Deep Vein Thrombosis and Pleural Effusion as Initial Manifestations of Systemic Lupus Erythematosus with Secondary Antiphospholipid Syndrome in a Male: A Case Report

Deep Vein Thrombosis and Pleural Effusion as Initial Manifestations of Systemic Lupus Erythematosus with Secondary Antiphospholipid Syndrome in a Male: 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 Deep Vein Thrombosis and Pleural Effusion as Initial Manifestations of Systemic Lupus Erythematosus with Secondary Antiphospholipid Syndrome in a Male: A Case Report Saad Rehman, Amna Arif, Hammad Khalid, Muhammad Tanveer Alam, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9506236/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Introduction: Systemic lupus erythematosus (SLE) with secondary antiphospholipid syndrome (APS) is an uncommon cause of unprovoked thrombosis and serosal inflammation, especially in males. Early recognition of autoimmune etiologies in thrombotic presentations is essential to prevent recurrence and long-term morbidity. Case Presentation: A 34-year-old male presented with 1 month history of high-grade fever, followed by relatively acute onset left-sided pleuritic chest pain and rapidly progressive, painful swelling of the left lower limb. Imaging revealed a left-sided pleural effusion and extensive deep vein thrombosis (DVT), with laboratory evaluations showing positive antinuclear antibodies (ANA), lupus anticoagulant, and anti-β2-glycoprotein I antibodies. Together with the patient’s clinical manifestations, these findings established the diagnosis of SLE with secondary APS. The patient was treated with low-molecular-weight heparin for acute DVT, intravenous antibiotics, proton pump inhibitors, inhaled bronchodilators, corticosteroids, and supportive care. Over a week, the patient experienced complete resolution of fever, significant reduction in leg swelling, and improvement in pleuritic chest pain. He was discharged on long-term anticoagulation with a plan for rheumatology follow-up for immunomodulatory therapy. Conclusion This case illustrates a diagnostically challenging presentation of SLE with secondary APS in males, mimicking infectious or thromboembolic conditions. Early autoimmune work-up in young patients with unexplained thrombosis or serositis can facilitate timely treatment and prevent recurrence. Systemic Lupus Erythematosus Antiphospholipid Syndrome Deep Vein Thrombosis Pleural Effusion Autoimmune Disease Secondary APS Figures Figure 1 INTRODUCTION Antiphospholipid syndrome (APS) is an autoimmune prothrombotic disorder characterized by the presence of antiphospholipid antibodies and clinical manifestations of recurrent venous or arterial thromboembolic events ( 1 , 2 ). When occurring in the context of systemic lupus erythematosus (SLE), it is called secondary APS ( 3 , 4 ). Although SLE predominantly affects women of childbearing age, men may also experience severe thrombotic events ( 5 – 7 ). Respiratory involvement, such as pleural effusion, can coexist with thrombosis and mimic infectious processes, leading to delayed diagnosis and perhaps treatment ( 8 , 9 ). This case report describes a young male patient presenting with deep vein thrombosis (DVT) and pleural effusion as the first manifestation of SLE with APS, underscoring the importance of maintaining a broad differential in thromboembolic presentations. CASE PRESENTATION A married 34-year-old male, a fisherman by occupation, with a 14-pack-year smoking history and no known comorbidities, presented with complaints of one month of high-grade fever, left-sided chest pain for 12 days, and progressive swelling of the left lower limb for 5 days. The fever was documented as high grade (102°F), was sudden in onset, intermittent, and associated with chills, body aches, and a productive cough. The chest pain was sharp, non-radiating, and aggravated by coughing but relieved by postural change. The leg swelling appeared suddenly, progressed to involve the entire limb, and was painful on walking. There was no history of trauma, prolonged immobilization, recent surgery, or any chronic illness. Sexual history was positive for multiple partners, and there was no family history of autoimmune or thromboembolic disorders. On examination, the patient was alert, well oriented, and vitally stable with a blood pressure of 120/70 mmHg, a pulse of 80 beats per minute, and a respiratory rate of 18 breaths per minute, and he maintained an oxygen saturation of 98% at room temperature. Mild pallor and right inguinal sub-centimetric lymph nodes were noted. Local examination of the left lower limb revealed pitting pedal edema extending up to the shins, associated with tenderness, warmth, and erythema. The left calf measured 38 cm in circumference, compared with 30 cm on the right. Pedal pulses were difficult to palpate because of edema, but there was no sensory or motor deficit. Respiratory exam demonstrated stony dull percussion, reduced air entry, and bronchial breathing with decreased vocal resonance at the left lung base. The rest of the systemic examination was unremarkable. Significant laboratory results included a total leukocyte count of 17,000 cells/µL, ESR of 100 mm/hr, CRP of 205 mg/L, ferritin of 1992 ng/mL, serum iron level of 17 mcg/dL, and LDH of 263 U/L. An ultrasound Doppler of the left lower limb revealed echogenic foci representing thrombus seen in the common femoral vein, extending to the superficial femoral and popliteal veins. Echocardiography showed a pulmonary artery pressure of 25 mmHg, while the rest of the scan was unremarkable. An X-ray of the chest revealed a homogeneous opacity in the left lower lung zone with blunting of the left costophrenic angle and obscuration of the left hemidiaphragm, consistent with a left-sided pleural effusion. ( Fig. 1 ) . A CT scan of the chest, abdomen, and pelvis revealed a left-sided pleural effusion, round atelectasis in the lateral basal segment of the left lower lobe, and no evidence of pulmonary embolism. Immunologic testing revealed a positive ANA, positive lupus anticoagulant and markedly elevated anti-β2 glycoprotein I IgM levels, which, in combination with patient’s clinical manifestations supported the diagnosis of SLE with secondary APS. ( Table 1 , 2 ) Table 1 Summary of the 2019 EULAR/ACR systemic lupus erythematosus (SLE) classification criteria and the patient’s respective clinical and immunologic findings. Domain 2019 EULAR/ACR Criteria (Points) Patient Finding Score Entry criterion ANA ≥ 1:80 required ANA positive (1:320) Yes Constitutional Fever ( 2 ) Fever for 30 days 2 Hematologic Leukopenia ( 3 ), Thrombocytopenia ( 4 ), Autoimmune hemolysis ( 4 ) None 0 Neuropsychiatric Delirium ( 2 ), psychosis ( 3 ), seizure ( 5 ) None 0 Mucocutaneous Oral ulcers ( 2 ), Nonscarring alopecia ( 2 ), Acute cutaneous lupus ( 6 ), Subacute cutaneous OR discoid lupus ( 4 ) None 0 Serosal Pleural/pericardial effusion ( 5 ), acute pericarditis ( 6 ) Left-sided pleural effusion 5 Musculoskeletal Joint involvement ( 6 ) None 0 Renal Proteinuria > 0.5 g/day ( 4 ), Class II–V lupus nephritis ( 8 – 10 ) None 0 Immunologic: Antiphospholipid Anticardiolipin, anti-β2GPI, lupus anticoagulant ( 2 ) Anti-β2GPI & lupus anticoagulant positive 2 Immunologic: Complement Low C3 or low C4 ( 3 ), both low ( 4 ) None 0 Immunologic: SLE-specific antibodies Anti-dsDNA ( 6 ), Anti-Sm ( 6 ) None 0 TOTAL ≥ 10 = SLE Definite SLE 9 Table 2 2006 Revised Sapporo (Sydney) Criteria with corresponding patient findings. Category Criteria Patient finding Clinical Vascular thrombosis ≥ 1 clinical episode of arterial, venous, or small-vessel thrombosis confirmed by imaging (e.g., Doppler, CT, MRI) or histopathology Acute left-leg DVT confirmed clinically and by Doppler findings Pregnancy morbidity ≥ 1 unexplained deaths of a morphologically normal fetus at ≥ 10 weeks gestation Not applicable ≥ 1 premature birth < 34 weeks due to eclampsia, severe pre-eclampsia, or placental insufficiency. ≥ 3 consecutive unexplained spontaneous miscarriages 40 GPL/MPL or > 99th percentile present on ≥ 2 occasions ≥ 12 weeks apart Negative Anti-β2 Glycoprotein I IgG/IgM > 99th percentile present on ≥ 2 occasions ≥ 12 weeks apart Positive APS is present if ≥ 1 clinical criteria and ≥ 1 laboratory criteria are met. The patient was treated with intravenous piperacillin/tazobactam 4.5 g three times daily, low-molecular-weight heparin (enoxaparin 40 mg subcutaneously twice daily), intravenous omeprazole 40 mg once daily, nebulized bronchodilators (ipratropium bromide and salbutamol every 6 hours), and inhaled corticosteroid (beclomethasone every 8 hours), along with oral folic acid 5 mg daily. Over one week, the fever subsided, the chest pain resolved, and the leg swelling markedly improved. The patient was discharged in stable condition on anticoagulation therapy and advised to follow up with rheumatology for initiation of long-term immunomodulatory treatment. DISCUSSION APS is a hypercoagulable state characterized by the presence of vascular thrombosis and/or obstetrical events in addition to the presence of autoantibodies, including lupus anticoagulant, anticardiolipin antibodies, and anti-β2-glycoprotein 1 antibodies ( 12 , 13 ). Most patients with APS are diagnosed between the ages of 15 and 50 years ( 14 , 15 ). When APS occurs with underlying systemic lupus erythematosus (SLE), it is termed secondary APS. The coexistence of these two debilitating disorders substantially increases the risk of thromboembolic events and potential end-organ damage ( 16 ). A 34-year-old male, presented with unprovoked deep vein thrombosis (DVT) and left-sided pleural effusion, which led to the diagnosis of SLE with secondary APS. Although SLE mostly affects women, men are often diagnosed at an older age and may even exhibit more severe disease manifestations, including renal and thromboembolic complications ( 17 ). The mechanisms of thrombosis in APS involve activation of endothelial cells, deposition of complement proteins, platelet aggregation, and suppression of natural anticoagulant pathways ( 18 ). These processes collectively create a hypercoagulable environment that predisposes to venous and arterial thrombosis. When superimposed on SLE-related immune dysregulation, the risk of thromboembolic complications increases several fold. Pleural effusion is the most common thoracic manifestation in SLE, reported in up to 50% of cases, often resulting from immune-complex–mediated pleuritis. However, in some cases, the effusion may be due to pulmonary embolism secondary to APS ( 19 ). In our patient, pleural effusion was exudative in nature, most likely due to inflammatory pleuritis, although a thromboembolic mechanism could not be entirely excluded. Secondary APS should be suspected when DVT or pulmonary embolism occurs alongside systemic symptoms such as fever, serositis, or cytopenias. Early identification is critical because thrombotic events in APS carry a high recurrence rate without adequate anticoagulation ( 20 ). The mainstay of treatment for APS-associated thrombosis is long-term anticoagulation, traditionally with warfarin, although low-molecular-weight heparin (LMWH) is recommended during acute management. In cases secondary to SLE, immunomodulatory therapy is indicated to control systemic inflammation and prevent further antibody-mediated vascular injury ( 21 ). Our patient was treated with LMWH, antibiotics, and supportive therapy, with a good clinical response. Long-term management should include a smooth transition to oral anticoagulation and rheumatology follow-up for disease-modifying agents such as hydroxychloroquine or corticosteroids. In the literature, a case report has described a rare presentation of systemic lupus erythematosus (SLE) with massive bilateral pleural effusions as the initial manifestation in a previously healthy 20-year-old soldier. Initial investigations were inconclusive; however, within three months, the patient developed the full clinical features of SLE and showed marked improvement following treatment with corticosteroids and cyclophosphamide, leading to complete resolution of the pleural effusions ( 22 ). A case series documented four cases of systemic lupus erythematosus (SLE) presenting with pleuritis as the initial disease manifestation; surprisingly, all of them were men ( 23 ). Another case was reported of a 31-year-old Black male who presented with recurrent pleural effusions secondary to active systemic lupus erythematosus (SLE ) ( 24 ). A case report described a 38-year-old male with antiphospholipid syndrome (APS) who presented with deep vein thrombosis (DVT) and pleural effusion ( 8 ). CONCLUSION This case illustrates that SLE with secondary APS can present in males with isolated venous thrombosis and pleural effusion. The presentation emphasizes the need for autoimmune screening in young patients with unprovoked DVT or serositis. Early immunological evaluation and timely initiation of anticoagulation are key to preventing recurrence and improving outcomes. Clinicians should remain vigilant for atypical presentations of autoimmune thrombotic disease, especially in high-risk environments where infectious etiologies are common mimickers and can delay diagnosis and thus treatment. Abbreviations APS Antiphospholipid Syndrome SLE Systemic Lupus Erythematosus DVT Deep Vein Thrombosis ESR Erythrocyte Sedimentation Rate CRP C-Reactive Protein LDH Lactate Dehydrogenase ANA Antinuclear Antibody IgA Immunoglobulin A IgM Immunoglobulin M IgG Immunoglobulin G LMWH Low Molecular Weight Heparin Declarations Conflicting interests: All authors declare that they have no competing financial or personal interests that could have influenced the preparation of this manuscript. Funding: This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Consent to participate and publication: I nformed consent to be included in the research and publication Ethical approval: This case report was reviewed and deemed exempt from formal ethical approval by the Institutional Review Board of Dr. Ruth K. M. Pfau Civil Hospital Karachi . Permission for data collection and publication was obtained from the head of the department Availability of data and material: All data relevant to this case are contained within the manuscript. Code availability: Not applicable Compliance with Care Guidelines: This report was prepared in accordance with the CARE (Consensus-based Clinical Case Reporting) guidelines; the completed CARE checklist is available upon request. Contributorship : SR contributed to the conception and design of the study, acquisition of clinical data, and drafting of the manuscript. AA contributed to literature review, data interpretation, and manuscript drafting. HK contributed to data collection, literature review, and manuscript preparation. MTA contributed to critical revision of the manuscript for important intellectual content. SMK contributed to supervision, data interpretation, and critical review of the manuscript. UY contributed to the conception of the study, overall supervision, critical revision, and final approval of the manuscript. Acknowledgements: None Written informed consent for participation and publication of anonymized clinical details was obtained from the patient. References Wysokinska E, Ortel TL. Antiphospholipid syndrome. In: Elsevier eBooks [Internet]. 2019 [cited 2026 Feb 12]. pp. 374–95. Available from: https://doi.org/10.1016/b978-0-323-46202-0.00020-0 Ivan GP. An insight into the pathophysiology of thrombosis in antiphospholipid syndrome. Frontiers in Bioscience [Internet]. 2007 Jan 1 [cited 2026 Feb 12];12(8–12):3093. Available from: https://doi.org/10.2741/2297 Rodríguez-Pintó I, Espinosa G, Cervera R. The catastrophic antiphospholipid syndrome. In: Rare diseases of the immune system [Internet]. 2014 [cited 2026 Feb 12]. pp. 249–62. Available from: https://doi.org/10.1007/978-3-319-11044-8_20 Agmon-Levin N, Shoenfeld Y. The spectrum between antiphospholipid syndrome and systemic lupus erythematosus. Clinical Rheumatology [Internet]. 2014 Jan 16 [cited 2026 Feb 12];33(3):293–5. Available from: https://doi.org/10.1007/s10067-014-2486-5 Singhal S, Jotwani P, Gupta S, Srikaram P, Desai D, Styler M. Prevalence, demographics, and mortality/morbidity of thrombotic events: A nationwide study of SLE patients in the United States. Journal of Thrombosis and Thrombolysis [Internet]. 2025 Oct 25 [cited 2026 Feb 12]; Available from: https://doi.org/10.1007/s11239-025-03200-4 Specker C, Becker A, Lakomek HJ, Bach D, Grabensee B. [Systemic lupus erythematosus in men–a different prognosis?]. 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Antiphospholipid syndrome: Clinical and immunologic manifestations and patterns of disease expression in a cohort of 1,000 patients. Arthritis & Rheumatism [Internet]. 2002 Apr 1[cited 2026 Feb 12];46(4):1019–27. Available from: https://doi.org/10.1002/art.10187 Capelusnik D, Ramiro S, Nikiphorou E, Maksymowych WP, Magrey M, Marzo-Ortega H, AB0198 THRESHOLDS OF PRESENTEEISM MEASUREMENT INSTRUMENTS FOR UNACCEPTABLE WORK PARTICIPATION AND FUTURE ADVERSE WORK OUTCOMES IN RA. Annals of the Rheumatic Diseases [Internet]. 2023 Jun 1[cited 2026 Feb 12];82:1281–2. Available from: https://doi.org/10.1136/annrheumdis-2023-eular.2823 Garcia-Diaz J, Escudero-Salamanca M, Alvarez-Santana R, Espinola-Zavaleta N. Catastrophic Antiphospholipid Syndrome Associated With Systemic Lupus Erythematosus: A case-based Review. Future Cardiology [Internet]. 2020 Nov 3[cited 2026 Feb 12];17(6):985–90. Available from: https://doi.org/10.2217/fca-2020-0145 Specker C, Becker A, Lakomek HJ, Bach D, Grabensee B. [Systemic lupus erythematosus in men — a different prognosis?]. Z Rheumatol. 1994;53(6):339–45. PMID: 7871906. [cited 2026 Feb 12]. Pierangeli SS, Vega-Ostertag M, Liu X, Girardi G. Complement activation: a novel pathogenic mechanism in the antiphospholipid syndrome. Annals of the New York Academy of Sciences [Internet]. 2005 Jun 1[cited 2026 Feb 12];1051(1):413–20. Available from: https://doi.org/10.1196/annals.1361.083 Mulherin D, Bresnihan B. Systemic lupus erythematosus. Baillière S Clinical Rheumatology [Internet]. 1993 Feb 1[cited 2026 Feb 12];7(1):31–57. Available from: https://doi.org/10.1016/s0950-3579(05)80267-5 Koike T. Anticardiolipin Antibodies in NZW x BXSB F1 Mice. Lupus [Internet]. 1994 Aug 1[cited 2026 Feb 12];3(4):241–6. Available from: https://doi.org/10.1177/096120339400300407 Hewagama A, Richardson B. The genetics and epigenetics of autoimmune diseases. Journal of Autoimmunity [Internet]. 2009 Apr 6 [cited 2026 Feb 12];33(1):3–11. Available from: https://doi.org/10.1016/j.jaut.2009.03.007 Stamm E. Die Insulinempfindlichkeit des nichtdiabetischen Menschen und ihre Beziehung zum vegetativen Nervensystem. Digestion [Internet]. 1930 Jan 1[cited 2026 Feb 12];48(1–2):104–24. Available from: https://doi.org/10.1159/000195982 Edahiro Y, Ando J, Suzuki T, Fukumura Y, Masuda A, Sakayori S et al. Multiple Placental Infarcts in a Pregnant Woman with Essential Thrombocythemia. Internal Medicine [Internet]. 2018 Aug 9 [cited 2026 Feb 12];57(24):3647–50. Available from: https://doi.org/10.2169/internalmedicine.1311-18 Kaine JL. Refractory massive pleural effusion in systemic lupus erythematosus treated with talc poudrage. Annals of the Rheumatic Diseases [Internet]. 1985 Jan 1[cited 2026 Feb 12];44(1):61–4. Available from: https://doi.org/10.1136/ard.44.1.61 Additional Declarations No competing interests reported. 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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-9506236","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":630561540,"identity":"a2a608b4-73bb-4343-856c-8384ab77784a","order_by":0,"name":"Saad Rehman","email":"","orcid":"","institution":"Dow University of Health Sciences","correspondingAuthor":false,"prefix":"","firstName":"Saad","middleName":"","lastName":"Rehman","suffix":""},{"id":630561541,"identity":"7093f924-65fc-4973-b855-286f918942de","order_by":1,"name":"Amna Arif","email":"","orcid":"","institution":"Dow University of Health Sciences","correspondingAuthor":false,"prefix":"","firstName":"Amna","middleName":"","lastName":"Arif","suffix":""},{"id":630561542,"identity":"284af398-5ea8-4348-916e-1bc3d14ddb3d","order_by":2,"name":"Hammad Khalid","email":"","orcid":"","institution":"Dow University of Health Sciences","correspondingAuthor":false,"prefix":"","firstName":"Hammad","middleName":"","lastName":"Khalid","suffix":""},{"id":630561543,"identity":"31b4c75d-47b5-4854-aee5-b44f29e2034f","order_by":3,"name":"Muhammad Tanveer Alam","email":"","orcid":"","institution":"Dow University of Health Sciences","correspondingAuthor":false,"prefix":"","firstName":"Muhammad","middleName":"Tanveer","lastName":"Alam","suffix":""},{"id":630561544,"identity":"beffa1a3-143a-4da2-a2e5-2bfebed8acb5","order_by":4,"name":"Syed Muhammad Kashif","email":"","orcid":"","institution":"Dow University of Health Sciences","correspondingAuthor":false,"prefix":"","firstName":"Syed","middleName":"Muhammad","lastName":"Kashif","suffix":""},{"id":630561545,"identity":"dd0c68d5-45bf-48dd-ba47-41f17c94d19b","order_by":5,"name":"Uzair Yaqoob","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA90lEQVRIie3RsUrEMBjA8S9k6PJJ5uNEXyFy0MWCg4/hEhDqVCi4BFwyXZc+QKe7V7hDcG4IVIeAq9DF4gsoLjeImHQU2jg65E+WhPwISQBisX9aC5DhaVLpt3FKqfoLyY/Panu9AuCOkDBxmQxeRLocCQQIY2YwEgySRuR3pfy6YpUjB/kwSRaq49rCDSY4dH1jedEYokht+0nCtXIDzpFUIu+P1rxQjlCyniEmeXeEIrQivfVkGyQd+lMuEZ5ESj3ZhciixtKRHP0jL9Guir0jeu4ujD3efyjILvxXfqI8KTbPRr8e5DQZI9+/Ftr5/bFYLBYL9QMKhlhirdUplgAAAABJRU5ErkJggg==","orcid":"","institution":"Shaheed Mohtarma Benazir Institute of Trauma","correspondingAuthor":true,"prefix":"","firstName":"Uzair","middleName":"","lastName":"Yaqoob","suffix":""}],"badges":[],"createdAt":"2026-04-23 11:39:01","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-9506236/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9506236/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":108101745,"identity":"164e499c-1017-4f38-918e-f78c401cfd1e","added_by":"auto","created_at":"2026-04-29 11:00:52","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":131252,"visible":true,"origin":"","legend":"\u003cp\u003eChest X-ray demonstrating homogeneous opacity in the left lower lung zone with blunting of the left costophrenic angle and obscuration of the left hemidiaphragm, consistent with a left-sided pleural effusion.\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-9506236/v1/d88e49a8378fce6b978c2e45.png"},{"id":108976683,"identity":"59eaa6f6-f07a-48aa-ac90-25f4d67b1614","added_by":"auto","created_at":"2026-05-11 11:28:02","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":358398,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9506236/v1/25b06d1b-98d0-4523-a0d0-bf7e0b9070bb.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Deep Vein Thrombosis and Pleural Effusion as Initial Manifestations of Systemic Lupus Erythematosus with Secondary Antiphospholipid Syndrome in a Male: A Case Report","fulltext":[{"header":"INTRODUCTION","content":"\u003cp\u003eAntiphospholipid syndrome (APS) is an autoimmune prothrombotic disorder characterized by the presence of antiphospholipid antibodies and clinical manifestations of recurrent venous or arterial thromboembolic events (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). When occurring in the context of systemic lupus erythematosus (SLE), it is called secondary APS (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eAlthough SLE predominantly affects women of childbearing age, men may also experience severe thrombotic events (\u003cspan additionalcitationids=\"CR6\" citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). Respiratory involvement, such as pleural effusion, can coexist with thrombosis and mimic infectious processes, leading to delayed diagnosis and perhaps treatment (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). This case report describes a young male patient presenting with deep vein thrombosis (DVT) and pleural effusion as the first manifestation of SLE with APS, underscoring the importance of maintaining a broad differential in thromboembolic presentations.\u003c/p\u003e"},{"header":"CASE PRESENTATION","content":"\u003cp\u003eA married 34-year-old male, a fisherman by occupation, with a 14-pack-year smoking history and no known comorbidities, presented with complaints of one month of high-grade fever, left-sided chest pain for 12 days, and progressive swelling of the left lower limb for 5 days. The fever was documented as high grade (102\u0026deg;F), was sudden in onset, intermittent, and associated with chills, body aches, and a productive cough. The chest pain was sharp, non-radiating, and aggravated by coughing but relieved by postural change. The leg swelling appeared suddenly, progressed to involve the entire limb, and was painful on walking. There was no history of trauma, prolonged immobilization, recent surgery, or any chronic illness. Sexual history was positive for multiple partners, and there was no family history of autoimmune or thromboembolic disorders.\u003c/p\u003e \u003cp\u003eOn examination, the patient was alert, well oriented, and vitally stable with a blood pressure of 120/70 mmHg, a pulse of 80 beats per minute, and a respiratory rate of 18 breaths per minute, and he maintained an oxygen saturation of 98% at room temperature. Mild pallor and right inguinal sub-centimetric lymph nodes were noted. Local examination of the left lower limb revealed pitting pedal edema extending up to the shins, associated with tenderness, warmth, and erythema. The left calf measured 38 cm in circumference, compared with 30 cm on the right. Pedal pulses were difficult to palpate because of edema, but there was no sensory or motor deficit. Respiratory exam demonstrated stony dull percussion, reduced air entry, and bronchial breathing with decreased vocal resonance at the left lung base. The rest of the systemic examination was unremarkable.\u003c/p\u003e \u003cp\u003eSignificant laboratory results included a total leukocyte count of 17,000 cells/\u0026micro;L, ESR of 100 mm/hr, CRP of 205 mg/L, ferritin of 1992 ng/mL, serum iron level of 17 mcg/dL, and LDH of 263 U/L.\u003c/p\u003e \u003cp\u003eAn ultrasound Doppler of the left lower limb revealed echogenic foci representing thrombus seen in the common femoral vein, extending to the superficial femoral and popliteal veins. Echocardiography showed a pulmonary artery pressure of 25 mmHg, while the rest of the scan was unremarkable. An X-ray of the chest revealed a homogeneous opacity in the left lower lung zone with blunting of the left costophrenic angle and obscuration of the left hemidiaphragm, consistent with a left-sided pleural effusion. \u003cb\u003e(\u003c/b\u003eFig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e1\u003c/span\u003e\u003cb\u003e)\u003c/b\u003e. A CT scan of the chest, abdomen, and pelvis revealed a left-sided pleural effusion, round atelectasis in the lateral basal segment of the left lower lobe, and no evidence of pulmonary embolism.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eImmunologic testing revealed a positive ANA, positive lupus anticoagulant and markedly elevated anti-β2 glycoprotein I IgM levels, which, in combination with patient\u0026rsquo;s clinical manifestations supported the diagnosis of SLE with secondary APS. \u003cb\u003e(\u003c/b\u003eTable\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e, \u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e\u003cb\u003e)\u003c/b\u003e\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eSummary of the 2019 EULAR/ACR systemic lupus erythematosus (SLE) classification criteria and the patient\u0026rsquo;s respective clinical and immunologic findings.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDomain\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003e2019 EULAR/ACR Criteria (Points)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003ePatient Finding\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eScore\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eEntry criterion\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eANA\u0026thinsp;\u0026ge;\u0026thinsp;1:80 required\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eANA positive (1:320)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eYes\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eConstitutional\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFever (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eFever for 30 days\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eHematologic\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eLeukopenia (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e), Thrombocytopenia (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e), Autoimmune hemolysis (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNone\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eNeuropsychiatric\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eDelirium (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e), psychosis (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e), seizure (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNone\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eMucocutaneous\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eOral ulcers (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e), Nonscarring alopecia (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e), Acute cutaneous lupus (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e), Subacute cutaneous OR discoid lupus (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNone\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eSerosal\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ePleural/pericardial effusion (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e), acute pericarditis (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eLeft-sided pleural effusion\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e5\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eMusculoskeletal\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJoint involvement (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNone\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eRenal\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eProteinuria\u0026thinsp;\u0026gt;\u0026thinsp;0.5 g/day (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e), Class II\u0026ndash;V lupus nephritis (\u003cspan additionalcitationids=\"CR9\" citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNone\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eImmunologic: Antiphospholipid\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAnticardiolipin, anti-β2GPI, lupus anticoagulant (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eAnti-β2GPI \u0026amp; lupus anticoagulant positive\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eImmunologic: Complement\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eLow C3 or low C4 (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e), both low (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNone\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eImmunologic: SLE-specific antibodies\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAnti-dsDNA (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e), Anti-Sm (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNone\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e0\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eTOTAL\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;10\u0026thinsp;=\u0026thinsp;SLE\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eDefinite SLE\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003e\u003cb\u003e9\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003e2006 Revised Sapporo (Sydney) Criteria with corresponding patient findings.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"3\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCategory\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCriteria\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003ePatient finding\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\" morerows=\"5\" rowspan=\"6\"\u003e \u003cp\u003e\u003cb\u003eClinical\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c3\" namest=\"c2\"\u003e \u003cp\u003e\u003cem\u003eVascular thrombosis\u003c/em\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;1 clinical episode of arterial, venous, or small-vessel thrombosis confirmed by imaging (e.g., Doppler, CT, MRI) or histopathology\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eAcute left-leg DVT confirmed clinically and by Doppler findings\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"2\" nameend=\"c3\" namest=\"c2\"\u003e \u003cp\u003e\u003cem\u003ePregnancy morbidity\u003c/em\u003e\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;1 unexplained deaths of a morphologically normal fetus at \u0026ge;\u0026thinsp;10 weeks gestation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\" morerows=\"2\" rowspan=\"3\"\u003e \u003cp\u003eNot applicable\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;1 premature birth\u0026thinsp;\u0026lt;\u0026thinsp;34 weeks due to eclampsia, severe pre-eclampsia, or placental insufficiency.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u0026ge;\u0026thinsp;3 consecutive unexplained spontaneous miscarriages\u0026thinsp;\u0026lt;\u0026thinsp;10 weeks gestation\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\" morerows=\"2\" rowspan=\"3\"\u003e \u003cp\u003e\u003cb\u003eLaboratory\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eLupus anticoagulant present on \u0026ge;\u0026thinsp;2 occasions\u0026thinsp;\u0026ge;\u0026thinsp;12 weeks apart\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003ePositive\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAnticardiolipin IgG/IgM\u0026thinsp;\u0026gt;\u0026thinsp;40 GPL/MPL or \u0026gt;\u0026thinsp;99th percentile present on \u0026ge;\u0026thinsp;2 occasions\u0026thinsp;\u0026ge;\u0026thinsp;12 weeks apart\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAnti-β2 Glycoprotein I IgG/IgM \u0026gt;\u0026thinsp;99th percentile present on \u0026ge;\u0026thinsp;2 occasions\u0026thinsp;\u0026ge;\u0026thinsp;12 weeks apart\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003ePositive\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colspan=\"3\" nameend=\"c3\" namest=\"c1\"\u003e \u003cp\u003eAPS is present if\u0026thinsp;\u0026ge;\u0026thinsp;1 clinical criteria and \u0026ge;\u0026thinsp;1 laboratory criteria are met.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eThe patient was treated with intravenous piperacillin/tazobactam 4.5 g three times daily, low-molecular-weight heparin (enoxaparin 40 mg subcutaneously twice daily), intravenous omeprazole 40 mg once daily, nebulized bronchodilators (ipratropium bromide and salbutamol every 6 hours), and inhaled corticosteroid (beclomethasone every 8 hours), along with oral folic acid 5 mg daily. Over one week, the fever subsided, the chest pain resolved, and the leg swelling markedly improved. The patient was discharged in stable condition on anticoagulation therapy and advised to follow up with rheumatology for initiation of long-term immunomodulatory treatment.\u003c/p\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eAPS is a hypercoagulable state characterized by the presence of vascular thrombosis and/or obstetrical events in addition to the presence of autoantibodies, including lupus anticoagulant, anticardiolipin antibodies, and anti-β2-glycoprotein 1 antibodies (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Most patients with APS are diagnosed between the ages of 15 and 50 years (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e). When APS occurs with underlying systemic lupus erythematosus (SLE), it is termed secondary APS. The coexistence of these two debilitating disorders substantially increases the risk of thromboembolic events and potential end-organ damage (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eA 34-year-old male, presented with unprovoked deep vein thrombosis (DVT) and left-sided pleural effusion, which led to the diagnosis of SLE with secondary APS. Although SLE mostly affects women, men are often diagnosed at an older age and may even exhibit more severe disease manifestations, including renal and thromboembolic complications (\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e). The mechanisms of thrombosis in APS involve activation of endothelial cells, deposition of complement proteins, platelet aggregation, and suppression of natural anticoagulant pathways (\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). These processes collectively create a hypercoagulable environment that predisposes to venous and arterial thrombosis. When superimposed on SLE-related immune dysregulation, the risk of thromboembolic complications increases several fold.\u003c/p\u003e \u003cp\u003ePleural effusion is the most common thoracic manifestation in SLE, reported in up to 50% of cases, often resulting from immune-complex\u0026ndash;mediated pleuritis. However, in some cases, the effusion may be due to pulmonary embolism secondary to APS (\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e). In our patient, pleural effusion was exudative in nature, most likely due to inflammatory pleuritis, although a thromboembolic mechanism could not be entirely excluded. Secondary APS should be suspected when DVT or pulmonary embolism occurs alongside systemic symptoms such as fever, serositis, or cytopenias. Early identification is critical because thrombotic events in APS carry a high recurrence rate without adequate anticoagulation (\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eThe mainstay of treatment for APS-associated thrombosis is long-term anticoagulation, traditionally with warfarin, although low-molecular-weight heparin (LMWH) is recommended during acute management. In cases secondary to SLE, immunomodulatory therapy is indicated to control systemic inflammation and prevent further antibody-mediated vascular injury (\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e). Our patient was treated with LMWH, antibiotics, and supportive therapy, with a good clinical response. Long-term management should include a smooth transition to oral anticoagulation and rheumatology follow-up for disease-modifying agents such as hydroxychloroquine or corticosteroids.\u003c/p\u003e \u003cp\u003eIn the literature, a case report has described a rare presentation of systemic lupus erythematosus (SLE) with massive bilateral pleural effusions as the initial manifestation in a previously healthy 20-year-old soldier. Initial investigations were inconclusive; however, within three months, the patient developed the full clinical features of SLE and showed marked improvement following treatment with corticosteroids and cyclophosphamide, leading to complete resolution of the pleural effusions (\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e). A case series documented four cases of systemic lupus erythematosus (SLE) presenting with pleuritis as the initial disease manifestation; surprisingly, all of them were men (\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e). Another case was reported of a 31-year-old Black male who presented with recurrent pleural effusions secondary to active systemic lupus erythematosus (SLE\u003cb\u003e)\u003c/b\u003e (\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e). A case report described a 38-year-old male with antiphospholipid syndrome (APS) who presented with deep vein thrombosis (DVT) and pleural effusion (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e).\u003c/p\u003e"},{"header":"CONCLUSION","content":"\u003cp\u003eThis case illustrates that SLE with secondary APS can present in males with isolated venous thrombosis and pleural effusion. The presentation emphasizes the need for autoimmune screening in young patients with unprovoked DVT or serositis. Early immunological evaluation and timely initiation of anticoagulation are key to preventing recurrence and improving outcomes. Clinicians should remain vigilant for atypical presentations of autoimmune thrombotic disease, especially in high-risk environments where infectious etiologies are common mimickers and can delay diagnosis and thus treatment.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eAPS\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eAntiphospholipid Syndrome\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eSLE\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eSystemic Lupus Erythematosus\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eDVT\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eDeep Vein Thrombosis\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eESR\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eErythrocyte Sedimentation Rate\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eCRP\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eC-Reactive Protein\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eLDH\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eLactate Dehydrogenase\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eANA\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eAntinuclear Antibody\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eIgA\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eImmunoglobulin A\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eIgM\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eImmunoglobulin M\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eIgG\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eImmunoglobulin G\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eLMWH\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eLow Molecular Weight Heparin\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eConflicting interests:\u003c/strong\u003e All authors declare that they have no competing financial or personal interests that could have influenced the preparation of this manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding:\u003c/strong\u003e This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent to participate and publication: I\u003c/strong\u003enformed consent to be included in the research and publication \u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthical approval:\u003c/strong\u003e This case report was reviewed and deemed exempt from formal ethical approval by the Institutional Review Board of\u003cstrong\u003e\u0026nbsp;Dr. Ruth K. M. Pfau Civil Hospital Karachi\u003c/strong\u003e.\u0026nbsp;Permission for data collection and publication was obtained from the head of the department\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and material:\u0026nbsp;\u003c/strong\u003eAll data relevant to this case are contained within the manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCode availability:\u0026nbsp;\u003c/strong\u003eNot applicable\u0026nbsp;\u003c/p\u003e\n\u003ch3\u003e\u003cstrong\u003eCompliance with Care Guidelines:\u003c/strong\u003e\u003c/h3\u003e\n\u003cp\u003eThis report was prepared in accordance with the CARE (Consensus-based Clinical Case Reporting) guidelines; the completed CARE checklist is available upon request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eContributorship\u003c/strong\u003e: \u003cstrong\u003eSR\u0026nbsp;\u003c/strong\u003econtributed to the conception and design of the study, acquisition of clinical data, and drafting of the manuscript. \u003cstrong\u003eAA\u0026nbsp;\u003c/strong\u003econtributed to literature review, data interpretation, and manuscript drafting. \u003cstrong\u003eHK\u0026nbsp;\u003c/strong\u003econtributed to data collection, literature review, and manuscript preparation. \u003cstrong\u003eMTA\u0026nbsp;\u003c/strong\u003econtributed to critical revision of the manuscript for important intellectual content. \u003cstrong\u003eSMK\u0026nbsp;\u003c/strong\u003econtributed to supervision, data interpretation, and critical review of the manuscript. \u003cstrong\u003eUY\u0026nbsp;\u003c/strong\u003econtributed to the conception of the study, overall supervision, critical revision, and final approval of the manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements:\u003c/strong\u003e None\u003cstrong\u003e\u003c/strong\u003e\u003c/p\u003e\u003cp\u003eWritten informed consent for participation and publication of anonymized clinical details was obtained from the patient.\u003c/p\u003e\n"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eWysokinska E, Ortel TL. 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Available from: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1136/ard.44.1.61\u003c/span\u003e\u003cspan address=\"10.1136/ard.44.1.61\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Systemic Lupus Erythematosus, Antiphospholipid Syndrome, Deep Vein Thrombosis, Pleural Effusion, Autoimmune Disease, Secondary APS","lastPublishedDoi":"10.21203/rs.3.rs-9506236/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9506236/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eIntroduction:\u003c/h2\u003e \u003cp\u003eSystemic lupus erythematosus (SLE) with secondary antiphospholipid syndrome (APS) is an uncommon cause of unprovoked thrombosis and serosal inflammation, especially in males. Early recognition of autoimmune etiologies in thrombotic presentations is essential to prevent recurrence and long-term morbidity.\u003c/p\u003e\u003ch2\u003eCase Presentation:\u003c/h2\u003e \u003cp\u003eA 34-year-old male presented with 1 month history of high-grade fever, followed by relatively acute onset left-sided pleuritic chest pain and rapidly progressive, painful swelling of the left lower limb. Imaging revealed a left-sided pleural effusion and extensive deep vein thrombosis (DVT), with laboratory evaluations showing positive antinuclear antibodies (ANA), lupus anticoagulant, and anti-β2-glycoprotein I antibodies. Together with the patient\u0026rsquo;s clinical manifestations, these findings established the diagnosis of SLE with secondary APS. The patient was treated with low-molecular-weight heparin for acute DVT, intravenous antibiotics, proton pump inhibitors, inhaled bronchodilators, corticosteroids, and supportive care. Over a week, the patient experienced complete resolution of fever, significant reduction in leg swelling, and improvement in pleuritic chest pain. He was discharged on long-term anticoagulation with a plan for rheumatology follow-up for immunomodulatory therapy.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eThis case illustrates a diagnostically challenging presentation of SLE with secondary APS in males, mimicking infectious or thromboembolic conditions. Early autoimmune work-up in young patients with unexplained thrombosis or serositis can facilitate timely treatment and prevent recurrence.\u003c/p\u003e","manuscriptTitle":"Deep Vein Thrombosis and Pleural Effusion as Initial Manifestations of Systemic Lupus Erythematosus with Secondary Antiphospholipid Syndrome in a Male: A Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-04-29 11:00:42","doi":"10.21203/rs.3.rs-9506236/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"03da4451-165b-4e5a-9d37-bd7d392d6419","owner":[],"postedDate":"April 29th, 2026","published":true,"recentEditorialEvents":[{"type":"decision","content":"Rejected","date":"2026-04-30T07:29:58+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-04-30T04:58:13+00:00","index":"","fulltext":""}],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2026-04-30T07:40:57+00:00","versionOfRecord":[],"versionCreatedAt":"2026-04-29 11:00:42","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9506236","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9506236","identity":"rs-9506236","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}