The increasing global prevalence of obesity and type 2 diabetes (T2D) has prompted significant advancements in pharmacological treatments, with glucagon-like peptide-1 (GLP-1) receptor agonists and dual agonists representing key innovations. Semaglutide, a GLP-1 receptor agonist, and tirzepatide, a novel dual agonist targeting both GLP-1 and glucose-dependent insulinotropic peptide (GIP) receptors, have shown remarkable efficacy in improving glycemic control and promoting weight loss. This review synthesizes the latest clinical evidence on the efficacy and safety of semaglutide and tirzepatide in the management of obesity and T2D, highlighting the findings from recent pivotal trials. In patients with T2D, semaglutide has consistently demonstrated superior glycemic control and weight loss compared to traditional therapies, as evidenced by the SUSTAIN trials [1]. Similarly, tirzepatide has emerged as a more efficacious option, with the SURPASS trials demonstrating greater reductions in HbA1c and more substantial weight loss compared to semaglutide. This positions tirzepatide as a potential first-line therapy for T2D.[2]. Both therapies have shown a favorable safety profile, with gastrointestinal side effects being the most common, and cardiovascular benefits observed in both drug classes. Given their dual mechanism of action, tirzepatide has shown unique potential in addressing both glycemic control and obesity, with emerging evidence supporting its use in non-diabetic patients with obesity [3].This review highlights the potential of these agents to revolutionise the management of obesity and T2D, with tirzepatide emerging as a promising next-generation treatment for metabolic diseases.

Netherton syndrome (NS) is a rare, autosomal recessive genodermatosis resulting from mutations in the SPINK5 gene, which encodes the LEKTI (Lympho-Epithelial Kazal-type-related inhibitor) protein. This deficiency leads to dysregulated epidermal protease activity, primarily of kallikrein-related peptidases (KLKs), causing severe skin barrier defects, abnormal desquamation, and a complex immune dysregulation involving the T_H2 and T_H17 pathways. Clinically, NS is characterised by a triad of ichthyosiform erythroderma (often evolving from congenital ichthyosiform erythroderma to ichthyosis linearis circumflexa); pathognomonic hair shaft abnormalities, such as trichorrhexis invaginata ("bamboo hair"); and atopic manifestations with elevated serum IgE. Diagnosis can be challenging due to symptomatic overlap with other inflammatory dermatoses, congenital ichthyosis, and primary immunodeficiencies. Confirmation relies on clinical findings, trichoscopic hair examination, and SPINK5 genetic testing. Management is currently largely supportive, focusing on emollients, antiseptics, and cautious use of topical anti-inflammatory agents. While traditional systemic treatments have limitations, emerging targeted therapies, including biologics and gene therapy, show promise, but require further investigation through robust clinical trials to establish their efficacy and safety. This review highlights the diagnostic intricacies and evolving therapeutic landscape of this complex disorder.

Nijmegen breakage syndrome (NBS) is a rare autosomal recessive defect of immunity, characterised by chromosomal instability and radiation sensitivity with a high predisposition to malignancy. The clinical manifestations of this condition include microcephaly, combined immunodeficiency, growth retardation and a range of additional abnormalities, including facial, skeletal and skin anomalies (such as café au lait spots and vitiligo). It is estimated that 40% of patients will develop cancer before reaching the age of 21 years. [1-2] The aetiology of this syndrome can be attributed to a mutation in the NBS1 gene, which is localised on chromosome 8q21 and is responsible for the production of the protein nibrin. [3] The most common mutation responsible for NBS (c.657_661del5) is consistent with a founder effect, with the majority of registered patients originating from Central and Eastern Europe and the largest cohort diagnosed in Poland. [4] This article provides an overview of Nijmegen breakage syndrome (NBS), including epidemiology, symptoms, diagnostic pathway and patient management, as well as treatment options. The objective of this study is to enhance awareness of this condition in order facilitate an early diagnosis and screening for malignancy in patients.

Background/Objectives: Psoriasis is a chronic immune-mediated disease frequently accompanied by systemic inflammation and metabolic disturbances. Nutrition plays a crucial role in modulating inflammatory pathways, yet the impact of baseline dietary status on systemic therapy outcomes remains underexplored. Methods: A total of 37 patients (20 men, 17 women; mean age 47.8 ± 4.87 years) scheduled for cyclosporine A (CsA) therapy underwent dietary assessment using 24 h recall and food frequency questionnaires. Intake was compared with dietary reference values. Psoriasis severity was measured by using the Psoriasis Area and Severity Index (PASI) and Body Surface Area (BSA) at baseline, day 42, and day 84. Mixed-effects regression models adjusted for body mass index (BMI), age, and sex assessed associations between nutrient adequacy and clinical outcomes. Results: Participants exhibited frequent dietary imbalances, including low polyunsaturated fatty acids, fiber, vitamin D, folate, and minerals such as magnesium and zinc, alongside excess saturated fat and sodium. Adequate intake of fiber, eicosapentaenoic acid (EPA)+ docosahexaenoic acid (DHA), and vitamins A and D, folate, magnesium, and zinc was independently associated with a lower baseline PASI/BSA and faster improvement during CsA therapy (p < 0.05). Higher BMI, older age, and male sex predicted poorer outcomes. Conclusions: Pre-treatment nutritional inadequacies are common in psoriasis and independently predict diminished therapeutic response to CsA. Early nutritional optimization may enhance treatment efficacy and support long-term disease control. Integrating dietary assessment in psoriasis management represents a feasible, impactful adjunct to pharmacotherapy.

Background: Since antiquity, honey has been recognised for its healing and antibacterial properties. Recently, Manuka honey (MH) has been identified as possessing antioxidant, anti-inflammatory, antimutagenic, and anticarcinogenic effects. Objective: This review examines the potential benefits of manuka honey, its bioactive components, and their effects on cancerogenesis, cancer growth, and development. Methods: The PubMed and Google Scholar databases were searched, and 46 studies were identified as most relevant to the research objective. Results: The accompanying papers posit that MH may impede carcinogenesis by regulating various molecular pathways and cancer cell progression. A substantial body of scientific evidence indicates that a range of honey types, including MH, can facilitate the release of reactive oxygen species and cytokines (predominantly IL-1β, IL-6, and TNF-α) by innate immune system cells. Furthermore, studies have demonstrated that honey can stimulate T lymphocytes and macrophages' proliferation and functions while also inducing apoptosis and cell cycle arrest in cancer cells. Conclusion: The body of evidence attesting to the anticarcinogenic properties of MH continues to grow. Several studies have demonstrated the significant role of manuka honey and its properties in promoting innate and adaptive immunity, which is essential for eliminating cancer cells. Nevertheless, further research is required to provide comprehensive data regarding the active constituents of Manuka honey and their potential efficacy in cancer therapy.

Buerger's disease, also known as thromboangiitis obliterans (TAO), is a rare but serious condition that primarily affects the blood vessels in the limbs. This inflammatory vascular disease is characterised by the formation of blood clots in the small and medium-sized arteries and veins, which results in a reduction in blood flow. Patients typically present with symptoms such as pain in the extremities, ulcers, and in severe cases, gangrene. The disease is most commonly observed in young male smokers, which highlights the strong correlation between tobacco use and the onset of this condition. A comprehensive understanding of Buerger's disease is essential for prompt diagnosis and effective management. This review will examine the historical context, symptoms, diagnostic criteria, therapeutic approaches, and future directions in research and treatment.