ABSTRACT
Background: Coronavirus disease-2019 (COVID-19) has caused a pandemic that has recently affected every aspect of life. Fortunately, many vaccines with high safety and efficacy profiles were developed timely to face this pandemic. In a very short time, billions of people were vaccinated. In the meantime, a wide range of neurological syndromes are being reported. Guillain-Barre syndrome (GBS) which is a rare immune-mediated post-infectious peripheral neuropathy was reported after both the COVID-19 infection itself and many types of its vaccines. Method(s): We are reporting a case of post-AstraZeneca vaccine GBS and reviewing the literature of all reported post-COVID-19 vaccines GBS till July 2021. Result(s): 29 adult patients were reported. Of them 58.6% were males. Their mean age is 58.2 years. The median time to clinical onset after vaccine administration was 13.2 days. 86.2% of patients had their symptoms following immunization with the 1st dose of AstraZeneca vector-based covid vaccine. Facial palsy was the most predominant single symptom in 75.8% of patients. Conclusion(s): Guillain-Barre syndrome is a well-recognized but still rare adverse event following vaccination against COVID-19. Although preliminary data incriminates viral vector-based vaccines more than the other types, active post-vaccination surveillance and more powerful statistics are mandatory to reach a solid conclusion regarding the presence of a causal relation.Copyright © 2022
ABSTRACT
Introduction The Syndrome of Inappropriate ADH Secretion (SIADH) is one of the most common causes of hyponatremia among medical inpatients. The evolution of SARS-CoV-2 infection over recent years has led to atypical presentations, one being in the form of acute symptomatic hyponatremia secondary to isolated SIADH not associated with pneumonia. CASES We report a series of three unusual cases of Category 2 COVID-19 infection presenting with acute symptomatic hyponatremia secondary to SIADH. All three patients presented with symptoms of acute severe hyponatremia and coincidentally tested positive for SARSCoV- 2 virus without respiratory tract symptoms and normal chest imaging. All patients were fully vaccinated and boosted at least 3 months before the presentation. Clinical and biochemical workup confirmed SIADH in all three patients. They were treated with hypertonic saline in the initial phase, followed by fluid restriction as per recommendations. It was postulated that the inappropriate ADH secretion was mediated by increased inflammatory cytokines, especially interleukin 6 may be a direct effect of the SARS-CoV-2 infection itself. Conclusion In the context of the ongoing COVID-19 pandemic, acute symptomatic hyponatremia without an obvious cause could be an atypical, isolated manifestation of SARS-CoV-2 infection. Awareness of these uncommon presentations is important so that specific treatment protocols or recommendations can be created and instituted to address this likely reversible but potentially fatal presentation of COVID-19.
ABSTRACT
Cerebral Salt Wasting Syndrome (CSW) is an uncommon cause of hypotonic hyponatremia associated to central nervous system disease (especially subarachnoid hemorrhage) and characterized by hypovolemia due to renal sodium loss. The main differential diagnosis is SIADH, a much more common form of hyponatremia without signs of hypovolemia. The treatment is based on filling with isotonic or hypertonic saline. We report the case of a 50-year-old chinese man with a history of arterial hypertension presenting to the ER for headache and fever after vaccination for SARS-CoV-2. In the ER he was hemodynamically stable without neurological deficits. Blood tests showed severe hypoosmolar hyponatremia. Brain CT revealed multiple hypodense oval areas of uncertain nature with peripheral contrast enhancement. The main microbiological tests were negative. In the suspicion of paraneoplastic SIADH, water restriction was prescribed and a total body CT scan was performed, resulting normal. Nevertheless, hyponatremia got worse. Brain MRI revealed signs of subacute intracranial bleeding and angiography showed an anterior cerebral artery aneurysm. An echocardiography revealed collapse of the inferior vena cava, therefore, given the hypovolemia, hypotonic hyponatremia and the signs of recent brain injury, diagnosis of CSW was made. Treatment was based on endovascular coiling of the aneurysm and correction of hypovolemic hyponatremia using isotonic saline. It is essential to differentiate between CWS and SIADH since the treatment is categorically different. Their key distinguishing feature is volemia.
ABSTRACT
Background: COVID-19 is an infectious disease caused by the SARS-CoV-2 virus, particularly known for its respiratory symptoms. Nevertheless, a wide variety of clinical manifestations has been associated with COVID-19, including Kawasaki disease, Guillain- Barré syndrome and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Clinical Case: A 55-years-old woman, affected by immune thrombocytopenia on prednisone therapy, presented with intense fatigue, hyporexia and vomit. She had no fever, no cough, nor other symptoms. She referred a quick prednisone decalage in previous days. ABG showed metabolic alkalosis, severe hyponatremia and hypokalemia. The patient tested positive for SARS-CoV-2. Further investigation showed euvolemic hyponatremia (102 mEq/L) with normal urine osmolality (275 mOsm/Kg), findings consistent with COVID-19-related SIADH. We set a corticosteroid therapy with Prednisone 37,5 mg/die for 5 days, then 25 mg/die for 2 days. After 7 days of hospitalization, the patient tested negative for SARS-CoV-2. In the meantime, kalemia and natremia were back in range. Conclusions: Despite COVID-19 being identified as severe respiratory viral infection, progressively many relevant endocrine manifestations have been reported greatly contributing to the severity of the clinical presentation. There is the urgent need to collect in international multicentric efforts data on all these aspects of the pituitary involvement in COVID-19 patients.