We report a case of endogenous lipoid pneumonia secondary to long-term use of amiodarone (> 30 years) for atrial fibrillation in a 76-year-old Caucasian woman, presenting with cough and dyspnea. Endogenous Lipoid pneumonia is a rare underdiagnosed condition more prevalent in adults. It is usually asymptomatic and a diagnosis is generally made in patients who have become clinically unstable or when an abnormal lung shadow is found on a chest X-ray. In the case here described it was diagnosed by fiberoptic bronchoscopy with bronchoalveolar lavage (BALF) where fat-laden macrophages (oil red O stain) were identified. Since a history of use of oil-based products had been ruled out, amiodarone was deemed to be the most likely cause of lipoid pneumonia. The patient was managed with the replacement of amiodarone with digoxin and treated with oral prednisolone. The patient has remained clinically stable with radiological improvement during a follow-up of two years.
Wir berichten über einen Fall endogener Lipidpneumonie infolge Langzeitanwendung (≥ 30 Jahre) von Amiodaron zur Behandlung von Vorhofflimmern bei einer 76-jährigen Patientin kaukasischer Abstammung, die sich mit Husten und Dyspnoe bei uns vorstellte. Die endogene Lipidpneumonie ist eine seltene und unterdiagnostizierte Krankheit, die häufiger bei Erwachsenen auftritt. Sie verläuft normalerweise asymptomatisch und wird meist bei Patienten diagnostiziert, die klinisch instabil geworden sind, oder wenn im Thoraxröntgenbild eine abnorme Verschattung der Lunge erkennbar ist. In dem hier vorgestellten Fall erfolgte die Diagnosestellung durch fiberoptische Bronchoskopie mit Gewinnung von Flüssigkeit nach bronchoalveolärer Lavage (BALF), in der fettbeladene Makrophagen (Oil-Red-O-Färbung) zu finden waren. Da die Anwendung ölhaltiger Produkte anamnestisch ausgeschlossen worden war, wurde Amiodaron für die wahrscheinlichste Ursache der Lipidpneumonie gehalten. Die Behandlung wurde von Amiodaron auf Digoxin umgestellt und die Patientin erhielt oral Prednisolon. Während der 2-jährigen Nachbeobachtungsdauer blieb die Patientin klinisch stabil und die radiologischen Zeichen gingen zurück.
Background Growing evidence focuses on the role of hypoalbuminemia in the COVID-19 course and the role of vascular inflammation in the progression to Capillary Leak Syndrome (CLS). CLS may be mediated by a derangement of endothelial barrier following vascular endothelial dysfunction. We investigated the role of cardiometabolic risk factors in the association of hypoalbuminemia with endothelial dysfunction of hospitalized COVID-19 patients. Methods In this cross-sectional study, patients hospitalized for COVID-19 at the medical ward or Intensive Care Unit (ICU) were enrolled. Medical history and laboratory examinations were collected while the endothelial function was assessed by brachial artery flow-mediated dilation (FMD) between the first 24–72 hours of their admission to the hospital. According to the body mass index, history of hypertension, dyslipidemia, and diabetes mellitus, COVID-19 patients were categorized in those with Cardiometabolic Risk Factors (CRFact) or without CRFact (no-CRFact). From the study population, we excluded subjects with established cardiovascular disease. Results Sixty-six patients with COVID-19 (37% admitted in ICU) were recruited. From the study population, 41 were in the group of CRFact and 25 in the no-CRFact. Patients with CFRact were older (65±9 years vs. 53±14 years, p<0.001), had more impaired FMD (1.16±2.13% vs. 2.60±2.44%, p=0.01), and lower serum albumin levels (3.10±0.68 g/dL vs. 3.52±0.26 g/dL, p=0.006) compared to the no-CRFact group. Between CRFact and no-CRFact, there was no difference in CRP and IL-6 levels. Interestingly, serum albumin in patients with CRFact was significantly lower than the lower reference limit (LRL) (=3.5 g/dl) of albumin (p=0.001), while no such finding was noted in subjects with no CRFact (p=0.64). Furthermore, regression analysis revealed that, even after adjustment for age, the presence of CRFact was associated with decreased serum albumin levels by 0.31mg/dl (95% CI 0.08 to 0.63, p=0.04). In the CRFact population, there was a correlation of albumin with FMD (R=0.29, p=0.05) and an inverse correlation with CRP (rho=−0.48, p=0.02) and IL-6 (rho=−0.66, p<0.001), while in the no-CRFact group no such correlation were observed (p=NS for all). Conclusion COVID-19 patients with cardiometabolic risk factors present with low serum albumin levels early at the course of the disease, which may be driven by endothelial dysfunction and vascular inflammation. This data gives insights into the potential association of a dysfunctional endothelial layer and the progression to capillary leak syndrome. Funding Acknowledgement Type of funding sources: None.
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