, gut microbiota, and gastrointestinal motility. Diagnostic methods are limited, and treatment strategies primarily involve dietary modifications, lactase supplementation, and probiotics. Conclusion: Lactose intolerance presents significant clinical challenges, often underrecognized and misdiagnosed. Despite diagnostic advancements further research is needed to refine diagnostic accuracy. Treatment focuses on dietary adjustments, enzyme supplementation, and probiotics. Balancing symptom relief with nutritional adequacy is essential. Future studies should explore the role of gut microbiome modulation in lactose intolerance management through clinical trials. [ABSTRACT FROM AUTHOR]