Misdiagnosis of ANCA-associated vasculitis in patients with cocaine/levamisole –associated autoimmune syndrome and Cocaine-Induced Midline Destructive Lesions: A case series.

Misdiagnosis of ANCA-associated vasculitis in patients with cocaine/levamisole –associated autoimmune syndrome and Cocaine-Induced Midline Destructive Lesions: A case series. | Authorea try { document.documentElement.classList.add('js'); } catch (e) { } var _gaq = _gaq || []; _gaq.push(['_setAccount', 'G-8VDV14Y67G']); _gaq.push(['_trackPageview']); (function() { var ga = document.createElement('script'); ga.type = 'text/javascript'; ga.async = true; ga.src = ('https:' == document.location.protocol ? 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Authors : Kehinde Sunmboye 0000-0003-4824-1340 [email protected] , Ameen Jubber , Maumer Durrani , Jeremy Royle , and Shireen Shaffu Authors Info & Affiliations https://doi.org/10.22541/au.174413355.53224578/v1 Published Immunity, Inflammation and Disease Version of record Peer review timeline 564 views 255 downloads Contents Abstract Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Background: Cocaine/Levamisole-Associated Autoimmune Syndrome (CLAAS) encompasses a spectrum of autoimmune and vasculitic phenomena, which includes Cocaine-Induced Midline Destructive Lesions (CIMDL), which can mimic ANCA-associated vasculitis (AAV) due to overlapping clinical features and the potential for ANCA positivity. These similarities can lead to misdiagnosis and inappropriate immunosuppressive therapy. Methods: This study highlights a case series of seven patients (from 2015 to 2024) with CLAAS with its subset of CIMDL, initially misdiagnosed as active AAV, in patients who were referred to various clinicians in the Rheumatology unit of a Tertiary Hospital in the United Kingdom. Results: All patients presented with nasal symptoms, and they all exhibited additional systemic manifestations consistent with CLAAS. Five were ANCA-positive at initial evaluation, leading to the initiation of immunosuppressive therapy; however, symptoms persisted. The diagnoses were then revised to CIMDL in all cases within the broader context of CLAAS following the identification of cocaine use after further patient enquiry and urine toxicology for drug of abuse (DOA) screening found cocaine metabolites. Conclusion: A comprehensive drug history and urine toxicology screening are crucial in patients with suspected AAV, as ANCA positivity can occur in CLAAS as well as its subset of CIMDL, complicating the diagnosis. Differentiating between AAV and CIMDL related to CLAAS is essential to avoid unnecessary immunosuppression. Introduction The emergence of cocaine/levamisole-associated autoimmune syndrome (CLAAS), alongside its subset of cocaine-induced midline destructive lesions (CIMDL), has significantly complicated the diagnostic landscape, particularly in the evaluation of patients presenting with symptoms suggestive of vasculitis. These syndromes introduce new challenges due to the clinical overlap between drug-induced conditions and genuine autoimmune disorders, such as antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), most notably granulomatosis with polyangiitis (GPA). The shared clinical manifestations between CIMDL and AAV—such as nasal crusting, epistaxis, and septal perforation—make it difficult to distinguish between these two conditions based solely on clinical presentation (Shoji et al., 2023; Gill et al., 2022; Berman et al., 2016). CLAAS, which is a systemic manifestation of cocaine induced disease can also cause constitutional symptoms that can occur in AAV. CIMDL, the localised manifestation of CLAAS can create diagnostic dilemmas as it can cause epistaxis, nasal crusting and facial pain (Shoji et al., 2023). Patients with CLASS as well as CIMDL can also tests positive for ANCA, a serological marker traditionally associated with active AAV, particularly with the cytoplasmic ANCA (c-ANCA) directed against proteinase-3 (PR3), which can blur the diagnostic boundaries between drug-induced and autoimmune processes (Gill et al., 2022; McGrath et al., 2011). This overlap in clinical and serological findings often leads to misdiagnoses, which may result in the inappropriate administration of immunosuppressive therapies. These treatments, while essential for managing AAV, expose patients to unnecessary risks, including increased susceptibility to infections and other complications, when misapplied in cases of substance-induced disease (Berman et al., 2016). Levamisole, a common adulterant found in street cocaine, has been increasingly implicated in the pathogenesis of autoimmune-like phenomena seen in both CLAAS and CIMDL, including ANCA positivity and vasculitis-like syndromes. Levamisole can induce a variety of vasculitis-like syndromes that closely mimic AAV, complicating the diagnostic process further (Graf et al., 2011; Cascio & Jen, 2018; Jin et al., 2018). The pathophysiological mechanisms underlying CLAAS as well as CIMDL, particularly the contributions of both cocaine and its adulterants like levamisole in inducing ANCA positivity, are areas of ongoing research that warrant careful clinical scrutiny (Shoji et al., 2023; Graf et al., 2011; Cascio & Jen, 2018). Studies have demonstrated that both cocaine and levamisole can activate neutrophils, leading to the formation of neutrophil extracellular traps (NETs), a process implicated in the promotion of inflammation and the development of autoimmunity (Shoji et al., 2023; Cascio & Jen, 2018). The presence of levamisole in cocaine has been particularly associated with a distinctive clinical syndrome characterized by purpura, skin necrosis, and a high prevalence of autoantibodies, including ANCAs (Jin et al., 2018). This association between levamisole and autoimmune-like phenomena adds to the diagnostic complexity, as patients often present with clinical features characteristic of both CIMDL and AAV, necessitating a nuanced and thorough evaluation (Shoji et al., 2023; Gill et al., 2022; Cascio & Jen, 2018). In the context of therapeutic interventions, it is critical to recognize that patients with CIMDL frequently do not respond to conventional immunosuppressive therapies that are typically effective for AAV. This resistance to standard treatment further complicates patient management, as clinicians may continue to escalate immunosuppressive regimens in the mistaken belief that they are dealing with a refractory case of AAV (Gill et al., 2022; Berman et al., 2016). However, cessation of cocaine use has been shown to significantly improve clinical outcomes in patients with CLAAS as well as CIMDL, limiting disease progression and enhancing surgical recovery when necessary (Trimarchi et al., 2021). Therefore, a critical component of improving diagnostic accuracy and patient management involves taking a thorough drug use history, including detailed inquiries about cocaine (often with levamisole exposure), and incorporating routine urine toxicology screening into the diagnostic workup within the clinic setting. This case series therefore aims to emphasize the importance of urine toxicology in the diagnostic process for all patients with AAV and optimize patient care by emphasizing the importance of distinguishing between drug-induced vasculitis and true autoimmune vasculitis. We have also set out to see if there is any pattern of clinical or biochemical features unique to this cohort of patients. The discussion will also focus on key clinical and histopathological differences between CLAAS as well as CIMDL and AAV, as well as the patterns of ANCA positivity that may aid clinicians in making an accurate diagnosis. Additionally, this study underscores the need for a multidisciplinary approach, involving rheumatologists, otolaryngologists, and addiction specialists, to ensure that patients with suspected drug induced vasculitidies receive appropriate care and avoid the risks associated with misdiagnosis (Veronese et al., 2016). Case Series: not-yet-known not-yet-known not-yet-known unknown Case 1: Patient A Case Summary A 26-year-old woman presented with pulmonary haemorrhage, arthralgia affecting the small joints of her hands, and a history of constitutional symptoms. She also reported numbness and neuropathic pain in her limbs. Diagnostic Workup The admitting respiratory team did not initially document a history of recreational drug use. Blood tests revealed elevated inflammatory markers without eosinophilia. A chest X-ray showed bilateral haziness across the lung fields (Figure 1), and chest CT imaging confirmed the presence and extent of pulmonary involvement (Figure 2). The combination of radiographic changes and raised C-reactive protein levels (see Table 1) prompted a provisional diagnosis of active ANCA-associated vasculitis (AAV), although ANCA testing returned negative. A more detailed social history later revealed regular cocaine use. Urine toxicology confirmed the presence of benzoylecgonine (a cocaine metabolite) and cannabinoids, establishing recent drug exposure. Treatment and Outcome Clinicians initially administered high-dose intravenous methylprednisolone for suspected AAV. However, following confirmation of cocaine exposure, they revised the diagnosis to pulmonary haemorrhage secondary to cocaine/levamisole-associated autoimmune syndrome (CLAAS). The patient’s symptoms resolved without the need for further immunosuppressive therapy. She did not require ongoing specialist follow-up. The team provided education about the health risks of continued drug use and referred her to addiction support services. not-yet-known not-yet-known not-yet-known unknown Figure 1: Chest x-ray for patient A, showing Bilateral lung field haziness. not-yet-known not-yet-known not-yet-known unknown Figure 2: Chest CT for patient A showing ground glass shadowing at the level of the tracheal bifurcation. Case 2: Patient B Case Summary A 31-year-old woman presented with several months of recurrent nasal crusting and episodes of epistaxis. She also reported bilateral sensorineural hearing loss and arthralgia affecting the small joints of her hands. Diagnostic Workup Her laboratory tests showed normal inflammatory markers but revealed eosinophilia on her full blood count. Chest imaging was unremarkable. A nasal biopsy demonstrated moderately severe inflammation, raising suspicion for ANCA-associated vasculitis (AAV). Serological testing confirmed elevated PR3-ANCA levels at 12 IU/mL (normal <3.5 IU/mL) (see Table 1). At the time of initial evaluation, the team did not obtain a history of recreational drug use. Treatment and Outcome She began immunosuppressive treatment with methotrexate, which was later switched to azathioprine due to persistent symptoms. As her condition remained refractory, clinicians escalated treatment to rituximab. Despite this, she continued to experience nasal crusting, recurrent epistaxis, and worsening joint pain. A regional specialist centre subsequently reviewed her case. Urine toxicology testing detected benzoylecgonine, confirming recent cocaine use. This led to a reassessment of her diagnosis, which was revised to cocaine-induced midline destructive lesions (CIMDL). Her clinical team discontinued rituximab, and she has since remained off immunosuppressive therapy. She received counselling about the health risks of ongoing drug use and was referred to addiction support services. Patient age (in years) Gender eGFR (ml/min/1.73m 2 ) Eosinophila at presentation (Highest Value of Eosinophilia) Normal: less than 0.4 X 10 9 /L) C-reactive protein level (mg/L) (Normal <5) ANCA result Peak PR3-ANCA levels (if applicable) Normal value for PR3-ANCA (90 No 13 Negative Not applicable Yes Benzoylecgonine, Cannabinoids Discharge from Hospital care 31 Female >90 Yes (0.58) Normal Positive (C-ANCA) PR3-ANCA (12 IU/ml) No Benzoylecgonine Discharge from Hospital care 33 Female >90 Yes (0.52) 19 Positive (C-ANCA) PR3-ANCA (119 IU/ml) No Benzoylecgonine and norcocaine Under clinical surveillance not on treatment 34 Male >90 Yes (0.90) Normal Negative Not applicable No benzoylecgonine, morphine,codeine, norcodeine and hydrocodone Discharge from Hospital care 44 Female >90 Yes (1.09) 11 Positive (C-ANCA) PR3-ANCA (40 IU/ml) No Pregabalin, benzoylecgonine and norcocaine, Tramadol and metabolite(o-desmethyltramadol) Discharge from Hospital care 47 Male 86 Yes (0.61) 16 Positive (C-ANCA) PR3-ANCA (23 IU/ml) No Benzoylecgonine) and cannabinoid metabolite (THC-COOH) Discharge from Hospital care 58 Male >90 Yes (0.99) 31 Positive (C-ANCA) PR3-ANCA (38 IU/ml) Yes Cocaine, Benzoylecgonine, Under clinical surveillance on conventional synthetic disease modifying herapy not-yet-known not-yet-known not-yet-known unknown Table 1: Table showing patient demographics, renal function, blood eosinophilia, ANCA positivity and subtype and urine metabolite products. not-yet-known not-yet-known not-yet-known unknown Case 3: Patient C Case Summary A 33-year-old woman presented with nasal crusting, a history of nasal septal perforation, and polyarthralgia. She had previously received ENT care for her nasal symptoms but was referred to the rheumatology team due to persistent and refractory issues. Diagnostic Workup Her blood tests showed elevated inflammatory markers and eosinophilia on full blood count. Serological testing revealed a markedly elevated PR3-ANCA level of 119 IU/mL (normal <3.5 IU/mL). The rheumatology team performed a routine urine toxicology screen, which detected cocaine and its metabolites—benzoylecgonine and norcocaine. Following these results, the patient disclosed a history of recreational drug use. Treatment and Outcome Although the referral was based on a working diagnosis of active ANCA-associated vasculitis, the combination of persistent nasal disease and positive toxicology findings prompted a revision of the diagnosis to cocaine-induced midline destructive lesions (CIMDL). She continues treatment with methotrexate for ongoing inflammatory joint symptoms and nasal involvement. However, her management has not escalated to rituximab. The team provided counselling on the health risks associated with continued drug use and referred her to addiction support services. Case 4: Patient D Case Summary A 34-year-old man presented with several years of nasal congestion that improved with both inhaled and oral corticosteroids. He also experienced purulent nasal discharge, a sensation of nasal fullness, and worsening symptoms when steroids were withdrawn. He had a history of recurrent visits to ENT services for nasal obstruction and intermittent sinus blockage. Diagnostic Workup Laboratory tests showed normal inflammatory markers and eosinophilia on full blood count. A nasal biopsy demonstrated moderately severe inflammation but no histological evidence of vasculitis. His initial ANCA result was positive but became negative on repeated testing. Urine toxicology identified multiple drug metabolites, including benzoylecgonine (cocaine), morphine, codeine, norcodeine, and hydrocodone, raising strong suspicion of drug-induced nasal injury consistent with CIMDL. Treatment and Outcome Clinicians had initially treated him with corticosteroids based on a presumed diagnosis of limited ANCA-associated vasculitis. However, the confirmation of recent cocaine use prompted a diagnostic revision to cocaine-induced midline destructive lesions (CIMDL). His team discontinued steroids and transitioned to conservative management. He was counselled about the health risks associated with ongoing drug use and referred to addiction support services. Case 5: Patient E Case Summary A 44-year-old woman presented with a nasal septal perforation. She had a known diagnosis of multiple sclerosis and was receiving natalizumab infusions as part of her treatment. She also reported ongoing nasal symptoms, including nasal crusting and dryness. Diagnostic Workup Blood tests revealed slightly elevated inflammatory markers and eosinophilia on full blood count. Further serological testing showed a positive PR3-ANCA result at 40 IU/mL (normal <3.5 IU/mL). Urine toxicology confirmed the presence of multiple drug metabolites, including benzoylecgonine and norcocaine (cocaine metabolites), as well as tramadol, o-desmethyltramadol, and pregabalin. Treatment and Outcome Although she was initially evaluated for possible ANCA-associated vasculitis, the detection of cocaine use on toxicology testing led to a revised diagnosis of cocaine-induced midline destructive lesions (CIMDL). Her clinical team did not initiate immunosuppressive therapy. She received counselling on the risks of continued drug use and was referred to addiction support services. Case 6: Patient F Case Summary A 47-year-old man presented with persistent nasal crusting and epistaxis, along with polyarthralgia affecting multiple joints. Diagnostic Workup Blood tests showed elevated inflammatory markers and eosinophilia on full blood count. Serology confirmed a persistently positive PR3-ANCA at 23 IU/mL (normal <3.5 IU/mL). At the time of initial assessment, clinicians did not obtain a social drug history. Treatment and Outcome He received multiple immunosuppressive therapies, including methotrexate, azathioprine, and mycophenolate mofetil. Due to lack of response, his treatment was escalated to rituximab. Despite ongoing rituximab and corticosteroid therapy, his nasal and systemic symptoms worsened. A urine toxicology screen was eventually performed and detected benzoylecgonine (cocaine metabolite) and THC-COOH (cannabinoid metabolite). Following this result, he disclosed ongoing cocaine use. Clinicians revised his diagnosis to cocaine/levamisole-associated autoimmune syndrome (CLAAS) with associated cocaine-induced midline destructive lesions (CIMDL). Rituximab and corticosteroids were discontinued. He remains on mycophenolate mofetil for management of CLAAS. He was counselled on the risks of continued drug use and referred to addiction support services. not-yet-known not-yet-known not-yet-known unknown Case 7: Patient G Case Summary A 58-year-old man presented to ENT services with several years of recurrent sinusitis, nasal discharge, crusting, and epistaxis. He also reported polyarthralgia and had a documented history of ocular inflammation, specifically uveitis. CT imaging of the sinuses revealed a nasal septal perforation (Figure 3). Diagnostic Workup Laboratory testing showed elevated inflammatory markers and eosinophilia on full blood count. Serological analysis revealed a positive PR3-ANCA result at 38 IU/mL (normal <3.5 IU/mL). At the time of initial evaluation, the clinical team did not obtain a social drug history. Treatment and Outcome Based on his ocular involvement and positive ANCA serology, clinicians initiated treatment with rituximab for suspected ANCA-associated vasculitis (AAV). Despite therapy, he remained symptomatic, and his PR3-ANCA titres continued to rise. A urine toxicology screen later detected both cocaine and its metabolite benzoylecgonine. In light of this finding, clinicians attributed his persistent ANCA positivity to ongoing cocaine exposure. They discontinued rituximab and administered intravenous methylprednisolone to manage acute symptoms. No additional immunosuppressive agents were started. He received counselling regarding the impact of cocaine use on his health and was referred to addiction support services. Figure 3: CT sinus (axial view), with the red arrow showing nasal perforation. not-yet-known not-yet-known not-yet-known unknown Discussion The cases presented highlight the complex diagnostic challenges involved in distinguishing cocaine/levamisole-associated autoimmune syndrome (CLAAS) and cocaine-induced midline destructive lesions (CIMDL) from ANCA-associated vasculitis (AAV). This challenge is especially evident in patients who test positive for ANCA, a marker long considered central to diagnosing AAV. However, this assumption can mislead clinicians when assessing patients with recent or ongoing cocaine exposure (Gill et al., 2022; Shoji et al., 2023). This is made even more imperative with the recent increase in recreational drug use in many countries in the world (OECD, 2023). Overlapping features—such as nasal crusting, epistaxis, septal perforation, and constitutional symptoms—commonly appear in both CIMDL and AAV (Bruce et al., 2022; Green et al., 2020). Clinicians often attribute these signs to idiopathic vasculitis without exploring substance-related causes. In several of the cases in this series, patients tested positive for PR3-ANCA with cytoplasmic (C-ANCA) patterns. One patient had a PR3-ANCA titre of 119 IU/mL. While PR3-ANCA is typically associated with granulomatosis with polyangiitis, its presence is increasingly observed in drug-induced syndromes (Cosola et al., 2021; Pendolino, 2023). This is especially true when atypical ANCA reactivities such as elastase antibodies are also involved—a known feature of CIMDL and CLAAS (Cohen Tervaert & Damoiseaux, 2012; Milman & Smith, 2011). The absence of elastase ANCA testing across these cases represents a limitation. Human neutrophil elastase antibodies help distinguish CIMDL and would have strengthened diagnostic accuracy (Shoji et al., 2023; McGrath et al., 2011). Although P-ANCA patterns with MPO or elastase specificity are more typical in CIMDL, five of the seven patients in this series showed C-ANCA with PR3-ANCA, further confounding the clinical picture. Some may have had idiopathic AAV with incidental cocaine use, but others likely had drug-induced vasculitis that mimicked AAV serologically as they were consequently discharged from hospital care without sequelae. These overlaps highlight the need to interpret ANCA results within context. PR3-ANCA alone should not confirm AAV in the absence of thorough drug history and toxicology testing (Cohen Tervaert & Damoiseaux, 2012; Pendolino, 2023). In all seven cases, clinicians revised their diagnoses only after identifying cocaine metabolites such as benzoylecgonine, or other substances including cannabinoids, opioids, and tramadol, via urine toxicology when the clinical course of the patient and poor response to therapy necessitated a review. Omitting routine toxicology screening delayed accurate diagnosis and led to inappropriate immunosuppression in several patients. High-dose corticosteroids, methotrexate, azathioprine, mycophenolate mofetil, and rituximab were used before drug exposure was confirmed. These treatments carry serious risks when misapplied (Bruce et al., 2022; Ortiz-Seller et al., 2021). It is worth noting that it may be necessary to use immunosuppressive therapy in cases where systemic features predominate (Berman et al. 2016 and van der Veer et al. 2015). While immunosuppression is generally ineffective in CIMDL, selected patients with CLAAS may benefit if systemic features are a dominant clinical phenotype. However, the default use of these therapies without confirming aetiology must be avoided (Veronese et al., 2016). The presence of eosinophilia can further complicate diagnosis. All patients in this series had eosinophilia, which may suggest eosinophilic granulomatosis with polyangiitis or drug-induced hypersensitivity (Challa et al., 2023). Eosinophilic infiltration may mimic granulomatous vasculitis histologically and be misinterpreted as AAV (Gill et al., 2022; Blaise et al., 2016). However Levamisole is known to have immunostimulatory properties which can contribute to eosinophilia in either CLAAS or CIMDL (Arora et al., 2012; Abdul-Karim et al., 2013). In this cohort, several patients had PR3-ANCA alongside eosinophilia—which is an unusual pairing in idiopathic AAV. These discrepancies demand broader differential diagnoses. Atypical ANCA, such as anti-elastase antibodies, frequently co-occur with PR3 in drug-induced disease (Milman & Smith, 2011). As Cohen Tervaert and Damoiseaux (2012) emphasize, clinicians must interpret ANCA pattern and antigen specificity together, especially when drug exposure is suspected. As cocaine is frequently adulterated with levamisole, which induces vasculitis-like syndromes including neutropenia, purpura, and arthralgia (Veer et al., 2015; Arora et al., 2012) any patient with non-organ threatening or ENT limited disease should have urine toxicology assessments. Although urine toxicology has a limited detection window as cocaine metabolites typically clear within 72 hours, patients who are chronic users of cocaine may have persistent positive urine toxicology (Lawrence et al., 2014). A negative test also does not rule out recent use (Lawrence et al., 2014). Hair testing offers a more reliable measure of chronic exposure, including to levamisole. In the case by van der Veer et al. (2015), hair testing provided critical diagnostic clarity when urine results were negative. To improve diagnostic accuracy, clinicians should implement structured protocols that include routine drug screening during the initial evaluation of suspected AAV—especially in patients with predominant sinonasal disease. Delayed toxicology testing not only leads to misdiagnosis but also misses the chance to intervene on substance misuse (Lawrence et al., 2014; Veronese et al., 2016). The complexity of these presentations supports the need for multidisciplinary care, involving rheumatologists, otolaryngologists, pathologists, and addiction specialists (Green et al., 2020). Further research should quantify ANCA prevalence in drug-using populations and explore immune responses to cocaine and levamisole. Large prospective studies comparing idiopathic AAV with CLAAS may reveal novel biomarkers, similar to elastase ANCA, that improve diagnostic discrimination (Rees et al., 2023; Blanco et al., 2022). not-yet-known not-yet-known not-yet-known unknown Conclusion This case series demonstrates the diagnostic complexity surrounding cocaine/levamisole-associated autoimmune syndrome (CLAAS) and cocaine-induced midline destructive lesions (CIMDL), particularly in patients with ANCA positivity and sinonasal symptoms. Misdiagnosis as idiopathic ANCA-associated vasculitis (AAV) can lead to unnecessary and potentially harmful immunosuppressive treatment. Accurate diagnosis depends on careful ANCA interpretation, awareness of atypical serologic patterns, and systematic toxicology screening. Clinicians must recognize the immunological effects of cocaine and levamisole, especially amid rising recreational drug use. A structured, multidisciplinary approach—including addiction assessment—can prevent misdirected treatment and ensure patients receive care aligned with their underlying pathology. Acknowledgements To the patients whom gave us the privilege and trust to take care of the medical condition. Ethics Committee Approval: Ethics committee approval was received for this study from the Leicester, Leicesteshire and Rutland ethics committee of Institutional Review Board Informed Consent: Consent was obtained from patients who participated in this study. Data availability The data supporting the findings of this study are not publicly available due to ethical restrictions Author Contributions: Concept – K.S., S.S., J.R.; Design - KS., S.S., J.R; Supervision -K.S; Resources – K.S.,S.S.J.R,A.J, M.D; Materials -K.S.,S.S.J.R,A.J, M.D; Data Collection and/or Processing - K.S.,S.S.J.R,A.J, M.D; Analysis and/or Interpretation - K.S.,S.S.J.R,A.J, M.D; Literature Search – K.S., S.S., J.R. 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Collection Immunity, Inflammation and Disease Keywords antibodies autoimmunity human inflammation Authors Affiliations Kehinde Sunmboye 0000-0003-4824-1340 [email protected] University of Leicester View all articles by this author Ameen Jubber University Hospitals of Leicester NHS Trust View all articles by this author Maumer Durrani University Hospitals of Leicester NHS Trust View all articles by this author Jeremy Royle University Hospitals of Leicester NHS Trust View all articles by this author Shireen Shaffu University Hospitals of Leicester NHS Trust View all articles by this author Metrics & Citations Metrics Article Usage 564 views 255 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Kehinde Sunmboye, Ameen Jubber, Maumer Durrani, et al. Misdiagnosis of ANCA-associated vasculitis in patients with cocaine/levamisole –associated autoimmune syndrome and Cocaine-Induced Midline Destructive Lesions: A case series.. Authorea . 08 April 2025. 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