European journal of case reports in internal medicine最新文献

{"title":"Unmasking Macrophage Activation Syndrome in Vexas Syndrome: A Diagnostic Challenge.","authors":"Alexandre Boissais, Baptiste Farrulo, Thomas Moulinet, Valentin Lacombe, Alexandra Audemard-Verger","doi":"10.12890/2026_007266","DOIUrl":"10.12890/2026_007266","url":null,"abstract":"<p><strong>Introduction: </strong>Vacuoles, E1 Enzyme, X-linked, Auto-inflammatory, Somatic (VEXAS) syndrome is a late-onset autoinflammatory disease caused by somatic mutations in the UBA1gene. Macrophage activation syndrome (MAS) is a rare but life-threatening hyperinflammatory condition whose association with VEXAS syndrome remains poorly described.</p><p><strong>Case description: </strong>We report three cases of MAS occurring in men aged 65 to 72 years with genetically confirmed VEXAS syndrome. In all cases, MAS was characterized by fever, recent-onset cytopenias, marked hyperferritinaemia, and a high probability of MAS according to the H-score (>93%). Bone marrow examination demonstrated haemophagocytosis in two patients and numerous activated macrophages in one. Extensive investigations failed to identify infectious, malignant, or drug-related triggers. In one patient, MAS preceded the diagnosis of VEXAS syndrome by several years. In the two others, MAS occurred during the course of established VEXAS disease and was considered a manifestation of disease flare. Treatment included high-dose corticosteroids, with additional anakinra in one patient and etoposide in another, resulting in rapid clinical and biological improvement. One patient experienced MAS relapse following granulocyte colony-stimulating factor exposure during azacitidine treatment, whereas no recurrence was observed in the other two patients during follow-up.</p><p><strong>Conclusion: </strong>MAS appears to be an underrecognized and potentially severe complication of VEXAS syndrome that may occur in the absence of an identifiable infectious or malignant trigger. Diagnostic overlap between both conditions may delay recognition. MAS should be suspected in VEXAS patients presenting with acute cytopenias, marked hyperferritinaemia, and organ involvement. Early use of the H-score, bone marrow examination, and prompt immunosuppressive treatment are essential to improve outcomes.</p><p><strong>Learning points: </strong>Macrophage activation syndrome (MAS) may represent a severe flare manifestation of Vacuoles, E1 Enzyme, X-linked, Auto-inflammatory, Somatic (VEXAS) syndrome, even in the absence of an identifiable infectious, malignant, or drug-related trigger.The diagnosis of MAS can be challenging in VEXAS syndrome because both conditions share overlapping features, including systemic inflammation, cytopenias, hyperferritinaemia, and bone marrow abnormalities.Recent-onset cytopenias, marked hyperferritinaemia, and organ involvement in patients with VEXAS syndrome should prompt early assessment for MAS using the H-score and bone marrow examination, allowing rapid initiation of immunosuppressive therapy.</p>","PeriodicalId":11908,"journal":{"name":"European journal of case reports in internal medicine","volume":"13 9","pages":"007266"},"PeriodicalIF":0.0,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13561133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesalazine-Induced Myocarditis Following Dose Escalation in Ulcerative Colitis: A Diagnostic Challenge.","authors":"Alfonso Vidal López, María Asunción Esteve Pastor, Manuel Romero Martínez, Lidia María Carrillo Mora, Joaquín Salinas García, Carmen Agulló López, Domingo Andrés Pascual Figal","doi":"10.12890/2026_007204","DOIUrl":"10.12890/2026_007204","url":null,"abstract":"<p><strong>Introduction: </strong>Mesalazine (5-aminosalicylic acid, 5-ASA) is the cornerstone treatment for mild-to-moderate ulcerative colitis. Although generally well tolerated, rare cases of drug-induced myocarditis have been reported. Distinguishing mesalazine-induced myocarditis from myocarditis related to inflammatory bowel disease is essential, as management differs substantially.</p><p><strong>Case description: </strong>A 43-year-old man with recently diagnosed ulcerative colitis presented with acute chest pain, fever and elevated cardiac biomarkers eight days after initiation of oral mesalazine (3 g/day). Electrocardiography demonstrated diffuse ST-segment elevation, while echocardiography showed preserved left ventricular systolic function; coronary angiography excluded obstructive coronary artery disease. During hospitalisation, worsening gastrointestinal symptoms prompted escalation of mesalazine to 4.8 g/day. Within 24 hours, the patient developed recurrent chest pain, fever and a marked increase in troponin, inflammatory markers and NT-proBNP. Viral and autoimmune investigations were negative. The close temporal relationship between symptom recurrence and dose escalation raised suspicion of mesalazine-induced myocarditis. Following discontinuation of mesalazine, rapid clinical and biochemical improvement was observed. A cardiac magnetic resonance imaging (MRI) performed on day 7 demonstrated myocardial oedema on T2-weighted sequences and non-ischaemic epicardial late gadolinium enhancement involving the apical and inferolateral segments. This fulfilled both T2-based and T1-based criteria of the 2018 modified Lake Louise criteria for acute myocarditis. At follow-up, the patient remained asymptomatic with complete recovery of ventricular function.</p><p><strong>Conclusion: </strong>Mesalazine-induced myocarditis is an uncommon but potentially serious adverse reaction that may mimic an extraintestinal manifestation of ulcerative colitis. Early recognition, careful assessment of drug exposure chronology and prompt withdrawal of mesalazine are crucial to prevent complications. Cardiac MRI plays a central role in confirming the diagnosis.</p><p><strong>Learning points: </strong>Mesalazine-induced myocarditis is a rare but potentially life-threatening adverse effect that should be suspected in any patient with inflammatory bowel disease presenting with chest pain shortly after treatment initiation or dose escalation.Differentiating drug-induced myocarditis from myocarditis related to inflammatory bowel disease is crucial, as continuation of mesalazine may worsen cardiac injury.Prompt withdrawal of mesalazine usually leads to complete clinical recovery, while cardiac MRI plays a key role in confirming the diagnosis.</p>","PeriodicalId":11908,"journal":{"name":"European journal of case reports in internal medicine","volume":"13 9","pages":"007204"},"PeriodicalIF":0.0,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13561128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Splenic Artery Embolization, A Therapy that Can be Life-Saving for Small Bowel Variceal Bleeding.","authors":"Rached Radwan, Marianne Ghantous, Johny Salem, Joe Khoury, Antoine Geagea, Khalil Chidiac","doi":"10.12890/2026_007245","DOIUrl":"10.12890/2026_007245","url":null,"abstract":"<p><strong>Introduction: </strong>Small bowel varices are a rare manifestation of portal hypertension, accounting for only 1-5% of variceal gastrointestinal bleeding. Their diagnosis and management remain challenging because of their uncommon occurrence, difficult anatomical accessibility, and lack of standardized treatment strategies. We report a case of refractory small bowel variceal bleeding successfully treated with splenic artery embolization after failure of conventional therapeutic options.</p><p><strong>Case presentation: </strong>A 45-year-old man with liver cirrhosis, cholangiocarcinoma with bone metastases, ulcerative colitis, and previous partial hepatectomy presented with haemorrhagic shock secondary to severe lower gastrointestinal bleeding. Endoscopic evaluation suggested a small bowel source, while computed tomography angiography demonstrated portal vein stenosis, superior mesenteric vein thrombosis, portal hypertension, and actively bleeding small bowel varices. Portal vein stenting failed to control the haemorrhage, and transjugular intrahepatic portosystemic shunt (TIPS) placement was unsuccessful because of extensive hepatic vein thrombosis related to tumour burden. Salvage splenic artery embolization was subsequently performed using two vascular plugs, resulting in immediate haemostasis without recurrent bleeding. Follow-up imaging confirmed the absence of active bleeding. The only post-procedural complication was partial splenic infarction, which was managed conservatively.</p><p><strong>Discussion: </strong>Splenic artery embolization reduces portal venous inflow by decreasing splenic blood flow, thereby lowering portal pressure and decompressing ectopic varices. Although primarily described for esophagogastric varices and other complications of portal hypertension, its use in small bowel variceal bleeding remains rarely reported. This case highlights splenic artery embolization as an effective rescue therapy when TIPS is technically impossible or unsuccessful.</p><p><strong>Conclusion: </strong>Splenic artery embolization may represent a safe, minimally invasive, and life-saving therapeutic option for refractory small bowel variceal bleeding in carefully selected patients who are not candidates for conventional interventions. Multidisciplinary collaboration is essential to optimize outcomes, and further studies are needed to better define the role of this technique in the management of ectopic variceal bleeding.</p><p><strong>Learning points: </strong>Small bowel ectopic varices account for only 1-5% of cases of gastrointestinal bleeding.Due to its rarity in clinical practice, therapy is challenging.</p>","PeriodicalId":11908,"journal":{"name":"European journal of case reports in internal medicine","volume":"13 9","pages":"007245"},"PeriodicalIF":0.0,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13561139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contrast-Induced Neurotoxicity Following Mechanical Thrombectomy for Acute Left MCA Occlusion: A Reversible Radiological Mimic of Intracranial Haemorrhage.","authors":"Abdelrahman Shehata, Sachin Syal, Nazia Akhtar, Sania Akhtar, Thuslim Sheik, Salama Mohamed Karamastaji","doi":"10.12890/2026_007261","DOIUrl":"10.12890/2026_007261","url":null,"abstract":"<p><strong>Introduction: </strong>Neurotoxicity due to contrast extravasation and disruption of the blood-brain barrier is a rare event in neuroendovascular procedures called contrast-induced neurotoxicity (CIN). Although a correct diagnosis may be difficult after mechanical thrombectomy, radiologically, CIN may be similar to haemorrhage or malignant oedema.</p><p><strong>Case description: </strong>A 59-year-old male with a history of hypertension, paroxysmal atrial fibrillation and recent non-ST-elevation myocardial infarction presented with acute ischemic stroke secondary to distal left middle cerebral artery occlusion. There was successful reperfusion with mechanical thrombectomy. The immediate post-procedure computed tomography scan revealed hyper attenuation of the left frontotemporal gyral with oedema, but no evidence of haemorrhage, which matched with the diagnosis of CIN. Rapid healing of hyper attenuation and evolution to a stable infarct was observed on serial computed tomography scans obtained over 24-48 hours. The patient needed prolonged ventilatory support, which was provided by a tracheostomy and there was no haemorrhagic transformation.</p><p><strong>Conclusion: </strong>This case serves as an example of a benign radiological mimic after thrombectomy, namely CIN. Understanding its imaging appearances and the need for serial CT imaging helps to prevent misdiagnosis and unnecessary discontinuation if anti-thrombotic treatment. There is no evidence of self-limitation and there is support for management of CIN.</p><p><strong>Learning points: </strong>Mechanical thrombectomy can also cause rare and reversible side effects of contrast-induced neurotoxicity (CIN) that can mimic immediately post-procedure computed tomography (CT) scan findings of intracranial bleeding.Non-contrast CT imaging is crucial to rule out malignant cerebral oedema or haemorrhagic transformation of the stroke lesion, especially in the case of serial imaging, to avoid unnecessary interventions.In patients with cardioembolic stroke and high-risk, antithrombotic therapy can be continued at the time of recognition of CIN.</p>","PeriodicalId":11908,"journal":{"name":"European journal of case reports in internal medicine","volume":"13 9","pages":"007261"},"PeriodicalIF":0.0,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13561130/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Familial Hypocalciuric Hypercalcemia and Early Severe Aortic Stenosis in A Patient with two Different Heart Failure Episodes.","authors":"Ana Margarida Fonseca, Mariana Lobo Oliveira, Ana Cordeiro Gomes, Luis Nogueira-Silva, Joana Pereira, Jorge Almeida, Patrícia Lourenço","doi":"10.12890/2026_006953","DOIUrl":"10.12890/2026_006953","url":null,"abstract":"<p><strong>Introduction: </strong>Familial hypocalciuric hypercalcemia (FHH) is a rare hereditary cause of mild hypercalcemia that usually follows a benign clinical course. Calcific aortic stenosis (AS) in a trileaflet aortic valve is uncommon before 65 years of age. Emerging evidence suggests that disturbances in calcium metabolism may contribute to aortic valve calcification.</p><p><strong>Case description: </strong>A 58-year-old woman presented in 2012 with acute heart failure (HF) and left ventricular ejection fraction (LVEF) of 32%. Coronary angiography was normal, and endomyocardial biopsy was not suggestive of myocarditis. She achieved complete recovery with guideline-directed medical therapy, consistent with resolved idiopathic cardiomyopathy. Echocardiography at that time showed only mild aortic valve thickening. She had chronic mild hypercalcemia consistent with FHH, supported by family history, normal parathyroid hormone levels, and fractional excretion of calcium <1%. Genetic testing was negative. During the following decade, progressive aortic valve calcification was documented. In 2023, echocardiography revealed severe AS with a functionally bicuspid valve (peak/mean gradients 105/69 mmHg; valve area 0.5 cm²) and LVEF of 41%, presenting with a second episode of acute HF. She underwent surgical aortic valve replacement with full symptomatic recovery.</p><p><strong>Conclusion: </strong>This case suggests a possible association between FHH and accelerated valvular calcification leading to premature severe AS. It is also notable for two separate HF episodes caused by different aetiologies: reversible cardiomyopathy initially, followed a decade later by severe AS. Although FHH is generally considered benign, chronic hypercalcemia may justify closer long-term cardiovascular surveillance.</p><p><strong>Learning points: </strong>Familial hypocalciuric hypercalcemia may be associated with accelerated valvular calcification and premature severe aortic stenosis.Serial imaging over 10 years documented progression from mild valve thickening to severe calcific aortic stenosis.The case describes two distinct episodes of heart failure caused by different underlying mechanisms.</p>","PeriodicalId":11908,"journal":{"name":"European journal of case reports in internal medicine","volume":"13 9","pages":"006953"},"PeriodicalIF":0.0,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13561145/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lymphocytic Variant Hypereosinophilic Syndrome Overlaps with Angioimmunoblastic T-Cell Lymphoma: A Case Report and Literature Review.","authors":"Nabil Belfeki, Omaima El Koudssi, Pierre Isnard, Guillaume Lefevre","doi":"10.12890/2026_007269","DOIUrl":"10.12890/2026_007269","url":null,"abstract":"<p><strong>Introduction: </strong>Lymphocytic-variant of hypereosinophilic syndrome (L-HES) is a clonal T-cell disorder driven by an aberrant Th2 response, typically featuring CD3- CD4+ T-cell expansion, eosinophil-mediated tissue injury, most commonly skin lesions, and lymphadenopathy. Angioimmunoblastic T-cell lymphoma (AITL) is an aggressive peripheral T-cell lymphoma of follicular helper T-cell origin; it can present with similar clinical features such as lymphadenopathy, rash and eosinophilia. Histological and immunophenotypic features may also be common in both diseases, thus creating a diagnostic overlap.</p><p><strong>Case description: </strong>We report the case of a 53-year-old man with a medical history of allergic rhinitis who developed a diffuse, persistent maculopapular rash with pruritis. Physical examination revealed inguinal lymphadenopathy without organomegaly, laboratory investigations demonstrated marked eosinophilia, and hypergammaglobulinemia, while additional testing excluded any infectious or autoimmune aetiologies. Lymphocytic immunophenotyping on peripheral blood and skin biopsy revealed a high proportion of CD3-CD4+ cells exhibiting a classic TH2 phenotype, consistent with L-HES. However, lymph node histology demonstrated architectural remodelling with intrafollicular infiltration by atypical T lymphocytes showing a T-cell follicular helper phenotype, findings indicative of AITL. The coexistence of L-HES and AITL was established. The patient underwent polychemotherapy, resulting in rapid clinical improvement of skin lesions with sustained remission at 6 months of follow up.</p><p><strong>Conclusion: </strong>L-HES and AITL may coexist, or L-HES may precede overt lymphoma, suggesting clonal evolution within a shared biological spectrum. This case highlights diagnostic pitfalls and emphasizes the need for integrated clinical, pathological, flow cytometric and molecular evaluation.</p><p><strong>Learning points: </strong>Lymphocytic-variant of hypereosinophilic syndrome (L-HES) may precede or be associated with T malignant lymphoproliferation.Physician awareness of L-HES conditions presenting with tumoral syndrome is necessary to rule out malignant lymphoproliferation.Histological samples and biological investigations are mandatory to distinguish L-HES from angioimmunoblastic T-cell lymphoma.</p>","PeriodicalId":11908,"journal":{"name":"European journal of case reports in internal medicine","volume":"13 9","pages":"007269"},"PeriodicalIF":0.0,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13561141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spontaneous Pneumomediastinum in Rheumatoid Arthritis Associated Interstitial Lung Disease and Bronchiectasis: A Three-Component Pathophysiologic Framework.","authors":"Rahaf Jereisat, Stephanie Ammari, Nawras Ibrahim","doi":"10.12890/2026_007257","DOIUrl":"10.12890/2026_007257","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Spontaneous pneumomediastinum is a recognized complication of connective tissue disease associated interstitial lung disease, most extensively described in dermatomyositis. Despite rheumatoid arthritis being the most common connective tissue disease with pulmonary involvement, spontaneous pneumomediastinum in rheumatoid arthritis associated lung disease has been reported only once previously. Rheumatoid arthritis uniquely causes two distinct forms of structural lung injury (interstitial lung disease and bronchiectasis) both linked to seropositive autoimmunity. An 83-year-old woman, a never-smoker with seropositive rheumatoid arthritis, progressive pulmonary fibrosis, left lower lobe bronchiectasis, low body mass index, and iatrogenic lymphopenia developed extensive pneumomediastinum during community-acquired pneumonia. Computed tomography scan demonstrated pneumomediastinum with subcutaneous emphysema, emphysematous lungs with diffuse interstitial scarring, bronchiectasis, and lobar consolidation. Conservative management with antibiotics achieved complete radiographic resolution at 8 weeks with no recurrence at 12 weeks. We hypothesize a three-component pathophysiologic framework: structural alveolar fragility from interstitial lung disease and emphysema may provide the substrate for alveolar rupture, while infection-driven coughing from true airway bronchiectasis may serve as the mechanical trigger via the Macklin effect. In rheumatoid arthritis, all three components appear driven by a shared seropositive autoimmune process. This mechanistic profile may differ fundamentally from dermatomyositis, where spontaneous pneumomediastinum is thought to reflect rapidly progressive parenchymal destruction, suggesting that dermatomyositis-derived mortality data may not be directly applicable to rheumatoid arthritis. Spontaneous pneumomediastinum in seropositive rheumatoid arthritis may follow a favourable trajectory when the mechanical trigger is reversible. High titer seropositivity, low body mass index, and iatrogenic immunosuppression may identify a convergent risk phenotype.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Learning points: &lt;/strong&gt;Seropositive rheumatoid arthritis uniquely drives two distinct forms of structural lung injury (interstitial lung disease [ILD] and bronchiectasis) that may converge to create a substrate for spontaneous pneumomediastinum via the Macklin effect. Internists should recognize that rheumatoid arthritis (RA) patients with high-titer rheumatoid factor and anti- cyclic citrullinated peptide are at increased risk for both manifestations, and their coexistence may lower the threshold for alveolar rupture during infection-driven coughing.Not all pneumomediastinum in connective tissue diseases carries the same prognosis. When spontaneous pneumomediastinum (SPM) occurs in the setting of a reversible mechanical trigger such as acute pneumonia, conservative management with targeted antibiotics may achieve complete resolution, in contrast to the progr","PeriodicalId":11908,"journal":{"name":"European journal of case reports in internal medicine","volume":"13 9","pages":"007257"},"PeriodicalIF":0.0,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13561146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roxadustat-Associated Cholestatic Jaundice in Haemodialysis Patients with Positive Rechallenge.","authors":"Xiaosu Ke, Churong Liu","doi":"10.12890/2026_007262","DOIUrl":"https://doi.org/10.12890/2026_007262","url":null,"abstract":"<p><p>Roxadustat, an oral hypoxia-inducible factor prolyl hydroxylase inhibitor, is widely used for anaemia in chronic kidney disease. While pivotal trials reported low risks of transaminase elevations, detailed clinical case reports substantiating a causal link with cholestatic jaundice remain scarce. We report a series of four haemodialysis patients who developed cholestatic jaundice after roxadustat initiation, characterized by predominant elevations of direct bilirubin and bile acids with persistently normal transaminases. Notably, two patients had positive rechallenges. Common causes of cholestasis were excluded, and biochemical recovery occurred after drug discontinuation. This case report suggests a causal association between roxadustat and cholestatic jaundice in haemodialysis patients and highlights the value of monitoring cholestatic parameters during therapy.</p><p><strong>Learning points: </strong>This case series provides clinical evidence supporting a causal association between roxadustat and cholestatic jaundice in haemodialysis patients, warranting clinical awareness of this potential adverse effect.</p>","PeriodicalId":11908,"journal":{"name":"European journal of case reports in internal medicine","volume":"13 8","pages":"007262"},"PeriodicalIF":0.0,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13479847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitral Valve Vegetation and Embolic Stroke in Newly Diagnosed Granulomatosis with Polyangiitis: A Diagnostic Challenge Mimicking Culture-Negative Endocarditis.","authors":"Noor Farhoud, Hussam Farhoud","doi":"10.12890/2026_006960","DOIUrl":"https://doi.org/10.12890/2026_006960","url":null,"abstract":"<p><strong>Introduction: </strong>Granulomatosis with polyangiitis (GPA) is an antineutrophil cytoplasmic antibody (ANCA)-associated small- to medium-vessel vasculitis that most commonly affects the respiratory tract and kidneys. Cardiac involvement is uncommon, and valvular manifestations are rare. Distinguishing GPA-related valvular involvement from infective endocarditis (IE) presents a significant diagnostic challenge, particularly because ANCA positivity may also occur in IE.</p><p><strong>Case description: </strong>We report a 60-year-old man who presented with necrotic lower-extremity ulcers, acute kidney injury, and elevated inflammatory markers. Serologic evaluation demonstrated positive ANCA with proteinase-3 specificity, while kidney biopsy confirmed pauci-immune necrotizing crescentic glomerulonephritis, supporting a diagnosis of GPA. Despite initiation of immunosuppressive therapy, he developed acute focal neurologic deficits, and brain magnetic resonance imaging demonstrated multifocal ischemic infarcts consistent with an embolic process. Transoesophageal echocardiography revealed a mitral valve mass with moderate-to-severe regurgitation. Blood cultures and serologic evaluation for fastidious organisms remained negative.</p><p><strong>Conclusion: </strong>This case highlights a rare presentation of GPA with suspected sterile valvular involvement complicated by embolic stroke and underscores the importance of distinguishing ANCA-associated vasculitis from culture-negative infective endocarditis.</p><p><strong>Learning points: </strong>Antineutrophil cytoplasmic antibody (ANCA) positivity does not exclude infective endocarditis, as significant clinical overlap exists between these conditions.Kidney biopsy and careful microbiologic evaluation may help distinguish ANCA-associated vasculitis from infection-associated mimics.Cardiac imaging should be considered in patients with granulomatosis with polyangiitis who develop unexplained focal neurologic deficits.</p>","PeriodicalId":11908,"journal":{"name":"European journal of case reports in internal medicine","volume":"13 8","pages":"006960"},"PeriodicalIF":0.0,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13479844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>Ascaris Lumbricoides</i> through an Intercostal Chest Tube in A Case with Hodgkin's Lymphoma.","authors":"Ayşe Öz, Sultan Aydın","doi":"10.12890/2026_007276","DOIUrl":"https://doi.org/10.12890/2026_007276","url":null,"abstract":"<p><strong>Introduction: </strong><i>Ascaris lumbricoides</i> typically mimics pneumonia during its larval migration phase. However, its presentation with pleural effusion and the recovery of a live adult worm through an intercostal chest tube is extraordinarily rare. This case highlights a unique opportunistic parasitic infection in an immunocompromised paediatric patient, emphasising the need to consider parasitic aetiologies in refractory pulmonary symptoms within oncology settings.</p><p><strong>Case description: </strong>A 15-year-old female with stage IIIA Hodgkin's lymphoma presented with fever, cough and respiratory distress five days after completing her second cycle of COPDAC chemotherapy. Despite broad-spectrum antibiotics and bilateral chest tube insertion for persistent pleural effusion, her clinical condition remained refractory. A live, 15-cm adult <i>A. lumbricoides</i> was unexpectedly recovered from the right chest tube. Following a 21-day course of albendazole, the patient showed complete clinical and radiological resolution.</p><p><strong>Conclusion: </strong>In paediatric oncology patients, standard treatments for pneumonia may fail when atypical pathogens are involved. This case underscores that clinicians should maintain a high index of suspicion for helminthic infections in immunocompromised hosts presenting with atypical or refractory pleural and pulmonary findings.</p><p><strong>Learning points: </strong><b>Atypical parasitic presentation</b> Clinicians should consider parasitic aetiologies, such as <i>Ascaris lumbricoides</i>, in immunocompromised paediatric oncology patients presenting with refractory pneumonia and severe pleural effusion that do not respond to standard antimicrobial therapies.<b>Chemotherapy-induced vulnerability</b> Severe immunosuppression and corticosteroid use associated with lymphoma protocols can alter standard biological barriers, facilitating aberrant migration pathways for helminths into the pleural cavity.<b>Diagnostic vigilance</b> The unexpected extraction of a live adult worm from an intercostal chest tube emphasises the critical need for comprehensive screening and high clinical suspicion for atypical pathogens in endemic regions.</p>","PeriodicalId":11908,"journal":{"name":"European journal of case reports in internal medicine","volume":"13 8","pages":"007276"},"PeriodicalIF":0.0,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13479875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}