Pheochromocytoma is a rare catecholamine-secreting tumor that can cause major cardiovascular complications, including acute heart failure, arrhythmias, and stress-induced cardiomyopathy. Takotsubo syndrome (TTS) is an acute non-ischemic cardiomyopathy characterized by transient left ventricular systolic dysfunction without obstructive coronary artery disease, often mimicking acute coronary syndrome. Catecholamine excess plays a central role in its pathophysiology, leading to myocardial stunning, hemodynamic instability, and arrhythmias. The association between pheochromocytoma and TTS is uncommon and frequently associated with severe clinical presentations. We report the case of a 52-year-old woman with poorly controlled hypertension treated with a calcium channel blocker, who presented with chest pain, dyspnea, and palpitations. On admission, blood pressure was 178/122 mmHg, and heart rate was 102 bpm. The patient described recurrent episodes of headache and palpitations occurring two to three times monthly and lasting 30 to 60 minutes, suggesting secondary hypertension. Electrocardiography showed 1 mm ST-segment elevation in the anterior leads without reciprocal changes and a prolonged QTc interval (480 ms). Peak high-sensitivity troponin reached 1880 ng/L (reference <35 ng/L), while brain natriuretic peptide (BNP) was 450 pg/mL (reference <125 pg/mL). Transthoracic echocardiography revealed a left ventricular ejection fraction of 45% with apical akinesia and basal hyperkinesia, consistent with Takotsubo syndrome. Left ventriculography confirmed typical apical ballooning, and coronary angiography showed no obstructive coronary artery disease. During hospitalization, the patient developed rapid atrial fibrillation with hemodynamic instability, requiring electrical cardioversion and amiodarone therapy. Labile blood pressure and paroxysmal symptoms raised suspicion of catecholamine excess, subsequently confirmed by elevated plasma and urinary metanephrines. Abdominal CT identified a 30 × 25 × 28 mm left adrenal mass with attenuation >10 HU and intense heterogeneous contrast enhancement, highly suggestive of pheochromocytoma. Preoperative treatment with phenoxybenzamine was progressively titrated to achieve hemodynamic stabilization before surgical resection. After surgery, left ventricular systolic function completely recovered, with ejection fraction improving to 58%. At the sixth-week follow-up, plasma and urinary metanephrines had normalized, confirming complete biochemical remission and successful tumor removal. Blood pressure also normalized postoperatively. This case highlights the importance of considering pheochromocytoma in patients with Takotsubo syndrome complicated by severe arrhythmias or labile hypertension, as early diagnosis may improve management and prognosis.

A previously healthy lady in her mid-30s presented to the medical emergency with recurrent episodes of flushing, rash, wheezing, chest tightness, palpitations, dyspnoea, and loss of consciousness. After five months of intensive medical investigations, she was referred to the gynaecological team, and a detailed clinical history made it clear that these episodes always occurred after unprotected penetrative sexual intercourse. The patient was thoroughly investigated with cardiological evaluation and imaging. Eventually, a semen allergy test was performed by injecting 1 cc of semen subcutaneously in the forearm, which pushed the patient into anaphylactic shock. The patient was treated with hydrocortisone, adrenaline, and an antihistamine. The patient recovered within 24 hours. The patient was diagnosed with a semen allergy. After the diagnosis, the patient was given an EpiPen and instructed to use condoms for sexual intercourse. Barrier contraception prevented any further episodes.

Background: Pulmonary arterial hypertension is a rare but life-threatening condition in children, with hereditary forms often being linked to mutations in genes such as bone morphogenetic protein receptor type 2 (BMPR2), caveolin 1 (CAV1), and potassium channel subfamily K member 3 (KCNK3). Among these, CAV1 mutations are associated with severe disease phenotypes, though cases resulting from de novo heterozygous CAV1 mutations with multi-system involvement remain rarely reported. The CAV1 mutation (c.424C > T, p.Q142X) disrupts caveolin-1 function, leading to dysregulated pulmonary vascular remodeling and multi-system abnormalities. Methods: This was a retrospective case study of a pediatric patient with hereditary PAH. The patient was followed at our hospital from initial presentation until death. Clinical data were collected from medical records, including physical examinations, laboratory tests, echocardiography, chest X-ray, computed tomography pulmonary angiography (CTPA), and genetic analysis. The patient was treated sequentially with various PAH-targeted medications. This report also includes a review of the relevant literature on CAV1-associated PAH. Results: A female aged 3 years and 11 months was diagnosed with hereditary PAH associated with a de novo heterozygous CAV1 mutation (c.424C > T, p.Q142X). Both parents underwent genetic testing and were negative for the mutation, confirming its de novo origin. Clinical manifestations included special facial features, congenital telangiectasia, cutis marmorata (marbled skin), congenital cataract, hereditary lipodystrophy, and severe PAH. The patient presented with progressive exercise intolerance, syncope, and worsening dyspnea over nine years. Echocardiography revealed pulmonary hypertension with an estimated pulmonary artery systolic pressure of 69-105 mmHg, right heart enlargement, right ventricular hypertrophy, and moderate tricuspid regurgitation. Blood and urine metabolic screenings were normal. A chest X-ray showed progressive enlargement of the cardiac silhouette and bulging of the pulmonary artery segment. CTPA demonstrated pulmonary hypertension, secondary right heart dysfunction, decompensated right ventricular function, and mosaic perfusion in both lungs, suggestive of small arterial branch occlusion. Right heart catheterization was declined by the parents. Thus, the diagnosis of PAH was established based on clinical, echocardiographic, CTPA, and genetic findings. The patient was hospitalized four times and lost to follow-up from 2017 to 2023. She received sequential treatment with digoxin, hydrochlorothiazide, tadalafil, ambrisentan, selexipag, and treprostinil. Despite these therapies, pulmonary artery pressure continued to rise with progressive clinical deterioration. The patient ultimately died at 13 years of age due to a pulmonary hypertensive crisis and multiple organ failure following a severe episode of gastroenteritis. Conclusions: Despite aggressive treatment with multiple targeted reduced pulmonary artery pressure drug therapies, managing hereditary PAH caused by CAV1 mutations in children remains a significant challenge, with a high mortality rate. Early genetic diagnosis, regular follow-up, and individualized treatment are crucial. It requires the joint efforts of patients, parents, and healthcare providers.

Chlorhexidine is a widely used antiseptic in healthcare settings, particularly for catheter site preparation in hemodialysis patients. While generally considered safe, chlorhexidine can rarely cause severe IgE-mediated anaphylactic reactions. Here we report the case of a 47-year-old man on maintenance hemodialysis who experienced two episodes of severe allergic reactions during dialysis sessions. During the first episode the patient presented with dyspnea, hypotension, and pruritus, which we initially attributed to the dialyzer membrane reaction. After changing the dialyzer membrane, the patient remained asymptomatic for 19 sessions. However, a second, more severe episode occurred with urticaria, profound hypotension, and respiratory distress requiring intravenous adrenaline. Retrospective analysis revealed chlorhexidine antisepsis at the tunneled catheter site as the causative agent, confirmed by elevated serum IgE (285 IU/mL), with complete resolution after switching to povidone-iodine as an antiseptic instead. This case demonstrates a concept called "sensitization window" where compromised skin integrity at the catheter exit site facilitated chlorhexidine penetration despite three years of uneventful exposure of the same during fistula use. This case highlights the importance of considering chlorhexidine hypersensitivity in such unexplained dialysis-related allergic reactions. Early recognition and prompt antiseptic substitution are thereby crucial to prevent potentially fatal anaphylactic episodes in this vulnerable population.

BACKGROUND Pulmonary alveolar proteinosis (PAP) is a rare lung disease characterized by the accumulation of surfactant within the alveoli. Its reported prevalence ranges from 3.7 to 40 cases per million. Because of its rarity and nonspecific clinical presentation, PAP is frequently misdiagnosed as more common respiratory conditions such as recurrent pneumonia. Accurate etiological classification is essential but can be challenging in routine clinical practice. CASE REPORT We report the case of a 79-year-old female non-smoker who presented with dyspnea and a history of unsuccessfully treated multiple pneumonia episodes. A computed tomography (CT) scan revealed a crazy paving pattern. Bronchoscopy showed the bronchoalveolar lavage fluid (BALF) had a milky appearance and became progressively opaque upon standing. The diagnosis of PAP was made based on a characteristic CT pattern and typical BALF analysis. Anti-granulocyte-macrophage colony-stimulating factor (GM-CSF) antibodies were negative, excluding autoimmune PAP. Extensive evaluation did not identify secondary causes such as hematologic disorders, immunodeficiency, chronic infection, or relevant environmental exposure. Genetic testing for hereditary PAP was not available; therefore, this subtype could not be definitively excluded. The patient subsequently underwent whole-lung lavage (WLL), leading to resolution of her symptoms and radiological features after 6 months of follow-up. CONCLUSIONS PAP can present with nonspecific respiratory symptoms and be misdiagnosed as recurrent pneumonia. Diagnosis relies on characteristic CT findings and BALF analysis, while determination of the PAP subtype requires systematic exclusion of autoimmune and secondary causes. This case highlights the diagnostic challenges of PAP classification in routine clinical practice.

Background/Objectives: The clinical determinants and functional relevance of persistent lung ultrasound (LUS) abnormalities after COVID-19 pneumonia remain poorly characterized. We aimed to identify determinants of qualitative LUS abnormalities and global lung involvement assessed by the LUS score, and to evaluate their association with persistent dyspnoea. Methods: We conducted a prospective observational study that included 261 patients who were hospitalized for COVID-19 pneumonia and were assessed 1-6 months after discharge. A standardized 14-zone LUS protocol was used to assess qualitative abnormalities (pleural line irregularity, ≥3 B-lines, and subpleural consolidations) and to calculate the LUS score. Associations with clinical variables, including dyspnoea assessed by the modified Medical Research Council (mMRC) scale, were analyzed using multivariable logistic regression. Results: The severity of the acute pneumonia episode emerged as the strongest determinant of qualitative LUS abnormalities and elevated LUS score (>6). Increasing age was independently associated with ultrasound findings. Persistent dyspnoea (mMRC ≥ 1) was associated with all qualitative abnormalities and with a higher prevalence of elevated LUS score (56.6% vs. 22.1%; p < 0.001). A graded association was observed between dyspnoea severity and both qualitative findings and LUS score. An increase in dyspnoea from baseline (ΔmMRC ≥ 1) remained independently associated with an elevated LUS score. Conclusions: Persistent LUS abnormalities are strongly associated with the severity of the acute episode. The LUS score provides a robust, clinically meaningful measure of residual lung involvement and shows a stronger association with persistent dyspnoea than qualitative findings, supporting its role in follow-up and risk stratification.