Authors:Sathesh BaskaranDr. G. Saravanakumar M.S., D.A., F.P.SAffiliation:  Madurai foot care Centre, Madurai, Tamil Nadu, IndiaCorresponding Author:Sathesh BaskaranEmail: sbaskaran@newvision.gePhone: +918754673570

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A document by Katelyn Kirves. Click on the document to view its contents.

A document by doueryunyun Dou. Click on the document to view its contents.

Background: Spondylolisthesis is a frequent cause of low back pain but is seldomly associated with infectious causes and multisystem failure. Case Presentation: We present a patient who complained of severe low back pain and acute onset of neurological deficits that progressed to cardiovascular collapse and developed into a complex diagnostic and

A document by Shuanglin Lei. Click on the document to view its contents.

Title: Rare case of Dutasteride induced reversible acute necrotising myopathyDr. Sujatha Kamalaksha 1, 2, Professor Catriona McLean3, Dr. H. M. Meththananda Herath2, 4Affiliations1 - Consultant Rheumatologist, Southwest Healthcare, Warrnambool, VIC Australia 32802 – Affiliate Senior Lecturer; Deakin Clinical School Warrnambool campus, VIC, Australia 32803 - Professor and Head Department of Anatomical Pathology, Alfred Health, Melbourne, VIC, Australia4 – Consultant Physician, Southwest Healthcare, Warrnambool, VIC, Australia 3280

ECG with Anterior T-wave inversion in Caucasian Healthy Athletes: Cardiomyopathy or Athlete’s Heart?Lista Patricia1; Pin Riccardo1; Muzzarelli Stefano2; Menafoglio Andrea3; Di Valentino Marcello1-4.1 Department of Cardiology, Clinica Luganese Moncucco, 6900 Lugano, Switzerland2 Cardiocentro Ticino Institute, Ente Ospedaliero Cantonale, 6600 Locarno, Switzerland3 Cardiocentro Ticino Institute, Ente Ospedaliero Cantonale, 6500 Bellinzona, Switzerland4 Faculty of Biomedical Sciences, Università della Svizzera italiana, 6900 Lugano, SwitzerlandCorrespondence: Patricia Lista (patricia.lista@moncucco.ch)Keywords: ECG, athletes, T-wave inversion, cardiomyopathy

Targeting BRAF V600E in Malignant Phyllodes Tumor: Evidence for Precision Oncology in a Rare Breast SarcomaJonathan Chi, Kamalesh K. Sankhala, Amin Mirhadi, Mark AgulnikKey Words: oncology, genetics and genomics, pathology and laboratory medicine, radiology and imaging, surgeryKey Clinical Message: Comprehensive genomic profiling identified a BRAF V600E mutation in malignant phyllodes tumor, enabling effective use of BRAF/MEK–targeted therapy. This case supports precision oncology as a viable strategy to reduce tumor burden and extend disease control in rare breast sarcomas.AbstractTargeted therapies are an accepted standard transformative approach in oncology, offering precision-based treatment strategies that are both less toxic and highly effective in reducing or eradicating tumor burden. We present the case of a patient with a malignant phyllodes tumor who, following mastectomy, underwent comprehensive genomic profiling through Foundation One sequencing, which identified a BRAF V600E mutation. On this basis, she was enrolled in the Targeted Agent and Profiling Utilization Registry (TAPUR) trial and initiated therapy with the BRAF inhibitor vemurafenib in combination with the MEK inhibitor cobimetinib—an FDA established regimen for melanoma but rarely applied in the context of breast malignancies or sarcomas. This report represents one of the first documented cases evaluating the efficacy of vemurafenib-cobimetinib in a breast sarcoma subtype. In conjunction with definitive surgery, adjuvant radiation, and microwave ablation, this targeted regimen was associated with a favorable toxicity profile and a measurable reduction in tumor burden. Taken together, this case underscores the critical role of next-generation sequencing in uncovering actionable genomic alterations and highlights the expanding potential of precision oncology in a rare breast sarcoma subtype.IntroductionPhyllodes tumors (PT) of the breast are rare fibroepithelial neoplasms, often difficult to clinically distinguish from fibroadenomas due to overlapping histologic features. The World Health Organization (WHO) classifies PT into three categories based on histological analysis: benign, borderline, and malignant.1 The distinguishing factors separating these categorizations are subjective, defined by stromal cellularity, stromal atypia, mitosis, stromal overgrowth, and tumor margin.2 This histologic ambiguity frequently contributes to diagnostic uncertainty and adds to existing challenges in establishing reliable primary breast sarcoma diagnosis.3The mainstay of treatment for malignant PT is surgical resection, while the role of adjuvant radiotherapy remains controversial with respect to improving disease-free survival.4 Local recurrence is a central concern with surgery alone, with results varying based on resection margins. Although a negative margin of ≥1 cm is generally considered adequate for borderline and malignant PT, this is not always surgically achievable.5 Despite optimal surgery and adjuvant radiation, malignant phyllodes tumors have a risk of metastatic disease, particularly to the lungs, though the risk is lower for borderline and benign types. A significant portion of these malignant tumors (up to 27%) can metastasize.6 And given this, there is a need for effective therapies in the metastatic setting. Current chemotherapeutic approaches are suboptimal.7,8These limitations highlight the need for novel, patient-specific therapeutic strategies to optimize outcomes.The expanding characterization of the PT genomic landscape has created opportunities for targeted therapies that may be less morbid than surgery and more tolerable than conventional sarcoma directed chemotherapy.We present a case of a patient with a malignant PT harboring a BRAF V600E mutation. This mutation results in constitutive activation of the BRAF kinase within the RTK/RAF/RAS signaling cascade. Unlike wild-type RAF isoforms, BRAF V600E signals as a monomer, bypassing the requirement for dimerization, and thereby drives persistent MAPK pathway activation, enhanced tumor proliferation, and oncogenic progression.9 Defining the clinical relevance of BRAF V600E in PT may yield actionable therapeutic insights, expand treatment options beyond chemotherapy, and further inform the development of histology-agnostic precision oncology strategies.10Case History/ExaminationWe present the case of a female who presented at age 49 with a left breast mass. Of note, the patient had a past medical history relevant for poliomyelitis, diagnosed at age 1. The patient was in her usual state of health until 2016, when she experienced bleeding from her left nipple and observed an increasing nodule in her left breast.Differential Diagnosis, Investigations, and TreatmentAn initial biopsy of the left breast mass was consistent with a benign phyllodes tumor. However, due to increased tumor growth and concern for malignancy, she underwent lumpectomy in November 2017 to excise a 7 cm malignant phyllodes tumor of the left breast and a 2.2 cm malignant phyllodes tumor of the superior left breast (Figure 3). Margins from the larger tumor were involved with disease. Patient was advised to undergo a left breast mastectomy on January 23, 2018 because of a positive margin at her initial surgery (Figure 3).In March 2018, the patient noticed 2 new nodules in her left chest wall near her prior surgical site. These enlarged rapidly. Biopsy was done and pathology confirmed recurrent sarcoma of the left breast with underlying infiltrate or sarcomatous malignancy invading into the skin dermis. This diagnosis was consistent with malignant PT with extensive sarcomatoid overgrowth.In 2018, Foundation One genetic profiling revealed a BRAF mutation in the tumor (Figure 1). The patient then enrolled in TAPUR: Testing the Use of FDA Approved Drugs That Target a Specific Abnormality in a Tumor Gene in People With Advanced Stage Cancer (TAPUR) NCT02693535. In May 2018, she initiated targeted therapy with vemurafenib (960 mg orally twice daily) in combination with cobimetinib (60 mg orally once daily, administered on days 1–21 of each 28-day cycle) (Figure 3).Figure 1Foundation 1 genetic profiling for the initial Phyllodes tumorPatient received treatment with dose reduction (vemurafenib 25% dose reduction and cobimetinib 33% dose reduction) due to recurrent skin rash. She briefly discontinued treatment in September 2018 and underwent surgery for the chest wall recurrence (Figure 3). Pathology showed no evidence of residual malignancy. The patient received adjuvant radiation therapy following surgery, to the chest wall, in October 2018 (Figure 3). Following radiation in February 2019, the patient resumed her targeted therapy with vemurafenib in combination with cobimetinib, at a modified dose until June 2019 (Figure 3). After a disease free interval of 6 months, a CT scan of the chest, abdomen, and pelvis, revealed new lung metastases, confirmed on core needle biopsy to be a spindle cell tumor, consistent with metastasis from malignant Phyllodes tumor of breast (Figure 2A). She resumed vemurafenib 25% dose reduction and cobimetinib 33% dose reduction in December 2019, and underwent microwave ablation of the enlarging left upper lobe lung lesion in January 2021, showing improvement in tumor size (Figure 2B, 3)Figure 2

Title: Whipple’s disease in a young Nepalese Mongolian male without rheumatological findings: A case report

Congenital Hepatic Fibrosis Complicated with Polycystic Kidney Disease and Extensive Portomesenteric Venous Thrombosis: A Case Report and Literature ReviewAuthors: Liu, Dandan ¹*; Xu, Gang ¹; Li, Xinglan ¹; Tang, Baijie ¹¹ University of Electronic Science and Technology of China Sichuan Provincial People’s Hospital*Corresponding author: Liu, Dandan, E-mail: hb_ldd@qq.com;ORCID: 0009-0003-3803-8645Key Clinical Message: Adults with portal hypertension and renal cysts, even with a history of alcohol use, should be evaluated for congenital hepatic fibrosis; pathological re‑evaluation helps correct misdiagnosis, and prompt anticoagulation is critical for thrombotic complications.IntroductionCongenital hepatic fibrosis (CHF) is a rare autosomal recessive fibrocystic liver disease caused by ductal plate malformation, often associated with ciliopathy‑related disorders such as polycystic kidney disease (PKD) and Caroli’s disease [1]. Adult‑onset CHF is prone to misdiagnosis due to atypical clinical manifestations and confounding factors such as alcohol consumption or viral hepatitis [2]. Its core clinical feature is portal hypertension, with symptoms overlapping those of alcoholic or viral cirrhosis [3]. The main complications of CHF are cholangitis and portal hypertension [4], whereas extensive portomesenteric venous thrombosis is extremely rare and rarely reported.We present an adult case of CHF misdiagnosed as alcoholic cirrhosis for nearly 6 years, complicated with PKD, Caroli’s disease, and extensive portomesenteric venous thrombosis, aiming to highlight diagnostic clues, avoid clinical anchoring bias [5], and provide a reference for the clinical management of such rare cases.Case History and ExaminationA 38‑year‑old male with a 10‑year history of alcohol consumption (50 g ethanol per occasion, 2–3 times weekly) and a 10‑year history of untreated gouty arthritis was admitted to our hospital five times. There was no family history of hereditary hepatorenal diseases.Initial Admission and Subsequent Treatment in 2020In July 2020, he was admitted with hematemesis and melena for 14 days, accompanied by dizziness, fatigue, and orthostatic hypotension. Physical examination revealed pale conjunctiva and skin, and splenomegaly (3 cm below the left costal margin). Laboratory tests showed anemia, thrombocytopenia, cholestatic liver dysfunction, elevated tumor markers, and elevated D‑dimer. Gastroscopy showed severe esophagogastric fundal varices. Abdominal contrast‑enhanced CT suggested liver cirrhosis, splenomegaly, mild intrahepatic bile duct dilatation, and bilateral renal cysts.He was diagnosed with acute upper gastrointestinal bleeding and decompensated alcoholic cirrhosis (Child–Pugh class A). Emergency endoscopic variceal ligation plus tissue adhesive injection was performed, and bleeding was controlled. Due to recurrent mild hematemesis, a second endoscopic variceal ligation (August 2020) and a third endoscopic sclerotherapy (March 2021) were performed, with no further bleeding thereafter.Admission and Surgery in 2024In January 2024, he was admitted with recurrent abdominal distension and aggravated splenomegaly, with persistent thrombocytopenia and leukopenia suggesting hypersplenism. He underwent splenectomy + portaazygos devascularization + liver biopsy. Intraoperative findings showed mild hepatic surface nodularity (without typical cirrhotic nodules) and mild intrahepatic bile duct dilatation. The initial pathological diagnosis of the liver biopsy was nodular cirrhosis. Postoperative recovery was uneventful, and he remained asymptomatic during 2 years of follow‑up.Admission and Examinations in 2026In January 2026, he presented with persistent dull upper abdominal pain (worse after meals), nausea, and anorexia. Three days before admission, he developed paroxysmal colic, abdominal distension, and constipation. Physical examination showed low‑grade fever, tachycardia, and tenderness, rebound tenderness, and guarding in the upper abdomen and periumbilical region.Laboratory tests revealed leukocytosis, hypokalemia, aggravated cholestatic liver dysfunction, elevated inflammatory markers, tumor markers, and D‑dimer. Serological tests for viral hepatitis and autoimmune liver disease were negative. Abdominal MRI + MRCP and CTA showed heterogeneous hepatic parenchyma, cystic dilatation of the intrahepatic bile ducts (Figure 1), extensive thrombosis of the main portal vein (Figure 2) and superior mesenteric vein (Figure 3) with cavernous transformation, and diffuse bilateral renal cysts of varying sizes (Figure 4).Differential Diagnosis, Investigations and TreatmentPathological Re‑evaluationTwo senior pathologists retrospectively re‑evaluated the 2024 liver biopsy specimen with HE, Masson, and immunohistochemical staining. Findings included:No pathological evidence of alcoholic liver disease (no steatosis, ballooning degeneration, Mallory bodies, or perisinusoidal fibrosis) [3]; Severe periportal fibrosis with chronic inflammatory cell infiltration, forming broad and loose fibrous septa, without typical cirrhotic nodules; Marked irregular proliferation of small bile ducts in the portal tracts, focal cholestasis, cystic dilatation of large bile ducts, and shedding of biliary epithelium into the lumen (Figure 5); Proliferating bile ducts were positive for CK7 and CK19.Masson staining confirmed obvious periportal fibrosis with broad fibrous septa around the portal tracts (Figure 6).Differential DiagnosisAlcoholic cirrhosis: Excluded due to absence of steatosis, Mallory bodies, perisinusoidal fibrosis, and the presence of ductal plate malformation, the core feature of CHF [3].Idiopathic noncirrhotic portal hypertension: Excluded due to lack of portal vein abnormalities or nodular regenerative hyperplasia, and presence of bile duct proliferation [6].Autoimmune cholangitis: Excluded due to negative autoantibodies and absence of inflammatory bile duct injury or ductal plate malformation [7].Polycystic liver disease: Excluded due to presence of periportal fibrosis and portal hypertension, which are absent in this disease [8].Final DiagnosisCongenital hepatic fibrosis complicated with Caroli’s disease, polycystic kidney disease, and extensive portomesenteric venous thrombosis.TreatmentThe patient received anticoagulation therapy (low‑molecular‑weight heparin followed by long‑term rivaroxaban), combined with anti‑infection, electrolyte correction, hepatoprotection, and nutritional support. This anticoagulation regimen was selected based on evidence for portal vein thrombosis after splenectomy [9].Conclusion and ResultsAfter anticoagulation and supportive treatment, the patient’s acute abdominal pain, distension, and constipation completely resolved. Inflammatory markers normalized, liver function improved, and vital signs were stable. He was discharged in a stable condition.After discharge, the patient was advised to receive long‑term standardized anticoagulation and regular follow‑up (liver and renal function, coagulation function, abdominal imaging). At the latest follow‑up, the patient had no recurrent abdominal pain, bleeding, or thrombotic events, with significantly improved quality of life and no progressive hepatic or renal impairment.DiscussionCHF is a rare fibrocystic liver disease caused by ductal plate malformation, mostly related to PKHD1 gene mutations [10], and often comorbid with Caroli’s disease and PKD [1]. To our knowledge, this is the first reported case in China of adult CHF with extensive portomesenteric venous thrombosis, enriching the clinical spectrum of the disease.Diagnostic Clues and Causes of MisdiagnosisThe long‑term alcohol history and initial variceal bleeding led to a 6‑year misdiagnosis of alcoholic cirrhosis, reflecting clinical anchoring bias [5]. Overlooked diagnostic clues for CHF included: bilateral renal cysts at first admission progressing to typical PKD [1]; persistent cholestatic liver dysfunction without significant elevation of transaminases or bilirubin; mild hepatic nodularity without typical cirrhotic nodules during surgery; and no pathological evidence of alcoholic liver disease on biopsy [3].This highlights that CHF should be considered in adults with portal hypertension and renal cysts, even with a history of alcohol use [1].Significance of Pathological DiagnosisPathological examination is the gold standard for CHF diagnosis, with classic features of ductal plate malformation and periportal fibrosis without typical cirrhotic nodules [4]. Retrospective pathological re‑evaluation of the liver biopsy was critical in correcting the misdiagnosis. Cystic dilatation of the intrahepatic bile ducts confirmed the CHF–Caroli complex, which results from persistent embryonic ductal plate malformation [4].In resource‑limited settings, comprehensive clinical, imaging, and pathological evaluation is a practical approach for diagnosing rare CHF [10].Thrombotic Complications: Risk Factors and ManagementExtensive portomesenteric venous thrombosis in this case was associated with multiple risk factors: hemodynamic abnormalities caused by long‑standing portal hypertension (slow venous flow, cavernous transformation) [11]; hypercoagulable state after splenectomy (elevated platelets) [9]; mechanical compression of the portal and mesenteric veins by enlarged polycystic kidneys [1]; and systemic inflammation activating the coagulation cascade.Timely anticoagulation achieved a satisfactory outcome, indicating that high vigilance for thrombotic complications and prompt anticoagulation are essential in CHF patients.Clinical Management and PrognosisNo curative treatment exists for CHF; management focuses on controlling complications [1,3]: endoscopic or surgical intervention for portal hypertension, antibiotics for cholangitis [11], supportive care for PKD‑related renal insufficiency, and anticoagulation for thrombotic complications [9].Liver transplantation is the only curative option for end‑stage CHF (refractory portal hypertension, liver failure) [12], and combined liver‑kidney transplantation is indicated for concurrent end‑stage renal disease [13]. Adult‑onset CHF generally progresses slowly, and early intervention for complications improves long‑term prognosis [14].Molecular genetic testing was not performed in this case due to financial constraints. In resource‑limited settings, comprehensive clinical, imaging, and pathological evaluation remains a practical diagnostic strategy for CHF [10].Patient PerspectiveThe 6‑year misdiagnosis caused recurrent symptoms, multiple endoscopic and surgical procedures, and heavy physical and economic burdens, with significant anxiety for the patient and his family. After definitive diagnosis and targeted treatment, his symptoms were completely relieved and quality of life greatly improved.The patient fully understands the chronic and hereditary nature of the disease, adheres to long‑term treatment and follow‑up, and is willing to share his experience to raise awareness of this rare disease and provide a reference for clinicians and other patients.Author contributions: Liu, Dandan (corresponding author) conceived the study, drafted and revised the manuscript; Xu, Gang collected and organized the patient’s clinical and imaging data; Li, Xinglan and Tang, Baijie performed retrospective pathological re‑evaluation of the liver biopsy specimen and provided professional pathological opinions; all authors reviewed and approved the final version of the manuscript.Conflict of interest: All authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.Patient consent statement: Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.References1. Alsomali MI, Yearsley MM, Levin DM, et al. Diagnosis of congenital hepatic fibrosis in adulthood. Am J Clin Pathol. 2020;153(1):119–125.2. Chen IY, Whitney-Miller CL, Liao X. Congenital hepatic fibrosis and its mimics: a clinicopathologic study of 19 cases at a single institution. Diagn Pathol. 2021;16(1):81.3. European Association for the Study of the Liver. EASL Clinical Practice Guidelines: management of cholestatic liver diseases. J Hepatol. 2009;51(2):237–267.4. Hasbaoui BE, Rifai Z, Saghir S, et al. Congenital hepatic fibrosis: case report and review of literature. Pan Afr Med J. 2021;38:188.5. Croskerry P. Clinical cognition and diagnostic error: applications of a dual process model of reasoning. Adv Health Sci Educ Theory Pract. 2009;14(Suppl 1):27–35.6. Fiel MI, Schiano TD. Idiopathic noncirrhotic portal hypertension. Semin Diagn Pathol. 2019;36(6):395–403.7. Gleeson D, Bornand R, Brownlee A, et al. British Society of Gastroenterology guidelines for diagnosis and management of autoimmune hepatitis. Gut. 2025;74(9):1364–1409.8. Norcia LF, Watanabe EM, Hamamoto Filho PT, et al. Polycystic Liver Disease: Pathophysiology, Diagnosis and Treatment. Hepat Med. 2022;14:135–161.9. Lin YK, Cai XR, Hong HJ, et al. Risk factors of portal vein system thrombosis after splenectomy: a meta-analysis. ANZ J Surg. 2023;93(12):2806–2819.10. Liu Y, Zhu P, Tian J. Case report: Rare genetic liver disease – a case of congenital hepatic fibrosis in adults with autosomal dominant polycystic kidney disease. Front Med. 2024;11:1344151.11. Zohud A, Akram M, Khamaise Y, et al. Splenic artery embolization in a patient with advanced Caroli’s syndrome complicated with portal hypertension: a case report. J Med Case Rep. 2025;19(1):536.12. Wu WK, Ziogas IA, Izzy M, et al. Liver transplantation for congenital hepatic fibrosis. Transpl Int. 2021;34(7):1281–1292.13. Khan K, Agostini T, Desale S, et al. Improved patient and graft survival from kidney transplantation in liver transplants for congenital hepatic fibrosis and Caroli’s disease. J Hepatol. 2020;73:S267–S268.14. Shorbagi A, Bayraktar Y. Experience of a single center with congenital hepatic fibrosis: a review of the literature. World J Gastroenterol. 2010;16(6):683–690.ImagesFigure 1. Abdominal imaging showing cystic dilatation of intrahepatic bile ducts (black arrow).Figure 2. Abdominal imaging showing thrombosis in the main portal vein (black arrow).Figure 3. Abdominal imaging demonstrating thrombosis in the superior mesenteric vein (black arrow).Figure 4. Abdominal imaging showing multiple cysts in bilateral kidneys (black arrow).Figure 5. Liver biopsy (HE staining, ×100) showing ductal plate malformation, cystic dilatation of intrahepatic bile ducts, and partial shedding of epithelium into the lumen (black arrows).Figure 6. Liver biopsy (Masson staining, ×100) showing broad fibrous septa around the portal tracts (blue staining).

A Case Report and Literature Review: Malignant Transformation of Colonic Polyps in Cronkhite–Canada SyndromeLei Liu | Congcong Min | Hao Chen | Chen Jiang | Zibin Tian | Xiaoyan YinDepartment of Gastroenterology, Affiliated Hospital of Qingdao University, Qingdao, Shandong, ChinaCorrespondence: Xiaoyan Yin ( yxy4503@163.com)ABSTRACTCronkhite–Canada syndrome (CCS) is a rare, acquired, nonhereditary gastrointestinal polyposis syndrome associated with an increased risk of gastrointestinal malignancy, including colorectal neoplasia. Early colorectal neoplasia in CCS may be difficult to recognize endoscopically because diffuse inflammatory polyposis and background mucosal edema can obscure subtle malignant changes. We report a case of CCS complicated by early colorectal neoplasia detected during endoscopic surveillance. Colonoscopy identified a 10 × 8 mm lesion at the rectosigmoid junction with focal erythema at the lesion base and surface glandular dilation in a background of diffuse inflammatory polyps. Endoscopic mucosal resection was performed, and histopathology confirmed high-grade intraepithelial neoplasia with intramucosal carcinoma. This case highlights the diagnostic challenge of identifying early colorectal cancer in CCS and emphasizes the importance of careful endoscopic surveillance and timely endoscopic intervention for suspicious lesions.

A document by Jun Yang. Click on the document to view its contents.

This case report presents the successful implantation of a left bundle area pacing lead in a 64-year-old male with a history of bundle branch ventricular tachycardia and consequent therapeutic ablation of the right bundle branch. Despite extensive conduction disease, effective physiological pacing was achieved as part of a cardiac synchronisation pacing

A 50-year-old man with untreated severe psychotic depression presented with a one-week history of gradually worsening lower abdominal pain and intermittent non-bilious vomiting. He was afebrile and hemodynamically stable, with focal abdominal tenderness and no signs of peritonitis. Laboratory investigations were unremarkable.Foreign body ingestion is more frequently encountered in adults with psychiatric disorders and is associated with a higher risk of complications such as gastrointestinal perforation, particularly with sharp or elongated objects.¹,²Contrast-enhanced computed tomography (CT) of the abdomen demonstrated multiple elongated metallic foreign bodies within the terminal ileum. One nail appeared to breach the bowel wall, with surrounding fat stranding and localized omental inflammatory changes consistent with a sealed perforation (Figure 1). CT is the imaging modality of choice for detecting retained foreign bodies and associated complications, including perforation.¹,³Exploratory laparotomy revealed multiple metallic nails within the terminal ileum and ileocecal region. One nail was found penetrating the ileal wall, associated with localized inflammatory changes but no gross contamination (Figure 2). Segmental ileal resection with ileocolic anastomosis was performed. Fourteen metallic nails were retrieved, the largest measuring 10 cm in length (Figure 3). A separate metallic nail lodged in the pylorus was removed through an anterior gastrotomy. The remaining bowel was intact.Postoperative recovery was uneventful. The patient was referred for psychiatric assessment following surgery.

Hybrid Field Variables C. R. Gimarelli (December 25, 2025) A Case Report and Treatment Experience of Extracorporeal Shock Wave Lithotripsy for Urachal CalculusHE Junyu1 Wang Yanzhao2 REN Hailin2 ZHANG Baolin2

A document by Rifah Anjum Samiha. Click on the document to view its contents.

Penile Metastasis from Dedifferentiated Prostate Cancer with Low PSA Levels: A Case Report