ECE2021 Audio Eposter Presentations Adrenal and Cardiovascular Endocrinology (80 abstracts)
Hypokalemia in a patient with severe SARS-CoV-2 infection
Kostoglou Athanasiou Ifigenia 1 , Sofia Nikolakopoulou 2 , Alexandra Konstantinou 2 , Lambros Athanassiou 2 , Alexandros Spyrantis 2 , Olga-Maria Spyropoulou 2 , Olga Mascha 3 , Charilaos Samaras 2 , Ioannis Bliziotis 2 & Panagiotis Athanassiou 4
1Asclepeion Hospital, Voula, Department of Endocrinology, Athens, Greece; 2Asclepeion Hospital, Voula, Covid Department, Athens, Greece; 3Asclepeion Hospital, Voula, Department of Biochemistry, Athens, Greece; 4St. Paul’s Hospital, Department of Rheumatology, Thessaloniki, Greece
Hypokalemia has been observed in cases of the new SARS-CoV-2 infection. It has been suggested that hypokalemia may be a sensitive biomarker of disease severity and the requirement for invasive mechanical ventilation requirement in COVID-19 pneumonia. The aim was to describe the case of a patient with severe SARS-CoV-2 pneumonia who developed severe hypokalemia. A patient, male, aged 52, presented with fever and dry cough. He was found to be positive for the SARS-CoV-2 infection. He was hospitalized. During his hospitalization he was found to have hypokalemia, serum K+ 3.2 mmol/l. His condition stabilized and he was discharged to be followed-up at home. The patient did not have an adrenal adenoma or hyperplasia or history of hypokalemia. However, 2 days later he developed fever and his cough deteriorated. He was hospitalized again. He was found to have pneumonia. K+ was 2.9 mmol/l, plasma renin 1.0 pg/ml and aldosterone 17 ng/dl. Potassium was administered. A CT of the abdomen was performed which did not show any evidence of an adrenal adenoma or adrenal hyperplasia. Diuretics were not administered. Hypokalemia persisted despite potassium administration and spironolactone was administered along with dexamethasone for the treatment of pneumonia. Following discharge from the hospital the patient recovered and spironolactone was discontinued. The SARS-CoV-2 virus invades cells via a spike which attaches to the ACE2 receptor. The attachment of the virus to the ACE2 receptor causes an imbalance between angiotensin II and angiotensin I systems favoring the angiotensin II system. This imbalance may result in the development of frank hyperaldosteronism in cases of severe SARS-CoV-2 virus infection. This increase in activity of the angiotensin II system causes systemic inflammation and may be involved in the pathogenesis of dry cough characterizing the infection. Hypokalemia has been proposed as a marker of disease severity in the new SARS-CoV-2 infection. However, results are as yet inconclusive and more studies are needed to assess the relationship between SARS-CoV-2 severity infection and hypokalemia.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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