ABSTRACT
Case Report: Protein losing enteropathy (PLE) occurs when proteins leak from the gastrointestinal (GI) system more rapidly than they are produced. Inflammation of the GI tract facilitates increased membrane permeability of gastric mucosa, leading to excess protein leakage. 1 PLE in children has been associated with CMV, rotavirus, COVID-19, HIV, C. difficile, and autoimmune diseases like Crohn's Disease. 2-6 Norovirus is a known cause of PLE in immunocompromised pediatric patients. 7-8 However, to our knowledge, there are no case reports about PLE precipitated by norovirus in immunocompetent pediatric patients. The purpose of this case report is to present a case of PLE precipitated by a norovirus infection in a 4- year-old previously healthy child. While the above gastrointestinal viruses have been proposed as precipitators for this disease, PLE precipitated by norovirus infection has not been well described. This case also highlights the importance of early diagnosis and management to avoid complications. Method(s): Our patient initially presented with two days of abdominal pain, diarrhea, emesis, reduced urine output, and swelling of the lower extremities. He was exposed to several sick family members-his sister had upper respiratory symptoms and his grandmother had gastrointestinal symptoms. Physical exam was notable for diminished breath sounds in the right lower lobe, abdominal distension with diffuse tenderness and dullness to percussion, significant scrotal and penile edema, and bilateral lower extremity pitting edema. Laboratory results revealed leukocytosis, hypoalbuminemia, hyponatremia, elevated aspartate aminotransferase (AST), and elevated serum alpha-1-antitrypsin, as well as low Immunoglobulins G and M. CD3 and CD4 levels were low reflecting cellular immune dysregulation seen in patients with PLE. IgA and Tissue Transglutaminase (TTF) were within normal limits. Ebstein Barr Virus and cytomegalovirus IgM antibodies were negative. COVID IgG was negative as well. His Polymerase chain reaction (PCR) gastrointestinal panel was positive for norovirus. A chest X-ray showed a large right pleural effusion. Abdominal CT revealed large ascites slightly more predominant in the upper abdomen, mesenteric lymphadenitis, and bilateral pleural effusions. Echocardiogram showed small anterior and apical pericardial effusions. Result(s): Based on the patient's elevated serum alpha-1 antitrypsin levels, hypoalbuminemia, low levels of immunoglobulins and lymphocytes, and clinical manifestations of ascites, bilateral pleural effusions, pericardial effusion, and dependent edema, along with a positive PCR for norovirus, the diagnosis of PLE secondary to Norovirus was made. Conclusion(s): This case demonstrates the importance of recognizing viruses like Norovirus as potential causes of PLE to avoid a delay in diagnosis and initiation of therapy, and to avoid unnecessary additional testing. Copyright © 2023 Southern Society for Clinical Investigation.
ABSTRACT
Background and Aim: Whilst most commonly recognised as a res-piratory pathogen, COVID-19 can also result in a variety of extrapulmonary manifestations including myocardial dysfunction and arrhythmia. We report a case of a 15 year old girl with repaired atrioventricular septal defect, presenting with arrhythmia and sud-den severe cardiac failure masked by COVID-19 positivity. Method(s): A 15 year old girl with repaired atrioventricular septal defect and tetralogy of Fallot, under regular follow up with asymp-tomatic moderate to severe atrioventricular valve dysfunction, pre-sented with one month's history of progressive breathlessness to her local hospital. Onset of illness coincided with typical COVID-19 symptoms;her family, attributing her deterioration to this, delayed seeking medical help. She was rapidly referred to our unit. The heart failure severity, which included diffuse dependent oedema, large pleural effusion and severe biventricular dysfunc-tion, could not be attributed to major valve function change. Moreover, deterioration had occurred rapidly without apparent ongoing cause, after extensive diagnostics. Tachyarrhythmia was suspected;initial adenosine challenge via peripheral vein was inconclusive. Diuretics, inotrope and empirical administration of amiodarone provided limited response;the patient was therefore ventilated, enabling further adenosine challenge via central line, which revealed atrial flutter. Shortly after conversion to sinus rhythm and pleural drainage, her biventricular function improved to near normal. Result(s): Redo surgery was undertaken. Firstly, this included mechanical valve replacement of left and right atrioventricular valves and ablation of the isthmus. Secondly, a permanent pace-maker was inserted a few days later. The patient made a quick and uneventful recovery and was discharged on day 10 with good biventricular function on minimal medical therapy and no symptoms. Conclusion(s): Our case highlights delayed presentation as a hidden effect of the COVID-19 pandemic, and that sudden deterioration in stable children with repaired congenital heart disease should prompt the clinician to exclude all reversible causes of de-stabili-sation, and in particular to maintain high suspicion of arrhythmia.