- D3.527 - Multisystem Inflammatory Syndrome in Children (MIS-C) as a Condition Resulting from Immune Dysregulation: What has Coronavirus Infection Taught Us? (Case Study)

The spread of coronavirus infection began in 2019 and soon covered many countries. However, after the transfer of COVID-19, damage to many organs was detected. The clinical manifestation included symptoms characteristic of KAWASAKI disease; multisystem inflammatory syndrome, which was characterized by damage to many organs in pediatric age, was a significant challenge for doctors. It is known as Kawasaki-like multisystem inflammatory syndrome. It was first observed in Pakistan, Lahore and Islamabad, later in Great Britain; in Georgia, Tbilisi, at the M. Iashvili Children's Central Clinic, the number of such cases is about 150 during 2019-2022.

The aim of the study was to compare pediatric patients with multisystem inflammatory syndrome and patients with Kawasaki disease. We studied the history of 40 patients, 30 with multisystem inflammatory syndrome and 10 with Kawasaki disease. The patients were of both sexes and were up to 16 years of age.

The exact etiopathogenesis of multisystem inflammatory syndrome and Kawasaki disease is unknown. According to the results of our study, the average age of patients with multisystem inflammatory syndrome was 10, and of Kawasaki disease - 2. Gastrointestinal problems, such as diarrhea, abdominal distension, and pain, were the leading symptoms in patients with MIS-C, while this was observed in only 1 patient with Kawasaki disease. Myocarditis was observed in 5 out of 30 patients, while cardiovascular problems were not detected in Kawasaki disease. According to paraclinical data, troponin, ferritin, and C-reactive protein were increased in 25 out of 30 patients, and in the case of Kawasaki disease, only C-reactive protein in 3 patients. Lymphopenia was detected in 20 out of 30 patients. Lymphopenia was not detected in Kawasaki disease. The overall presentation of MIS-C appears to overlap with KD. However, there are still great differences between the syndromes, and it is controversial to say whether MIS-C is a new entity or is a “severe type” of KD.

Several clinical features overlap between MIS-C and KD. These 2 entities share inflammatory characteristics, indicating that MIS-C and KD may belong to the same broad umbrella of inflammatory disorders involving the master cytokine IL-1β, but differ in many aspects of etiology, demography, epidemiology, clinical and laboratory findings, as well as pathology. The intensity of the inflammatory response and long-term cardiovascular sequelae diverge between KD and MIS-C. Whereas MIS-C presents with a more intense inflammatory syndrome, KD vasculitis is associated with pathologic changes in the coronary arteries and associated with long-term cardiovascular sequelae. The 2 to 6 weeks delay between SARS-CoV-2 exposure and MIS-C development may account for the development of the autoinflammatory response involving dysregulated B and T cell responses, plasmablast differentiation, and autoantibody production. While the general hypothesis is that KD is triggered by a viral infectious agent(s), the causative agents remain unidentified, and whether KD can be considered a postinfectious syndrome, like MIS-C, remains unclear. In conclusion, the data available so far support the hypothesis that MIS-C and KD belong to the same broad spectrum of inflammatory disorders but with clearly distinct etiopathology.