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12MEDICAL SCIENCES
A CASE OF MULTISYSTEM INFLAMMATORY SYNDROME IN AN ADULT PATIENT
Ospanbekova N.
Kazakh-Russian Medical University, Department of Infectious Diseases, Head of the Department, Associate Professor
Suleimenova Z. KRMU, Associate Professor,
Doskozhaeva S.
KRMU, D.m.s, Associate Professor Dmitrovskiy A. D.m.s., Professor
Ospanbekova A
KazNMU, teacher
Abstract
The new MERS-COV-2 infection causes the development of multisystem inflammatory syndrome not only in children, but also in adults. General practitioners involved in the diagnosis and treatment of patients with COVID-19 should take into account the possibility of developing this syndrome in adult patients using the criteria of SDS.
Keywords: multisystem inflammatory syndrome, COVID-19 coronavirus infection.
The U.S. Centers for Disease Control and Prevention (CDC) has reported cases of Multisystem Inflammatory Syndrome (MIS) in adults. CDC experts suggest that a syndrome similar to MIS may develop in adults of all ages during or after coronavirus infection, clinical manifestations of MIS may develop 2-5 weeks after the manifest form of COVID-19. The interval between infection and the development of MIS is not completely clear. There are isolated cases without previous respiratory symptoms, which makes it difficult to determine the date of initial infection.
The purpose of the study: to familiarize general practitioners with the clinical manifestations of Multisystem Inflammatory Syndrome in adults.
According to the review published by the SDS on 27 cases of Multisystem Inflammatory Syndrome in adults (MIS-A), criteria for making this diagnosis were identified (1):
- severe disease requiring hospitalization in persons 21 years and older;
- positive test result for current infection or previous SARS-COV-2 infection (determination of genetic material or antibodies) during hospitalization or in the previous 12 weeks;
- severe dysfunction of 1 or more organ systems, with the exception of respiratory (for example: hypotension or shock, cardiac dysfunction arterial or venous thrombosis or thromboembolism, acute liver damage);
- laboratory signs of severe inflammation (elevated levels of CRP, ferritin, D-dimer, interleukin 6);
- absence of severe respiratory disease (to exclude a patient whose inflammation and organ dysfunction may be associated with tissue hypoxia).
respiratory symptoms, which makes it difficult to determine the date of initial infection.
Material and methods.
Male, 42 yers old, was admitted to inpatient treatment 1 month after the onset of the disease.
History of disease: Has been acutely ill since the first days of December 2020. There were abdominal pains, subfebrile body temperature, without chills and sweats and loose stools 3 times a day, for 3 days. At the same time, he noted a skin, non-itchy rash with a predominant location on the face (figure), stiffness after nights, swelling of the hands and face appeared.
Figure. Rash on the face
He sought medical help at his place of residence, was diagnosed with ARVI and prescribed appropriate therapy, without any effect. During the tests, hematuria was recorded. Due to the lack of effect from the treatment, the patient was admitted to inpatient treatment in Almaty.
A hospital examination revealed changes in the general blood test (table).
The dynamics of general blood tests
Table.
№ Red blood cells, 10A12/l Hemoglobin, g/l Platelets, 10A9/l Leukocytes, 10A9/l r- sh.n1, % s.n2% Lymphocytes, % (10A9/l) Monocytes, % ESR, mm/h
1 3,45 98 116 4,2 11 72 16 (0,672) 1 47
2 3,0 92 140 2,7 TNG 3+ 6 62 24 (0,648) 7 45
3 3,2 95 129 3,0 TNG 3+ 5 64 25 (0,750) 6 45
1 r-sh.n - rod - shaped neutrophils, 2c/a - segmented neutrophils, 3TNG - toxic neutrophils granularity
There was the presence of hypochromic anemia, thrombocytopenia, leukopenia with absolute lympho-penia, which indicated a significant inflammatory process with bone marrow damage. This, in turn, was indicated by neutrophilosis, a rod-shaped shift of the formula to the left, sharply accelerated ESR and the presence of toxic neutrophil granularity.
The study of the general urinalysis revealed the following changes: albuminuria (0.66; 0.099; 0.033 ppm), hematuria (25-30 cells in f/v; 7-10 cells in f/v; 17-18-23 cells in f/v) with mostly unchanged erythrocytes (altered erythrocytes were within 5-7 in f/v, 1-2 in f/v, 3-4 in f/v), cylindrical due to hyaline cylinders (0-1-2 in f/v; 2-3 in f/v; 0-1 in f/v). A urine test by the Nechiporenko method found an increased content of red blood cells 3000 in f/v and leukocytes 4250 in f/v, indicating kidney damage by the type of glomerulone-phritis.
Indicators of biochemical liver samples twice showed an increased content of blood amylase (106 units, 118 units) without any pancreatitis clinic and an increase in the thymol sample (8.55 units). Indicators of ALT, AST, total bilirubin and total protein were within normal limits.
The results of the coagulogram revealed multidirectional, moderate changes: an undefined increase in the activated partial thromboplastin time (APTT) index to 40.7 seconds. and a slight decrease in the indicator of prothrombin time to 9.7 seconds. and increased fibrinogen content up to 4.66 g/l.
Total protein was reduced to 59.3 g/l, albumin - to 45.8 g/l; gamma globulin - increased to 32 g/l. The A/G ratio is 0.84.
Blood ferritin was 604 mcg/l, streptolysin O was 200 IU/ml, procalcitonin was negative, D-dimer was 500 ng/ml. That is, there was not bacterial inflammatory syndrome.
ELISA for antibodies to SARS CoV 2 revealed the presence of IgM - 1834 AU/ml and IgG - 54 351 AU/ml antibodies. These results obtained a month after the onset of the disease confirm the diagnosis of COVID-19.
There are several hypotheses for the development of MIS-A, for example, antibodies that are produced against COVID-19 disrupt the body's work, when it is not the virus itself that kills the macroorganism, but the immune response to it" (2).
Ultrasound examination revealed a compaction and increased echolithicity of the hepar parenchyma, a cyst of the right kidney. The presence of fluid around the kidneys, hepatic (1140 ml), spleen (380 ml), pelvis
(380 ml), pleural cavities (500-600 ml on the right, 480500 ml on the left), pericardium (170 ml) was also revealed.
Echocardiography noted the presence of an increase in the size of the left ventricle and an effusion into the pericardium.
Computed tomography revealed basal pneu-mosclerosis.
Additional examinations excluded the presence of other infectious diseases.
Thus, it can be concluded that a patient who has suffered an acute COVID-19 infection has developed a multisystem inflammatory syndrome, which is primarily indicated by clinical symptoms of the disease, prolonged subfebrility, abdominal pain with diarrhea, skin lesions and multiple organ pathology:
- lungs: basal pneumosclerosis;
- heart: an increase in the size of the left ventricle with fluid effusion into the pericardium;
- kidneys: changes in the type of glomerulonephri-
tis;
- pancreas: twice elevated blood amylase levels;
- polyserositis: fluid in the pelvis, pericardium, pleural cavities, around the kidneys, hepar, spleen;
- hepar: violation of protein metabolism;
- morning stiffness in large joints and swelling of the hands and face;
- skin: hemorrhagic rash, more on the face, not itchy, with different sizes of elements;
- typical blood changes (hypochromic anemia, leukopenia, thrombocytopenia, lymphopenia);
- high rates of IgM and IgG to SARS CoV 2.
When COVID-19 at any age often develop autoimmune diseases and pathology of the lungs and other organs and tissues caused not only by the action of the virus, but also autoimmune reaction (2).
Thus, in this case according to the criteria of the CDC, the patient had the presence of antibodies to SARS-COV-2, verifying the presence of infection, multiple organ lesions, elevated ferritin and D-dimer.
Later, positive results of the examination for autoimmune diseases were revealed: antinuclear factor 1:1280 and antibodies to ds DNA for Critidia luciliae 1:160 (norm 1:10).
Exacerbation of chronic diseases may be added to the multi-inflammatory syndrome in adults, and coro-navirus can serve as both a cause and a trigger for exacerbation of diseases (2).
Conclusion
A clinical case of Multisystem Inflammatory Syndrome in an adult patient who developed a month after
the onset of the disease is the result of SARS-COV-2, which subsequently led to an autoimmune disease.
References
1. Case Series of Multisystem Inflammatory Syndrome in Adults Associated with SARS-CoV-2 Infection — United Kingdom and United States, March-
August 2020. Weekly / October 9, 2020 / 69(40);1450-1456.
2. Izvestiaiz.ru. June 14, 2021. COVID's shadow: a dangerous syndrome affects 4 organ systems of those who have been ill. Why patients develop multi-inflammation.
