Minimally Invasive Aortic Valve Replacement Using a Bioprosthesis in a Young Adult With Wunderlich Syndrome and Bicuspid Aortic ValveSantiago Orozco Martinez1, Manuela Orozco Martinez21. General Physician, S.E.S Hospital Universitario de Caldas. Manizales, Colombia. Orcid 0009-0000-5651-6987. Santiom2001@gmail.com2. Internal Medicine Resident, Universidad de Manizales. Manizales, Colombia. Orcid 0009-0000-9132-0533. Manuelaorozco29@hotmail.com

A document by Jad Kabbara. Click on the document to view its contents.

Aesthetic study on the repair of earlobe cleft combined with one-stage reconstruction of ear holeKuan Wang, MD, Ping Zhang, MD, Jie Zou, MDDepartment of Plastic and Burns Surgery, The First Affiliated Hospital of Chengdu Medical College, Chengdu, Sichuan, ChinaCorrespondence to: Jie Zou; Email: 947200956@qq.comKey Clinical Message: Our novel double-opposing lingual flap technique enables single-stage repair of earlobe clefts with simultaneous ear hole reconstruction. This approach eliminates the need for re-piercing, achieves natural aesthetics, and allows immediate earring use, significantly enhancing patient satisfaction.Keywords: Auricular Lobe Cleft; Auricular Hole; Lingual FlapAuricular lobe clefts are predominantly caused by trauma, leading to facial aesthetic impairment and the inability to wear earrings, thus prompting a strong desire for repair. Postoperative recurrence, auricular swelling, auricular deformity, loss of the auricular hole, and scar formation are common challenges in auricular lobe cleft correction. This article introduces a new method of double-opposing lingual flaps for repairing auricular lobe clefts and simultaneously reconstructing the auricular hole.Case Report: A 34-year-old female presented with a complete right auricular lobe laceration sustained over five years prior. Examination revealed a deformed right auricular lobe with a complete cleft and visible scarred healing. After admission and completion of preoperative assessments to rule out surgical contraindications, outpatient surgery was performed. Postoperative care included regular dressing changes, and sutures were removed after 5-7 days. The incision healed with first-class union, the flap blood supply was adequate, the reconstructed auricular hole appeared natural, and the color and texture of the auricular lobe closely matched the surrounding area. Follow-ups were scheduled at 1, 3, and 6 months postoperatively. The preoperative, intraoperative, postoperative and follow-up photos of the patients are shown in Figure 1

Duodenal obstruction resulting from the annular pancreas：One case reportWen-Kang Yuan1*, Chao Zhang, Chong Zhang1#1Department of General Surgery, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, China.#Corresponding author: Chong Zhang, Email: chongzhang93@126.comTelephone: +8613965053990

Title PageTitle:Not All Leg Swelling Is Volume: A Case Report on the Role of Point-of-Care Ultrasound in Fluid Assessment After Combined Heart-Kidney TransplantManuscript type: Case reportAuthors and Affiliations:Rebecca BoyleStanford Hospital and ClinicsDepartment of NephrologyPalo Alto, CA, United StatesNeev Patel, MBBSStanford UniversityDepartment of NephrologyPalo Alto, CA, United StatesCorresponding Author:Neev Patel, MBBSPGY-5 FellowStanford NephrologyPalo Alto, CA, United Statesneevp@stanford.eduEthics and Integrity Statements:Patient Consent Statement: Written informed consent was obtained from the patient for publication of this case report and accompanying images.Conflict of Interest Disclosure: The authors declare no conflicts of interest.Funding Statement: The authors received no funding for this work.Ethics Approval Statement: Not applicable. This is a retrospective, de-identified clinical case with no intervention outside standard care.Data Availability Statement: No datasets were generated or analyzed for this case report.Permission to Reproduce Material: Not applicable. No third-party material was reproduced.Clinical Trial Registration: Not applicable.Key Clinical Message : Not all edema reflects hypervolemia. In transplant patients, drug-induced lymphedema can mimic volume overload. Point-of-care ultrasound (POCUS) enables accurate bedside volume assessment and avoids misdirected treatment.Abstract : A 65-year-old man one year post combined heart-kidney transplant presented with AKI, dyspnea, and progressive leg edema unresponsive to escalating diuretics. Despite suspicion for volume overload, point-of-care ultrasound (POCUS) revealed a collapsible IVC and dry lungs, suggesting hypovolemia. The edema was ultimately attributed to sirolimus-associated lymphedema. Diuretic de-escalation improved renal function. This case illustrates the diagnostic utility of POCUS in volume status evaluation, preventing harm from empiric diuresis, and recognizing sirolimus-induced lymphedema.Introduction: Leg edema is a common presentation in post-transplant patients, and it is often presumed to indicate volume overload. However, the differential for edema is broad and includes lymphatic obstruction, venous insufficiency, hypoalbuminemia, and medication-related causes. In patients with complex immunosuppressive regimens and multiple comorbidities, distinguishing these etiologies becomes even more important to guide therapy and avoid potential harm. Point-of-care ultrasound (POCUS) has emerged as a valuable tool in the bedside assessment of volume status, enabling rapid, non-invasive insights into intravascular volume. We present a case of sirolimus-associated lymphedema in a combined heart-kidney transplant recipient, initially misattributed to volume overload, where POCUS clarified the diagnosis and prevented further iatrogenic injury.Case Presentation : A 65-year-old man with cardiac and renal sarcoidosis underwent simultaneous heart-kidney transplant one year prior. His post-transplant course was complicated by recurrent renal sarcoidosis, leukopenia, and indeterminate cardiac allograft biopsies. Due to persistent leukopenia and concern for cardiac allograft vasculopathy, his immunosuppression was changed from mycophenolate to sirolimus while continuing tacrolimus and prednisone.Four months after initiating sirolimus, the patient developed progressive bilateral lower extremity edema and worsening kidney function. Outpatient diuretic therapy was escalated with minimal improvement. Serum creatinine rose from a baseline of 1.3 to 1.9 mg/dL. He was referred to the emergency department with new exertional dyspnea, edema, and concern for fluid overload.On presentation, vital signs were stable: temperature 36.8°C, BP 153/81 mmHg, HR 86 bpm, and SpO2 96% on room air. His weight had decreased by 3 kg over three weeks. Physical examination revealed asymmetric pitting edema of both lower extremities with warm extremities and no jugular venous distension. Lung auscultation was clear without rales or rhonchi. Cardiac exam showed regular rate and rhythm without murmurs. There was no ascites or hepatomegaly.POCUS was performed at the bedside to assess volume status. Lung ultrasound revealed bilateral A-lines with no B-lines or effusions, consistent with absence of pulmonary edema (Figure 1). The inferior vena cava (IVC) measured less than 1.5 cm in diameter with greater than 50% collapsibility during inspiration (Figure 2), suggesting a low right atrial pressure. Cardiac views from the apical four-chamber window demonstrated normal biventricular chamber sizes, preserved systolic function, and no septal flattening (Figures 3a & 3b). There was no evidence of right ventricular dilation or dysfunction.Given the absence of sonographic signs of hypervolemia, the etiology of edema was reconsidered. The temporal relationship between sirolimus initiation and the onset of symptoms raised suspicion for sirolimus-associated lymphedema. A right heart catheterization was performed to confirm volume status and further evaluate cardiac function. Hemodynamics revealed right atrial pressure of −2 mmHg, pulmonary artery pressure of 22/5 mmHg, pulmonary capillary wedge pressure of 3 mmHg, and a Fick-derived cardiac output and index of 6.3 L/min and 3.0 L/min/m², respectively. These findings confirmed a low-filling pressure, high-output state.Diuretic therapy was de-escalated, and the patient was transitioned from sirolimus to everolimus. Serum creatinine improved from 1.9 mg/dL to 1.4 mg/dL at discharge. He was referred to a multidisciplinary lymphedema clinic for further evaluation and management.Discussion : Edema in transplant recipients is commonly attributed to fluid overload, particularly in the setting of dyspnea and rising creatinine. However, this case underscores the importance of re-evaluating such assumptions. Sirolimus, an mTOR inhibitor used for immunosuppression, has been associated with peripheral lymphedema through mechanisms involving impaired lymphangiogenesis and lymphatic endothelial injury. [1, 2] This adverse effect is underrecognized and can mimic signs of volume overload, leading to inappropriate therapy.The reported latency between sirolimus initiation and onset of lymphedema ranges from 4 months to 3 years, aligning with this patient’s presentation. [3, 4, 5] In this case, escalating diuretic therapy—based on presumed volume overload—contributed to prerenal azotemia and acute kidney injury. POCUS findings, including bilateral A-line pattern and a highly collapsible IVC, suggested a low effective circulating volume, prompting a critical shift in management. [6, 7]The diagnostic utility of POCUS in transplant patients is especially valuable. These individuals often have complex volume status, abnormal renal handling of sodium, and overlapping cardiac pathology. Traditional markers such as weight, jugular venous pressure, or even chest X-ray can be misleading. POCUS allows direct visualization of the lungs, IVC, and cardiac function in real time, improving clinical accuracy and reducing reliance on invasive diagnostics.Right heart catheterization further validated the POCUS assessment, demonstrating low filling pressures and adequate cardiac output. The improvement in kidney function following diuretic de-escalation confirms the iatrogenic contribution of overdiuresis. This case not only illustrates the potential harms of assumption-based therapy but also highlights POCUS as a pivotal diagnostic and educational tool in transplant medicine.References :Sinnathamby ES, Urban BT, Clark RA, Roberts LT, De Witt AJ, Wenger DM, et al. Etiology of drug-induced edema: a review of dihydropyridine, thiazolidinedione, and other medications causing edema. Cureus. 2024 Feb 1;16(2):e53400. doi:10.7759/cureus.53400. PMID: 38435190; PMCID: PMC10908346.Desai N, Heenan S, Mortimer PS. Sirolimus-associated lymphoedema: eight new cases and a proposed mechanism. Br J Dermatol. 2009 Jun;160(6):1322–6. doi:10.1111/j.1365-2133.2009.09098.x. PMID: 19302070.Romagnoli J, Citterio F, Nanni G, Tondolo V, Castagneto M. Severe limb lymphedema in sirolimus-treated patients. Transplant Proc. 2005 Mar;37(2):834–6. doi:10.1016/j.transproceed.2004.12.180. PMID: 15848530.Aboujaoude W, Milgrom ML, Govani MV. Lymphedema associated with sirolimus in renal transplant recipients. Transplantation. 2004 Apr 15;77(7):1094–6. doi:10.1097/01.TP.0000118406.01509.75. PMID: 15087794.Rashid-Farokhi F, Afshar H. Lymphedema of the transplanted kidney and abdominal wall with ipsilateral pleural effusion following kidney biopsy in a patient treated with sirolimus: a case report and review of the literature. Am J Case Rep. 2017 Nov 9;18:1370–6. doi:10.12659/AJCR.905272. PMID: 29125545; PMCID: PMC5700623.Brennan JM, Blair JE, Goonewardena S, Ronan A, Shah D, Vasaiwala S, et al. Reappraisal of the use of inferior vena cava for estimating right atrial pressure. J Am Soc Echocardiogr. 2007 Jul;20(7):857–61. doi:10.1016/j.echo.2007.01.005. PMID: 17467685.Tsou PY, Wong JS, Taghizadeh A, Graglia RP, Nahmod K, Ramkumar S, et al. Basics of point-of-care lung ultrasonography. N Engl J Med. 2023 Feb 9;388(6):556–564. doi:10.1056/NEJMvcm2108203. PMID:36722223.

Nevoid melanoma is a rare and diagnostically challenging variant of malignant melanoma that closely mimics benign melanocytic nevi both clinically and histologically. We report a case of a 72-year-old male who presented with an 8 mm pearlescent papule on the forehead. Histopathological analysis of the shave biopsy revealed a biphasic intradermal

Peritoneal Extramedullary Hematopoiesis in Myelofibrosis: A Case Report and Literature ReviewAuthors: Shadi Baba Ali1*, MD, Erfan Barootchi2, MD, Saeed Nazarbeigi3, MD, Pardis Zamani4, MD1. Corresponding author : Department of Internal Medicine, Imam Khomeini Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran,Email: sh.babaali@yahoo.comORCID: 0009-0005-5648-84412. Imam Khomeini Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran, Tehran, Iran, Email: e.baroot4@gmail.comhttps://orcid.org/0000-0001-6439-78183. Department of Gastroenterology and Hepatology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran, Email: saeednazarbeigi@yahoo.com4. Imam Khomeini Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran, Tehran, Iran, Email: pardiszamani7@gmail.comORCID: 0009-0005-1121-1596Full title : Extramedullary Hematopoiesis in Myelofibrosis: A Case Report and Literature ReviewShort title : Peritoneal Extramedullary Hematopoiesis in MyelofibrosisKey clinical message: Peritoneal extramedullary hematopoiesis is a rare manifestation of myelofibrosis, which can mimic malignancy or cirrhosis. Understanding this presentation is essential to avoid misdiagnosis, especially in patients with ascites, splenomegaly, and atypical blood smear findings.Word count : 92 for abstract and 1488 for main textNumber of figures and tables : 1 Table and 2 FiguresConflict of interest : No conflicts of interest declaredCompeting interests : The authors have no competing interestsPatient Consent Statement: Written informed consent was obtained from all the patients to publish this report.Keywords: Myelofibrosis, extramedullary hematopoiesis, Hydroxyurea, AscitesReference count : 23Author contributions :Shadi Baba Ali : Designed and supervised the research study, reviewed the draft.Erfan Barootchi: Did the investigation and wrote the original draft.Saeed Nazarbeigi : Investigated and reviewed the draft.Pardis Zamani : Validated the research and wrote the original draft

PTEN and WDR19 Variants in an African Neonate with Brain and Cutaneous Anomalies

Some Heart Breaks Are Worse Than Others: A Rare Case of Mid-Ventricular Takotsubo Cardiomyopathy Resulting in Cardiogenic Shock in the Context of MDMA Use.Ma’in Abumuhfouz1, Yazan Almohtasib1, Uttsav Sandesara 2, Rebecca Adler1, David Gonzalez 1, Taiyeb Khumri3, Mohammed Saghir 3.1: University of Missouri - Kansas City (UMKC), Kansas City, Missouri, USA.2: Wake Forest University School of Medicine3: Saint Luke’s Hospital of Kansas City, Kansas City, Missouri, USA.Corresponding Author:Main AbumahfouzDepartment of Internal Medicine,University of Missouri - Kansas City (UMKC), Kansas City, USA2411 Holmes St, Kansas City, MO 64108E-mail: maenabumahfuth95@gmail.comPhone #: 816-305-8514Authors contributions:Ma’in Abumuhfouz, M.DWriting – original draftYazan Almohtasib, M.DConceptualized and designed the study.Uttsav Sandesara, M.DConceptualized and designed the study.Writing – review and editingRebecca Adler, D.ODavid Gonzalez, M.DWriting – review and editingTaiyeb Khumri, M.DMohammed Saghir, M.DProject administrationAbbreviations:TTC: Takotsubo cardiomyopathyMDMA: 3,4-methylenedioxymethamphetamineGAD: Generalized Anxiety DisorderMDD: Major Depressive DisorderConflict of interest:No conflict of interest to report.Keywords:Takotsubo cardiomyopathy, Cardiogenic Shock, Cardiac MRI.Key clinical message:Mid-ventricular Takotsubo cardiomyopathy can present with cardiogenic shock, especially following MDMA use. Early recognition, hemodynamic support, and advanced cardiac imaging are crucial for diagnosis and management. This case highlights the reversible nature of stress cardiomyopathy and the importance of considering recreational drug use in young patients with acute cardiac dysfunction.Introduction:Takotsubo cardiomyopathy (TTC), also known as stress-induced cardiomyopathy, is characterized by transient regional systolic dysfunction of the left ventricle, often mimicking acute coronary syndrome but without obstructive coronary artery disease. While the classic apical ballooning pattern is most frequently observed, mid-ventricular variants have been increasingly recognized and may be associated with more severe hemodynamic compromise, including cardiogenic shock. The pathophysiology of TTC is incompletely understood but is thought to involve catecholamine-mediated myocardial stunning, with both emotional and physical stressors serving as triggers [14].Sympathomimetic agents, including amphetamines and their derivatives such as 3,4-methylenedioxymethamphetamine (MDMA, ”ecstasy”), have been implicated in the development of TTC and other forms of acute cardiac injury [10-12]. MDMA exerts its cardiovascular toxicity through multiple mechanisms, including increased catecholamine release, oxidative stress, mitochondrial dysfunction, and disruption of cardiac gene expression and gap junction integrity [9][13]. Acute MDMA intoxication has been associated with arrhythmias, myocardial infarction, and both acute and chronic cardiomyopathy, with case reports and experimental data supporting its potential to precipitate severe cardiac events even in young, otherwise healthy individuals [9-10].Although TTC is generally considered a reversible condition, the mid-ventricular variant, particularly when complicated by cardiogenic shock, poses significant diagnostic and therapeutic challenges. The intersection of MDMA use and TTC is rare but clinically significant, underscoring the importance of recognizing this entity in patients presenting with acute heart failure or shock following sympathomimetic exposure [14].This case report describes a rare presentation of mid-ventricular TTC with cardiogenic shock in the context of recent MDMA use, highlighting the need for vigilance regarding the cardiovascular risks associated with recreational drug use and the expanding clinical spectrum of stress cardiomyopathy.Case History and Examination:A 29-year-old woman with a past medical history of Generalized Anxiety Disorder (GAD) and Major Depressive Disorder (MDD) presented to our care as a transfer from an outside hospital with cardiogenic shock following MDMA use. The patient arrived intubated, with an Impella CP device and pulmonary artery catheter in place, requiring vasopressor support with norepinephrine. Her partner reported progressive shortness of breath, chest pain, and altered mental status prior to admission at the referring facility with frequent use of MDMA. On arrival at the outside hospital, the patient was hypothermic, tachycardic (130–140 bpm), and hypoxic, requiring high-flow nasal cannula oxygen.Differential diagnosis, investigations, and treatment:Laboratory results revealed markedly elevated troponin levels (>17,000 ng/L). Echocardiography demonstrated severe left ventricular dysfunction with an ejection fraction of 20%, and cardiac catheterization showed normal coronary arteries but hemodynamics consistent with cardiogenic shock. Post-catheterization, the patient experienced cardiac arrest, reportedly requiring multiple rounds of CPR. An Impella CP device and norepinephrine were initiated prior to transfer to our institution for advanced care.At our facility, the patient remained tachycardic with adequate mean arterial pressures (90–100 mmHg) on low-dose norepinephrine. She self-extubated early during her stay, transitioned to nasal cannula oxygen, and tolerated gradual weaning of vasopressor support. Echocardiography demonstrated an improvement in ejection fraction to 45%. Cardiac MRI findings were consistent with mid-ventricular variant stress cardiomyopathy [Figure 1-A].Neurology evaluation identified an acute infarction in the right parietal lobe and a subacute infarction in the left cerebellum, likely embolic in etiology due to severe cardiomyopathy. Despite mild orthostatic hypotension, the patient was hemodynamically stable after initiation of midodrine. PT/OT assessments deemed the patient safe for discharge.Conclusion and Results:The patient condition had improved significantly with gradual return to her baseline, and she expressed eagerness to return home. She was discharged home with family support and instructions for outpatient follow-up. At discharge, she reported complete resolution of symptoms.The patient was followed up 6 months after discharge and was completely asymptomatic at that time. A repeat cardiac MRI demonstrated normalization of left ventricular ejection fraction (45% → 71%), resolution of mid-ventricular wall motion abnormalities, normalization of T1 and T2 mapping relaxation times, and resolution of patchy late gadolinium enhancement, except for a small subendocardial area likely representing residual fibrosis [Figure 1-B].Discussion:The presented case highlights a rare instance of mid-ventricular Takotsubo cardiomyopathy (TTC) associated with MDMA use, emphasizing the need for heightened awareness of this condition’s unique pathophysiology, clinical presentation, and management challenges.Takotsubo cardiomyopathy, commonly referred to as stress cardiomyopathy, typically involves transient left ventricular dysfunction precipitated by acute emotional or physical stress. The pathophysiological mechanisms underlying TTC remain complex, with catecholamine excess playing a pivotal role in inducing myocardial stunning [3]. Elevated levels of catecholamines, as in this case, can cause direct myocardial toxicity, vascular dysfunction, and microvascular spasm, all of which contribute to the development of the condition [2]. The mid-ventricular variant, although less common than the apical type, is associated with distinct features and often a more severe clinical course [4].The use of MDMA has been implicated in drug-induced Takotsubo cardiomyopathy, likely due to its potent sympathomimetic effects, which exacerbate catecholaminergic surges [5]. In this patient, the development of cardiogenic shock underscores the potential severity of the mid-ventricular variant, which has been reported to occur in up to 10% of TTC cases [6].Advanced imaging modalities, such as cardiac MRI, proved invaluable in this case for confirming the diagnosis and identifying the pattern of myocardial involvement, including the global hypokinesis of mid-ventricular segments with sparing of the apical and basal regions. This imaging pattern is a hallmark of the mid-ventricular variant and serves as a key diagnostic clue [4]. Structural analyses have demonstrated that TTC involves transient myocardial edema and inflammation during the acute phase, which resolves with recovery, further supporting the reversibility of this condition [7].The patient’s remarkable recovery, marked by improved hemodynamics and left ventricular function, aligns with prior studies indicating a favorable prognosis for most TTC cases, provided that complications such as cardiogenic shock are promptly managed [8]. Temporary mechanical circulatory support, as used here, can be lifesaving in severe cases of shock [6]. Nevertheless, the association between the mid-ventricular variant and adverse outcomes warrants further research to refine management strategies and improve long-term prognosis [1].In conclusion, this case underscores the importance of early recognition of TTC and its variants, particularly in patients with drug-induced triggers such as MDMA. Comprehensive understanding of its pathophysiological mechanisms and the use of advanced imaging modalities are paramount in optimizing patient outcomes. Further studies are needed to elucidate the long-term implications of the mid-ventricular variant and refine treatment approaches for this complex syndrome.Ethics approval:Our institution does not require ethical approval for reporting individual cases or case series.Informed consent:Written informed consent was obtained from the patient(s) for their anonymized information to be published in this article.References:Pelliccia F, Greco C, Vitale C, Rosano G, Gaudio C, Kaski JC. Takotsubo syndrome (stress cardiomyopathy): an intriguing clinical condition in search of its identity. Am J Med. 2014 Aug;127(8):699-704. doi: 10.1016/j.amjmed.2014.04.004. Epub 2014 Apr 19. PMID: 24754972.Al Houri HN, Jomaa S, Jabra M, Alhouri AN, Latifeh Y. Pathophysiology of stress cardiomyopathy: A comprehensive literature review. Ann Med Surg (Lond). 2022 Sep 15;82:104671. doi: 10.1016/j.amsu.2022.104671. PMID: 36268377; PMCID: PMC9577654.Lyon AR, Rees PS, Prasad S, Poole-Wilson PA, Harding SE. Stress (Takotsubo) cardiomyopathy–a novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat Clin Pract Cardiovasc Med. 2008 Jan;5(1):22-9. doi: 10.1038/ncpcardio1066. PMID: 18094670.Grigorov M, Spindel J, Katrapati P, Stoddard M, Varbanova M. Stress Cardiomyopathy: The Midventricular Variant. CASE (Phila). 2022 Aug 26;6(9):406-410. doi: 10.1016/j.case.2022.06.008. PMID: 36451868; PMCID: PMC9703095.Kido K, Guglin M. Drug-Induced Takotsubo Cardiomyopathy. Journal of Cardiovascular Pharmacology and Therapeutics. 2017;22(6):552-563. doi:10.1177/1074248417708618Medina de Chazal H, Del Buono MG, Keyser-Marcus L, Ma L, Moeller FG, Berrocal D, Abbate A. Stress Cardiomyopathy Diagnosis and Treatment: JACC State-of-the-Art Review. J Am Coll Cardiol. 2018 Oct 16;72(16):1955-1971. doi: 10.1016/j.jacc.2018.07.072. PMID: 30309474; PMCID: PMC7058348.Nef HM, Möllmann H, Kostin S, Troidl C, Voss S, Weber M, Dill T, Rolf A, Brandt R, Hamm CW, Elsässer A. Tako-Tsubo cardiomyopathy: intraindividual structural analysis in the acute phase and after functional recovery. Eur Heart J. 2007 Oct;28(20):2456-64.Jurisic, S.; Gili, S.; Cammann, V.L.; Kato, K.; Szawan, K.A.; D’Ascenzo, F.; Jaguszewski, M.; Bossone, E.; Citro, R.; Sarcon, A.; et al. Clinical Predictors and Prognostic Impact of Recovery of Wall Motion Abnormalities in Takotsubo Syndrome: Results from the International Takotsubo Registry. J. Am. Heart Assoc.  2019 , 8 , e011194.Fonseca DA, Ribeiro DM, Tapadas M, Cotrim MD. Ecstasy (3,4-methylenedioxymethamphetamine): Cardiovascular effects and mechanisms. Eur J Pharmacol. 2021 Jul 15;903:174156. doi: 10.1016/j.ejphar.2021.174156. Epub 2021 May 8. PMID: 33971177.Bozkurt B, Colvin M, Cook J, Cooper LT, Deswal A, Fonarow GC, Francis GS, Lenihan D, Lewis EF, McNamara DM, Pahl E, Vasan RS, Ramasubbu K, Rasmusson K, Towbin JA, Yancy C; American Heart Association Committee on Heart Failure and Transplantation of the Council on Clinical Cardiology; Council on Cardiovascular Disease in the Young; Council on Cardiovascular and Stroke Nursing; Council on Epidemiology and Prevention; and Council on Quality of Care and Outcomes Research. Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association. Circulation. 2016 Dec 6;134(23):e579-e646. doi: 10.1161/CIR.0000000000000455. Epub 2016 Nov 3. Erratum in: Circulation. 2016 Dec 6;134(23):e652. doi: 10.1161/CIR.0000000000000474. PMID: 27832612.Cotinet PA, Bizouarn P, Roux F, Rozec B. Management of cardiogenic shock by circulatory support during reverse Tako-Tsubo following amphetamine exposure: A report of two cases. Heart Lung. 2021 May-Jun;50(3):465-469. doi: 10.1016/j.hrtlng.2020.10.007. Epub 2020 Nov 24. PMID: 33243478.Lavonas EJ, Akpunonu PD, Arens AM, Babu KM, Cao D, Hoffman RS, Hoyte CO, Mazer-Amirshahi ME, Stolbach A, St-Onge M, Thompson TM, Wang GS, Hoover AV, Drennan IR; American Heart Association. 2023 American Heart Association Focused Update on the Management of Patients With Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2023 Oct 17;148(16):e149-e184. doi: 10.1161/CIR.0000000000001161. Epub 2023 Sep 18. PMID: 37721023.Tiangco DA, Halcomb S, Lattanzio FA Jr, Hargrave BY. 3,4-Methylenedioxymethamphetamine alters left ventricular function and activates nuclear factor-Kappa B (NF-κB) in a time and dose dependent manner. Int J Mol Sci. 2010;11(12):4843-63. doi: 10.3390/ijms11124743. Epub 2010 Nov 26. PMID: 21614177; PMCID: PMC3100831.Templin C, Ghadri JR, Diekmann J, Napp LC, Bataiosu DR, Jaguszewski M, Cammann VL, Sarcon A, Geyer V, Neumann CA, Seifert B, Hellermann J, Schwyzer M, Eisenhardt K, Jenewein J, Franke J, Katus HA, Burgdorf C, Schunkert H, Moeller C, Thiele H, Bauersachs J, Tschöpe C, Schultheiss HP, Laney CA, Rajan L, Michels G, Pfister R, Ukena C, Böhm M, Erbel R, Cuneo A, Kuck KH, Jacobshagen C, Hasenfuss G, Karakas M, Koenig W, Rottbauer W, Said SM, Braun-Dullaeus RC, Cuculi F, Banning A, Fischer TA, Vasankari T, Airaksinen KE, Fijalkowski M, Rynkiewicz A, Pawlak M, Opolski G, Dworakowski R, MacCarthy P, Kaiser C, Osswald S, Galiuto L, Crea F, Dichtl W, Franz WM, Empen K, Felix SB, Delmas C, Lairez O, Erne P, Bax JJ, Ford I, Ruschitzka F, Prasad A, Lüscher TF. Clinical Features and Outcomes of Takotsubo (Stress) Cardiomyopathy. N Engl J Med. 2015 Sep 3;373(10):929-38. doi: 10.1056/NEJMoa1406761. PMID: 26332547.

A document by Kazem Dalaie. Click on the document to view its contents.

Introduction Pembrolizumab is a monoclonal antibody used to treat various cancers via monotherapy or in conjunction with other chemotherapeutic regimens. Randomized-control trials report adrenal insufficiency in approximately 0.7% of patients on pembrolizumab. This number may be an underestimation considering patients’ nonspecific symptoms on presentation, making diagnosis difficult. Case Presentation A 38-year-old

Young Adult with Malignant Phyllodes Undergoing Adjuvant Radiotherapy with Bolus

Key Clinical MessageClinical significance of Double axillary vein is often minimal, however it can be of concern in surgical procedures, particularly those involving axillary dissection. Injury to one of the veins could lead to severe bleeding or venous congestion, complicating the surgical outcome. Therefore, Surgeons should be aware of this variation.

A document by Bhumika GC. Click on the document to view its contents.

SummaryThe coexistence of endometrioid carcinoma and endometriosis with lymph node metastasis can lead to difficulties in pathological diagnosis and even misdiagnosis.Endometrioid carcinoma and endometriosis share potential molecular mechanisms and metastatic pathways, emphasizing the necessity of combined immunohistochemical staining (PAX-2/Ki-67/MMR) for accurate differential diagnosis.

Diagnosis and Treatment of Middle Colic Artery Aneurysm Rupture: A Clinical Case ReportXiancong Wu1，Xiaoqin Wu2，De Kang11Department of Emergency , Zhangzhou Affiliated Hospital of Fujian Medical University, China.2Department of Emergency, The 909th Hospital, School of Medicine, Xiamen University, China.First Author:Xiancong WuDepartment of Emergency , Zhangzhou Affiliated Hospital of Fujian Medical University, China.Email:king21405@163.comCorresponding authors:De KangDepartment of Emergency , Zhangzhou Affiliated Hospital of Fujian Medical University, China.Email:cdkant@163.comORCID：0000-0002-4395-2146Other author’s email:Xiaoqin Wu，13055351917@163.com

A document by Yasmeen Imtiaz G. Click on the document to view its contents.

TitleA Diagnostic Challenge: Non-Giant Cell Arteritis Presenting as Fever of Unknown Origin