<p>Rheumatology is facing an expanding care gap, as the number of newly referred patients continues to outpace the availability of rheumatologists [<span>1</span>], resulting in longer diagnostic delays—often weeks to months—that lead to irreversible damage, poorer treatment outcomes, and higher societal costs [<span>2</span>]. Patients and physicians alike struggle with fluctuating, often nonspecific symptoms (e.g., joint pain), and this challenge is compounded by limited awareness of rheumatic diseases among both the general population and general practitioners. The poor specificity of referrals and the inability of traditional triage approaches to improve the situation widen the care gap further. Although patient education is integral to rheumatology care, it remains underutilized due to inadequate reimbursement and workforce shortages, leaving many patients feeling poorly informed about their disease. Clinicians also face a significant time burden with clinical documentation [<span>3</span>], especially for newly referred patients.</p><p>In response to these multifaceted challenges, digital health technologies (DHT) have emerged as a promising cornerstone to enhance diagnosis, information provision, patient education, documentation and alleviating workforce shortages. With the rapid proliferation of smartphones and advanced DHT, traditional care delivery models should be reevaluated to leverage these innovations [<span>4</span>]. Task-shifting is increasingly being implemented to mitigate workforce shortages, wherein tasks are delegated from physicians to nurses, medical students, or other healthcare professionals. However, task-shifting remains limited in scale and cost-efficiency and DHT could significantly leverage widespread implementation [<span>5</span>].</p><p>Currently increasing numbers of rheumatic patients turn to online platforms for initial symptom assessment [<span>6</span>], and diagnostic decision support systems (DDSS), that can empower patients to receive preliminary diagnoses within minutes. Although computer-aided diagnosis for rheumatologists has existed for decades [<span>7</span>], adoption has been hindered by poor usability [<span>8</span>], including time-intensive data entry [<span>9</span>] and restricted querying options. These limitations also affect patient education, as static, often printed information leaves patients scrolling through lengthy materials rather than engaging in open-ended, personalized exploration. To bridge these limitations recently made advancements in large-language-model-technology (LLM) can be used for unprecedented scalability and multimodal data processing. Therefore DHT usability, performance, and the patient-provider relationship could be significantly improved by integrating LLM-driven decision support within a collaborative digital health triad [<span>4</span>]. By continuously processing patient- and provider-generated data, LLMs can deliver more personalized, accessible, and dynam
{"title":"Harnessing Large Language Models for Rheumatic Disease Diagnosis: Advancing Hybrid Care and Task Shifting","authors":"Fabian Lechner, Sebastian Kuhn, Johannes Knitza","doi":"10.1111/1756-185X.70124","DOIUrl":"https://doi.org/10.1111/1756-185X.70124","url":null,"abstract":"<p>Rheumatology is facing an expanding care gap, as the number of newly referred patients continues to outpace the availability of rheumatologists [<span>1</span>], resulting in longer diagnostic delays—often weeks to months—that lead to irreversible damage, poorer treatment outcomes, and higher societal costs [<span>2</span>]. Patients and physicians alike struggle with fluctuating, often nonspecific symptoms (e.g., joint pain), and this challenge is compounded by limited awareness of rheumatic diseases among both the general population and general practitioners. The poor specificity of referrals and the inability of traditional triage approaches to improve the situation widen the care gap further. Although patient education is integral to rheumatology care, it remains underutilized due to inadequate reimbursement and workforce shortages, leaving many patients feeling poorly informed about their disease. Clinicians also face a significant time burden with clinical documentation [<span>3</span>], especially for newly referred patients.</p><p>In response to these multifaceted challenges, digital health technologies (DHT) have emerged as a promising cornerstone to enhance diagnosis, information provision, patient education, documentation and alleviating workforce shortages. With the rapid proliferation of smartphones and advanced DHT, traditional care delivery models should be reevaluated to leverage these innovations [<span>4</span>]. Task-shifting is increasingly being implemented to mitigate workforce shortages, wherein tasks are delegated from physicians to nurses, medical students, or other healthcare professionals. However, task-shifting remains limited in scale and cost-efficiency and DHT could significantly leverage widespread implementation [<span>5</span>].</p><p>Currently increasing numbers of rheumatic patients turn to online platforms for initial symptom assessment [<span>6</span>], and diagnostic decision support systems (DDSS), that can empower patients to receive preliminary diagnoses within minutes. Although computer-aided diagnosis for rheumatologists has existed for decades [<span>7</span>], adoption has been hindered by poor usability [<span>8</span>], including time-intensive data entry [<span>9</span>] and restricted querying options. These limitations also affect patient education, as static, often printed information leaves patients scrolling through lengthy materials rather than engaging in open-ended, personalized exploration. To bridge these limitations recently made advancements in large-language-model-technology (LLM) can be used for unprecedented scalability and multimodal data processing. Therefore DHT usability, performance, and the patient-provider relationship could be significantly improved by integrating LLM-driven decision support within a collaborative digital health triad [<span>4</span>]. By continuously processing patient- and provider-generated data, LLMs can deliver more personalized, accessible, and dynam","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70124","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143248694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Geoffrey Littlejohn, Nithila Anbumurali, Catherine O'Sullivan, Tegan Smith, Tina Racunica, Peta Pentony, Suren Jayaweera, Laila Girgis, Christine M. Smyth, Claire T. Deakin
{"title":"The Relationship Between Patient-Reported Quality of Life and Physician-Derived Clinical Outcomes in Rheumatoid Arthritis in the Australian OPAL Dataset","authors":"Geoffrey Littlejohn, Nithila Anbumurali, Catherine O'Sullivan, Tegan Smith, Tina Racunica, Peta Pentony, Suren Jayaweera, Laila Girgis, Christine M. Smyth, Claire T. Deakin","doi":"10.1111/1756-185X.70123","DOIUrl":"https://doi.org/10.1111/1756-185X.70123","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143111916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Correction for Figure 2: Revise the measurement of the apical diameter of the capillaries.
We apologize for this error.
{"title":"Correction to “Alterations on Nailfold Videocapillaroscopy in Myelodysplastic Syndrome and Onychomycosis in a Female Smoker: Microvascular Dysfunction Without Connective Tissue Disease” A. Nigro, “ Alterations on Nailfold Videocapillaroscopy in Myelodysplastic Syndrome and Onychomycosis in a Female Smoker: Microvascular Dysfunction Without Connective Tissue Disease,” International Journal of Rheumatic Diseases 27 (2024): e70000.","authors":"","doi":"10.1111/1756-185X.70122","DOIUrl":"https://doi.org/10.1111/1756-185X.70122","url":null,"abstract":"<p>Correction for Figure 2: Revise the measurement of the apical diameter of the capillaries.</p><p>We apologize for this error.</p>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70122","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143111915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Estelle Noonan, Matthew Verheyden, Hwei Choo Soh, Alexander Dunn, Christina Liang, Mitchell Lycett, Leticia Deveza
{"title":"Case Report: Inflammatory Myositis Presenting as Dropped Head Syndrome in a Patient With Rheumatoid Antibodies","authors":"Estelle Noonan, Matthew Verheyden, Hwei Choo Soh, Alexander Dunn, Christina Liang, Mitchell Lycett, Leticia Deveza","doi":"10.1111/1756-185X.70098","DOIUrl":"https://doi.org/10.1111/1756-185X.70098","url":null,"abstract":"","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143111914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wanping Lv, Huixiang Chen, Pan Zhou, Aihua Du, Yu Lei
Hyperuricemia (HUA) is a metabolic condition resulting from an abnormality in the process of purine metabolism. Its occurrence has been on the rise globally. The results of relevant studies show that 5% to 12% of HUA patients will eventually develop gout, and one-third of these patients may involve the kidneys and develop kidney disease. Although the severe renal health hazards associated with excessive uric acid levels are well known, the specific molecular mechanisms remain unknown. Therefore, this paper provides insights into the mechanisms and related chain reactions of HUA leading to renal injury from three perspectives: imbalance of intestinal homeostasis, oxidative stress response, and NLRP3 inflammasome. In addition, standing against the background of the strong side effects and high tolerability disadvantages of commercially available uric acid-lowering drugs such as allopurinol, benzbromarone, and febuxostat, the development of a new active anti-hyperuricemic drug with fewer side effects is justified. This article reviews the progress of research on natural actives (probiotics, dietary polyphenols, peptides) with a high safety profile, multi-targeting, and integrative modulatory effects, in an attempt to provide some ideas for drug developers.
{"title":"Mechanisms Associated With Renal Injury in Hyperuricemia and Strategies for the Development of Natural Active Substances","authors":"Wanping Lv, Huixiang Chen, Pan Zhou, Aihua Du, Yu Lei","doi":"10.1111/1756-185X.70096","DOIUrl":"10.1111/1756-185X.70096","url":null,"abstract":"<div>\u0000 \u0000 <p>Hyperuricemia (HUA) is a metabolic condition resulting from an abnormality in the process of purine metabolism. Its occurrence has been on the rise globally. The results of relevant studies show that 5% to 12% of HUA patients will eventually develop gout, and one-third of these patients may involve the kidneys and develop kidney disease. Although the severe renal health hazards associated with excessive uric acid levels are well known, the specific molecular mechanisms remain unknown. Therefore, this paper provides insights into the mechanisms and related chain reactions of HUA leading to renal injury from three perspectives: imbalance of intestinal homeostasis, oxidative stress response, and NLRP3 inflammasome. In addition, standing against the background of the strong side effects and high tolerability disadvantages of commercially available uric acid-lowering drugs such as <i>allopurinol</i>, <i>benzbromarone</i>, and <i>febuxostat</i>, the development of a new active anti-hyperuricemic drug with fewer side effects is justified. This article reviews the progress of research on natural actives (probiotics, dietary polyphenols, peptides) with a high safety profile, multi-targeting, and integrative modulatory effects, in an attempt to provide some ideas for drug developers.</p>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To explore the relationship between an innovative anoikis-related gene signature and inflammatory infiltrates in patients with osteoarthritis.
Methods
Gene expression profiles (GSM1248759 and GSE200843) were curated from the Gene Expression Omnibus database, followed by the construction of a protein–protein interaction network. Functional and genomic enrichment analyses were conducted using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. The CIBERSORT method was employed to investigate immune cell infiltration differences between osteoarthritic and control tissues. Additionally, the ConsensusClusterPlus package in R software was utilized to identify distinct anoikis patterns (Cluster C1 and Cluster C2) and conduct molecular biological investigations.
Results
Analysis revealed two distinct anoikis patterns (Cluster C1 and Cluster C2), with Cluster C2 patients exhibiting varying immune cell levels compared to Cluster C1 patients. Molecular investigations identified 84 DEGs enriched in specific pathways such as adipocytokine signaling, cytokine–cytokine receptor interaction, ECM–receptor interaction, and the PPAR signaling pathway. qPCR experiments confirmed the elevated expression levels of specific genes, including SOD2, MAPK14, CEACM3, LAMB3, COL13A1, TLR3, NOTCH3, and KLF12, in the IL-1β-induced group compared with the osteoarthritis group.
Conclusion
This study highlights the role of anoikis-related genes and immune infiltration differences in osteoarthritis, enhancing our understanding of its development.
{"title":"An Innovative Anoikis Signature With Inflammatory Infiltrates in Osteoarthritis","authors":"Ze-Hao Sheng, Xin-Yi Gong, Peng-Peng Huang, Qi-Yu Xu, Wen-Jie Zhang, Feng-Bao Sun, Kai-yi Song, Du-Chun Zeng","doi":"10.1111/1756-185X.70093","DOIUrl":"10.1111/1756-185X.70093","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>To explore the relationship between an innovative anoikis-related gene signature and inflammatory infiltrates in patients with osteoarthritis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Gene expression profiles (GSM1248759 and GSE200843) were curated from the Gene Expression Omnibus database, followed by the construction of a protein–protein interaction network. Functional and genomic enrichment analyses were conducted using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. The CIBERSORT method was employed to investigate immune cell infiltration differences between osteoarthritic and control tissues. Additionally, the ConsensusClusterPlus package in R software was utilized to identify distinct anoikis patterns (Cluster C1 and Cluster C2) and conduct molecular biological investigations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Analysis revealed two distinct anoikis patterns (Cluster C1 and Cluster C2), with Cluster C2 patients exhibiting varying immune cell levels compared to Cluster C1 patients. Molecular investigations identified 84 DEGs enriched in specific pathways such as adipocytokine signaling, cytokine–cytokine receptor interaction, ECM–receptor interaction, and the PPAR signaling pathway. qPCR experiments confirmed the elevated expression levels of specific genes, including <i>SOD2</i>, <i>MAPK14</i>, <i>CEACM3</i>, <i>LAMB3</i>, <i>COL13A1</i>, <i>TLR3</i>, <i>NOTCH3</i>, and <i>KLF12</i>, in the IL-1β-induced group compared with the osteoarthritis group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study highlights the role of anoikis-related genes and immune infiltration differences in osteoarthritis, enhancing our understanding of its development.</p>\u0000 </section>\u0000 </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shiuan-Tzuen Su, Yung-Heng Lee, Yuan-Chih Tsai, Po-Cheng Shih
<p>Type 2 diabetes mellitus (T2DM) is a long-term metabolic disorder marked by persistent hyperglycemia, mainly due to insulin resistance and impaired insulin production. Rising rates of obesity and sedentary behavior have fueled a global increase in T2DM. While complications such as cardiovascular disease, nephropathy, neuropathy, and retinopathy are well known, recent research highlights a notable link between T2DM and bone health. Patients with T2DM face a higher risk of fractures, even with normal or increased bone mineral density (BMD), primarily due to compromised bone quality and a greater likelihood of falls.</p><p>In a study conducted in Finland using rat bone marrow, short-term hyperglycemia (lasting 1 or 3 days) was found to stimulate osteoblast activity. However, when hyperglycemia persisted for a longer duration (10 days), it led to increased production of reactive oxygen species (ROS), which ultimately impaired osteoblast function [<span>1</span>], highlights the dual effects of hyperglycemia on bone health, with transient elevations possibly supporting bone formation, while prolonged exposure contributes to oxidative stress and compromised osteoblast performance.</p><p>In a longitudinal study conducted in the United States, Ballato et al. examined 169 T2DM male patients and found that poor glycemic control over 1 year was linked to reduced bone turnover and impaired bone microarchitecture [<span>2</span>]. Further analysis of 51 male T2DM patients indicated that poorly managed long-term blood sugar levels were associated with an increase in circulating osteogenic progenitor (COP) cells, potentially hindering the maturation of these cells into osteoblasts [<span>3</span>]. This disruption in cellular development may contribute to weakened bone formation and structure, underscoring the impact of glycemic control on bone health in T2DM patients.</p><p>Chronic hyperglycemia leads to the accumulation of advanced glycation end products (AGEs), which impair bone formation by promoting osteoblast apoptosis [<span>4</span>]. A systematic review of 66 studies found that hyperglycemia decreases osteoblast and osteoclast activity, also resulting in reduced bone turnover and increased fracture risk in T2DM [<span>5</span>]. However, the BMD of patients with T2DM is generally normal to higher compared to non-diabetics [<span>4</span>]. The elevated risk of fractures may not directly correlate with BMD in T2DM.</p><p>Older patients had a higher osteoporosis fracture risk. This finding suggests that factors beyond BMD may contribute to the heightened fracture risk in patients with T2DM. Here, we explore some of these potential reasons.</p><p>Reduced physical activity causes sarcopenia through loss of type II fast-twitch muscle, which impairs glucose uptake by skeletal muscle, and T2DM is associated with sarcopenia [<span>6</span>]. A UK study found reduced proximal leg muscle strength in 20 T2DM patients with diabetic polyneuropathy compared to 20
{"title":"Glycemic Control and Fracture Risk in Patients With Type 2 Diabetes Mellitus","authors":"Shiuan-Tzuen Su, Yung-Heng Lee, Yuan-Chih Tsai, Po-Cheng Shih","doi":"10.1111/1756-185X.70103","DOIUrl":"10.1111/1756-185X.70103","url":null,"abstract":"<p>Type 2 diabetes mellitus (T2DM) is a long-term metabolic disorder marked by persistent hyperglycemia, mainly due to insulin resistance and impaired insulin production. Rising rates of obesity and sedentary behavior have fueled a global increase in T2DM. While complications such as cardiovascular disease, nephropathy, neuropathy, and retinopathy are well known, recent research highlights a notable link between T2DM and bone health. Patients with T2DM face a higher risk of fractures, even with normal or increased bone mineral density (BMD), primarily due to compromised bone quality and a greater likelihood of falls.</p><p>In a study conducted in Finland using rat bone marrow, short-term hyperglycemia (lasting 1 or 3 days) was found to stimulate osteoblast activity. However, when hyperglycemia persisted for a longer duration (10 days), it led to increased production of reactive oxygen species (ROS), which ultimately impaired osteoblast function [<span>1</span>], highlights the dual effects of hyperglycemia on bone health, with transient elevations possibly supporting bone formation, while prolonged exposure contributes to oxidative stress and compromised osteoblast performance.</p><p>In a longitudinal study conducted in the United States, Ballato et al. examined 169 T2DM male patients and found that poor glycemic control over 1 year was linked to reduced bone turnover and impaired bone microarchitecture [<span>2</span>]. Further analysis of 51 male T2DM patients indicated that poorly managed long-term blood sugar levels were associated with an increase in circulating osteogenic progenitor (COP) cells, potentially hindering the maturation of these cells into osteoblasts [<span>3</span>]. This disruption in cellular development may contribute to weakened bone formation and structure, underscoring the impact of glycemic control on bone health in T2DM patients.</p><p>Chronic hyperglycemia leads to the accumulation of advanced glycation end products (AGEs), which impair bone formation by promoting osteoblast apoptosis [<span>4</span>]. A systematic review of 66 studies found that hyperglycemia decreases osteoblast and osteoclast activity, also resulting in reduced bone turnover and increased fracture risk in T2DM [<span>5</span>]. However, the BMD of patients with T2DM is generally normal to higher compared to non-diabetics [<span>4</span>]. The elevated risk of fractures may not directly correlate with BMD in T2DM.</p><p>Older patients had a higher osteoporosis fracture risk. This finding suggests that factors beyond BMD may contribute to the heightened fracture risk in patients with T2DM. Here, we explore some of these potential reasons.</p><p>Reduced physical activity causes sarcopenia through loss of type II fast-twitch muscle, which impairs glucose uptake by skeletal muscle, and T2DM is associated with sarcopenia [<span>6</span>]. A UK study found reduced proximal leg muscle strength in 20 T2DM patients with diabetic polyneuropathy compared to 20","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>Chronic nonbacterial osteitis (CNO) represents an infrequent, chronic, and relapsing inflammatory affliction of the bone with an undetermined cause. It is distinguished by a persistent state of inflammation within the bone marrow, a condition that is not instigated by bacterial infections [<span>1</span>]. Necrobiosis gangrenosum, a rare inflammatory skin disease within the spectrum of neutrophilic dermatoses, is primarily characterized by painful ulcers [<span>2</span>]. In some instances, CNO may manifest in the form of pyoderma gangrenosum. This is predominantly attributable to the nature of CNO as an autoinflammatory disorder [<span>1</span>]. Previous studies have demonstrated the efficacy of Janus kinase inhibitors (JAKis) in the treatment of necrobiosis gangrenosum [<span>2</span>]. Here, we report a case of CNO predominantly manifested by necrobiosis gangrenosum, which showed significant improvement following treatment with abrocitinib.</p><p>The patient is a middle-aged male presenting with extensive skin rashes on the hands and trunk (Figure 1A1,A3), accompanied by pain in the upper chest and buttocks. Laboratory tests revealed a C-reactive protein (CRP) level of 17.8 mg/L, while a 99mTc bone image showed localized increased metabolic activity in the sternum and sacrococcygeal region (Figure 1B). Skin pathology confirmed the diagnosis of necrobiosis gangrenosum (Figure 1C), leading to a final diagnosis of CNO. The patient was initially treated with a nonsteroidal anti-inflammatory drug (NSAID) in combination with tofacitinib at a dosage of 5 mg twice daily for a duration of 6 months. Although there was relief from bone pain, the skin rash did not improve. Subsequently, the treatment regimen was changed to abrocitinib at a dosage of 200 mg once daily. After 6 months of this therapy, there was a marked improvement in the skin rash (Figure 1A2,A4).</p><p>Currently, JAKis have been widely utilized in treating SAPHO syndrome, consistently demonstrating favorable therapeutic outcomes [<span>3</span>]. Given that SAPHO syndrome's osteomyelitis is part of the CNO spectrum, we postulate that JAKis may also have comparable therapeutic effectiveness in treating CNO. Regarding the treatment of pyoderma gangrenosum, JAKis are regarded as a promising alternative therapeutic approach [<span>4</span>]. However, conventional literature suggests that abrocitinib can effectively treat pyoderma gangrenosum [<span>5</span>]. Against this backdrop, we commenced treating a patient with abrocitinib at a dosage of 200 mg once daily. After 3 months, a marked improvement was observed in the rashes on the patient's hands and trunk. After an additional 6 months of treatment, the skin lesions on the trunk showed even more significant alleviation compared to earlier evaluations. These results highlight the substantial advantage of abrocitinib in managing the skin manifestations of CNO, especially when pyoderma gangrenosum is the predominant feature. However, it is
{"title":"Investigating the Efficacy Variability of Different JAK Inhibitors in Chronic Nonbacterial Osteitis (CNO) Presenting Primarily With Pyoderma Gangrenosum","authors":"Ruitian Ma, Zhi Ye, Chen Li, Zhenhua Ying","doi":"10.1111/1756-185X.70110","DOIUrl":"10.1111/1756-185X.70110","url":null,"abstract":"<p>Chronic nonbacterial osteitis (CNO) represents an infrequent, chronic, and relapsing inflammatory affliction of the bone with an undetermined cause. It is distinguished by a persistent state of inflammation within the bone marrow, a condition that is not instigated by bacterial infections [<span>1</span>]. Necrobiosis gangrenosum, a rare inflammatory skin disease within the spectrum of neutrophilic dermatoses, is primarily characterized by painful ulcers [<span>2</span>]. In some instances, CNO may manifest in the form of pyoderma gangrenosum. This is predominantly attributable to the nature of CNO as an autoinflammatory disorder [<span>1</span>]. Previous studies have demonstrated the efficacy of Janus kinase inhibitors (JAKis) in the treatment of necrobiosis gangrenosum [<span>2</span>]. Here, we report a case of CNO predominantly manifested by necrobiosis gangrenosum, which showed significant improvement following treatment with abrocitinib.</p><p>The patient is a middle-aged male presenting with extensive skin rashes on the hands and trunk (Figure 1A1,A3), accompanied by pain in the upper chest and buttocks. Laboratory tests revealed a C-reactive protein (CRP) level of 17.8 mg/L, while a 99mTc bone image showed localized increased metabolic activity in the sternum and sacrococcygeal region (Figure 1B). Skin pathology confirmed the diagnosis of necrobiosis gangrenosum (Figure 1C), leading to a final diagnosis of CNO. The patient was initially treated with a nonsteroidal anti-inflammatory drug (NSAID) in combination with tofacitinib at a dosage of 5 mg twice daily for a duration of 6 months. Although there was relief from bone pain, the skin rash did not improve. Subsequently, the treatment regimen was changed to abrocitinib at a dosage of 200 mg once daily. After 6 months of this therapy, there was a marked improvement in the skin rash (Figure 1A2,A4).</p><p>Currently, JAKis have been widely utilized in treating SAPHO syndrome, consistently demonstrating favorable therapeutic outcomes [<span>3</span>]. Given that SAPHO syndrome's osteomyelitis is part of the CNO spectrum, we postulate that JAKis may also have comparable therapeutic effectiveness in treating CNO. Regarding the treatment of pyoderma gangrenosum, JAKis are regarded as a promising alternative therapeutic approach [<span>4</span>]. However, conventional literature suggests that abrocitinib can effectively treat pyoderma gangrenosum [<span>5</span>]. Against this backdrop, we commenced treating a patient with abrocitinib at a dosage of 200 mg once daily. After 3 months, a marked improvement was observed in the rashes on the patient's hands and trunk. After an additional 6 months of treatment, the skin lesions on the trunk showed even more significant alleviation compared to earlier evaluations. These results highlight the substantial advantage of abrocitinib in managing the skin manifestations of CNO, especially when pyoderma gangrenosum is the predominant feature. However, it is","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 2","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1756-185X.70110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143079963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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