Drug-induced hypersensitivity reaction presenting as systemic capillary leak-like syndrome with polyserositis: a case report

Drug-induced hypersensitivity reaction presenting as systemic capillary leak-like syndrome with polyserositis: a case report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Drug-induced hypersensitivity reaction presenting as systemic capillary leak-like syndrome with polyserositis: a case report Ninh Xuan Nguyen, Ngoc Tien Pham, Huong Thi Thanh Le, Quoc Viet Tran, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6511758/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 01 Jul, 2025 Read the published version in BMC Rheumatology → Version 1 posted 11 You are reading this latest preprint version Abstract Background Systemic capillary leak syndrome (SCLS) is a rare disorder characterized by increased vascular permeability leading to third-spacing of fluids and protein. Drug-induced hypersensitivity reactions can mimic SCLS clinically and radiologically. Case Presentation: A 42-year-old Vietnamese man developed abdominal distension, facial edema, and dyspnea after initiation of Helicobacter pylori eradication therapy. Imaging revealed pleural, pericardial, and peritoneal effusions, periportal edema, and interstitial pulmonary edema. Laboratory results showed hyponatremia, hypoalbuminemia, and mild anemia. Autoimmune screening revealed ANA positivity (1:80, speckled) and lupus anticoagulant, though extractable nuclear antigens were negative. The patient improved rapidly with corticosteroids and antihistamines. Conclusion This case highlights a systemic hypersensitivity reaction mimicking capillary leak syndrome, likely drug-induced, and occurring in a patient with subclinical autoimmune predisposition. It underscores the importance of immune surveillance and early immunomodulatory therapy. Drug hypersensitivity systemic capillary leak polyserositis autoimmune gastritis lupus anticoagulant ANA cytokine-mediated reaction Figures Figure 1 Figure 2 Figure 3 Background Systemic capillary leak syndrome (SCLS) is a rare, life-threatening condition that results in plasma extravasation into interstitial and serosal compartments. While idiopathic SCLS is classically defined by the triad of hypotension, hemoconcentration, and hypoalbuminemia, secondary forms—particularly those induced by drugs—may present atypically and are underrecognized. Hypersensitivity reactions to antimicrobial or proton pump inhibitor therapy can result in systemic capillary leak-like features through endothelial dysfunction and cytokine storm [2]. Case Presentation A 42-year-old Vietnamese man presented with progressive abdominal distension, dyspnea, and periorbital edema 5 days after initiating a second-line Helicobacter pylori eradication regimen including esomeprazole, amoxicillin, levofloxacin, bismuth, and Bacillus clausii , along with desloratadine. He had previously experienced mild eyelid and extremity swelling after a prior regimen including esomeprazole, rifaximin, and antacid therapy. On admission, he was normotensive, afebrile, and alert. Examination revealed ascites, bilateral pedal edema, and decreased breath sounds at the bases. Lab work showed hyponatremia (Na 121 mmol/L), hypoalbuminemia (31.6 g/L), elevated CRP (16.6 mg/L), and normocytic anemia. Chest X-ray showed bilateral basal infiltrates and cardiomegaly (Fig. 1) . CT showed bilateral pleural effusions, interstitial pulmonary edema, periportal edema, pericardial effusion, and gallbladder wall thickening ( Fig. 2 ). ANA was positive (1:80, speckled), and lupus anticoagulant was positive on repeat testing. Tryptase was within normal limits, ruling out anaphylaxis. Gastric biopsies showed chronic gastritis with intestinal metaplasia and features suggestive of early autoimmune gastritis. He was treated with IV methylprednisolone (80 mg/day) and oral desloratadine. Symptoms improved significantly within 48 hours, and electrolytes normalized. He was discharged on day 4 with outpatient follow-up ( Fig. 3 ). Investigations: Hematology: Normocytic anemia, leukocytosis, elevated CRP Biochemistry: Hyponatremia, hypoalbuminemia, normal liver enzymes Autoimmunity: ANA 1:80, lupus anticoagulant (+), normal complements Histopathology: Gastritis with intestinal metaplasia and glandular atrophy (suggestive of autoimmune gastritis) Imaging: See Fig. 1 , Fig. 2 ; causality assessment summarized in Table 1 Insert Figure 1 here Insert Figure 2 here Differential Diagnosis: Idiopathic SCLS: no hypotension, no hemoconcentration → unlikely DRESS syndrome: no eosinophilia, rash, or hepatic injury Autoimmune disease (SLE/APS): ANA and LAC positive but below classification threshold Nephrotic syndrome: proteinuria not in nephrotic range Drug-induced systemic hypersensitivity: most consistent with clinical and laboratory findings ( Table 1 , Fig. 2 ) Treatment: IV methylprednisolone 80 mg/day × 3 days Oral desloratadine 5 mg BID Hypertonic saline for hyponatremia Discontinuation of offending agents Outcome and Follow-up: Rapid clinical improvement was observed, with resolution of edema and normalization of sodium. At 1-month follow-up, ANA and LAC remained positive but no autoimmune clinical manifestations emerged. Further rheumatology follow-up planned ( Fig. 3 ). Insert Figure 3 here Discussion This case underscores the clinical complexity and diagnostic challenge of drug-induced systemic hypersensitivity reactions that can phenotypically resemble systemic capillary leak syndrome (SCLS). While classic idiopathic SCLS is defined by hypotension, hypoalbuminemia, and hemoconcentration [1], drug-induced variants—especially those involving cytokine-mediated endothelial dysfunction—may lack the full triad. The patient presented with multisystem fluid shifts including pleural effusions, pericardial fluid, and ascites—consistent with a capillary leak-like phenomenon ( Fig. 2 ). The absence of hypotension and elevated hematocrit argued against idiopathic SCLS but aligned more closely with hypersensitivity-mediated endothelial permeability dysfunction. Imaging revealed periportal edema, interstitial pulmonary changes, and gallbladder wall thickening—all indicative of systemic inflammatory insult ( Fig. 2 ). A notable feature in this case was the temporal association between the H. pylori eradication regimen and symptom onset. The patient had received amoxicillin, levofloxacin, and esomeprazole—drugs known to elicit hypersensitivity reactions, though rarely manifesting as diffuse capillary leak [2,3]. We utilized the Naranjo algorithm to assess causality, resulting in a total score of +5, suggesting a “probable” link to drug-induced etiology ( Table 1 ) [4]. Notably, the patient had experienced milder edema during the first drug course, suggesting sensitization. Insert Table 1 here The absence of eosinophilia and rash reduces the likelihood of DRESS syndrome. However, cytokine release syndromes (CRS)—an increasingly recognized adverse drug reaction—present with similar systemic inflammatory features. IL-6, TNF-α, and VEGF have been implicated in capillary leak pathogenesis [5]. Although cytokine assays were not performed in this case, the patient’s rapid response to corticosteroids and antihistamines supports an immune-mediated mechanism. Further, serological findings of ANA (1:80, speckled) and lupus anticoagulant positivity suggest transient autoimmune activation. ANA seropositivity in the absence of systemic features may result from drug exposure and typically resolves upon withdrawal of the offending agent [6]. Lupus anticoagulant, however, has implications for hypercoagulability and warrants longitudinal monitoring [7]. In this case, follow-up serology at one month remained positive, though the patient was asymptomatic. In parallel, gastric histopathology demonstrated moderate chronic gastritis with intestinal metaplasia and glandular atrophy, raising suspicion for early-stage autoimmune gastritis. Autoimmune gastritis is characterized by chronic inflammation of the gastric body mucosa, loss of parietal cells, and eventual hypochlorhydria, often accompanied by autoantibodies against parietal cells and intrinsic factor. It is frequently associated with other autoimmune conditions, including systemic lupus erythematosus, autoimmune thyroiditis, and type 1 diabetes mellitus [8]. Although anti-parietal cell antibodies and serum vitamin B12 levels were not assessed in this case, the histological features—combined with the presence of transient ANA and lupus anticoagulant positivity—suggest a background of latent immune dysregulation. This may have predisposed the patient to an exaggerated immunologic response to drug exposure. Early recognition of autoimmune gastritis is important, not only for surveillance of micronutrient deficiencies but also because it may serve as a harbinger of systemic autoimmunity [9]. Differential diagnoses such as nephrotic syndrome were ruled out due to sub-nephrotic proteinuria. Idiopathic SCLS was deemed unlikely in the absence of shock or hemoconcentration. Serosal tuberculosis and viral causes were excluded based on cultures, imaging, and inflammatory markers. While one might question the incomplete exclusion of autoimmune diseases (e.g., early SLE or MCTD), the lack of systemic features or high-titer autoantibodies diminishes this probability. In sum, this case presents a compelling example of drug-induced hypersensitivity with systemic manifestations mimicking capillary leak, set against a background of latent autoimmune predisposition. Early recognition and immunomodulation are crucial to avoid escalation to multi-organ failure. Future reports should emphasize the inclusion of cytokine profiling, sequential autoantibody titers, and lymphocyte transformation tests when feasible to delineate drug causality more precisely. Conclusion Clinicians should maintain high suspicion for systemic hypersensitivity reactions in patients presenting with unexplained capillary leak, particularly when immune markers and drug history support a reactive etiology. This case highlights the role of immune dysregulation in atypical drug reactions and suggests the need for longitudinal monitoring for autoimmune sequelae. Learning Points: Systemic hypersensitivity can mimic SCLS with polyserositis without classical features. Naranjo scoring and temporal correlation assist in suspecting drug-induced causes. Transient ANA/LAC positivity may reflect immune activation during hypersensitivity reactions. Coexistent autoimmune gastritis may predispose patients to exaggerated drug responses. Corticosteroids and antihistamines can reverse severe manifestations effectively Declarations Ethics approval and consent to participate: Not applicable (case report; observational data from routine clinical care). Consent for publication: Written informed consent for publication of this case report and accompanying images was obtained from the patient. Availability of data and materials: All data generated or analyzed during this study are included in this published article. Competing interests: The authors declare that they have no competing interests. Funding: No funding was received for this study. Authors' contributions: Ninh Xuan Nguyen conceived the case report, supervised clinical care, and led the drafting of the manuscript. Ngoc Tien Pham and Huong Thi Thanh Le contributed to immunological data interpretation and literature review. Quoc Viet Tran and Hang Ngoc Thuy Tran were responsible for data collection, imaging documentation, and manuscript editing. An Thien Do provided expert input on immunological aspects and critically revised the manuscript. All authors read and approved the final version of the manuscript. Acknowledgements: The authors wish to thank the Department of Internal Medicine and Immunology, Vinmec Central Park Hospital, for their clinical support. Authors' information (optional): Dr. Ninh Xuan Nguyen is the Head of the Emergency Department at Vinmec Central Park International Hospital (Ho Chi Minh City, Vietnam). His clinical interests include systemic inflammatory disorders, drug-induced autoimmunity, and diagnostic challenges in internal medicine. References Druey KM, Parikh SM. Idiopathic systemic capillary leak syndrome. N Engl J Med. 2017;376(26):2456–2467. https://doi.org/10.1056/NEJMra1612647 González-Díaz SN, Zavala-Cerna MG, Vargas-Ramírez R, et al. Hypersensitivity reactions to antibiotics in pediatrics. J Investig Allergol Clin Immunol. 2022;32(2):84–93. https://doi.org/10.18176/jiaci.0769 Kim MH, Kang HR. Proton pump inhibitors and hypersensitivity: overview. World Allergy Organ J. 2020;13(3):100108. https://doi.org/10.1016/j.waojou.2020.100108 Naranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30(2):239–245. https://doi.org/10.1038/clpt.1981.154 Ogawa K, Morito T, Sugai S, et al. Cytokine profiles in patients with DRESS and other severe drug eruptions. J Am Acad Dermatol. 2021;84(2):466–475. https://doi.org/10.1016/j.jaad.2020.04.122 Tozzoli R, Bizzaro N, Tonutti E, et al. Guidelines for the laboratory use of autoantibody tests in autoimmune diseases. Autoimmun Rev. 2020;19(4):102510. https://doi.org/10.1016/j.autrev.2020.102510 Ruiz-Irastorza G, Crowther M, Branch W, Khamashta MA. Antiphospholipid syndrome. Lancet. 2010;376(9751):1498–1509. https://doi.org/10.1016/S0140-6736(10)60709-X Hershko C, Ronson A, Eliakim R. Autoimmune gastritis: pathogenesis and clinical implications. World J Gastroenterol. 2022;28(8):748–759. https://doi.org/10.3748/wjg.v28.i8.748 Neumann WL, Coss E, Rugge M, Genta RM. Autoimmune atrophic gastritis: pathogenesis, pathology and management. Nat Rev Gastroenterol Hepatol. 2013;10(9):529–541. https://doi.org/10.1038/nrgastro.2013.101 Table 1 Table 1. Naranjo Adverse Drug Reaction Probability Score applied to this case Question Answer Score Are there previous conclusive reports on this reaction? Yes +1 Did the adverse event appear after the suspected drug was administered? Yes +2 Did the adverse reaction improve when the drug was discontinued? Yes +1 Did the adverse reaction reappear when the drug was readministered? Not done 0 Are there alternative causes that could have caused the reaction? Possible -1 Did the reaction reappear with a placebo? Not done 0 Was the drug detected in blood (toxic concentration)? No 0 Was the reaction more severe when the dose was increased? No 0 Did the patient have a similar reaction to the same or similar drugs? Yes +1 Was the adverse event confirmed by any objective evidence? Yes +1 Total Score +5 (Probable) Scoring tool used to assess the likelihood of drug-induced adverse reactions. A score of +5 in this case indicates a probable causal relationship between drug exposure and systemic hypersensitivity manifestations Additional Declarations No competing interests reported. Cite Share Download PDF Status: Published Journal Publication published 01 Jul, 2025 Read the published version in BMC Rheumatology → Version 1 posted Editorial decision: Revision requested 02 Jun, 2025 Reviews received at journal 30 May, 2025 Reviewers agreed at journal 30 May, 2025 Reviews received at journal 22 May, 2025 Reviewers agreed at journal 22 May, 2025 Reviewers agreed at journal 22 May, 2025 Reviewers invited by journal 20 May, 2025 Editor assigned by journal 20 May, 2025 Editor invited by journal 19 May, 2025 Submission checks completed at journal 15 May, 2025 First submitted to journal 15 May, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6511758","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":459600801,"identity":"15a937b5-82b4-40fe-9b4d-0c23a6c5bb2e","order_by":0,"name":"Ninh Xuan Nguyen","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAuUlEQVRIiWNgGAWjYJCCA4wNDAz8DCCSJC2SDaRoAZtvcIBY1QYHeA8eLtxxJ3HzjeS2Rzcq7Bj427sTCGjhSzg888wzY7Mbie3GOWeSGSTOnN2AV4tkA4/BYd62w3JmZw62See2HWAwkMglTguPcQ9Iyz8itPAzQG0xYG8EamkgRgszRIuxxHGglpxjyTwE/cLG3mP8Gaglsb+Z/Zl0To2dHH97L34tDMxofB78ykfBKBgFo2AUEAUA9fxFIdUvQd0AAAAASUVORK5CYII=","orcid":"","institution":"Vinmec Central Park International Hospital","correspondingAuthor":true,"prefix":"","firstName":"Ninh","middleName":"Xuan","lastName":"Nguyen","suffix":""},{"id":459600802,"identity":"3657c642-51b9-4c5d-a9c6-c3b7ecf162be","order_by":1,"name":"Ngoc Tien Pham","email":"","orcid":"","institution":"Vinmec Central Park International Hospital","correspondingAuthor":false,"prefix":"","firstName":"Ngoc","middleName":"Tien","lastName":"Pham","suffix":""},{"id":459600803,"identity":"14257e8b-97c6-4b01-b219-7a37b3599092","order_by":2,"name":"Huong Thi Thanh Le","email":"","orcid":"","institution":"Vinmec Central Park International Hospital","correspondingAuthor":false,"prefix":"","firstName":"Huong","middleName":"Thi Thanh","lastName":"Le","suffix":""},{"id":459600804,"identity":"b9a115cf-53fa-4236-a2e0-2ff47badffdd","order_by":3,"name":"Quoc Viet Tran","email":"","orcid":"","institution":"Vinmec Central Park International Hospital","correspondingAuthor":false,"prefix":"","firstName":"Quoc","middleName":"Viet","lastName":"Tran","suffix":""},{"id":459600805,"identity":"093b2008-5eba-423f-a4fa-a25a65b205cc","order_by":4,"name":"Hang Ngoc Thuy Tran","email":"","orcid":"","institution":"Vinmec Central Park International Hospital","correspondingAuthor":false,"prefix":"","firstName":"Hang","middleName":"Ngoc Thuy","lastName":"Tran","suffix":""},{"id":459600806,"identity":"3c1c5d8c-7ec0-49ad-a0de-22c4c48b4011","order_by":5,"name":"An Thien Do","email":"","orcid":"","institution":"Vinmec Central Park International Hospital","correspondingAuthor":false,"prefix":"","firstName":"An","middleName":"Thien","lastName":"Do","suffix":""}],"badges":[],"createdAt":"2025-04-23 10:38:21","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6511758/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6511758/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1186/s41927-025-00535-6","type":"published","date":"2025-07-01T15:58:27+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":83436171,"identity":"ce8d2986-c367-4ac5-9ee8-dc6d54ce5b7a","added_by":"auto","created_at":"2025-05-26 08:32:45","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":297907,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eChest X-ray on admission.\u003c/strong\u003e\u003cbr\u003e\nFrontal chest radiograph showing bilateral basal interstitial infiltrates involving the lower third of both lungs. The costophrenic angles appear preserved. Cardiomegaly is evident with an enlarged cardiac silhouette.\u003c/p\u003e","description":"","filename":"Figure1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6511758/v1/32072324eade4b3230beb570.jpg"},{"id":83437186,"identity":"d874e9e7-3129-46db-a532-f5f66019b731","added_by":"auto","created_at":"2025-05-26 08:40:45","extension":"jpg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":389848,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eContrast-enhanced CT of the thorax and abdomen.\u003c/strong\u003e\u003cbr\u003e\nAxial CT images demonstrate periportal hypoattenuating edema, mild ascites, bilateral pleural effusions, interlobular septal thickening, dependent ground-glass opacities in lower lung zones, and a small pericardial effusion. Gallbladder wall thickening is also present. These findings suggest systemic capillary hyperpermeability secondary to hypersensitivity reaction.\u003c/p\u003e","description":"","filename":"Figure2.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6511758/v1/6c554f47c7e7c3c37c8996d6.jpg"},{"id":83437435,"identity":"5dcb4300-6124-4cc5-9042-e9c9e7741975","added_by":"auto","created_at":"2025-05-26 08:48:45","extension":"jpg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":391781,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eClinical timeline.\u003c/strong\u003e\u003cbr\u003e\nTimeline summarizing key clinical events from initial drug exposure, onset of symptoms, hospital course, to follow-up evaluation.\u003c/p\u003e","description":"","filename":"Figure3.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6511758/v1/3f683fc998a6ab6b04148af5.jpg"},{"id":86179881,"identity":"ee3a1118-e5e0-443a-9a2a-8ca9777eb492","added_by":"auto","created_at":"2025-07-07 16:20:16","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1673811,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6511758/v1/96f4282d-8e2d-4079-a8f4-530b20f4b9c5.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Drug-induced hypersensitivity reaction presenting as systemic capillary leak-like syndrome with polyserositis: a case report","fulltext":[{"header":"Background","content":"\u003cp\u003eSystemic capillary leak syndrome (SCLS) is a rare, life-threatening condition that results in plasma extravasation into interstitial and serosal compartments. While idiopathic SCLS is classically defined by the triad of hypotension, hemoconcentration, and hypoalbuminemia, secondary forms\u0026mdash;particularly those induced by drugs\u0026mdash;may present atypically and are underrecognized. Hypersensitivity reactions to antimicrobial or proton pump inhibitor therapy can result in systemic capillary leak-like features through endothelial dysfunction and cytokine storm [2].\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eA 42-year-old Vietnamese man presented with progressive abdominal distension, dyspnea, and periorbital edema 5 days after initiating a second-line \u003cem\u003eHelicobacter pylori\u003c/em\u003e eradication regimen including esomeprazole, amoxicillin, levofloxacin, bismuth, and \u003cem\u003eBacillus clausii\u003c/em\u003e, along with desloratadine. He had previously experienced mild eyelid and extremity swelling after a prior regimen including esomeprazole, rifaximin, and antacid therapy.\u003c/p\u003e\n\u003cp\u003eOn admission, he was normotensive, afebrile, and alert. Examination revealed ascites, bilateral pedal edema, and decreased breath sounds at the bases. Lab work showed hyponatremia (Na 121 mmol/L), hypoalbuminemia (31.6 g/L), elevated CRP (16.6 mg/L), and normocytic anemia. Chest X-ray showed bilateral basal infiltrates and cardiomegaly \u003cstrong\u003e(Fig. 1)\u003c/strong\u003e. CT showed bilateral pleural effusions, interstitial pulmonary edema, periportal edema, pericardial effusion, and gallbladder wall thickening (\u003cstrong\u003eFig. 2\u003c/strong\u003e). ANA was positive (1:80, speckled), and lupus anticoagulant was positive on repeat testing. Tryptase was within normal limits, ruling out anaphylaxis. Gastric biopsies showed chronic gastritis with intestinal metaplasia and features suggestive of early autoimmune gastritis.\u003c/p\u003e\n\u003cp\u003eHe was treated with IV methylprednisolone (80 mg/day) and oral desloratadine. Symptoms improved significantly within 48 hours, and electrolytes normalized. He was discharged on day 4 with outpatient follow-up (\u003cstrong\u003eFig. 3\u003c/strong\u003e).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eInvestigations:\u003c/strong\u003e\u003c/p\u003e\n\u003cul type=\"disc\"\u003e\n \u003cli\u003eHematology: Normocytic anemia, leukocytosis, elevated CRP\u003c/li\u003e\n \u003cli\u003eBiochemistry: Hyponatremia, hypoalbuminemia, normal liver enzymes\u003c/li\u003e\n \u003cli\u003eAutoimmunity: ANA 1:80, lupus anticoagulant (+), normal complements\u003c/li\u003e\n \u003cli\u003eHistopathology: Gastritis with intestinal metaplasia and glandular atrophy (suggestive of autoimmune gastritis)\u003c/li\u003e\n \u003cli\u003eImaging: See \u003cstrong\u003eFig. 1\u003c/strong\u003e,\u003cstrong\u003e\u0026nbsp;Fig. 2\u003c/strong\u003e; causality assessment summarized in \u003cstrong\u003eTable 1\u003c/strong\u003e\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003e\u003cem\u003eInsert Figure 1 here\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eInsert Figure 2 here\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eDifferential Diagnosis:\u003c/strong\u003e\u003c/p\u003e\n\u003cul class=\"decimal_type\"\u003e\n \u003cli\u003eIdiopathic SCLS: no hypotension, no hemoconcentration \u0026rarr; unlikely\u003c/li\u003e\n \u003cli\u003eDRESS syndrome: no eosinophilia, rash, or hepatic injury\u003c/li\u003e\n \u003cli\u003eAutoimmune disease (SLE/APS): ANA and LAC positive but below classification threshold\u003c/li\u003e\n \u003cli\u003eNephrotic syndrome: proteinuria not in nephrotic range\u003c/li\u003e\n \u003cli\u003eDrug-induced systemic hypersensitivity: most consistent with clinical and laboratory findings (\u003cstrong\u003eTable 1\u003c/strong\u003e, \u003cstrong\u003eFig. 2\u003c/strong\u003e)\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003e\u003cstrong\u003eTreatment:\u003c/strong\u003e\u003c/p\u003e\n\u003cul\u003e\n \u003cli\u003eIV methylprednisolone 80 mg/day \u0026times; 3 days\u003c/li\u003e\n \u003cli\u003eOral desloratadine 5 mg BID\u003c/li\u003e\n \u003cli\u003eHypertonic saline for hyponatremia\u003c/li\u003e\n \u003cli\u003eDiscontinuation of offending agents\u003c/li\u003e\n\u003c/ul\u003e\n\u003cp\u003e\u003cstrong\u003eOutcome and Follow-up:\u003c/strong\u003e Rapid clinical improvement was observed, with resolution of edema and normalization of sodium. At 1-month follow-up, ANA and LAC remained positive but no autoimmune clinical manifestations emerged. Further rheumatology follow-up planned (\u003cstrong\u003eFig. 3\u003c/strong\u003e).\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eInsert Figure 3 here\u003c/em\u003e\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThis case underscores the clinical complexity and diagnostic challenge of drug-induced systemic hypersensitivity reactions that can phenotypically resemble systemic capillary leak syndrome (SCLS). While classic idiopathic SCLS is defined by hypotension, hypoalbuminemia, and hemoconcentration [1], drug-induced variants\u0026mdash;especially those involving cytokine-mediated endothelial dysfunction\u0026mdash;may lack the full triad.\u003c/p\u003e\n\u003cp\u003eThe patient presented with multisystem fluid shifts including pleural effusions, pericardial fluid, and ascites\u0026mdash;consistent with a capillary leak-like phenomenon (\u003cstrong\u003eFig. 2\u003c/strong\u003e). The absence of hypotension and elevated hematocrit argued against idiopathic SCLS but aligned more closely with hypersensitivity-mediated endothelial permeability dysfunction. Imaging revealed periportal edema, interstitial pulmonary changes, and gallbladder wall thickening\u0026mdash;all indicative of systemic inflammatory insult (\u003cstrong\u003eFig. 2\u003c/strong\u003e).\u003c/p\u003e\n\u003cp\u003eA notable feature in this case was the temporal association between the \u003cem\u003eH. pylori\u003c/em\u003e eradication regimen and symptom onset. The patient had received amoxicillin, levofloxacin, and esomeprazole\u0026mdash;drugs known to elicit hypersensitivity reactions, though rarely manifesting as diffuse capillary leak [2,3]. We utilized the Naranjo algorithm to assess causality, resulting in a total score of +5, suggesting a \u0026ldquo;probable\u0026rdquo; link to drug-induced etiology (\u003cstrong\u003eTable 1\u003c/strong\u003e) [4]. Notably, the patient had experienced milder edema during the first drug course, suggesting sensitization.\u003c/p\u003e\n\u003cp\u003e\u003cem\u003eInsert Table 1 here\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eThe absence of eosinophilia and rash reduces the likelihood of DRESS syndrome. However, cytokine release syndromes (CRS)\u0026mdash;an increasingly recognized adverse drug reaction\u0026mdash;present with similar systemic inflammatory features. IL-6, TNF-\u0026alpha;, and VEGF have been implicated in capillary leak pathogenesis [5]. Although cytokine assays were not performed in this case, the patient\u0026rsquo;s rapid response to corticosteroids and antihistamines supports an immune-mediated mechanism.\u003c/p\u003e\n\u003cp\u003eFurther, serological findings of ANA (1:80, speckled) and lupus anticoagulant positivity suggest transient autoimmune activation. ANA seropositivity in the absence of systemic features may result from drug exposure and typically resolves upon withdrawal of the offending agent [6]. Lupus anticoagulant, however, has implications for hypercoagulability and warrants longitudinal monitoring [7]. In this case, follow-up serology at one month remained positive, though the patient was asymptomatic.\u003c/p\u003e\n\u003cp\u003eIn parallel, gastric histopathology demonstrated moderate chronic gastritis with intestinal metaplasia and glandular atrophy, raising suspicion for early-stage autoimmune gastritis. Autoimmune gastritis is characterized by chronic inflammation of the gastric body mucosa, loss of parietal cells, and eventual hypochlorhydria, often accompanied by autoantibodies against parietal cells and intrinsic factor. It is frequently associated with other autoimmune conditions, including systemic lupus erythematosus, autoimmune thyroiditis, and type 1 diabetes mellitus [8]. Although anti-parietal cell antibodies and serum vitamin B12 levels were not assessed in this case, the histological features\u0026mdash;combined with the presence of transient ANA and lupus anticoagulant positivity\u0026mdash;suggest a background of latent immune dysregulation. This may have predisposed the patient to an exaggerated immunologic response to drug exposure. Early recognition of autoimmune gastritis is important, not only for surveillance of micronutrient deficiencies but also because it may serve as a harbinger of systemic autoimmunity [9].\u003c/p\u003e\n\u003cp\u003eDifferential diagnoses such as nephrotic syndrome were ruled out due to sub-nephrotic proteinuria. Idiopathic SCLS was deemed unlikely in the absence of shock or hemoconcentration. Serosal tuberculosis and viral causes were excluded based on cultures, imaging, and inflammatory markers. While one might question the incomplete exclusion of autoimmune diseases (e.g., early SLE or MCTD), the lack of systemic features or high-titer autoantibodies diminishes this probability.\u003c/p\u003e\n\u003cp\u003eIn sum, this case presents a compelling example of drug-induced hypersensitivity with systemic manifestations mimicking capillary leak, set against a background of latent autoimmune predisposition. Early recognition and immunomodulation are crucial to avoid escalation to multi-organ failure. Future reports should emphasize the inclusion of cytokine profiling, sequential autoantibody titers, and lymphocyte transformation tests when feasible to delineate drug causality more precisely.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eClinicians should maintain high suspicion for systemic hypersensitivity reactions in patients presenting with unexplained capillary leak, particularly when immune markers and drug history support a reactive etiology. This case highlights the role of immune dysregulation in atypical drug reactions and suggests the need for longitudinal monitoring for autoimmune sequelae.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLearning Points:\u003c/strong\u003e\u003c/p\u003e\n\u003cul\u003e\n \u003cli\u003eSystemic hypersensitivity can mimic SCLS with polyserositis without classical features.\u003c/li\u003e\n \u003cli\u003eNaranjo scoring and temporal correlation assist in suspecting drug-induced causes.\u003c/li\u003e\n \u003cli\u003eTransient ANA/LAC positivity may reflect immune activation during hypersensitivity reactions.\u003c/li\u003e\n \u003cli\u003eCoexistent autoimmune gastritis may predispose patients to exaggerated drug responses.\u003c/li\u003e\n \u003cli\u003eCorticosteroids and antihistamines can reverse severe manifestations effectively\u003c/li\u003e\n\u003c/ul\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate:\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;Not applicable (case report; observational data from routine clinical care).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication:\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;Written informed consent for publication of this case report and accompanying images was obtained from the patient.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials:\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;All data generated or analyzed during this study are included in this published article.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests:\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;The authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding:\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;No funding was received for this study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026apos; contributions:\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;Ninh Xuan Nguyen conceived the case report, supervised clinical care, and led the drafting of the manuscript. Ngoc Tien Pham and Huong Thi Thanh Le contributed to immunological data interpretation and literature review. Quoc Viet Tran and Hang Ngoc Thuy Tran were responsible for data collection, imaging documentation, and manuscript editing. An Thien Do provided expert input on immunological aspects and critically revised the manuscript. All authors read and approved the final version of the manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements:\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;The authors wish to thank the Department of Internal Medicine and Immunology, Vinmec Central Park Hospital, for their clinical support.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026apos; information (optional):\u003c/strong\u003e\u003cbr\u003e\u0026nbsp;Dr. Ninh Xuan Nguyen is the Head of the Emergency Department at Vinmec Central Park International Hospital (Ho Chi Minh City, Vietnam). His clinical interests include systemic inflammatory disorders, drug-induced autoimmunity, and diagnostic challenges in internal medicine.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eDruey KM, Parikh SM. Idiopathic systemic capillary leak syndrome. N Engl J Med. 2017;376(26):2456\u0026ndash;2467. https://doi.org/10.1056/NEJMra1612647\u003c/li\u003e\n\u003cli\u003eGonz\u0026aacute;lez-D\u0026iacute;az SN, Zavala-Cerna MG, Vargas-Ram\u0026iacute;rez R, et al. Hypersensitivity reactions to antibiotics in pediatrics. J Investig Allergol Clin Immunol. 2022;32(2):84\u0026ndash;93. https://doi.org/10.18176/jiaci.0769\u003c/li\u003e\n\u003cli\u003eKim MH, Kang HR. Proton pump inhibitors and hypersensitivity: overview. World Allergy Organ J. 2020;13(3):100108. https://doi.org/10.1016/j.waojou.2020.100108\u003c/li\u003e\n\u003cli\u003eNaranjo CA, Busto U, Sellers EM, Sandor P, Ruiz I, Roberts EA, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30(2):239\u0026ndash;245. https://doi.org/10.1038/clpt.1981.154\u003c/li\u003e\n\u003cli\u003eOgawa K, Morito T, Sugai S, et al. Cytokine profiles in patients with DRESS and other severe drug eruptions. J Am Acad Dermatol. 2021;84(2):466\u0026ndash;475. https://doi.org/10.1016/j.jaad.2020.04.122\u003c/li\u003e\n\u003cli\u003eTozzoli R, Bizzaro N, Tonutti E, et al. Guidelines for the laboratory use of autoantibody tests in autoimmune diseases. Autoimmun Rev. 2020;19(4):102510. https://doi.org/10.1016/j.autrev.2020.102510\u003c/li\u003e\n\u003cli\u003eRuiz-Irastorza G, Crowther M, Branch W, Khamashta MA. Antiphospholipid syndrome. Lancet. 2010;376(9751):1498\u0026ndash;1509. https://doi.org/10.1016/S0140-6736(10)60709-X\u003c/li\u003e\n\u003cli\u003eHershko C, Ronson A, Eliakim R. Autoimmune gastritis: pathogenesis and clinical implications. World J Gastroenterol. 2022;28(8):748\u0026ndash;759. https://doi.org/10.3748/wjg.v28.i8.748\u003c/li\u003e\n\u003cli\u003eNeumann WL, Coss E, Rugge M, Genta RM. Autoimmune atrophic gastritis: pathogenesis, pathology and management. Nat Rev Gastroenterol Hepatol. 2013;10(9):529\u0026ndash;541. https://doi.org/10.1038/nrgastro.2013.101\u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Table 1","content":"\u003cp\u003e\u003cstrong\u003eTable 1. Naranjo Adverse Drug Reaction Probability Score applied to this case\u003c/strong\u003e\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eQuestion\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAnswer\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eScore\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003eAre there previous conclusive reports on this reaction?\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003eYes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e+1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003eDid the adverse event appear after the suspected drug was administered?\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003eYes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e+2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003eDid the adverse reaction improve when the drug was discontinued?\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003eYes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e+1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003eDid the adverse reaction reappear when the drug was readministered?\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003eNot done\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003eAre there alternative causes that could have caused the reaction?\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003ePossible\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e-1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003eDid the reaction reappear with a placebo?\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003eNot done\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003eWas the drug detected in blood (toxic concentration)?\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003eWas the reaction more severe when the dose was increased?\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003eNo\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003eDid the patient have a similar reaction to the same or similar drugs?\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003eYes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e+1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003eWas the adverse event confirmed by any objective evidence?\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 90px;\"\u003e\n \u003cp\u003eYes\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e+1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 468px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eTotal Score \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" valign=\"top\" style=\"width: 156px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e+5 (Probable)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eScoring tool used to assess the likelihood of drug-induced adverse reactions. A score of +5 in this case indicates a probable causal relationship between drug exposure and systemic hypersensitivity manifestations\u003c/p\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-rheumatology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"brhm","sideBox":"Learn more about [BMC Rheumatology](http://bmcrheumatol.biomedcentral.com)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/brhm/default.aspx","title":"BMC Rheumatology","twitterHandle":"@BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Drug hypersensitivity, systemic capillary leak, polyserositis, autoimmune gastritis, lupus anticoagulant, ANA, cytokine-mediated reaction","lastPublishedDoi":"10.21203/rs.3.rs-6511758/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6511758/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eSystemic capillary leak syndrome (SCLS) is a rare disorder characterized by increased vascular permeability leading to third-spacing of fluids and protein. Drug-induced hypersensitivity reactions can mimic SCLS clinically and radiologically.\u003c/p\u003e\u003ch2\u003eCase Presentation:\u003c/h2\u003e \u003cp\u003eA 42-year-old Vietnamese man developed abdominal distension, facial edema, and dyspnea after initiation of Helicobacter pylori eradication therapy. Imaging revealed pleural, pericardial, and peritoneal effusions, periportal edema, and interstitial pulmonary edema. Laboratory results showed hyponatremia, hypoalbuminemia, and mild anemia. Autoimmune screening revealed ANA positivity (1:80, speckled) and lupus anticoagulant, though extractable nuclear antigens were negative. The patient improved rapidly with corticosteroids and antihistamines.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eThis case highlights a systemic hypersensitivity reaction mimicking capillary leak syndrome, likely drug-induced, and occurring in a patient with subclinical autoimmune predisposition. It underscores the importance of immune surveillance and early immunomodulatory therapy.\u003c/p\u003e","manuscriptTitle":"Drug-induced hypersensitivity reaction presenting as systemic capillary leak-like syndrome with polyserositis: a case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-05-26 08:32:40","doi":"10.21203/rs.3.rs-6511758/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2025-06-02T19:58:03+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-05-30T10:39:27+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"122681728268978052183297752336784118541","date":"2025-05-30T10:15:04+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-05-23T03:50:27+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"206164564454331397833036102903844679050","date":"2025-05-23T03:18:15+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"289598321249625206306031760428691986340","date":"2025-05-22T10:03:40+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-05-20T09:37:02+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-05-20T09:35:22+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-05-19T07:32:51+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-05-15T05:45:42+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Rheumatology","date":"2025-05-15T05:44:35+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-rheumatology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"brhm","sideBox":"Learn more about [BMC Rheumatology](http://bmcrheumatol.biomedcentral.com)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/brhm/default.aspx","title":"BMC Rheumatology","twitterHandle":"@BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"08980ce1-22dc-41ef-9591-93f9db0b74b2","owner":[],"postedDate":"May 26th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2025-07-07T16:12:41+00:00","versionOfRecord":{"articleIdentity":"rs-6511758","link":"https://doi.org/10.1186/s41927-025-00535-6","journal":{"identity":"bmc-rheumatology","isVorOnly":false,"title":"BMC Rheumatology"},"publishedOn":"2025-07-01 15:58:27","publishedOnDateReadable":"July 1st, 2025"},"versionCreatedAt":"2025-05-26 08:32:40","video":"","vorDoi":"10.1186/s41927-025-00535-6","vorDoiUrl":"https://doi.org/10.1186/s41927-025-00535-6","workflowStages":[]},"version":"v1","identity":"rs-6511758","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6511758","identity":"rs-6511758","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}