Immune-Mediated Inflammatory Diseases and Cancer - a dangerous liaison.

Patients with Immune-Mediated Inflammatory Diseases (IMIDs) are known to have an elevated risk of developing cancer, but the exact causative factors remain subject to ongoing debate. This narrative review aims to present the available evidence concerning the intricate relationship between these two conditions. Environmental influences and genetic predisposition lead to a dysregulated immune response resulting in chronic inflammation, which is crucial in the pathogenesis of IMIDs and oncogenic processes. Mechanisms such as the inflammatory microenvironment, aberrant intercellular communication due to abnormal cytokine levels, excessive reparative responses, and pathological angiogenesis are involved. The chronic immunosuppression resulting from IMIDs treatments further adds to the complexity of the pathogenic scenario. In conclusion, this review highlights critical gaps in the current literature, suggesting potential avenues for future research. The intricate interplay between IMIDs and cancer necessitates more investigation to deepen our understanding and improve patient management.

Comparative effectiveness of combined biologic agents versus standard therapies in the treatment of plaque psoriasis: a retrospective analysis.

Introduction: Plaque psoriasis is a persistent skin disorder that necessitates efficient management. This study investigates the therapeutic effectiveness and timeline for skin lesion resolution in plaque psoriasis patients treated with combined biologic agents compared to standard therapies. Methods: Conducted retrospectively between March 2020 and March 2023, the study included 162 patients with moderate to severe plaque psoriasis. Participants were divided into two groups: the Control Group, which received standard treatments, and the Combined Biologic Agent Group, which received additional biologic therapy with secukinumab. Participants in the Control Group received standard treatments, while those in the Combined Biologic Agent Group received standard treatments plus secukinumab. Results: The results showed that the Combined Biologic Agent Group experienced a significantly faster onset of therapeutic effects, with an average time of 3.04 ± 2.25 days compared to 6.12 ± 2.06 days in the Control Group. Additionally, skin lesion resolution occurred more rapidly in the biologic agent group (7.04 ± 2.13 days) than in the control group (14.56 ± 4.73 days). By week 24, the Psoriasis Area and Severity Index (PASI) scores demonstrated a more substantial reduction in the biologic agent group, decreasing from 26.98 ± 11.28 to 2.48 ± 3.01, whereas the control group showed a reduction from 25.82 ± 10.47 to 10.40 ± 7.63. The overall effectiveness rate was higher in the biologic agent group, with no cases of ineffectiveness, compared to a 20.99% ineffectiveness rate in the control group. Furthermore, there was no recurrence of the disease in the biologic agent group, while the control group experienced an 11.11% recurrence rate. Both groups had a similar incidence of adverse reactions, indicating that the addition of biologic agents does not significantly increase the risk of adverse events. Discussion: These findings suggest that combined biologic agent therapy offers a more effective and faster treatment option for plaque psoriasis without compromising safety. However, larger-scale clinical trials are necessary to validate these results and establish the long-term benefits and safety of this treatment approach in diverse patient populations.

Refractory Dupilumab-Induced Inflammatory Arthritis Treated by Upadacitinib: A 'Janus Kinase (JAK)' of All Trades.

Dupilumab, a monoclonal interleukin (IL)-4 receptor α antagonist, is used to treat moderate-to-severe atopic dermatitis. Uncommonly, inflammatory arthritis and enthesitis may occur upon initiation of dupilumab. Upadacitinib, a Janus kinase (JAK) inhibitor, is an alternative medication approved for moderate-to-severe atopic dermatitis but is also used to treat inflammatory arthritis. We report a case of dupilumab-induced inflammatory arthritis that was refractory to oral nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids and was successfully treated by upadacitinib, which also treated the atopic dermatitis. A 40-year-old female with moderate-to-severe atopic dermatitis was treated with dupilumab for 10 months, showing improvement in her skin. However, she then developed recurrent right knee effusions, polyarthritis in her hands, feet, and knees, and prolonged stiffness. She noticed swelling which developed abruptly in her right knee, then progressed to multiple joints including fingers, wrists, ankles, and persisted for four weeks prior to seeking additional medical care. She denied any recent preceding trauma. Joint pain was worsened by movement and morning stiffness lasted over two hours. Trials of ibuprofen or celecoxib and application of ice did not alleviate it. She had an elevated erythrocyte sedimentation rate of 29 mm/hr and C-reactive protein of 21.6 mg/dL. She tested negative for antinuclear antibody, rheumatoid factor, anti-cyclic citrullinated protein, human leukocyte antigen B27, Lyme enzyme-linked immunosorbent assay (ELISA), and Western blot. She was initially treated with a prednisone taper, but the symptoms returned upon reaching 10 mg daily. She continued on dupilumab for four weeks, but stopped as the joint symptoms progressed. With cessation, her atopic dermatitis also became active again. Despite stopping the dupilumab, she continued to have diffuse swelling and tenderness in her hands, feet, knees, and wrists over the next 12 weeks. Upadacitinib, within one month of initiating, led to improvement in both joints and skin. She was able to taper off the corticosteroids. At five months, she continued to not have swelling or tenderness in her joints, and her skin was well-controlled. We report the first successful use of upadacitinib for the treatment of refractory dupilumab-induced inflammatory arthritis as well as atopic dermatitis. The use of JAK inhibitors should be considered to treat this uncommon condition, given that they also treat atopic dermatitis.

Tocilizumab Reduces Depression Risk in Rheumatoid Arthritis Patients: A Systematic Review and Meta-Analysis.

Depression is a possible cause of the increased mental health risks associated with rheumatoid arthritis (RA), including depression-related complications. Biological disease-modifying antirheumatic drug (bDMARDs) therapies have emerged as innovative anti-inflammatory drugs with positive effects on mental well-being. Tocilizumab is a bDMARDs commonly used to treat RA and its influence on depression needs to be studied. It targets interleukin-6 (IL-6) receptors, reducing inflammation, which may also alleviate depressive symptoms due to the role of inflammation in the pathophysiology of depression. Thus, its influence on depression needs to be studied. To assess the strength of the association between exposure to tocilizumab and the rate of development of depression in patients with RA and to evaluate tocilizumab as an exposure and depression as an outcome in these patients, a search was conducted in the MEDLINE, PreMEDLINE, Cochrane, and Scopus databases from January 1980 to April 2024. Inclusion criteria were studies that diagnosed RA according to the latest American College of Rheumatology/European League Against Rheumatism guidelines or a rheumatologist and provided information on tocilizumab exposure and diagnosed depression as an outcome. The present meta-analysis was conducted following the guidelines of the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) statement. These studies were assessed for eligibility by the author and an independent assessor. To summarize the findings, the meta-analysis combined the relative risk estimates from each study with raw data counts. Twelve studies in the meta-analysis fulfilled the inclusion criteria. Tocilizumab monotherapy exhibited a promising beneficial effect on the risk of depression, indicated by the decreased risk in RA patients (Relative risk 0.68, 95% CI 0.20, 2.31). Patients with RA on tocilizumab treatment had a lower risk of developing depression compared to those unexposed to tocilizumab treatment. Therefore, future longitudinal studies are needed to confirm the beneficial effect of tocilizumab on depression in the RA population.

The kynurenine pathway in patients with rheumatoid arthritis during tumor necrosis factor α inhibitors treatment.

Introduction: The importance of the kynurenine pathway in normal immune system function has led to an appreciation of its possible contribution to autoimmune disorders such as rheumatoid arthritis (RA). The aim of the study was to evaluate the effect of treatment with tumor necrosis factor α (TNF-α) inhibitors on the activity of the kynurenine pathway in patients with RA. Material and methods: This was an investigator-initiated, prospective, observational study. The study was performed on 30 RA patients (Caucasian, 11 male, 19 female; mean age 45 ±16 years) treated with TNF-α inhibitors. All patients were assessed before and after 6 months of therapy. As a control group, age- and sex-matched, 20 healthy volunteers were recruited. Disease activity was evaluated by the Modified Disease Activity Score with 28-joint count (DAS28). Inflammatory markers were assessed routinely by the hospital central laboratory. Serum concentrations of kynurenine, serotonin and tryptophan were measured with specific immunoassays. To estimate indoleamine 2,3-dioxygenase (IDO) activity, kynurenine-to-tryptophan ratio was calculated. Results: The results of our study showed changes in tryptophan metabolism in RA patients, compared with healthy controls. Surprisingly, RA patients had statistically significant decreased kynurenine-to-tryptophan ratio (p = 0.003), which could indicate diminished IDO activation in RA. Moreover, we found no significant changes in kynurenine-to-tryptophan ratio after treated with TNF-α inhibitors (p = 0.490), despite disease remission. Additionally, tryptophan metabolism activity did not correlate with objective markers of inflammation. Conclusions: The RA patients had altered tryptophan metabolism, compared with healthy controls. The mechanisms affecting tryptophan metabolism in RA may be complex. We believe that continuing elucidation of pathophysiological pathways relevant in RA offer substantial hope for the development of specific pharmacotherapy for treatment of RA - especially for comorbidity of RA and depression.

Therapeutic drug monitoring in inflammatory bowel disease: recent developments.

INTRODUCTION: Therapeutic Drug Monitoring (TDM) has an important role in the management of inflammatory bowel disease (IBD) patients on infliximab (IFX) or adalimumab and is recommended in IBD patients presenting a loss of response under anti TNF agent. But, TDM was not recommended for others biotherapies. AREAS COVERED: Analyzing all publications about TDM and biologics in IBD patients, we reported the major results for each biotherapy. EXPERT OPINION: Emerging data suggest that TDM will probably be similarly useful forIFX SC. In contrast, there is no demonstrated clinical benefit to the use of TDM with golimumab. For vedolizumab results for the use of both reactive and proactive TDM are discordant. For ustekinumab, data supports the existence of an exposure response relationship, albeit of a lesser magnitude than with anti-TNF agents. Finally, recent data from small case series suggests that TDM could be valuable in optimizing anti-IL23 agents, particularly risankizumab, but this requires further clarification. Consistent with the new concept of 'proactive' strategy, recent data support the utility of dashboard-driven model informed precision dosing (MIDP) of anti-TNF agents, in particular infliximab. Dashboards are software systems using Bayesian population pharmacokinetic modelling to individualize recommendations for target drug levels.

Ulcerative colitis: molecular insights and intervention therapy.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by abdominal pain, diarrhea, rectal bleeding, and weight loss. The pathogenesis and treatment of UC remain key areas of research interest. Various factors, including genetic predisposition, immune dysregulation, and alterations in the gut microbiota, are believed to contribute to the pathogenesis of UC. Current treatments for UC include 5-aminosalicylic acids, corticosteroids, immunosuppressants, and biologics. However, study reported that the one-year clinical remission rate is only around 40%. It is necessary to prompt the exploration of new treatment modalities. Biologic therapies, such as anti-TNF-α monoclonal antibody and JAK inhibitor, primarily consist of small molecules targeting specific pathways, effectively inducing and maintaining remission. Given the significant role of the gut microbiota, research into intestinal microecologics, such as probiotics and prebiotics, and fecal microbiota transplantation (FMT) shows promising potential in UC treatment. Additionally, medicinal herbs, such as chili pepper and turmeric, used in complementary therapy have shown promising results in UC management. This article reviews recent findings on the mechanisms of UC, including genetic susceptibility, immune cell dynamics and cytokine regulation, and gut microbiota alterations. It also discusses current applications of biologic therapy, herbal therapy, microecologics, and FMT, along with their prospects and challenges.

Osteopoikilosis in a young ankylosing spondylitis patient.

Osteopoikilosis (OPK) is a rare benign congenital genetic-mediated sclerosing skeletal disease, characterized by the formation of osteosclerosis foci. OPK is usually clinically asymptomatic, but some patients (15%~20%) may have arthralgia and synovitis. OPK may be associated with rheumatic diseases and might lead to unreasonable over-examination in real clinical practice. Single cases of the OPK together with ankylosing spondylitis (AS) have been described. Here we present a 33-year-old patient diagnosed with AS coexisting with OPK. In the case considered, the combination of AS and OPK accompanied with a high activity of inflammation, peripheral arthritis, a rapid rate of structural progression in axial skeleton, inefficiency of disease-modifying antirheumatic drugs and nonsteroidal anti-inflammatory drugs, a lack of response to anti interleukin-17 and a good response to a tumor necrosis factor inhibitor golimumab. We describe the important points of differential diagnosis associated with the identification of focal changes in bone tissue, especially neoplastic lesion. Foci revealed had typical localization, so, acquaintance of practicing doctors with such rare cases would minimize unnecessary examinations.

Neuropathic pain in spondyloarthritis: Decoding its prevalence, risk factors, and impact on disease activity.

OBJECTIVES: This study aimed to evaluate the prevalence and characteristics of neuropathic pain in patients with various subtypes of spondyloarthritis (SpA), including axial SpA (axSpA), psoriatic arthritis (PsA), and undifferentiated peripheral SpA (p-SpA). Additionally, the study sought to identify potential risk factors associated with the presence or severity of neuropathic pain and to investigate its impact on clinical disease activity assessment. METHODS: We conducted a cross-sectional study at two tertiary rheumatology centers, enrolling patients diagnosed with SpA. Data on demographic and clinical characteristics, comorbidities, and current therapies were collected. Neuropathic pain was assessed using the PainDETECT Questionnaire (PD-Q) and the Neuropathic Pain Symptom Inventory (NPSI). Statistical analyses included descriptive statistics, t-tests, and Pearson's correlations to evaluate the relationships between neuropathic pain scores and clinical disease activity indices. RESULTS: The study included 177 patients. Of these, 22.2% had a PD-Q score ≥19, showing a high likelihood of neuropathic pain, while 64.9% scored ≤12, suggesting the absence of significant neuropathic components. The mean PD-Q score was 11.5 ± 10.1. Subgroup analyses showed that females had significantly higher scores for paroxysmal and evoked pain (p < 0.05), and obese patients had significantly higher scores across all NPSI subscores (p < 0.05). Moderate positive correlations were found between neuropathic pain scores and clinical disease activity indices, such as DAPSA (r = 0.46, p < 0.0001) and ASDAS-CRP (r = 0.42, p < 0.01). CONCLUSIONS: Neuropathic pain is prevalent among patients with SpA and is significantly associated with disease activity assessments and management. This study highlights the importance of integrating neuropathic pain evaluation into the clinical assessment of SpA to tailor treatment approaches effectively and improve patient outcomes.

Agreement of Medication Information Derived From EHR Data Compared to Medicare Insurance Claims: An Analysis of Biologic Disease-Modifying Antirheumatic Drugs.

PURPOSE: Few studies have reported the agreement between medication information derived from ambulatory EHR data compared to administrative claims for high-cost specialty drugs. We used data from a national EHR-enabled registry, the Rheumatology Informatics System for Effectiveness (RISE), with linked Medicare claims in a population of patients with rheumatoid arthritis (RA) to investigate variations in agreement for different biologic disease-modifying agents (bDMARDs) between two data sources (RISE EHR data vs. Medicare claims), categorized by drug, route of administration, and patient insurance factors (dual eligibility). METHODS: Patients ≥ 65 years old, with ≥ 2 visits in RISE with RA ICD codes ≥ 30 days apart, and continuous enrollment in Medicare Parts B and D in 2017-2018 were included. We classified patients as bDMARD users or nonusers in Medicare claims or EHR data in 2018, and we calculated sensitivity, specificity, positive predicted value (PPV), and negative predicted value (NPV) of EHR data for identifying bDMARD users, using Medicare as the reference standard. We also calculated these metrics after stratifying by clinic-administered (Part B) versus. pharmacy-dispensed (Part D) bDMARDs and by patient dual-eligibility. RESULTS: A total of 26 097 patients were included in the study. Using Medicare claims as the reference standard, EHR data had a sensitivity of 75.0%-90.8% for identifying patients with the same medication and route. PPV for Part B bDMARDs was higher compared with Part D bDMARDs (range 94.3%-97.3% vs. 51.0%-69.6%). We observed higher PPVs for Part D bDMARDs among patients who were dual-eligible (range 82.4%-95.1%). CONCLUSION: The risk of misclassification of drug exposure based on EHR data sources alone is small for Medicare Part B bDMARDs but could be as high as 50% for Part D bDMARDs, in particular for patients who are not dually eligible for Medicare and Medicaid.

Does the Combined Arteritis Damage Score (CARDS) in the Diagnosis of Takayasu Arteritis Predict Prognosis and Need for Biologic Therapy?

BACKGROUND: We aimed to investigate the prognostic value of the combined arteritis damage score (CARDS) in Takayasu arteritis (TAK) patients to predict the need for biologic treatment at diagnosis and the possible contribution of wall thickness (WT). MATERIALS AND METHODS: Blind evaluation of MRA/CTA at the time of diagnosis was performed by a reader rheumatologist (RR) and an interventional radiologist (RIR). The CARDS damage score for 21 arterial regions was assessed as normal, mild or moderate/severe stenosis, occclusion or aneursym/dilatation. Additionally, WT was scored for all regions as present or absent. A modified CARDS (mCARDS) was calculated as the sum of CARDS and the number of WT areas. RESULTS: According to follow-up treatment, 10 patients with non-biologic treatment (non-BT) (F/M:8/2, median age 37.5 years) and 15 patients with biologic treatment (BT) (F/M:13/2, median age 30 years) were included. Indian Takatasu Arteritis Score (ITAS), CRP, and ESR levels were similar in both groups. CARDS (1.4 (0-7.2) vs 4.5 (.6-19), P: .003), WT (1.5 (0-8) vs 7 (1-21), P < .001), and mCARDS (4 (0-14.2) vs 11.4 (1.6-40), P < .001) scores were significantly higher in the BT group compared to nonBT group. Cohen's kappa coefficient between RR and RIR for WT was .99 with 99.6% aggrement, and CARDS was .98 with 99.6% agreement. The AUC values for CARDS, WT, and mCARDS scores were .748 (.605-.892), .837 (.723-.950), and .847 (.735-.958), respectively, and P value was <.0001. CONCLUSIONS: The prediction of prognosis and biologic treatment need at TAK diagnosis using non-invasive angiographic images can improve outcomes and prompt closer follow-up. The combination of CARDS and WT as mCARDS achieved the highest sensitivity and specificity, and all scores appear useful for predicting prognosis.

Bone-protective effects of neutralizing angiopoietin-like protein 4 monoclonal antibody in rheumatoid arthritis.

Despite recent advances, rheumatoid arthritis (RA) patients remain refractory to therapy. Dysregulated overproduction of angiopoietin-like 4 protein (ANGPTL4) is thought to be contributed to the disease development. ANGPTL4 was initially identified as a regulator of lipid metabolism, which is hydrolyzed to N-terminal (nANGPTL4) and C-terminal (cANGPTL4) fragments in vivo. cANGPTL4 is involved in several non-lipid-related processes, including angiogenesis and inflammation. The present study revealed that the level of ANGPTL4 was markedly elevated in the sera and synovial tissues from patients with RA versus controls. The administration of a neutralizing antibody against cANGPTL4 (anti-cANGPTL4 Ab) resulted in the inhibition of inflammatory processes and bone loss in animal models of collagen-induced arthritis (CIA) and adjuvant-induced arthritis (AIA). Transcriptomic and proteomic profiling of synovial tissues from AIA model indicated that the anti-cANGPTL4 Ab inhibited fibroblast-like synoviocytes (FLS) immigration and inflammatory-induced osteoclastogenesis. Mechanistically, the anti-cANGPTL4 Ab has been shown to inhibit TNF-α-induced inflammatory cascades in RA-FLS through the sirtuin 1/nuclear factor-κB signaling pathway. Moreover, the anti-cANGPTL4 Ab was found to block FLS invasion- and immigration-induced osteoclast activation. Collectively, these findings identify ANGPTL4 as a prospective biomarker for the diagnosis of RA, and targeting cANGPTL4 may represent a potential therapeutic strategy.

The Association of Interleukin-36 Staining Intensity and Response to Biologic Therapy in Patients With Psoriasis: A Retrospective Immunohistochemical and Chart Review Pilot Study.

BACKGROUND: There are limited surrogate biomarkers to identify the active inflammatory pathway in psoriasis to direct treatment with targeted biologic therapies. We investigated the association of interleukin (IL)-36 epidermal expression, a diagnostic marker of psoriasis, with response to biologic therapy in patients with psoriasis. METHODS: Retrospective immunohistochemical and chart review pilot study. RESULTS: Patients with psoriasis with low (scores 0-2) vs. high (scores 3-4) IL-36 expression did not have significantly different response rates to tumor necrosis factor α (TNFα), IL-17, and IL-12/23 or IL-23 inhibitors; and similarly, mean IL-36 expression scores did not significantly differ among responders vs. non-responders to each treatment mechanism. However, in patients with psoriasis treated with IL-12/23 or IL-23 inhibitors, there was a marked absolute difference in response rates in those with high vs. low IL-36 (84% vs. 50%, p = 0.12) and in mean IL-36 scores in responders vs. non-responders (3.35 vs. 2.57, p = 0.19). CONCLUSIONS: Patients with psoriasis with high IL-36 expression were more likely to respond to IL-12/23 and IL-23 inhibition than those with low IL-36, though these findings were not statistically significant. Additional studies with larger sample sizes are needed to validate and expand upon these findings.

2023 guidelines on the management of psoriasis by the Dermatological Society of Singapore.

Introduction: Psoriasis is a multisystem, chronic, inflammatory dermatological disease. In routine clinical practice, the management of psoriasis varies significantly. The current study aimed to develop a set of practice guidelines relevant to dermatology practice in Singapore. Method: The Psoriasis Therapeutic Guidelines Workgroup, comprising members of the Dermato-logical Society of Singapore with a subspecialisation in psoriasis, was convened to develop the guidelines. Clinical questions on selected topics were generated and refined by the workgroup. A literature search using PubMed was performed on their assigned topics from June 2013 to December 2023. The articles were included and graded based on the level of evidence. Results: The guidelines address topics ranging from clinical assessment to practical considerations in the management of mild, moderate and severe psoriasis, including delivery of care, referrals to specialists and adherence to treatment. The recommended therapies include phototherapy, methotrexate, acitretin, cyclosporine; apremilast; topical corticoste-roids, calcipotriol, topical calcineurin inhibitors; and biologics (i.e. adalimumab, infliximab, secukinumab, ixekizumab, ustekinumab, etanercept) either in combina-tion or as monotherapy. Common therapeutic concerns relating to biologic use were addressed. Recommendations on generalised pustular psoriasis, palmoplantar pustular psoriasis and psoriatic arthritis were also made. Patients on systemic therapy would receive appropriate vaccine counselling. Therapeutic implica-tions in special populations, such as pregnant/ lactating women, children, the elderly, those undergo-ing surgery and those suffering from specific infections and cancer were addressed. Conclusion: These guidelines were developed for dermatologists, family physicians, rheumatologists and other specialists to support their selection of appropriate management options.

A systematic review and meta-analysis of randomized controlled trials for the management of ventral hernia: biologic versus synthetic mesh.

An abdominal wall hernia near the location of a prior surgical incision is referred to as an incisional hernia. A midline incisional hernia is the most prevalent form. The management of incisional hernia includes many options, from conservative to surgical. The surgeon might consider using a synthetic or biological mesh when discussing surgical options with patients. Our aim through this study is to comprehensively compare synthetic and biological mesh in terms of complication and infection rates for managing elective incisional hernia. This systematic review was designed and conducted using PRISMA guidelines. The literature was systematically searched in January 2023 using the following databases: MEDLINE, Cochrane, and EMBASE. Among the terms used to aid the search were the following: incisional hernia, ventral hernia, ventral herniorrhaphy, biologic mesh, polypropylene mesh, absorbable mesh, permanent mesh, biomaterial mesh, biological mesh, and synthetic mesh. The review of the literature resulted in a total of 3115 publications. By applying our criteria, six articles were included in this study, with 949 participants. Our meta-analysis showed the overall complication incidence displaying a significant difference favouring the synthetic mesh group (IV = 1.25, 95% CI 1.11-1.42, P = 0.0002). The operation failure rate, defined as hernia recurrence, also significantly favoured synthetic mesh (IV = 2.42, 95% CI 1.66-3.52, P < 0.00001). In conclusion, the present study found that the synthetic mesh proved superior in overall complication rate and operation failure compared to biologic mesh. However, it had no significant differences in other complications.

Rheumatic Adverse Effects With Biologics Targeting Type 2 Inflammation In Severe Asthma: A Vigibase® Study.

CLINICAL IMPLICATIONS BOX: Biologics in severe asthma are associated with an excess reporting of rheumatic diseases and rheumatic symptoms in the WHO database. The profile of rheumatic adverse events varies according to biologics and their mechanisms of action.

Effectiveness and safety of tildrakizumab in individuals with HIV and psoriasis: A case series.

Psoriasis, a chronic inflammatory skin disease, presents unique challenges when co-occurring with HIV. Tildrakizumab, an IL-23p19 inhibitor, has demonstrated efficacy in treating moderate-to-severe psoriasis. This retrospective case series reports three individuals living with HIV and psoriasis treated with tildrakizumab. Clinical outcomes, including Psoriasis Area and Severity Index (PASI) and HIV viral load, were recorded over a year. All three patients achieved significant clinical improvements with tildrakizumab, with PASI scores improving by over 95%. No adverse effects were reported, and HIV viral loads remained undetectable. Tildrakizumab appears to be a safe and effective treatment option for psoriasis in individuals living with HIV, providing significant benefits without compromising HIV control.