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Background. Anifrolumab (ANI) is a monoclonal antibody directed against type 1 interferon receptor. Its use in the treatment of patients with systemic lupus erythematosus (SLE) is becoming more frequent in clinical practice. The aim of this study is to evaluate the efficacy of ANI in SLE without active renal involvement.   Methods. Data were prospectively collected from SLE patients (according to the ACR, SLICC, or EULAR/ACR classification criteria) undergoing treatment with ANI. Specifically, SLEDAI-2K, SLE Disease Activity Score (SLEDAS), painful/swollen joint count (SJT/TJC), and CLASI (Cutaneous LE Disease Area and Severity Index) were acquired before the start of therapy and subsequently every 3 months for the first year of therapy. Platelet count (PC) and lymphocyte count (LC), complement levels, anti-dsDNA antibody titers, and daily prednisone dose (PDN) were also collected at the same frequency. The SDI (SLICC/ACR damage index) was assessed at baseline and after 6 months. Finally, rates of remission (SLEDAI-2K=0 with PDN ≤5 mg/day), clinical remission (clinical SLEDAI-2K=0 with PDN ≤5 mg/day) and modified lupus low disease activity state (SLEDAI-2K ≤4 without major organ involvement and no new manifestations, with PDN≤7.5 mg/day) were obtained. The T-test and Wilcoxon test for paired data were used to compare the various timepoints.   Results. Since September 2023, 22 patients with SLE have been treated with ANI: of these, 11 (50%) for skin involvement, 10 (45%) for joint involvement, while hematological and serosal involvement were present in 4 (18%) and 2 (9%) patients, respectively. In 8 patients (36%), ANI was administered before conventional immunosuppressants (IS). Reductions in the mean SLEDAI-2K (p = 0.016 at 6 months and p = 0.007 at 9 months), SLEDAS (p < 0.001 at 6 months), CLASI (p = 0.008 at 6 months and p = 0.043 at 9 months), TCJ (p = 0.009 at 6 months and p = 0.033 at 9 months), SJC (p = 0.023 at 6 months) and LC (p = 0.021 at 6 months and p = 0.007 at 9 months) were encountered. No changes were found in PC, hypocomplementemia rates, elevated anti-dsDNA antibody titers or SDI at 6 months (Figure 1). A trend toward reduced prednisone use was observed. Rates of remission, clinical remission, and modified lupus low disease activity state are shown in Figure 2. Treatment was discontinued in 3 patients (2 due to ineffectiveness and 1 due to sepsis). There were no cases of herpes zoster.   Conclusions. ANI has been shown to reduce disease activity, with major impact in the cutaneous and articular domains. Further data are needed to evaluate its effect on hematological and serositis manifestations.

Background. Pulmonary involvement in systemic lupus erythematosus (SLE) is a heterogeneous and usually non-severe complication, affecting 50–70% of patients (and up to 4–5% at disease onset). Pleuro-parenchymal manifestations include pleuritis (30%), interstitial lung disease (ILD, 1–15%), and lupus pneumonitis (1–4%), the latter often requiring differential diagnosis from infectious forms. Vascular manifestations comprise pulmonary arterial hypertension (PAH, 0.5–17.5%), diffuse alveolar hemorrhage (DAH, 1–5.4%), and venous thromboembolism (VTE, 9%; 35–42% in the presence of antiphospholipid antibodies), as well as acute reversible hypoxemia (ARH). Rare forms include airway disease and shrinking lung syndrome. Anifrolumab, a monoclonal antibody that blocks the type I interferon receptor, has shown efficacy in moderate to severe SLE, particularly for mucocutaneous, articular, and serological manifestations. According to European guidelines, Anifrolumab is recommended as first-line therapy for extra-renal (non–major organ) manifestations, especially cutaneous, and as add-on therapy for severe disease. We report a case of SLE with lupus pneumonitis and antiphospholipid syndrome (APS) successfully treated with Anifrolumab.   Materials and Methods. A 45-year-old Caucasian man, with no significant past medical history, experienced three episodes of bilateral pneumonia (bibasilar consolidations) since mid-2022, all requiring hospitalization. One episode was complicated by pulmonary embolism and another by a generalized rash, both treated with antibiotics and corticosteroids. Laboratory findings revealed positivity for ANA (1:2560, homogeneous nuclear pattern), anti-dsDNA, anti-Ro52, anti-nucleosome, anti-histone antibodies, rheumatoid factor, and lupus anticoagulant. Rheumatologic assessment revealed Jaccoud arthropathy and widespread erythematous maculopapular lesions on the trunk, back, and limbs. Given the absence of infectious findings (including negative BAL), the pulmonary abnormalities were attributed to autoimmune disease. A diagnosis of SLE with cutaneous involvement (histologically confirmed subacute cutaneous lupus erythematosus), pulmonary and articular manifestations, and associated APS was established. The patient started oral anticoagulation, high-dose corticosteroids, hydroxychloroquine (discontinued due to cutaneous reaction), and rituximab (1 g × 2), achieving initial improvement. Rituximab was discontinued after the second course due to an adverse reaction, followed by recurrence of bilateral pneumonia and cutaneous flare. Consequently, Anifrolumab 300 mg every 4 weeks was initiated.   Results. After six months of Anifrolumab therapy, HRCT showed marked improvement, inflammatory markers normalized, and the patient reported substantial improvement in respiratory, cutaneous, and articular symptoms, allowing progressive corticosteroid tapering.   Conclusions. Anifrolumab represents a promising therapeutic option for patients with severe SLE manifestations who are refractory to or intolerant of conventional treatments. Modulation of the type I interferon signaling pathway may play a key role in achieving systemic disease control. In patients with pulmonary involvement, a multidisciplinary approach and careful differentiation from infectious causes are essential.

Background. The efficacy of anifrolumab has been documented in several studies (1,2), however data regarding its use in the haematological domain of SLE remain limited (3). The aim of this case series is to describe a single-centre experience with anifrolumab in patients with SLE predominantly affecting the haematological domain, particularly thrombocytopenia and haemolytic anaemia.   Materials and Methods. We retrospectively evaluated data from six patients with haematological involvement treated with intravenous anifrolumab at a dosage of 300 mg every four weeks. Assessments were performed at baseline (T0) and after one (T1), three (T3), and six months (T6) of therapy. Changes in complete blood counts and corticosteroid dosages were analysed.   Results. Among the six patients, five had thrombocytopenia and one had haemolytic anaemia. All patients were corticosteroid-dependent at baseline. The epidemiological and clinical characteristics of the cohort are detailed in Tables 1 and 2. Four patients with thrombocytopenia received anifrolumab therapy for at least six months. In these cases, an increase in platelet counts was observed, allowing a reduction in corticosteroid therapy — in two cases to a prednisone dose below 5 mg/day, and in one case complete discontinuation was achieved. At the time of reporting, one patient has been treated for three months, showing an improvement in platelet count after the first infusion and a reduction in corticosteroid dosage after the third one (Figure 1). A single patient was treated with anifrolumab for haemolytic anaemia and lymphopenia. At six months after treatment initiation, improvements were observed in lymphocyte counts, haemoglobin levels and haptoglobin values, previously undetectable, allowing a reduction in corticosteroid dosage (Figure 2). No significant adverse events occurred during treatment. In one case, therapy was discontinued after twelve months due to loss of efficacy and diagnosis of colon cancer. In this instance, a paraneoplastic aetiology as a contributing factor to the worsening and refractoriness of thrombocytopenia could not be entirely excluded.   Conclusions. Based on our data, haematological involvement in SLE may represent a potential therapeutic target for anifrolumab. However, the small number of cases precludes any definitive conclusions. Expanding data collection to a larger, multicentre cohort would be valuable to explore potential predictors of response, which could account for the observed variability in both the magnitude and timing of clinical responses.

Background. Anifrolumab is a biologic agent approved for the treatment of Systemic Lupus Erythematosus (SLE). Clinical trials evaluating its efficacy (TULIP-1 and TULIP-2) excluded patients with active neuropsychiatric manifestations (NPSLE). The aim of this study was to review the published cases of NPSLE treated with Anifrolumab (ANI) and to describe a clinical case from our cohort. Materials and Methods. A literature search was conducted on Medline/PubMed and Embase for reports of NPSLE patients treated with ANI. In addition, we describe a case from our local cohort. Results. The literature review identified seven published cases of NPSLE successfully treated with ANI, including two with confusional states, one with acute psychosis, one with headache, one with cerebral vasculitis, one with aseptic meningitis, and one with demyelinating polyneuropathy. The data are summarized in Table 1. We also report the case of a 63-year-old woman with a 26-year history of SLE and antiphospholipid syndrome (APS), who initially presented with polyarthritis, lymphopenia, an ischemic stroke, and positivity for ANA, anti-dsDNA, anti-Ro/SSA, lupus anticoagulant, anti-cardiolipin IgG, and hypocomplementemia. Over the years, she experienced a relapsing-remitting course characterized by cutaneous vasculitis of the hands and feet, thrombocytopenia, leukopenia, and epileptic seizures with spatiotemporal disorientation. Electroencephalography revealed left-hemispheric irritative electrical abnormalities, interpreted as secondary to ischemic damage. The patient’s treatment history included several immunosuppressants—cyclophosphamide, azathioprine, mycophenolate mofetil, belimumab, and hydroxychloroquine (discontinued due to gastrointestinal intolerance, INR abnormalities, and arrhythmia). Levetiracetam was escalated to 2500 mg/day due to worsening seizures, without achieving clinical remission (DORIS). In 2022, following prednisone tapering to 5 mg/day, disease flare occurred with hand vasculitis, malar rash, alopecia, leukopenia (1700/µl), and thrombocytopenia (95,000/µl). Anifrolumab was initiated, and prednisone was increased to 10 mg/day. At the 3-month follow-up, mucocutaneous and hematologic manifestations had resolved, and seizure frequency had decreased (from 2/week to 1 every 8 weeks). After 6 months of ANI treatment, the patient achieved complete clinical remission (CLASI = 0, cSLEDAI-2K = 0) with prednisone tapered to 2.85 mg/day. Conclusions. The results from both the literature review and our clinical case suggest that Anifrolumab may be effective in managing neuropsychiatric manifestations of SLE. In our experience, a remarkable improvement was also observed in the hematologic domain. Although these findings are encouraging, they warrant confirmation in dedicated clinical trials, emphasizing the need for personalized therapeutic strategies in SLE management.

Background. Belimumab (BEL) and Anifrolumab (ANI) are currently the only biologic drugs authorized for the treatment of Systemic Lupus Erythematosus (SLE). The aim of the study is to analyze the factors associated with the therapeutic choice between BEL and ANI in a monocentric cohort of patients affected by SLE.   Materials and Methods. We conducted a prospective observational study on consecutively enrolled patients affected by SLE and treated with BEL or ANI starting from June 2022, the date when the compassionate use of ANI began. Clinical, clinimetric, serological, and therapeutic data (prednisone, previous and concomitant therapy) were collected. Univariate analysis was performed using the chi-square or Fisher’s test for categorical variables and the Mann-Whitney or Student’s t test for continuous variables; for multivariate analysis, logistic regression models were created selecting variables with p<0.05.   Results. The study included 22 patients treated with ANI (21 women, 95.5%) and 39 with BEL (35 women, 89.7%). The demographic, clinical, and therapeutic characteristics of the two groups at baseline are reported in the table, together with the results of the univariate analysis. In multivariate analysis, the use of ANI was preferentially associated with a chronic-active disease course (OR 17.8; 95% CI 3.5-91.7; p<0.001) and with active cutaneous manifestations (OR 9.9; 95% CI 1.5-66.5; p<0.017). In particular, the sub-analysis of cutaneous involvement showed an association between the preferential use of ANI compared with BEL in patients with subacute lupus (OR 12.7; 95% CI 2.0-79.4; p<0.006) and alopecia with lupus hair (OR 6.2; 95% CI 1.7-22.0; p<0.005). The use of BEL was significantly associated with a relapsing-remitting disease course (OR 10.7; 95% CI 2.3-50.1; p=0.002) and with the presence of active arthritis (OR 5.3; 95% CI 1.2-23.0; p<0.002). In particular, the sub-analysis of articular involvement showed a preferential association between the use of BEL and the subtype of non-deforming and non-erosive arthritis (OR 6.5; 95% CI 1.8-23.8; p<0.004). Although univariate analysis showed more active serology, with anti-DNA positivity (p=0.015) and complement consumption (p=0.061), in patients treated with BEL, these differences were not significant in multivariate analysis. No significant differences emerged between the two groups in terms of corticosteroid dose and concomitant use of hydroxychloroquine (HCQ). However, a greater number of patients treated with ANI were taking methotrexate, in relation to the predominant cutaneous involvement.   Conclusions. The choice of biologic drug in patients with active SLE currently appears to be mainly guided by the clinical phenotype, in line with evidence from registration trials. Real-life studies and the development of predictive biomarkers of response to specific biologic drugs will allow for better personalization of therapy within the framework of precision medicine.

Background. to compare the clinical profile of patients prescribed with either BEL or ANI and assess preliminary efficacy of ANI in a monocentric cohort of systemic lupus erythematosus (SLE) patients.   Methods. we performed an observational study on consecutive patients with active SLE prescribed with a biological drug at our clinic between July 2023 to July 2024, with a follow-up of at least 6 months from baseline (start of biologic). Clinical, demographic and serological data were collected at baseline, at 3 and 6 months. Disease activity was measured through the SLE-disease activity index 2000 (SLEDAI-2K) and the SLE-disease activity score (SLEDAS) including assessment of active serology. For skin involvement, ANI patients had their CLASIa (Cutaneous LE Disease Area and Severity Index) calculated. Comparisons between continuous and categorical variables were carried out using parametric or non parametric tests as appropriate. We used Friedman’s test to repeat measures and compare paired samples. Categorical variables were expressed as n (%) and continuous variables as mean±standard deviation (SD).   Results. we included 15 SLE patients (Table 1) with a mean follow-up of 8.90 (6.10) months since start of biologic, receiving either BEL (7, 46.6%) or ANI (8, 53.4%). The main organ involvement encompassed skin rash and arthritis in the ANI group (both 62.5%), and skin rash (41%) and arthritis (71%) in the BEL group. BEL and ANI group did not differ in terms of baseline disease activity; more patients were serologically active (positive anti-dsDNA and/or low complement) in the BEL group while not reaching statistical significance. Organ damage was significantly lower at baseline in the BEL group. Out of 8 patients on ANI, 3 (37.5%) had to stop the drug after a mean time of 3.50±2.78 months due to inefficacy (1 case) or adverse events (2 cases: recurrent vaginal bleeding and pneumonia requiring ICU admission). No withdrawals were seen in the BEL group within the follow-up. Both SLEDAI-2K and SLEDAS decreased significantly in both ANI and BEL groups (Table 2). ANI patients further displayed a significant decrease in CLASIa as well between baseline and T6 (10.71±10.57 vs. 3.14±5.39, p=0.023), indicating improvement of skin involvement. Prednisone daily dosage was quickly tapered in the BEL group Relative to ANI group, patients prescribed with BEL had received a significantly lower number of traditional immunosuppressants before the initiation of the biological drug (p<0.001, Table 1); no patients on BEL had received any other biologic before.   Conclusions. in our consecutive cohort of SLE patients receiving biologics in the last 18 months, both drugs showed similar efficacy in decreasing disease activity. BEL was prescribed earlier than ANI in disease history and confirmed a steroid-sparing potential, underscoring the importance of early treatment in active SLE.

Background. Despite recent improvements in the management of systemic lupus erythematosus (SLE), patients still face a high risk of morbidity and mortality. Sustained remission is the goal of SLE management, although it is rarely achieved in clinical practice. When remission cannot be reached, the Lupus Low Disease Activity State (LLDAS) represents an alternative Treat-to-Target objective. In Italy, real-world data are lacking on the achievement and maintenance of LLDAS, remission, and corticosteroid tapering in patients treated with anifrolumab. Therefore, a study was designed with the primary objective of describing the proportion and characteristics of patients who achieve LLDAS5 and remission during treatment with anifrolumab in Italian clinical practice, and with the secondary objective of defining a glucocorticoid tapering scheme to inform clinical practice.   Materials and Methods. DAHLIA is an Italian, multicenter, prospective, observational cohort study conducted in accordance with Good Clinical Practice (GCP). The study population will include 245 Italian adult patients of both sexes with SLE, according to EULAR/ACR criteria, who are prescribed initiation of anifrolumab therapy for the first time in the context of routine Italian clinical practice, in line with the approved and reimbursed label. The primary objective is to describe the proportion and characteristics of patients who achieve LLDAS with a corticosteroid (prednisone) dose equal to or less than 5 mg (LLDAS5) at week 52. Secondary objectives include assessment of the estimated cumulative probability of achieving LLDAS5 over the course of the study; the percentage of flares following glucocorticoid reduction to a dose equal to or less than 5 mg/day; the cumulative probability of achieving DORIS remission; the persistence of DORIS remission; and the description of a glucocorticoid tapering scheme used in routine clinical practice. The sample size was estimated based on results from analyses of LLDAS achievement in the TULIP trials, the number of participating centers, and the potential study dropout rate. The study period for each participant will last 104 ± 1 weeks from treatment initiation or until discontinuation of anifrolumab, loss to follow-up, or death. Participating patients, who do not attend the visit after the first infusion, will be included only in the safety analysis. Data will be collected starting from the first day of anifrolumab treatment, as part of routine clinical practice.   Conclusions. The multicenter observational DAHLIA study will collect real-world evidence from Italian clinical practice, identifying the characteristics of patients treated with anifrolumab who achieve the LLDAS5 target and DORIS remission. In addition, it will help to identify a glucocorticoid tapering scheme in patients with SLE treated with anifrolumab.

Background. Systemic Lupus Erythematosus (SLE) is a chronic systemic autoimmune disease characterized by the interaction of genetic, environmental, and immunological factors. The type I interferon (IFN-I) pathway, particularly IFN-alpha, represents a central element in its pathogenesis. IFN-I is produced by pDCs and other cells in response to exposure to immune complexes containing DNA or RNA, and it promotes the activation and differentiation of B and T cells, the maturation of DCs, and the expression of pro-inflammatory cytokines. Anifrolumab is a human monoclonal antibody that binds to the type I interferon receptor (IFNAR1), inhibiting the activity of all type I interferons. Interferons, particularly IFN-gamma and type I IFN, also play a crucial role in the pathogenesis of psoriasis: pDCs can be activated by nucleic acids released from damaged keratinocytes or by immune complexes, producing IFN and contributing to the inflammation.   Methods and Results. A 57-year-old woman presented with a diagnosis of inverse psoriasis and undifferentiated connective tissue disease, previously treated with Hydroxychloroquine (discontinued due to an allergic reaction) and then with Methotrexate and Cyclosporine. Laboratory tests showed ANA positivity (1/640 speckled pattern), anti-dsDNA and anti-SSA/Ro60 positivity, ESR 44 mm/h, CRP 18.1 mg/L. On physical examination, she presented with erythematous, desquamative, and infiltrated lesions in the intergluteal fold, buttocks, submammary and retroauricular regions, alopecia and a malar rash. A diagnosis of Systemic Lupus Erythematosus was made, and initially treatment with Cyclosporine 300 mg/day was maintained. One year later, blood tests showed an increase in ESR and CRP, mild anemia, and 24-hour proteinuria of 884 mg/24h. The patient also presented with a painful swelling of the right sternoclavicular joint, and ultrasound documented inflammatory involvement (consistent with Tietze's syndrome). Cyclosporine therapy was suspended, and treatment with Methotrexate and Prednisone was initiated. One month later, at the follow-up visit, tests showed a reduction in proteinuria (168 mg/24h) and inflammatory markers, as well as the resolution of the sternoclavicular swelling, so prednisone taper was started. At subsequent follow-ups, the patient showed clinical stability in laboratory tests; however, a strong psoriatic component persisted with erythema in the submammary, inguinal, retroauricular, elbow, intergluteal fold, and left calf regions. An erythematous lesion also appeared on the V of the chest. Therefore, after screening to initiate biotechnological drug therapy, treatment with Anifrolumab 300 mg/month was scheduled.   Conclusions. Type I interferon is a common pathogenetic driver in both SLE and psoriasis. Anifrolumab, by blocking the type I IFN receptor, has demonstrated clear efficacy in SLE, reducing disease activity and improving clinical outcomes. Its targeted action on the IFN-I pathway suggests a potential benefit for psoriasis as well, by acting on a shared inflammatory mechanism. The introduction of Anifrolumab in this patient could offer a potential benefit for both conditions.

Background. Dermatomyositis is a rare autoimmune disease characterized by multisystem involvement. Treatment can be challenging, particularly in refractory cases unresponsive to conventional therapies, for which standardized management protocols are lacking. An increased activation of the type I interferon (IFN-I) pathway has been demonstrated in patients with dermatomyositis, providing a rationale for the use of anifrolumab, a monoclonal antibody targeting the IFN-I receptor, already approved for systemic lupus erythematosus and particularly effective on cutaneous manifestations. Materials and Methods We report the case of a 57-year-old woman with anti–TIF-1γ–positive dermatomyositis, diagnosed in May 2024, with a history of high-grade serous ovarian carcinoma treated with surgery and chemotherapy (August 2024–February 2025). At rheumatologic evaluation in March 2025, the disease was clinically active with extensive cutaneous involvement, including heliotrope rash, malar rash without sparing of the nasolabial folds, diffuse erythema of the limbs, back, and décolleté, palmar and facial telangiectasias, and distal ulcers on the hands and right ear (Cutaneous Dermatomyositis Disease Area and Severity Index – CDASI: Activity 29, Damage 5). The patient also reported disabling myalgia and progressive gait impairment (Medical Research Council scale – MRC 45/60). Previous treatments (steroids, hydroxychloroquine, mycophenolate mofetil, intravenous immunoglobulins, and anakinra) were ineffective or discontinued due to adverse events, while rituximab was considered inappropriate because of her oncologic history. Therefore, monthly intravenous anifrolumab therapy was initiated. Results. After two months of anifrolumab treatment, marked clinical improvement was observed in both cutaneous (CDASI Activity 12; Damage 4) (Figure 1A–C, Figure 2A–B) and muscular domains (MRC 50/60), with no adverse events reported, including serious infections. The improvement allowed progressive corticosteroid tapering (from 25 mg to 5 mg of prednisone) without elevation of muscle damage markers or disease flare. Conclusions. This case suggests that anifrolumab may represent a promising therapeutic option for refractory dermatomyositis. Controlled studies are warranted to confirm its efficacy and safety in this indication.  

Background and Objective. To describe our experience with the use of anifrolumab (AFM) in a small single-center cohort of patients (pts) with systemic lupus erythematosus (SLE), with particular focus on the management of refractory manifestations. SLE is a systemic autoimmune disease that can affect virtually any organ or system. Refractory manifestations represent an unmet need in disease management, as they are associated with higher glucocorticoid (GC) exposure, increased risk of cumulative organ damage, and reduced quality of life (QoL). Type I interferons (IFN-I) play a key role in antiviral defense; however, in SLE patients, IFN-I signaling pathways are upregulated both in genetic predisposition and in epigenetic changes characteristic of the disease, contributing to disease onset and activity. Several clinical and laboratory features of SLE—including lymphopenia—are associated with the overexpression of IFN-I–regulated genes, providing a strong rationale for targeting this pathway. Anifrolumab, a monoclonal antibody that inhibits the type I interferon receptor, offers new therapeutic perspectives in this setting.   Materials and Methods. We report on 5 female SLE patients aged 35–64 years, followed from September 2024 to the present. Four pts presented with cutaneous involvement: acute cutaneous lupus (n=2), subacute cutaneous lupus (SCLE)(n=1), and discoid lupus with scarring alopecia (DLE) (n=1). One pt exhibited predominant constitutional (persistent remittent fever up to 39.5°C for ~1 year, fatigue) and hematologic involvement (leukopenia–lymphopenia). These manifestations prompted initiation of AFM therapy. Previous manifestations (currently in remission) included articular (3 pts), serosal (pleural effusion, 1 pt), and renal involvement (class III glomerulonephritis, 1 pt). At the time of our observation, pts (previously followed in other Centers) were receiving hydroxychloroquine (except the pt with constitutional/hematologic involvement, due to intolerance) and GCs (except the pt with DLE, who had discontinued GCs due to lack of efficacy on cutaneous disease). Three of the five pts had a remote history of traditional immunosuppressant use. Anti-dsDNA antibodies were present in 3 pts, and C4 was reduced in 4 pts.   Results. Treatment with AFM led to improvement in all cutaneous manifestations, with complete remission in two cases, after only a few months of therapy. A marked clinical benefit was also observed in the DLE case, a notoriously refractory manifestation (CLASI score improved from 17 [T0] to 8 [T5]). The pt with persistent fever and leukopenia–lymphopenia—also typically refractory—experienced rapid resolution of symptoms and improvement in fatigue (SLEDAI decreased from 6 [T0] to 2 [T2]). All pts were able to taper GCs, with complete withdrawal achieved in two pts with cutaneous disease.   Conclusions. Our findings confirm the efficacy of AFM, as previously demonstrated in clinical trials, across selected SLE disease domains. They highlight the potential to extend precision medicine principles to SLE management and to consider AFM as a valuable therapeutic option for difficult-to-treat manifestations.