BACKGROUND Cryptococcosis is an infection caused by Cryptococcus species, an invasive fungus. The fungus is transmitted through the inhalation of spores, and causes opportunistic infection that affects the central nervous system, lungs, and skin. Soil, fruits, wood, and bird excreta commonly harbor the fungus. Two cryptococcal species are known to cause infection in humans. Cryptococcus neoformans is known to affect immunocompromised individuals, whereas C. gattii develops disease in immunocompetent individuals. CASE SUMMARY We report a case of disseminated cryptococcosis presenting as molluscoid skin lesions, followed by meningo-encephalitis. CONCLUSION Collaboration and communication among interdisciplinary teams is essential in the diagnosis of cryptococcosis. Any nonhealing skin lesion should be biopsied for histopathology. Although cryptococcosis is known to have a high case fatality ratio, in our patient, histopathological examination of skin lesions prompted the timely initiation of therapy, and hence, a favorable outcome was achieved.
BACKGROUND Hemophagocytic lymphohistiocytosis (HLH) is a rare, life-threatening hyperinflammatory syndrome driven by excessive cytokine release and uncontrolled immune activation. While HLH is commonly associated with infections, malignancies, and autoimmune diseases, its occurrence secondary to sarcoidosis is exceptionally rare. Sarcoidosis is a multisystem granulomatous disorder characterized by noncaseating granulomas, most frequently affecting the lungs and lymphatic system. Coexistence of these two conditions presents significant diagnostic and therapeutic challenges, particularly in adult populations in whom the established diagnostic criteria may be less sensitive. CASE SUMMARY We report the case of a 57-year-old man with a 2-year history of unexplained weight loss, recurrent nocturnal fever, generalized lymphadenopathy, and hepatosplenomegaly. His medical history included hypertension, type 2 diabetes mellitus, hyperlipidemia, and gout. Initial laboratory and imaging workup were inconclusive. Progressive clinical deterioration prompted further hematological evaluation, revealing pancytopenia with abnormal peripheral smear findings, although bone marrow biopsy was unremarkable. Serum angiotensin-converting enzyme levels were mildly elevated. Subsequent endoscopic ultrasound-guided fine needle aspiration of a subdiaphragmatic lymph node demonstrated florid noncaseating granulomatous inflammation consistent with sarcoidosis. Based on multidisciplinary team discussion and application of the HScore (174), a diagnosis of HLH secondary to systemic sarcoidosis was established. The patient was initiated on high-dose corticosteroid therapy, with a plan for gradual tapering and consideration of additional immunosuppressive therapy. Early recognition and prompt treatment were critical to prevent further clinical deterioration. CONCLUSION This case highlights a rare but important association between sarcoidosis and HLH, underscoring the need for maintaining a high clinical suspicion in patients presenting with systemic inflammatory features and granulomatous disease. Early multidisciplinary evaluation and timely initiation of immunosuppressive therapy are essential to improve outcomes in this potentially fatal condition.
Krishnan et al published in the World Journal of Clinical Cases report a case of probable fenbendazole-induced liver injury in a patient with metastatic colon cancer on nivolumab/relatlimab, concluding that fenbendazole caused the hepatotoxicity and recommending against its use in cancer patients receiving immune checkpoint inhibitor (ICI). We argue that the biochemical evidence presented is more consistent with immunogenic tumor cell death potentiated by benzimidazole-checkpoint inhibitor synergy than with primary drug hepatotoxicity. Three published mechanisms support this interpretation: Albendazole promotes ubiquitin-mediated proteasomal degradation of programmed cell death ligand-1 via ubiquilin-4 suppression; flubendazole downregulates programmed cell death protein-1 through signal transducer and activator of transcription-3 inhibition; and mebendazole demonstrates direct synergy with anti-programmed cell death protein-1 in syngeneic murine colorectal cancer models. The aspartate aminotransferase: Alanine aminotransferase ratio of 1.01 at peak injury in the reported case, the stable alkaline phosphatase, and the documented hepatic metastases with periportal edema on computed tomography may be more compatible with tumor cell onconecrosis than hepatocellular drug injury, though these findings do not exclude drug-induced injury. The ICI rechallenge result presented as key evidence for fenbendazole causality would also be consistent, under the immunogenic cell death potentiation model, with removal of the inducer — a hypothesis-generating alternative, not proof of isolated drug toxicity. We propose minimum methodological standards for future case reports and a diagnostic framework distinguishing drug-induced liver injury from onconecrosis in benzimidazole-treated cancer patients.
BACKGROUND Calcinosis cutis is a recognized manifestation of limited cutaneous systemic sclerosis (CREST syndrome), but extensive multifocal involvement of large joints and the trunk is rare. Diagnosis may be particularly challenging in patients with negative systemic sclerosis-specific autoantibodies. CASE SUMMARY A 59-year-old woman with extensive calcinosis cutis in the prepatellar region, elbows, and trunk, accompanied by Raynaud’s phenomenon. Despite persistently negative autoimmune serology results, a seronegative CREST variant was diagnosed based on calcinosis, Raynaud’s phenomenon, and clinically diagnosed sclerodactyly, together with histopathological evidence of chronic inflammation and fibrosis after excluding other differential diagnoses. Surgical excision of the prepatellar lesion resulted in complete resolution without recurrence. Histopathological examination revealed aggregated lymphocytes and fibrosis surrounding the calcified tissue, consistent with an autoimmune process. CONCLUSION CREST syndrome should not be excluded despite negative serology. Surgical excision may benefit symptomatic extensive calcinosis cutis.
BACKGROUND Percutaneous vertebroplasty is a widely used treatment for painful vertebral compression fractures. Cement leakage and infection are the most common complications, whereas vascular injury, particularly aortic puncture, is exceedingly rare but potentially fatal. Reports of major vascular injury during vertebroplasty remain scarce, and awareness of this complication remains limited among proceduralists. This case report describes an aortic pseudoaneurysm caused by inadvertent needle puncture during vertebroplasty, highlighting the recognition, endovascular management, and prevention of this complication. CASE SUMMARY A 74-year-old female with severe osteoporosis and prior vertebral compression fractures (L3 and L4) underwent percutaneous vertebroplasty for back pain refractory to conservative therapy. During needle advancement at L3, the needle inadvertently traversed the vertebral body, and retrograde blood flow through the needle prompted reflexive withdrawal. Cement injection was subsequently performed at the same level, and anterior cement extravasation was observed on lateral fluoroscopy during injection. Computed tomography angiography revealed a pseudoaneurysm of the infrarenal abdominal aorta with an associated retroperitoneal hematoma, and the hemoglobin level decreased from 12.8 g/dL to 9.6 g/dL. Urgent aortic angiography confirmed the pseudoaneurysm, which was successfully excluded with an endovascular stent-graft. The patient recovered uneventfully, and 6-month computed tomography angiography confirmed stable stent positioning without endoleak, thrombosis, or migration. CONCLUSION Aortic injury is a rare but life-threatening complication of vertebroplasty requiring continuous fluoroscopic monitoring throughout the procedure and prompt management.
Diabetes mellitus (type 1 diabetes mellitus and type 2 diabetes mellitus) results from a failure of pancreatic β cells at different velocities and time frames resulting insulin deficiency. Currently, management of type 1 diabetes mellitus relies on replacing insulin, without changing the natural course of progressive β cell loss. Stem cell therapy can prevent autoimmune destruction as well replenish pancreatic β cells. Among various sources, human umbilical cord mesenchymal stem cells (hUC-MSCs) have the advantage of generating progenitor cells, greater immunosuppression, cell proliferation and clonality. Further they are less immunogenic. Practical advantages for their use include painless extraction and potential of long term storage. In this review we provide a brief of interventions available to prevent and slow down immune destruction of pancreatic β cell cells, and discuss evidence obtained from cell and animal studies, combined use with adjuvants, their potential on microvascular complications, human clinical trials, meta-analysis and umbrella reviews. We then discuss the limitations and challenges, and offer future perspectives. Currently, hUC-MSC is a treatment with promise. Further large randomized clinical trials with diverse populations, proper trial protocol with inclusion criteria, treatment methods and pre-defined outcome measures in the long term are necessary to bring hUC-MSC therapy into mainstream clinical use.
BACKGROUND Lumbar degenerative disease affects nearly one-third of adults over 65 years old in the United States, a population expected to reach 89 million by 2050. Advances in minimally invasive spine surgery aim to address this growing demand by reducing blood loss, recovery time, and hospitalization. Robotic spine surgery improves hardware placement accuracy and reduces radiation exposure, while awake spine surgery performed under spinal anesthesia minimizes risks associated with general anesthesia and postoperative opioid use. However, reports describing the combined application of these techniques remain limited. CASE SUMMARY A 57-year-old male with hypertension presented with progressive neurogenic claudication and mechanical back pain refractory to conservative management. Magnetic resonance imaging demonstrated L4-L5 disc bulge with ligamentum flavum hypertrophy and central canal stenosis. After discussing operative options, the patient elected to undergo awake robotic-assisted L4-L5 decompression and fusion under spinal anesthesia. Preoperative thin-cut computed tomography was used for robotic trajectory planning. Intraoperatively, spinal anesthesia achieved adequate motor and sensory blockade, allowing prone positioning and robotic placement of cortical screws followed by decompression and fusion. The procedure was completed without complications, and postoperative imaging confirmed appropriate hardware placement. The patient recovered uneventfully and was discharged on postoperative day one. CONCLUSION Awake robotic lumbar decompression and fusion under spinal anesthesia is feasible and was completed without conversion to general anesthesia, supporting the combination of robotic precision with the recovery advantages of spinal anesthesia.
BACKGROUND Large cell neuroendocrine carcinoma (LCNEC) of the extrahepatic bile duct is an exceedingly rare and highly aggressive malignancy, accounting for < 0.2% of all extrahepatic bile duct tumors. Preoperative diagnosis is challenging, and early recurrence is common even after R0 resection. No standard treatment regimen has been established to date. Mismatch repair (MMR) status has important implications for immunotherapy indications; however, it has rarely been reported in biliary LCNEC. CASE SUMMARY A 73-year-old man presented with obstructive jaundice. Imaging revealed a distal common bile duct mass. After percutaneous transhepatic cholangial drainage for biliary decompression, laparoscopic pancreaticoduodenectomy was performed. Pathological analysis confirmed LCNEC with a minor adenocarcinoma component, positive bile duct margin, and proficient MMR (pMMR)/microsatellite stable (MSS) phenotype. The patient received six cycles of adjuvant etoposide plus (EP) cisplatin and remained progression-free at 12-months follow-up (April 25, 2026), with no evidence of recurrence on imaging. CONCLUSION Biliary LCNEC is a rare and aggressive tumor. The pMMR/MSS phenotype provides a molecular rationale for excluding immunotherapy and directs treatment toward platinum-based chemotherapy. Even with a positive margin (R1), individualized adjuvant EP chemotherapy can achieve short-term disease-free survival. Multidisciplinary-guided, molecularly driven individualized therapy is central to the management of such rare malignancies.
Chronic musculoskeletal pain (CMP) is one of the world's health problems affecting millions of people. As musculoskeletal pain is chronic, it changes from nociceptive pain to mixed pain mediated by peripheral and central sensitization. CMP is a biopsychosocial disorder in which psychological factors, including anxiety and depression, significantly affect the pain experience and disability. In addition to these factors, pain coping strategies and social determinants of health also play important roles in the experience of chronic pain. In the recent issue of World Journal of Clinical Cases , conducted by Hamed et al , investigated psychiatric disorders, coping strategies, and quality of life in patients with CMP to better understand the clinical and psychosocial aspects of CMP. This editorial letter aims to critically appraise the multidimensional nature of CMP in light of the findings by Hamed et al , with a particular focus on clinical heterogeneity, psychiatric comorbidities, psychosocial stressors, and key determinants of impaired quality of life.
BACKGROUND Dyspepsia encompasses a wide range of high-prevalence upper gastrointestinal symptoms, especially in patients with type 2 diabetes mellitus (T2DM) owing to diabetic autonomic neuropathy. Despite its disruption to daily life, limited studies have compared patients with dyspepsia with and without T2DM, largely due to high-cost, availability, and radiation exposure of the gold standard gastric emptying scintigraphy (GES). Although less accurate than GES, electrogastrography (EGG) examination is more affordable, non-invasive, and radiation-free instead, recording gastric myoelectrical activity to assess gastric motility dysfunction, and making it a promising preliminary evaluation tool for detecting gastric motility dysfunction. AIM To investigate gastric myoelectrical activity in patients with dyspepsia with and without T2DM using EGG. METHODS Clinical and demographic data of study participants were collected from August to December 2025 at Cipto Mangunkusumo National Hospital and Mitra Keluarga Hospital Kemayoran through consecutive sampling. Eligible subjects were patients who provided informed consent, had complete medical records, completed the Indonesian version of the Short-Form Leeds Dyspepsia Questionnaire, and underwent EGG recordings. Data were statistically analysed using SPSS version 26.0, including bivariate comparative analyses and multivariate analysis with robust variance estimation Poisson regression. RESULTS In total, 76 subjects (38 in each group) were included. Patients in the T2DM group were older (P = 0.001), predominantly obese (P = 0.006), and had higher rates of indigestion (P = 0.021) and bradygastria (P = 0.005). EGG results were similar across demographic characteristics (P > 0.05), while T2DM status remained independently associated with bradygastria in multivariate analysis. Compared with other forms of gastric myoelectrical activity, patients with T2DM had a higher likelihood of bradygastria (adjusted prevalence ratio: 1.739; 95%CI: 1.079-2.804; P = 0.023). Additionally, good glycaemic control (glycated haemoglobin of < 6.5%) in patients with T2DM was associated with milder dyspepsia (P = 0.036). CONCLUSION T2DM is significantly associated with bradygastria in patients with dyspepsia. Good glycaemic control is associated with milder dyspeptic symptoms in patients with T2DM.
BACKGROUND Neuromuscular choristoma (NMC) is a rare developmental anomaly characterised by the aberrant presence of mature skeletal muscle fibres within peripheral nerve fascicles. Involvement of the sciatic nerve is uncommon, with most reported instances limited to isolated case reports in paediatric patients. The natural history, long-term neurological stability, and optimal management of this condition remain poorly defined in the literature. CASE SUMMARY We describe a paediatric patient who was diagnosed in infancy with a sciatic nerve NMC, confirmed by open biopsy, and has been followed for over ten years. Neurologically, the patient remained stable, exhibiting only mild weakness in the left posterior compartment of the leg. Serial imaging over the follow-up period showed no significant progression or malignant transformation of the lesion. However, over time a progressive limb length discrepancy and lower limb muscle imbalance developed, eventually becoming the dominant clinical issues. A multidisciplinary evaluation supported continued conservative management of the nerve lesion. Ultimately, it was the orthopaedic sequelae, rather than any neurological deterioration, that necessitated intervention. As the patient approached puberty, a guided growth (epiphysiodesis) procedure was performed to address the limb length discrepancy. CONCLUSION Our case adds to the limited body of long-term follow-up data and supports a conservative management approach for NMC, with an emphasis on secondary musculoskeletal consequences.
BACKGROUND Arteriovenous malformations (AVMs) of the eyelid are rare vascular lesions that can be difficult to diagnose because they often present in unusual ways. While AVMs typically show signs of vascularity such as pulsation, bruit, or skin discoloration, some lesions may appear as simple painless eyelid swellings and closely resemble benign conditions like dermoid or epidermal inclusion cysts. Such atypical presentations can lead to misdiagnosis and unexpected challenges during surgery. CASE SUMMARY We report an atypical case of an AVM presenting as a cystic eyelid mass. An 18-year-old female presented with a progressively enlarging swelling of the left upper eyelid over a period of two years. Non-contrast computed tomography revealed a well-defined soft-tissue lesion, provisionally diagnosed as an epidermal inclusion cyst. The patient underwent excisional biopsy under general anesthesia. A greyish-brown mass was completely excised and submitted for histopathological examination, which confirmed the diagnosis of an AVM. The postoperative course was uneventful, and no recurrence was observed at one year of follow-up. This case highlights the variability in the clinical presentation of AVMs. CONCLUSION This case highlights how an eyelid AVM can closely mimic a benign cystic lesion such as a dermoid cyst, creating a significant diagnostic challenge. Even in the absence of obvious vascular signs, vascular malformations should be considered in atypical or progressively enlarging eyelid masses. Early recognition and careful surgical management can help prevent complications and achieve excellent cosmetic and functional outcomes.
Pulmonary embolism remains a major cause of cardiovascular morbidity and mortality, with management guided by risk stratification and the balance between thrombotic burden, right ventricular dysfunction and bleeding risk. Although anticoagulation remains the cornerstone of therapy, percutaneous catheter-based interventions have emerged as important alternatives or adjuncts in selected intermediate-risk and high-risk patients, particularly when systemic thrombolysis is contraindicated, has failed, or carries an unacceptable bleeding risk. These approaches include catheter-directed thrombolysis, ultrasound-assisted thrombolysis, mechanical thrombectomy, aspiration embolectomy and hybrid techniques, all aiming to achieve rapid hemodynamic improvement while limiting systemic thrombolytic exposure. Available trial and registry data suggest favorable effects on right ventricular function and pulmonary hemodynamics, with an acceptable safety profile in experienced centers, although recent comparative evidence for hard clinical endpoints remains limited. This review summarizes the current evidence, technical considerations and patient-selection principles for percutaneous therapies in acute pulmonary embolism and discusses their potential integration into evolving treatment algorithms and future research directions.
In this retraction note, we describe the World Journal of Clinical Cases Editorial Office’s decision and reason for retracting a published article titled "Lung imaging characteristics in a patient infected with Elizabethkingia miricola following cerebral hemorrhage surgery: A case report", World J Clin Cases 2024; 12(1): 169-175.
BACKGROUND Ampullary adenocarcinoma is often associated with favourable outcomes due to early presentation and high resectability. Small ampullary lesions are more commonly well-differentiated neuroendocrine tumours, which typically demonstrate indolent behaviour. In contrast, poorly differentiated neuroendocrine carcinomas, including large-cell neuroendocrine carcinoma (LCNEC), are exceptionally rare and biologically aggressive, challenging prognostic assumptions based on tumour size. CASE SUMMARY A 69-year-old woman presented with painless obstructive jaundice. Imaging revealed a small ampullary lesion without evidence of metastatic disease. Endoscopic cytology suggested adenocarcinoma, and pancreaticoduodenectomy was performed. Histopathological examination demonstrated LCNEC characterised by large polygonal cells, extensive necrosis, high mitotic activity, and a Ki-67 index up to 70%. Immunohistochemistry was positive for synaptophysin and chromogranin A. The patient completed six cycles of adjuvant carboplatin and etoposide and remains disease-free at 8 months postoperatively. CONCLUSION This case highlights the size-biology paradox in ampullary tumours, where small lesions may harbour highly aggressive histology. LCNEC of the ampulla of Vater remains rare and carries a potentially poor prognosis, warranting accurate pathological diagnosis and multidisciplinary management.
BACKGROUND Blau syndrome (BS) is a rare sporadic or autosomal dominant multi-system inflammatory condition attributable to mutations in the nucleotide binding oligomerization domain containing 2 gene. It classically manifests as a triad of skin rash, uveitis and arthritis, although the phenotype may vary and pose diagnostic dilemmas in the presence of systemic co-morbidities. CASE SUMMARY We describe two sporadic cases with different clinical profiles. Case 1: A 5-year-old male presented with a history of erythematous skin lesions all over the body since the age of 6 months and recurrent fever and knee and wrist joint pains for the past year, associated with progressive diminution of vision. He had dry, scaly skin, malar erythema and bilaterally swollen wrist, ankle and knee joints, bilateral band-shaped keratopathy, and bilateral post-uveitis cataracts. Case 2: An 11-year-old male previously diagnosed with polyarticular juvenile idiopathic arthritis, tubulointerstitial nephritis, seizure disorder, restrictive lung disease, and multidrug-resistant pulmonary tuberculosis, presented with bilateral granulomatous uveitis. Fundus examination of the right eye showed fibrovascular proliferation over the disc secondary to retinal vasculitis and exudative shallow retinal detachment. Both patients were diagnosed with BS and treated with corticosteroids and adalimumab, leading to improvement in systemic and ocular symptoms over the next 2 years. Case 1 underwent bilateral cataract surgery with a good visual outcome. CONCLUSION The diagnosis of BS is important to consider in very young children with arthritis and uveitis. Timely interdepartmental referral and collaboration is prudent. Prompt multidisciplinary management is required to prevent significant morbidity.
BACKGROUND Adenosine-sensitive focal atrial tachycardias (AT) arising from the anteroseptal region are uncommon and may be difficult to ablate safely because of their proximity to the atrioventricular (AV) conduction system. Failure of conventional right or left atrial ablation should prompt consideration of alternative anatomical sites. CASE SUMMARY A 64-year-old caucasian man with no structural heart disease presented with recurrent adenosine-sensitive supraventricular tachycardia. Electrophysiological study demonstrated a long-RP focal AT with intermittent AV block and earliest activation in the anteroseptal right atrium. High-density mapping and radiofrequency (RF) applications in both atria were ineffective. Mapping of the aortic root identified the earliest atrial signal in the non-coronary cusp, 36 milliseconds before the surface P wave, with a negative unipolar electrogram. RF delivery at this site terminated the tachycardia, and additional consolidation lesions prevented recurrence. The arrhythmia was no longer inducible under isoproterenol. At 3-year follow-up, the patient remains asymptomatic without antiarrhythmic therapy. CONCLUSION The non-coronary cusp is a safe and effective ablation target for anteroseptal focal atrial tachycardia.
BACKGROUND A considerable proportion of patients diagnosed with hypertrophic cardiomyopathy (HCM) or HCM-like phenotypes lack an identifiable genetic mutation and are classified as non-familial cases. This observation suggests that hormonal, autoimmune, and structural mechanisms may contribute to myocardial hypertrophy in selected patients. CASE SUMMARY A 45-year-old woman with a history of hypertension and hypothyroidism was evaluated and found to have hypokalemia, metabolic alkalosis, and asymmetric left ventricular hypertrophy. Transthoracic echocardiography revealed dynamic left ventricular outflow tract obstruction, while cardiac magnetic resonance imaging demonstrated diffuse asymmetric hypertrophy with mid-wall late gadolinium enhancement consistent with non-ischemic myocardial fibrosis. Hormonal evaluation showed markedly elevated aldosterone levels with suppressed renin activity, confirming primary hyperaldosteronism. Autoimmune testing and minor salivary gland biopsy established Sjögren’s syndrome. Abdominal imaging revealed a right adrenal adenoma and left-sided obstructive uropathy with severe unilateral renal dysfunction. CONCLUSION Endocrine and autoimmune disorders should be considered in patients presenting with HCM-like phenotypes.
