Febuxostat, initially developed as a xanthine oxidase inhibitor to address hyperuricemia in gout patients, has evolved into a versatile therapeutic agent with multifaceted applications. This review provides a comprehensive overview of febuxostat’s mechanism of action, its effectiveness in gout management, its cardiovascular safety profile, renal and hepatic effects, musculoskeletal applications, safety considerations, and emerging research prospects. Febuxostat’s primary mechanism involves selective inhibition of xanthine oxidase, resulting in reduced uric acid production. Its pharmacokinetics require personalized dosing strategies based on individual characteristics. In gout management, febuxostat offers a compelling alternative, effectively lowering uric acid levels, relieving symptoms, and supporting long-term control, especially for patients intolerant to allopurinol. Recent studies have demonstrated its cardiovascular safety, and it exhibits minimal hepatotoxicity, making it suitable for those with liver comorbidities. Febuxostat’s potential nephroprotective effects and kidney stone prevention properties are noteworthy, particularly for gout patients with renal concerns. Beyond gout, its anti-inflammatory properties hint at applications in musculoskeletal conditions and a broader spectrum of clinical contexts, including metabolic syndrome. Emerging research explores febuxostat’s roles in cardiovascular health, neurological disorders, rheumatoid arthritis, and cancer therapy, driven by its anti-inflammatory and antioxidative properties. Future directions include personalized medicine, combination therapies, mechanistic insights, and ongoing long-term safety monitoring, collectively illuminating the promising landscape of febuxostat’s multifaceted therapeutic potential.

Janus kinase (JAK) inhibitors have heralded a paradigm shift in the management of immune-mediated diseases. While their efficacy is well-established, the safety concerns associated with these agents, particularly regarding thromboembolic events (TE), remain a focus of extensive research and clinical scrutiny. This comprehensive literature review embarks on an exploration of the multifaceted landscape of JAK inhibitors, providing insights into their safety profiles across diverse immune-mediated diseases. The introduction highlights the transformative influence of JAK inhibitors in the treatment of immune-mediated diseases. Historically, the therapeutic arsenal for these conditions included corticosteroids, disease-modifying antirheumatic drugs (DMARDs), and biologics. The advent of JAK inhibitors has revolutionized this landscape, although concerns about their safety persist. This review strives to comprehensively evaluate their safety, amalgamating knowledge from multiple studies and trials. The subsequent sections delve into the safety of specific JAK inhibitors in the context of rheumatoid arthritis, inflammatory bowel diseases, and dermatologic conditions and their associations with venous thromboembolism. The evolving understanding of TE risk, particularly the intricate relationship between these agents and immune-mediated diseases, is meticulously unravelled. The concluding remarks underscore the dynamic nature of TE risk assessment with regard to immune-mediated diseases involving JAK inhibitors. It underscores that risk assessment is multifactorial, influenced not only by the choice of JAK inhibitor but also by the nuances of the underlying immune-mediated disease and the unique patient characteristics. This review offers a holistic perspective on TE risks associated with JAK inhibitors and contributes to the ongoing dialogue regarding their safety in the realm of immune-mediated diseases.

Aim: To establish the correlation between intraocular pressure (IOP) and thickness of extraocular muscles (EOM), the severity and activity of thyroid-associated orbitopathy (TAO). Materials and methods: 50 patients with TAO were included in the study. They all underwent a thorough ophthalmic examination, Goldmann tonometry (mm Hg) and computer tomography of the orbits, the muscle thickness sum (MTS) of each eye being measured in millimeters. According to the activity of TAO, the patients were divided into two groups – with and without activity, and according to the severity of the disease – into 6 groups: Group 1 (‘O’) had only subjective symptoms, group 2 (‘S’) had soft tissue symptoms, group 3 (‘P’) – proptosis, group 4 (‘E’) – ocular motility disorders, group 5 (‘C’) – corneal damage, and group 6 (‘Si’) – visual impairment; Results: TAO activity was registered in 21 patients (42 eyes, 42%) with MTS 23.39±3.81 and IOP 18.43±4.16. Twenty-nine patients (58 eyes, 58%) with MTS 19±3.21 and IOP 15.98±4.59 showed no TAO activity. The IOP within the groups, in terms of severity, was as follows: group 1 – 19.92+4.05; group 2 – 14.5±2.55; group 3 – 18.04±4.51; group 4 – 18.2±5.05; group 5 – 20.5±4.5; group 6 – 21.5±4.95. A correlation between the IOP and MTS was found. Conclusions: The IOP in patients with TAO depends on the thickness of the EOM, as well as on the activity and severity of the disease.

Seronegative sicca syndrome encompasses patients who present with xerostomia and/or keratoconjunctivitis sicca but lack anti-SSA/SSB antibodies and do not fulfill current classification criteria for primary Sjögren’s syndrome (pSS). Despite symptom overlap with pSS, these individuals remain diagnostically and therapeutically unclassified. This review studies the clinical, immunological, and pathological spectrum of seronegative sicca, highlighting its heterogeneity and the limitations of antibody-centric diagnostic frameworks. Histopathologic findings in some seronegative patients—including focal lymphocytic sialadenitis—mirror those seen in pSS, suggesting underlying immune-mediated glandular damage. In others, nonspecific or normal biopsy findings suggest non-immune mechanisms. New evidence of immune activity, such as elevated cytokines (BAFF, IFN-α), and novel autoantibodies (SP-1, CA-VI), further supports the concept of subclinical autoimmunity in a subset of these patients. Clinically, they often face significant burden, including dryness, fatigue, and pain, yet remain excluded from most research cohorts, therapeutic trials, and clinical guidelines. Their management is often individualized, relying on symptomatic therapies rather than immunomodulatory agents. The lack of validated diagnostic criteria and prognostic markers compounds the uncertainty surrounding disease evolution, as some patients may later seroconvert or develop systemic features. To address these gaps, a paradigm shift is needed—one that embraces the spectrum of sicca syndromes, incorporates advanced immunophenotyping, and allows inclusion of seronegative patients in research and care algorithms.

Acute retinal necrosis (ARN) is a devastating viral infection commonly associated with varicella zoster virus (VZV) and herpes simplex virus types 1 and 2 (HSV-1, HSV-2). Typically, ARN affects individuals without immune status disorders between the ages of 50-70. In two-thirds of the cases, one-eye involvement is observed and the inflammation can be presented as panuveitis. The most characteristic clinical manifestations are vitreitis, occlusion of the retinal arterioles, and peripheral necrotizing retinitis. Retinitis presents with the appearance of deep, multifocal, yellowish-white foci, typically localized in the peripheral retina. Systemic antivirals are the first treatment of choice for ARN. The goal of the therapy is to stop the viral replication and disease progression in the affected eye, as well as to prevent involvement of the healthy eye. The other eye can be attacked in an interval of 5 days to 30 years. The visual prognosis after illness is poor. Early diagnosis and timely initiation of treatment play an important role in maintaining visual acuity and preventing the other eye from being affected.

We report a case of subconjunctival invasion of Dirofilaria repens in a woman from Southern Bulgaria. Dirofilariasis is an extremely rare parasitic disease for Bulgaria. It occurs as an endemic parasitosis in the Mediterranean countries. It is caused by helminths of the genus Dirofilaria, which are parasites in dogs, cats, foxes, wolves – the final hosts of the parasite. It may very rarely occur in humans, the infection triggered by a bite of bloodsucking mosquitoes, which are the intermediate hosts of Dirofilaria. The clinical forms of dirofilariasis in humans are subcutaneous, pulmonary and ocular, the brain, testes and mammary glands being rarely affected. A 51-year-old patient presented with migrating edema in the area of the left temple and upper eyelid, with redness and swelling of the conjunctiva, as well as a subjective sense of movement under the eyelid of the left eye, lasting for about ten days. The subconjunctival localization of a moving 9.5-cm nematode was established, it was surgically removed and histologically studied. This case of ocular subconjunctival dirofilariasis is of clinical interest due to the rarely observed pathology.