A 33-year-old woman presented with progressive dysphagia and pleuritic chest pain, initially undergoing an unrevealing cardiopulmonary evaluation. Persistent symptoms prompted upper endoscopy, which demonstrated an ulcerated gastroesophageal junction lesion, with biopsy confirming invasive moderately to poorly differentiated adenocarcinoma. Immunohistochemical studies showed intact mismatch repair protein expression and negative human epidermal growth factor receptor 2 and Claudin 18.2, while programmed death-ligand 1 expression was markedly elevated (tumor proportion score 80%; combined positive score 80). Comprehensive next-generation sequencing revealed no actionable genomic alterations. Staging positron emission tomography demonstrated widespread metastatic disease, including involvement of the regional lymph nodes, liver, and ovary. The patient was treated with combination chemotherapy and immune checkpoint inhibition. This case highlights an atypical presentation of advanced gastroesophageal junction adenocarcinoma in a young adult and underscores the importance of early endoscopic evaluation in patients with persistent dysphagia, as well as recognition of uncommon metastatic patterns and the therapeutic implications of biomarker profiling.

Pleural-based lung masses can mimic lung cancer and differentiating malignancy from other causes remains a diagnostic challenge. We report a case of a 50-year-old man who presented with an acute onset pleuritic chest pain and a history of weight loss. Chest radiography and computed tomography scan showed a solitary pleural-based lung lesion that was suspicious for malignancy. Two sessions of computed tomography guided biopsies yielded only necrotic tissue. An endobronchial ultrasound-guided transbronchial needle aspiration showed inflammatory cells but was non-diagnostic. Video-assisted thoracoscopic surgery wedge resection of the lesion provided tissue revealing a chronic granulomatous mass which showed caseous necrosis and Langhans type giant cells on histopathology. A probable diagnosis of tuberculoma was made based on these findings when other investigations did not reveal a definitive diagnosis and the patient was treated with antitubercular medicines. This case report highlights the challenges encountered in diagnosing a pleural-based solitary lung mass. The key lesson learnt is that tuberculosis should remain in the differential diagnosis of pleural-based lung mass in endemic settings, especially when repeated biopsies show necrosis without malignant cells.

Pulmonary mucormycosis is an invasive fungal infection that can present with rapidly progressive pulmonary disease and may mimic bacterial pneumonia or lung abscess. This diagnostic overlap can lead to delayed recognition and treatment. We report the case of a 33-year-old woman with type 2 diabetes mellitus and a solitary functioning kidney, who presented with fever, productive cough, pleuritic chest pain, and progressive dyspnea. Serial chest radiographs demonstrated rapid progression of lung lesions from right-sided consolidation to cavitary necrosis with air-fluid level formation, consistent with lung abscess. Despite broad-spectrum antibiotic therapy, clinical and inflammatory markers worsened, prompting bronchoscopy evaluation. Histopathology revealed broad aseptate fungal hyphae with right-angle branching. Fungal culture confirmed Rhizopus species, compatible with the diagnosis of pulmonary mucormycosis. The patient was treated with intravenous liposomal amphotericin B for six weeks. The therapy was complicated by amphotericin-induced hypokalemia, hypomagnesemia, and transient liver enzyme derangement, necessitating close monitoring given her solitary functioning kidney. She demonstrated gradual clinical and biochemical improvement with appropriate antifungal therapy. This case highlights the importance of early suspicion of mucormycosis in diabetic patients with non-resolving pneumonia and underscores the challenges of managing antifungal therapy in patients with limited renal reserve.

Recurrent pericarditis (RP) remains challenging, especially in tuberculosis (TB)-endemic regions where empirical anti-TB therapy is often unnecessarily prolonged. We report a 35-year-old woman with three RP episodes over six months, presenting with pleuritic chest pain, elevated inflammatory markers, and moderate-to-large pericardial effusion. Extensive infectious (including TB), autoimmune, and malignancy workups were negative. Cardiac magnetic resonance revealed persistent pericardial late gadolinium enhancement despite clinical remission. Whole-exome sequencing identified a heterozygous MEFV c.442G>C (p.Glu148Gln) variant, suggesting an autoinflammatory predisposition. Although the patient finally achieved sustained symptom-free status for six months on a standardized low-dose colchicine regimen, still over 10% of patients have recurrent symptoms receiving colchicine in addition to conventional anti-inflammatory therapy with aspirin or ibuprofen. This case highlights the shifting paradigm from an infection-centered to an autoinflammatory framework for RP in TB-endemic countries, underscores the role of MEFV variants in idiopathic recurrent pericarditis, and illustrates the real-world gap between genetic insights and therapeutic accessibility to IL-1 inhibitors in resource-limited settings.

A man in his early 40s with peripheral arterial disease and prior ultrasound-assisted catheter-directed thrombolysis using the EKOS™ system (Boston Scientific) for arterial thrombosis presented with severe pleuritic chest pain. Initial evaluation demonstrated an acute right-sided segmental pulmonary embolism and a small-to-moderate pericardial effusion. His D-dimer was elevated at 2.8 µg/mL FEU, and his Wells' score was calculated at 6, indicating moderate-to-high clinical probability. He was treated with intravenous heparin and colchicine for pulmonary embolism with suspected pericarditis. Persistent severe pain prompted repeat imaging, which revealed a retained intravascular guidewire extending from the inferior vena cava into the right atrium, associated with fibrin sheath formation and interval enlargement of the pericardial effusion. Endovascular retrieval achieved partial removal, but a residual intracardiac fragment remained. Two weeks later, the patient re-presented with recurrent symptoms, and an additional 10 cm retained guidewire fragment was successfully retrieved. This rare case of a retained intravascular guidewire causing iatrogenic pericarditis highlights the importance of careful post-procedural imaging review, multidisciplinary management, and confirmation of complete foreign body removal.

Cardiac amyloidosis can present with troponin-positive chest pain and non-obstructive coronary arteries, mimicking acute coronary syndrome. When a concurrent treatable diagnosis, such as pericarditis, is identified, symptomatic improvement may lead to premature diagnostic closure and failure to pursue confirmatory testing for an underlying infiltrative cardiomyopathy.

Invasive pulmonary aspergillosis (IPA) is a fulminant fungal infection that predominantly occurs in immunocompromised patients; however, it may occasionally be encountered in immunocompetent individuals, often leading to diagnostic delay and unfavorable outcomes. We describe a case of invasive pulmonary aspergillosis (IPA) in an immunocompetent woman in her mid-20s who presented with productive cough, hemoptysis, low-grade fever, and pleuritic chest pain, closely resembling pulmonary tuberculosis at initial evaluation. While the chest x-ray was normal, high-resolution computed tomography of the chest demonstrated a characteristic halo sign in the right middle lobe. Further evaluation with bronchoscopy and bronchoalveolar lavage revealed a markedly elevated galactomannan index, and fungal culture grew Aspergillus flavus. Hence the patient was initiated on oral voriconazole in accordance with Infectious Diseases Society of America guidelines, resulting in complete clinico-radiological resolution. In immunocompetent patients with persistent respiratory symptoms and suggestive imaging results, this report emphasizes the significance of maintaining a high index of suspicion for IPA. It also emphasizes the importance of early intervention in the form of bronchoscopic evaluation and prompt antifungal therapy in achieving favorable outcomes.

We present a 19-year-old female, eight weeks postpartum, with a seven-week history of migratory arthralgias followed by progressive dyspnea and pleuritic chest pain. A large mass in her right lower lobe was discovered on computed tomography. Laboratory evaluation demonstrated elevated anti-proteinase 3 (PR3) antibody, along with elevated inflammatory markers. The bronchoalveolar lavage culture grew Cryptococcus neoformans, and serum cryptococcal antigen was positive. The patient was diagnosed with pulmonary cryptococcosis and treated with amphotericin and flucytosine, given the severity of her illness. Granulomatosis with polyangiitis was a part of the initial differential but was not diagnosed until she later developed transient hemoptysis, recurrent epistaxis, skin rash, and significant proteinuria. The skin biopsy was consistent with cutaneous vasculitis, and the kidney biopsy was positive for glomerulonephritis, confirming postpartum systemic vasculitis masked by a concurrent pulmonary cryptococcal infection.