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Background. To assess the influence of the co-presence of psoriasis (PsO) on the clinical and therapeutic pattern of a single-centre cohort of patients with spondyloarthritis (SpA) associated with chronic inflammatory bowel disease (IBD).   Methods. This study represents a preliminary phase of an ancillary analysis of the DIAMANTE project (Early diagnosis of spondyloarthritis in a cohort of patients with chronic inflammatory bowel disease), developed with the overall objective of determining the prevalence, predictors and outcomes of SpA in a cohort of subjects with IBD, in the context of close and structured collaboration between gastroenterologists and rheumatologists. Within the DIAMANTE cohort, two subgroups of patients were identified for the study: patients with SpA and a concomitant personal diagnosis of PsO (Group 1: IBD+SpA+PsO) and patients with a diagnosis of SpA alone (Group 0: IBD+SpA). For both groups, the following demographic, clinical and therapeutic data were recorded and compared: gender, association between IBD patterns, peripheral joint involvement, axial involvement, history of dactylitis, need for biological therapy, multi-resistance to targeted drugs (discontinuation due to ineffectiveness of at least two small molecule biological drugs). A significance threshold of p<0.05 was used with Fisher's and X² tests.   Results. Data from 665 consecutive patients with IBD recruited from November 2023 to April 2025 were analysed. Within this cohort, 95 (14%) had a concomitant diagnosis of SpA; among these, 21 (22%) also had a diagnosis of PsO (IBD+SpA+PsO group), while 74 (78%) had only SpA associated with IBD (IBD+SpA group). Comparative analysis of the two groups revealed significant, albeit only trending towards statistical significance, differences in terms of female prevalence (71% vs 54%, p=0.15), frequency of peripheral involvement (62% vs 49%, p=0.28) and use of biologic drugs (91% vs 77%; p=0.17). Most notably, a significantly higher frequency of multidrug resistance to biological drug treatment was observed in patients with concomitant PsA compared to patients with IBD and SpA alone (29% vs 11% p=0.04). No significant differences were observed in terms of destruction of the different IBD conditions (ulcerative colitis, Crohn's disease, undifferentiated forms) between the two study groups.   Conclusions. In patients with SpA associated with IBD, the simultaneous association with PsO, another extra-articular domain typical of the spectrum of spondyloarthropathies, was also frequently demonstrated. The results of this exploratory analysis suggest that it would be useful to investigate, in larger prospective case series, the impact that this dual combination of extra-articular manifestations may have on disease characteristics and, in particular, on treatment management.

Background. Lichen sclerosus (LS) is a chronic, immune-mediated inflammatory condition that predominantly affects mucocutaneous areas, particularly the anogenital region. Although the etiopathogenesis of LS remains poorly understood, autoimmune, genetic, infectious, and traumatic mechanisms have been hypothesized.¹ Large-scale epidemiological studies are limited, but the estimated prevalence in the general population ranges from 0.05% to 0.3%. ²,³ In Italy, LS is classified among rare diseases (prevalence 5/10,000; exemption code RL0060). LS has been associated with several dermatological and immune-mediated conditions, including Hashimoto’s thyroiditis, psoriasis, vitiligo, alopecia areata, ulcerative colitis, systemic lupus erythematosus (SLE), and systemic sclerosis. However, the relationship between LS and systemic autoimmune diseases warrants further investigation. Although some case reports have described overlap between LS and Sjögren’s disease (SjD), this potential association remains poorly explored.   Outcome: To further investigate the possible overlap between LS and SjD.   Materials and Methods: Medical records of patients with SjD and non-Sjögren sicca syndrome consecutively evaluated at the Sjögren Clinic of our Rheumatology Unit over the past 12 months were reviewed. During each visit, patients were specifically asked whether they had ever received a diagnosis of LS. Those reporting a prior diagnosis of LS were subsequently re-evaluated to confirm the diagnosis.   Results. A total of 378 patients with SjD (13 males, 365 females; mean age 55 years, range 24–79; mean disease duration since diagnosis 3.7 years) and 99 subjects with non-Sjögren sicca (6 males, 93 females; mean age 56.3 years, range 34–72; mean symptom duration 3.12 years) were included. Among patients with SD, 7/378 (1.8%) female patients had a confirmed diagnosis of LS (mean age 46.8 years, range 37–55). None of the subjects with non-Sjögren sicca had LS.   Conclusions. Although no statistically significant differences were observed between SjD and non-Sjögren sicca, the prevalence of LS among patients with SjD was higher than that reported in the general population. This observation supports the hypothesis of shared etiopathogenic mechanisms, likely immune-mediated, as further suggested by the reported occurrence of SjD in approximately 1.5% of patients with LS. This comorbidity should always be investigated in patients with SjD. References Singh N, Ghatage P. Etiology, clinical features, and diagnosis of vulvar lichen sclerosus: a scoping review. Obstet Gynecol Int. 2020; 2020:7480754. Murphy R. Lichen sclerosus. Dermatol Clin. 2010;28(4):707-15.  De Luca DA, Papara C, Vorobyev A, Staiger H, Bieber K, Thaçi D, Ludwig RJ. Lichen sclerosus: The 2023 update. Front Med (Lausanne). 2023;10:1106318. Guttentag A et al. Australas J Dermatol. 2025;66:135-141. Shiboski CH, Shiboski SC, Seror R, Criswell LA, Labetoulle M, Lietman TM, et al. The 2016 American College of Rheumatology and European League Against Rheumatism classification criteria for primary Sjögren's syndrome were developed through a consensus and data-driven methodology that involved three international patient cohorts. Arthritis Rheumatol. 2017;69(1):35-45.

Background. Primary Sjögren’s syndrome (pSS) is a chronic autoimmune inflammatory disease that typically develops in the absence of another systemic autoimmune disorder. Interstitial lung disease (ILD) represents the most frequent pulmonary manifestation of pSS and is associated with impaired lung function and potentially severe complications. Stratifying patients according to their risk of developing pSS-associated ILD (pSS-ILD) and identifying those at increased risk at an early stage may enable timely therapeutic intervention. Therefore, transcriptomic studies aimed at identifying differentially expressed genes across the three study groups may prove useful for the characterization of predictive disease factors.   Materials and Methods. Transcriptomic analyses of inflammatory and immune-related gene panels were performed on patients with ILD, pSS, and pSS-ILD using the NanoString nCounter platform. RNA was extracted from FFPE-embedded minor salivary gland samples obtained from eight patients in each group. Only RNA samples with the highest DV200 values, as assessed by Bioanalyzer, were used for further analysis. Data were processed using the nSolver software, and genes showing significant up- or down-regulation with p < 0.05 were considered differentially expressed.   Results. Gene expression analysis in patients with ILD revealed significant differences in immune and inflammatory responses compared to patients with isolated pSS. The up-regulation of TSLP, IL1RN, MAP2K6, JUN, IL1RL1, TNFRSF14, CXCL10, and IL7, along with the down-regulation of PIGR and ITGA6, signifies modified immunologic activity that may aid in clarifying the pathophysiology associated with ILD. Moreover, substantial gene expression variations were observed between pSS-ILD and isolated ILD. Elevated expression of HIF1A, NFATC3, FLT1, APP, and CD14, alongside diminished expression of transcription factors like MYC and FOS, indicates significant modifications in intracellular signaling pathways that may be involved in the pathogenesis of ILD. In addition, upregulation of HDAC4, C4A, and C7 in pSS-ILD patients compared to those with isolated pSS highlights further dysregulation of immune and inflammatory processes, suggesting the emergence of a profibrotic microenvironment capable of exacerbating lung injury. Conversely, down-regulation of CCL21 implies possible disturbances in lymphocyte trafficking and immune surveillance, further complicating disease pathogenesis.   Conclusions. It is noteworthy that not all patients with pSS develop ILD, suggesting the possible contribution of genetic or environmental factors to disease manifestation and progression. In summary, the transcriptomic landscape distinguishing ILD, pSS, and their comorbidity provides crucial insights into disease pathogenesis. The differential expression of genes—particularly HDAC4, C4A, C7, and CCL21—offers valuable clues for future research focused on targeted therapies and precision medicine approaches for these complex clinical phenotypes.

Background. Investigating the inflammatory response of synoviocytes in patients with psoriatic arthritis (PsA) is crucial due to their central role in disease pathogenesis. Recent studies have reported upregulation of interleukin-6 (IL-6) and activation of the transcription factor NF-κB as key mechanisms in PsA development. Although the role of dendritic-like CD14 synoviocytes remains unclear, these cells have been shown to contribute to the initiation and maintenance of inflammation. Furthermore, impaired dendritic cell function has been associated with dysregulated inflammatory responses that may promote chronic inflammation. Therefore, this study aimed to explore the molecular responses of non-dendritic CD14 synoviocytes under basal conditions and after stimulation with inflammatory mediators, and to characterize the basal molecular profile of CD14 synoviocytes. Materials and Methods. Fibroblast-like synoviocytes (FLS) were isolated from synovial membranes of healthy donors (h) and PsA patients. CD14 FLS were selected using immunomagnetic beads and cultured under basal conditions (wt), whereas CD14 FLS were stimulated for 24 hours with LPS and IFNγ. Cells were analyzed at passage 6 (P6) by real-time PCR. Healthy donor FLS were also analyzed by flow cytometry (FACS) at passages 2 (P2) and 6 (P6) for CD90 and CD14 expression. Results. Under basal conditions, healthy CD14 FLS (h-FLS CD14 ) exhibited higher CD64 expression than PsA CD14 FLS. Following inflammatory stimulation, h-FLS CD14 showed increased expression of all analyzed genes compared to PsA-FLS CD14 , except for HLA-DR (Fig. 1). In PsA-FLS CD14 , expression of macrophage-associated markers (CD14, Mer-TK, CD64) decreased, whereas all other genes were upregulated except CD90, CDH-11, and NF-κB (Fig. 2). FACS analysis prior to selection revealed that h-FLS wt at P2 consisted of CD14 /CD90 (67%), CD14 /CD90 (3%), and CD14 /CD90 (8%) populations. Upon activation, the CD14 /CD90 population remained nearly unchanged (64%), while CD14 /CD90 (5%) and CD14 /CD90 (15%) subsets increased. After magnetic selection and expansion (P6), h-FLS CD14 wt were predominantly CD14 /CD90 (93%), with minimal CD14 /CD90 (0.8%) and CD14 /CD90 (0.01%) populations (Fig. 3). Conclusions. The differential expression of surface markers and inflammatory genes between h-FLS and PsA-FLS highlights distinct responses to inflammatory stimuli. The higher expression of pro-inflammatory markers in h-FLS CD14 suggests a stronger inflammatory capacity compared with PsA-FLS CD14 , whereas PsA-FLS CD14 display a more inflammatory phenotype under basal conditions. These findings underscore the dynamic nature of synovial cell populations in response to inflammation and indicate that detailed phenotypic characterization of synoviocytes is essential for developing more effective therapeutic strategies in PsA management. Moreover, elucidating the phenotypic differences between CD14 and CD14 synoviocytes may aid in identifying novel biomarkers for early diagnosis and personalized treatment of PsA.

Background. Methotrexate (MTX) is the first-line Disease Modifying Anti-Rheumatic Drug (DMARD) in the treatment of rheumatoid arthritis (RA). According to EULAR guidelines, patients with RA should start immunosuppressive therapy at the time of diagnosis, achieve clinical improvement within 3 months, and remission within 6 months. The objective of this monocentric, retrospective, real-life study was to evaluate the achievement of the therapeutic target in a cohort of patients affected by early-onset RA treated with MTX. Further objectives were to evaluate the MTX ability to act as a “steroid sparing” agent, assess its safety, and the monotherapy maintenance rate.   Materials and Methods. Patients attending the Early Arthritis Clinic from 2006 to the present, affected by RA (ACR 2010 criteria) who had started MTX therapy within 24 weeks from symptom onset, were enrolled. Demographic, clinical, pharmacological, clinimetric indices, and any adverse events associated with therapy were recorded at baseline (T0) and during follow-up until MTX discontinuation or switch to biotechnological therapy.   Results. Table 1 reports demographic and clinical data of the 78 enrolled patients. Graph 2 shows disease activity according to DAS28-PCR and SDAI (2a; 2b) and the percentage of Boolean remission (2c) at follow-up. The median time to achieve remission or low disease activity was 3 months, both according to DAS28-PCR and SDAI (graph 3a). Referring to remission only, the median was 6 months according to DAS28-PCR, while it was 24 months according to SDAI and Boolean Remission 2.0 definition (graph 3b). It emerged that in patients treated with MTX, the mean prednisone dose progressively decreases by 0.08 mg per month, while the probability of continuing steroid therapy decreases by 10% for each month of treatment. Therapy persistence was 7 years in half of the patients (graph 4a), while the median MTX monotherapy maintenance was 6 years (graph 4b).   Conclusions. To our knowledge, this is the first monocentric study that evaluated in real life the efficacy and safety of MTX in early RA patients. MTX confirms its role as an anchor drug in the treatment of RA, with a probability of achieving the therapeutic target already at 3 months in two-thirds of patients with recent disease onset. Our data confirm the higher stringency of SDAI and Boolean Remission 2.0 compared to DAS28-PCR. MTX significantly reduces the steroid dose until discontinuation. Finally, in our cohort, it showed a good safety and clinical efficacy profile, with good therapy persistence.

Tumor necrosis factor inhibitors (TNFi) remain a cornerstone in the management of rheumatoid arthritis (RA), representing the first-line biologic therapy for most patients. This study aimed to assess the real-world effectiveness of TNFi in RA patients. To this purpose, we retrospectively analysed data from RA patients treated with TNFi and enrolled in an Italian national registry. Baseline demographic and clinical characteristics included age, sex, body mass index (BMI), tobacco use, comorbidities, rheumatoid factor and ACPA positivity, line of biologic therapy, VAS pain, patient and physician global assessment, DAS28, CDAI, SDAI, HAQ-DI, use of concomitant glucocorticoids (including dose), and csDMARD co-therapy. Changes in disease activity, quality of life, and steroid use were assessed at 12 months. Remission rates were evaluated at 3, 6, 12, 24, and 60 months. Drug survival was analyzed at 6, 12, 24, and 60 months. Discontinuations and reasons for treatment withdrawal were also recorded. Baseline demographic and clinical characteristics are summarized in Table 1. A significant reduction in disease activity (measured as DAS28, CDAI and SDAI), quality of life and proportion of patients in steroid therapy was observed at 12 months, with DAS28 remission rates of 36% at 3 months, 45%% at 6 months, 44%% at 12 months, 59% at 24 months, and 50% at 60 months. TNFi survival rates were 87.5% at 6 months, 76.8% at 12 months, 63.8% at 24 months, and 44.3% at 60 months. The overall drug survival is depicted in Figure 1A. A significant reduction in treatment survival was observed when TNFi were prescribed at third or further therapeutic line (Figure 1B), while co-therapy with csDMARDs had no influence on survival on treatment (Figure 1C). A total of 942 treatment discontinuations were recorded during follow-up. The main reason for treatment discontinuation was represented by loss of efficacy (30.5% of patients), while adverse events led to suspension in 11.6% of cases. In summary, in this real-world Italian cohort, TNFi therapy was associated with a sustained reduction in disease activity, increasing remission rates over time, and good long-term treatment persistence up to 5 years.

Background. Behçet's Disease (BD) is a rare multisystemic vasculitis that can result in life-threatening manifestations when involving the central nervous system or vascular system. Infliximab (IFX) is an immunosuppressive drug widely used for the treatment of BD with major organ involvement or refractory to therapies. The objective of the study was to evaluate the drug survival, discontinuation reasons, safety profile and disease activity of a cohort of patients diagnosed with BD receiving IFX.   Materials and Methods. We conducted a retrospective observational study examining all the patients affected by BD according to ISG criteria treated with Infliximab. Patient demographics and background data were collected. Disease activity was assessed using the BDCAF (Behçet’s Disease Current Activity Form 2006) index, and clinical remission was evaluated with a score <= 2 points; the safety outcomes were the incidence of adverse drug reactions (ADRs). IFX 5 mg/kg was administered as an intravenous infusion at weeks 0, 2, and 6, and at 6-8 week intervals thereafter. We performed statistical analysis using descriptive statistics (mean ± standard deviation), median (interquartile range IQR), Odds Ratio, Chi-square test, Student’s t-test or Mann Whitney test, statistical significance was assessed for p < 0.05.   Results. A total of 60 BD patients (56.7% female, 43.3% male) were treated with IFX from 2003 to 2025. Their mean age of disease onset was 30.9 years (range 8-63), with a mean age at the introduction of Infliximab of 41.6 years. The main cumulative reasons for starting therapy were: oral and genital recurrent aphthae (71.7% and 35%), cutaneous manifestations (35%), articular involvement (inflammatory arthralgias in 23.3% and arthritis in 23.3%), ocular involvement was found in 28% and SNC involvement in 15%. Analyzing the duration of treatment, it was observed that therapy is currently being followed by 27 patients (drug survival 45%) with a median treatment duration of 37 months (IQR 17-72); drug survival at one year is 78%, at two years of 63.3%, and at five years of 35%. The main causes of discontinuation of therapy were allergic reactions (13%), loss of efficacy (13%), inefficacy (13%), and de novo manifestations (12%) mainly because of recurrent aphthous manifestation. Analyzing the BDCAF index, it emerged that 92.6% of patients currently undergoing treatment with IFX show an improvement in BDCAF, as well as 89.3% of patients who discontinued treatment, with an average reduction of this index by 4 points.   Conclusions. This study showed that IFX is associated with low rates of discontinuation due to adverse events in patients with BD. Notably, 12% of patients experienced de novo organ manifestations. Drug survival was 45%, with a median treatment duration of 37 months. The drug led to a significant reduction in the BDCAF index in the analyzed patients, demonstrating a good safety profile and effectiveness in real life.

Background. This single-center study aimed to evaluate the clinical efficacy of upadacitinib (UPA) in patients with axial spondyloarthritis (axSpA) and to assess its long-term treatment persistence. A secondary objective was to identify potential predictors of treatment persistence with UPA.   Materials and Methods. All adult patients diagnosed with axSpA and treated with UPA for at least six months were included. Clinical data were retrospectively collected at baseline and after 3, 6, and 12 months of therapy. Outcome measures included changes in disease activity assessed by ASDAS-CRP and BASDAI, pain intensity evaluated using a visual analogue scale (VAS), and functional limitation measured with the BASFI. The UPA drug retention rate (DRR) at 18 months was estimated using Kaplan–Meier survival analysis, and the influence of potential modifying factors was assessed using the log-rank test.   Results. A total of 49 patients (35 F, 14 M) with a mean ± SD age at baseline of 50.3 ± 12.7 years were included. Median (IQR) baseline values were: ASDAS-CRP = 3.2 (1.2), BASDAI = 6.5 (3.2), BASFI = 4.1 (3.2), and VAS-pain = 7.0 (3.0). From month 3 onward, there was a statistically significant reduction in median ASDAS-CRP (p < 0.01), BASDAI (p < 0.01), BASFI (p = 0.047), ESR (p = 0.02), and VAS-pain (p < 0.01). At month 6, further decreases were observed in ESR (p < 0.01), ASDAS-CRP (p < 0.01), BASDAI (p < 0.01), and BASFI (p = 0.02). A significant improvement in BASFI (p < 0.01) was also recorded between months 6 and 12, while the other parameters reached a plateau (Fig. 1). At the last follow-up, 85.4% of patients remained on UPA therapy; seven patients had discontinued treatment (n = 1 primary inefficacy; n = 5 adverse events). The UPA DRR at 6, 12, and 18 months was 95.5%, 85%, and 81.3%, respectively (Fig. 2). Sex (p = 0.32), BMI (p = 0.07), radiographic SpA (p = 0.88), prior bDMARDs use (p = 0.54), and fibromyalgia (p = 0.08) did not significantly affect treatment persistence.   Conclusions. This study confirms the efficacy of upadacitinib in achieving a rapid reduction in disease activity and pain among patients with axSpA, with significant improvements detectable from month 3 and progressive enhancement of functional capacity up to month 12. The observed DRR indicates sustained long-term effectiveness and a favorable tolerability profile, which appear to be independent of sex, BMI, treatment line, or coexisting fibromyalgia.

Background. This work describes a clinical case of VEXAS syndrome associated with myelodysplastic neoplasm, aiming to highlight the clinical and diagnostic features and the importance of a multidisciplinary approach to optimize treatment and improve the patient's prognosis.   Materials and Methods. A 57-year-old male, with a medical history of type 2 diabetes and hypertension, presented between March and June 2024 with marked fatigue, migratory arthralgia in the lower limbs, subcutaneous nodules, an episode of left ear chondritis, and a 20 kg weight loss over 6 months, without fever or apparent infections. Laboratory findings included macrocytic anemia (Hb 6.8 g/dL, MCV 108 fl), without hemolysis, leukocytopenia (WBC 2270/mm³, PMN 1170/mm³), hyperferritinemia (842 µg/L), CRP 111 mg/L, and polyclonal hypergammaglobulinemia. Autoimmune markers (ANA, ENA, ANCA) and HCV/HBV serology were negative. CT scans of the head, chest, and abdomen (August 2024) revealed hepatosplenomegaly. In September, the patient developed a fever with chills, further weight loss, and petechiae at the base of all limbs. PET-CT showed increased lymph node, splenic, and skeletal uptake, while bone marrow biopsy identified myelodysplastic syndrome of the RAEB II subtype, with high IPSS and R-IPSS scores. Microscopic examination noted cytoplasmic vacuoles in granulocytes and blasts. VEXAS syndrome was confirmed by genetic testing identifying a mutation in the UBA1 gene (c.121A>G p.(Met41Val)). The treatment regimen included corticosteroids (methylprednisolone 1 mg/kg/day), with azacitidine as a bridge to transplant.   Results. During follow-up, the patient showed a satisfactory clinical and laboratory response to steroid and antineoplastic drugs, with normalization of inflammatory markers, blood count, and regression of clinical manifestations. In January 2025, he was hospitalized for influenza A pneumonia during neutropenia and treated with antivirals, antibiotics, and corticosteroids. The steroid dose was tapered to 10 mg/day of prednisone, maintaining satisfactory clinical and laboratory control. A follow-up chest CT (3 months later) revealed persistent fibrotic changes and ground-glass opacities, consistent with an inflammatory pattern related to the syndrome. Azacitidine therapy resulted in partial remission, and the option of allogeneic stem cell transplantation was contemplated owing to the patient's youth and the poor prognosis linked to myelodysplasia.   Conclusions. This case underscores the importance of early recognition of VEXAS syndrome, a rare autoinflammatory disorder that combines systemic inflammatory and hematological manifestations. Genetic diagnosis is essential for confirming the diagnosis and guiding treatment. A multidisciplinary approach, involving immunosuppressive therapy and consideration of allogeneic stem cell transplantation, is the most promising strategy to improve patient’s prognosis. Close clinical and radiological monitoring is crucial to manage infectious and inflammatory complications, optimizing the therapeutic choice and the patient's quality of life.

Background. Sarcoidosis is a multisystem disease of unknown etiology, characterized by the presence of non-necrotizing granulomas in multiple organs. It is a clinical condition capable of mimicking several disorders. For an accurate differential diagnosis, histopathological examination of the affected organ is crucial, in addition to clinical, radiological, and laboratory findings.   Case Report. We report the case of a patient with a suspected IgG4-related disease in a differential diagnosis of sarcoidosis. A 25-year-old Pakistani male, smoker, and stable worker was referred to rheumatologic evaluation in January 2025 for progressive, painless, bilateral periorbital and parotid swelling that had developed since November 2024. Ophthalmologic examination and subsequent orbital MRI confirmed the presence of bilateral glandular hypertrophy. The patient denied any infectious episodes preceding symptom onset. His past medical history included only a left-sided Bell’s palsy with lagophthalmos in 2021, occurring after the first dose of the SARS-CoV-2 vaccine, which resolved after a short course of corticosteroids. At the presentation, he denied dry cough, dyspnea, fever or low-grade fever, arthritis/arthralgia, visual impairment, erythema nodosum, cutaneous lesions, or gastrointestinal symptoms. Physical examination revealed painless swelling of the parotid, submandibular, and lacrimal glands, associated with conjunctival hyperemia and lagophthalmos. Palpable, non-tender, mobile lymph nodes were noted in the right retroauricular and left laterocervical regions; no joint inflammation was detected. Given the suspicion of an IgG4-related disease, hospital admission was planned. During hospitalization, the patient underwent • Laboratory tests: ESR 45 mm/h, CRP 0.5 mg/dL, ACE 66 U/L, severe vitamin D deficiency (<4 ng/mL), PTH 36.3 pg/mL; normal serum calcium, phosphate, and 24-hour urinary calcium (145.2 mg). The patient's IgG subclasses were within normal limits, and both autoimmune and infectious serologies were negative. • Whole-body FDG-PET: Increased radiotracer uptake in bilateral parotid glands, bilateral hilar and peribronchovascular regions, and ocular bulbs. • Abdominal ultrasound: Unremarkable. • Ocular immunology evaluation: There were no signs of granulomatous uveitis. Empirical treatment with oral prednisone (50 mg daily) was initiated. Subsequently, a biopsy of the left parotid gland was performed, showing a fibroinflammatory process with granulomas containing small necrotic foci, consistent with sarcoidosis. Chest CT revealed multiple peribronchovascular pulmonary nodules and hilar-mediastinal lymphadenopathy. A diagnosis of sarcoidosis involving the lacrimal and parotid glands, lymph nodes, and pulmonary parenchyma (Stage II) was therefore established. Corticosteroid therapy (prednisone 0.5 mg/kg/day) was maintained, and methotrexate 20 mg weekly was added as a steroid-sparing agent. At follow-up in March 2025, a marked clinical improvement was observed, with significant reduction of parotid and lacrimal gland swelling. This case highlights the importance of an appropriate differential diagnosis among granulomatous diseases and the pivotal role of histopathological confirmation in establishing a definitive diagnosis.