Chanika Assavarittirong

Background/Objectives: VEXAS (Vacuoles, E1-Enzyme, X-linked, Autoinflammatory, and Somatic) syndrome is a recently described adult-onset autoinflammatory disorder. It is characterized by somatic mutations in the UBA1 gene, systemic inflammation, macrocytic anemia, cytopenias, and bone marrow vacuolization and frequently overlaps with Sweet’s syndrome, relapsing polychondritis, and myelodysplastic syndrome (MDS). Because treatment options are evolving, we reviewed the current and latest evidence of clinical features and therapeutic methods. Methods: A comprehensive literature review was conducted using PubMed and MEDLINE for studies published between 1 January 2020 and 1 July 2025. Search terms included “VEXAS” and “treatment.” Eligible publications comprised clinical trials, multicenter and observational studies, and case reports containing therapeutic data. Findings were analyzed narratively with emphasis on treatment response, steroid-sparing effects, survival outcomes, and molecular responses. Results: Glucocorticoids remain the first-line therapy for acute management; however, this comes with near-universal steroid dependence. DMARDs and TNF-α inhibitors showed limited benefits. IL-6 inhibitors and JAK inhibitors showed improvement in overall response, with JAK inhibitors demonstrating a superior effect. Ruxolitinib showed a higher complete response rate and transfusion independence compared to other JAK inhibitors. Hypomethylating agents, particularly azacitidine, improved hematologic responses in patients with co-existing MDS and reduced UBA1 variant allele burden. Allogeneic hematopoietic stem cell transplantation may be the only current curative method, though with notable transplant-related mortality. Conclusions: JAK inhibitors and hypomethylating agents offer promising disease-modifying potential, while transplant may provide curative intent in selected patients. Ongoing clinical trials are taking place to dictate the treatment direction of VEXAS syndrome.

Fibromyalgia (FM) is characterized by chronic widespread musculoskeletal pain associated with sleep problems, fatigue, depression, and anxiety. The persistence of pain, impairment of cognitive function, and negative impact on the psychological state have caused a detrimental effect on the patients’ quality of life. However, to date, the treatment and mechanisms of this disease are yet to be established. Oxidative stress might play a critical role in FM pathophysiology. Increased levels of prooxidative factors such as nitric oxide, lipid peroxidation, and mitophagy can cause pain sensitization in fibromyalgia. Numerous studies have supported the hypothesis of beneficial antioxidative effects in FM. Due to the lack of effective therapy for fibromyalgia, many treatments are sought to reduce pain and fatigue and improve patients’ quality of life. This manuscript discusses the impact of various antioxidative procedures that can diminish fibromyalgia symptoms, such as hyperbaric oxygen therapy, modification of dietary habits, and physical activity.