ABSTRACT
Background: We report a severe hypersensitivity reaction due to warfarin in a COVID19 patient with sepsis. Case Report: An 86-year-old man was admitted for COVID19 pneumonia. He was vaccinated with 2 ComirNaty doses. He was affected by hypertension and CKD in emodialysis. At the admission he presented fever and tachypnea, the laboratory tests showed a septic state. We started administration of empiric therapy with piperacillina/tazobactam, it was replaced with meropenem and linezolid on the 29th day. After 10 days linezolid was stopped for thrombocitopenia. On the 14th day we prescribed warfarin for tromboembolic risk prevention when paroxysmal atrial fibrillation occurred . At the fifth week there was a clinic and laboratory worsening so we started target antibiotic therapy with cefiderocol and colistin due to positive blood cultures for A. Baumanii XDR. On the 24th day an inguinal erytema with blister-like lesion occurred and involved progressively face, neck, limbs, trunk and abdomen with extensive skin sloughing and crusted lesions appeared in the perioral and perinasal mucosa. Nikolsky sign was negative. Skin biopsy showed signs of inflammatory reaction. Warfarin was stopped and 1mg/kg methylprednisone was started with slow and progressive benefit. Conclusions: The patient has developed a warfarin linked hypersensitivity reaction with clinical features similar to toxic epidermal necrolysis. We assume that it was a borderline condition of hypersensitivity to warfarin in a patient with hyperactivation of immune system due to COVID19 and sepsis.
ABSTRACT
OBJECTIVE: In human pathology, SARS-CoV-2 utilizes multiple molecular pathways to determine structural and biochemical changes within the different organs and cell types. The clinical picture of patients with COVID-19 is characterized by a very large spectrum. The reason for this variability has not been clarified yet, causing the inability to make a prognosis on the evolution of the disease. MATERIALS AND METHODS: PubMed search was performed focusing on the role of ACE 2 receptors in allowing the viral entry into cells, the role of ACE 2 downregulation in triggering the tissue pathology or in accelerating previous disease states, the role of increased levels of Angiotensin II in determining endothelial dysfunction and the enhanced vascular permeability, the role of the dysregulation of the renin angiotensin system in COVID-19 and the role of cytokine storm. RESULTS: The pathological changes induced by SARS-CoV-2 infection in the different organs, the correlations between the single cell types targeted by the virus in the different human organs and the clinical consequences, COVID-19 chronic pathologies in liver fibrosis, cardiac fibrosis and atrial arrhythmias, glomerulosclerosis and pulmonary fibrosis, due to the systemic fibroblast activation induced by angiotensin II are discussed. CONCLUSIONS: The main pathways involved showed different pathological changes in multiple tissues and the different clinical presentations. Even if ACE2 is the main receptor of SARS-CoV-2 and the main entry point into cells for the virus, ACE2 expression does not always explain the observed marked inter-individual variability in clinical presentation and outcome, evidencing the complexity of this disorder. The proper interpretation of the growing data available might allow to better classifying COVID-19 in human pathology.