Evaluating dietary considerations in hidradenitis suppurativa: a critical examination of existing knowledge.

Hidradenitis suppurativa (HS) is a chronic condition that can overwhelm patients, and the effectiveness of supplementary dietary treatments remains uncertain. The primary aim of this review is to explore the connection between diet and HS progression. However, it is imperative to note that the evidence supporting a substantial role of the diet in HS remains weak. Dietary alterations alone should not be considered independent solutions for managing HS. Medical therapy continues to be indispensable for adequate treatment. Research indicates that the Mediterranean lifestyle and diet may provide cost-effective and beneficial adjustments when combined with traditional therapies. Conversely, foods with a high glycemic index and dairy could worsen HS symptoms, conceivably through mechanisms linked to insulin resistance and inflammation. Zinc, known for its antioxidant properties, shows promise as an adjunct therapy. Moreover, evidence suggests a connection between vitamin D deficiency and HS severity, although the findings are inconclusive. Brewer's yeast-free diet, B12 supplementation, intermittent fasting, and reducing the intake of refined sugar and dairy merit further investigation. In conclusion, this review highlights the need for additional research because of the lack of standardized reporting of clinical effects in the studies under scrutiny. A deeper exploration of the pathophysiology focusing on dietary modifications and their potential associations with HS severity is essential. Furthermore, it is crucial to recognize that patients' willingness to experiment with new diets makes them vulnerable to fraudulent interventions, highlighting the importance of evidence-based dietary guidance.

Oral mucosa involvement in pediatric patients with xeroderma pigmentosum: a comprehensive review.

BACKGROUND: Xeroderma pigmentosum (XP) is a rare autosomal recessive disorder presenting with an inability to repair UV-induced DNA damage. This can lead to the development of neoplasms affecting multiple organ systems, with onset often in childhood. Unfortunately, no cure currently exists for XP, and management strategies focus on sun protection and early intervention for malignancies. Although most skin problems in XP patients are UV induced, various oral lesions are also described. However, the literature has not extensively characterized the oral manifestations and their prognostic significance. METHODS: We conducted a comprehensive review to evaluate the prevalence and nature of oral mucosal lesions in pediatric XP patients. RESULTS: Our literature search yielded 130 pediatric XP patients with oral involvement and 210 associated tumoral or non-tumoral lesions. Squamous cell carcinoma was the most common type of oral mucosal tumor reported, with other malignancies including basal cell carcinoma, melanoma, angiosarcoma, fibrosarcoma, and trichilemmal carcinoma. CONCLUSION: Given the potential morbidity and mortality associated with oral mucosal tumors in XP patients, our study aims to raise awareness of these manifestations. Early diagnosis and treatment are crucial for managing these lesions effectively, and routine oral exams should be considered a critical component of dermatological evaluations for XP patients, especially in the pediatric age group.

Behçet's Disease: A Comprehensive Review on the Role of HLA-B*51, Antigen Presentation, and Inflammatory Cascade.

Behçet's disease (BD) is a complex, recurring inflammatory disorder with autoinflammatory and autoimmune components. This comprehensive review aims to explore BD's pathogenesis, focusing on established genetic factors. Studies reveal that HLA-B*51 is the primary genetic risk factor, but non-HLA genes (ERAP1, IL-10, IL23R/IL-12RB2), as well as innate immunity genes (FUT2, MICA, TLRs), also contribute. Genome-wide studies emphasize the significance of ERAP1 and HLA-I epistasis. These variants influence antigen presentation, enzymatic activity, and HLA-I peptidomes, potentially leading to distinct autoimmune responses. We conducted a systematic review of the literature to identify studies exploring the association between HLA-B*51 and BD and further highlighted the roles of innate and adaptive immunity in BD. Dysregulations in Th1/Th2 and Th17/Th1 ratios, heightened clonal cytotoxic (CD8+) T cells, and reduced T regulatory cells characterize BD's complex immune responses. Various immune cell types (neutrophils, γδ T cells, natural killer cells) further contribute by releasing cytokines (IL-17, IL-8, GM-CSF) that enhance neutrophil activation and mediate interactions between innate and adaptive immunity. In summary, this review advances our understanding of BD pathogenesis while acknowledging the research limitations. Further exploration of genetic interactions, immune dysregulation, and immune cell roles is crucial. Future studies may unveil novel diagnostic and therapeutic strategies, offering improved management for this complex disease.

Efficacy of Amikacin and Meropenem on Colistin-Induced Klebsiella pneumoniae Persisters.

Colistin-based antibiotic therapies have been recommended for the treatment of multidrug-resistant Klebsiella pneumoniae infections. During colistin treatment, persister cells that tolerate antibiotics may arise. Here we designed an in vitro study to assess the killing activity of colistin, meropenem, and amikacin on colistin-induced K. pneumoniae persisters in comparison with starvation-induced persisters. Colistin-induced persisters were generated under exposure to 10 × minimum inhibitory concentration dose of colistin, whereas starvation-induced persisters were produced by limitation of nutrients. In colistin-induced persisters, amikacin totally inhibited cell growth in 6 hours, whereas 98% of the cell population was inhibited by meropenem, and total eradication with meropenem was observed after 24 hours. Both antibiotics also inhibited metabolic activity >88%. The lack of killing effect under colistin exposure suggested to us that these cells could protect themselves from further colistin stress. There was no significant permeabilization change in the cellular membrane with all antibiotics. There was no killing effect on starvation-induced persister cells with the exposure to all antibiotics. In 6 hours, the metabolic activity of the persisters with meropenem and colistin increased 99% and 40%, respectively, whereas there was no increase with amikacin. The sustained inhibition with amikacin was an important finding for antipersister effect of amikacin. Amikacin had rapid and sustained antipersister activity on colistin-induced persister cells. During the colistin treatment of K. pneumoniae infection, the addition of amikacin to the regimen seems to be an effective approach to prevent a recurrence.