ABSTRACT
Case report: Chronic urticaria is defined as the presence of urticaria for a period exceeding six weeks. Infections are known as possible triggers for urticaria manifestations, and, as such, SARS-CoV- 2 infection can be recognized as causative. An 8-year- old boy, with a previous history of idiopathic chronic urticaria, came to the Emergency Department for the appearance of generalized urticaria and lips angioedema associated with vomit and shortening of breath normal vital signs by age. Thus, due to the significant reaction, intravenous corticosteroids and antihistamines were promptly administered, with a rapid improvement of symptoms. Since the systemic reaction, the tryptase dosage was performed with the identification of an elevation at the time of the arrival and a complete normalization after the twelfth hour from the beginning of the reaction. Figure 1 shows the kinetic of the tryptase over time. SARS-CoV2 swab was performed before hospitalization and a positive test was identified. To investigate the etiopathogenesis of reaction, the patient was submitted to the extensive clinical, laboratory, and instrumental investigations that revealed only a positive in vitro basophil activation test (BAT) as evidence of functional serum histamine-releasing autoantibodies that are directed against IgE or high-affinity IgE receptors. The viral infection did not need any medication, and the urticaria was resolute in a couple of days. Daily treatment with oral antihistamines was then prescribed, and no further urticarious episodes occurred. A negative SARS-CoV- 2 swab was detected within 12 days of beginning symptoms. Approximately 40% of patients with idiopathic chronic urticaria have circulating antibodies versus IgE epitopes or the IgE receptor, but as it occurs in many autoimmune conditions, the presence of autoantibodies does not necessarily result in a disease phenotype. It is demonstrated that infections can elicit an autoimmune condition, and as our report shows, SARS-CoV2 could explain the reaction observed in our patient. The autoimmune precondition could have been the primer of the systemic reaction, pre-activating the mastocyte degranulation, as the tryptase elevation demonstrated. On the other hand, the SARS-CoV2 virus reducing the ACE2 expression, due to virus endocytosis, could create an imbalance in the RAS system, increasing the bradykinin levels. Bystander activation of pre-activated mastocytes caused by an inflammatory environment could explain the systemic reaction described above.
ABSTRACT
OBJECTIVE: From September 2020, a second wave of COVID-19 pandemic started. We aimed at exploring the impact of SARS-CoV-2 infection in IBD patients during the two waves. PATIENTS AND METHODS: All IBD patients with a confirmed diagnosis of SARS-CoV-2 infection were enrolled. They were sorted into two groups (those infected before September 2020, and those from September 2020 to January 2021) and compared by demographic and clinical data. RESULTS: Twenty-five patients (out of about 600 with a follow-up visit) were infected with SARS-CoV-2 (4.1%). Sixteen were male and the mean age was 46.5 ± 14.3 years (range 24-74). Six were smokers and 11 had comorbidities; 2 were on steroids and 17 on immunosuppressants or biologics. Three patients (12%) needed hospitalization and other three patients were treated with azithromycin, steroids and LMWH, all of them during the second wave. No patient died or developed any sequelae. Two subjects were infected during the first wave (0.3 vs. 3.83, p<0.0001). Non-significant differences were found between the two groups. CONCLUSIONS: A higher number of IBD patients were infected during the second wave. No patient developed a severe form of pneumonia, even those treated with immunosuppressants or biologics. No risk factor for hospitalization was found.