The investigation of the relationship between hyperuricemia and hypertension is a captivating field in hypertension research. The final product of purine metabolism is uric acid (UA), and the elevation of serum UA (SUA) levels directly contributes to the development of hypertension. Numerous studies have substantiated that hyperuricemia is a significant risk factor for hypertension. Furthermore, initial clinical trials have demonstrated that therapeutic interventions aimed at reducing SUA levels lower blood pressure (BP) in individuals with hypertension attributed to hyperuricemia. Recent research has demonstrated that hyperuricemia can facilitate the onset of hypertension via multiple mechanisms, including oxidative stress, inflammation, diminished nitric oxide (NO) synthesis, activation of reactive oxygen species (ROS), insulin resistance, vascular smooth muscle proliferation, and renal impairment. Given the interconnectedness between hyperuricemia and hypertension, it is advantageous to identify potential therapeutic approaches for timely intervention in order to impede the advancement of hypertension in individuals with hyperuricemia. This article reviews the research progress on the pathogenesis of hyperuricemia-induced hypertension.

A prominent endocrine disorder linked to unhealthy lifestyle behaviors and increased visceral adiposity is Male Obesity Secondary Hypogonadism (MOSH). The pathogenesis of MOSH remains under investigation. However, recent evidence supports a direct role of leptin in affecting Leydig cells, reducing testosterone production, and increasing appetite. Conversely, testosterone deficiency is associated with comorbidities like hypertension, diabetes, and nonalcoholic fatty liver disease. A recently published study entitled “Relationship between sex hormones, markers of adiposity and inflammation in male patients with severe obesity undergoing bariatric surgery” describes evidence supportive of an inverse association between testosterone and serum leptin as well as levels of c-reactive protein (CRP) and IL-6, as well as a correlation between body mass index and CRP. The same study also provides novel insight retrieved from their in vitro findings, which reveal that testosterone exposure influences the expression of genes associated with adiposity, like fatty acid binding protein 4, peroxisome proliferation-activated receptor γ (PPARγ), leptin, and adiponectin, as well as von Willebrand factor, in human-derived adipocytes. Overall, the latest evidence highlights the importance of early identification of hypogonadism in obese males and the potential benefits of testosterone supplementation in alleviating complications associated with obesity, particularly chronic inflammation. These observations underscore the need for a holistic approach to managing severe obesity, addressing hormonal and inflammatory factors to reduce its overall burden on health.

The worldwide growing prevalence of diabetes and cancer led to an increase in subjects affected by both these diseases that share several of the involved risk factors and have a complex, multifactorial etiopathogenesis. Cancer therapies could have harmful effects on several organs, particularly in subjects also affected by diabetes and its related comorbidities. Moreover, cancer diagnosis often monopolizes the attention of both patients and caregivers, thus reducing the attention to pre-existent diseases. Retinopathy is one of the most frequent microvascular complications of diabetes, accounting for about 5% of legal blindness worldwide. The retinal neurovascular unit is dysfunctional in diabetes and could represent a frail site when cancer therapies are administered. Nevertheless, the short- and long-term effects of the different anticancer molecules on retinal tissue, especially in diabetic subjects, are poorly known, and no specific recommendations on their prevention and management are available. In this review, we summarised the current data on this topic, focusing on the different cancer class drugs involved in retinal damage: anti-oestrogen, classical cytolytic chemotherapy (alkylating agents, taxanes, topoisomerase inhibitors, and antimetabolites), mitogen-activated protein kinase, tyrosine-kinase, and vascular endothelial growth factor inhibitors are the cancer drugs associated with retinal damage and visual disturbance. However, further studies are necessary to improve knowledge on the molecular and clinical relation between cancer therapies and retinopathy, in order to provide clinicians with evidence-based protocols to optimise the management of these conditions and minimise vision loss occurrence, impaired quality of life, and public health expense.

Roux-en-Y gastric bypass (RYGB)-associated marginal ulceration (MU) poses significant challenges for both patients and clinicians. Persistent symptoms such as epigastric pain, nausea, and reduced oral intake complicate the clinical landscape. MU can lead to severe complications, including anastomotic strictures, bleeding, and perforations. The etiology of MU is intricate, likely stemming from a combination of technical and patient-related factors. Technical considerations involve ischemia, tension on the anastomosis causing tissue ischemia, anastomotic technique, gastric pouch size, foreign bodies, and gastrogastric fistulas. Patient factors encompass smoking, nonsteroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori (H. pylori), and uncontrolled medical comorbidities. Diagnosis primarily relies on upper endoscopy. Initial treatment typically involves proton pump inhibitors (PPI) and sucralfate. Should these measures prove insufficient, the addition of misoprostol and the implementation of endoscopic techniques, such as oversewing or stenting across the ulcer, may be considered to facilitate healing. Ultimately, if medical and endoscopic interventions fail, surgical options become imperative. These include transthoracic truncal vagotomy and revisional procedures such as resection of the ulcer with redo gastrojejunal anastomosis, resection of the ulcer and pouch with esophagojejunal anastomosis, or resection and reversal to normal anatomy. Surgical interventions demand expertise and should be conducted at qualified, high-volume centers. To support clinicians in comprehending the nuances of MU, we conducted a literature review, presenting a summary of our findings. Additionally, we propose an algorithm delineating the escalation of treatments for MU, ranging from medical to endoscopic to surgical therapies. This concise review aims to assist clinicians in both the prevention and treatment of marginal ulceration.

A recent study by Crudele et al. reported on the association between surrogate indices of liver fibrosis and risk of gynecological cancers among dysmetabolic women. To put this study in context, notions regarding sex dimorphism in nonalcoholic fatty liver disease (NAFLD) are discussed. Additionally, meta-analytic reviews regarding the risk of extrahepatic cancers are reviewed. Next, I discuss the relationship of metabolic dysfunction-associated fatty liver disease (MAFLD) with extrahepatic cancers, notably including the breast and cancers of the female reproductive systems in humans. The pathomechanisms potentially accounting for this association include genetics, deregulated sex hormones, chronic subclinical inflammatory state, dysmetabolic milieu, oxidative stress, gut dysbiosis, environmental pollution, and altered immune surveillance.

The era of precision medicine necessitates standardization in reporting outcomes, in order to provide a common ground of communication among specialists and yield objective measurements at the same time. Although metabolic bariatric surgery spearheads innovation and standardization with regard to technique, this is not the case when measuring outcomes, particularly regarding weight recurrence. The multitude of definitions of weight regain and insufficient weight loss stems not only from a lack of consensus but also from the inherent deficiencies of weight- and BMI-based formulas to incorporate a global and comprehensive assessment for obesity. In this Perspective, we investigate current knowledge as well as potential amendments that will ameliorate our ability to assess weight recurrence and improve the services that we offer to people living with obesity.