Severe Systemic Inflammatory Response Research Articles

Chinese Additive Anti-inflammatory Action for Aortopathy & Arteriopathy (5A)Registry protocol: rationale, design and methodology.

Acute aortic syndrome (AAS) is a life-threatening condition. Inflammation plays a key role in the pathogenesis, development and progression of AAS, and is associated with significant mortality and morbidity. Understanding the inflammatory responses and inflammation resolutions is essential for an appropriate management of AAS. Thirty Chinese cardiovascular centers have collaborated to create a multicenter observational registry (named Chinese Additive Anti-inflammatory Action for Aortopathy & Arteriopathy [5A] registry), with consecutive enrollment of adult patients who underwent surgery for AAS that was started on Jan 1, 2016 and will be ended on December 31, 2040. Specially, the impact of inflammation and anti-inflammatory strategies on the early and late adverse events are investigated. Primary outcomes are severe systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), Sequential Organ Failure Assessment (SOFA) scores at 7 days following this current surgery. Secondary outcomes are SISR, 30-day mortality, operative mortality, hospital mortality, new-onset stroke, acute kidney injury, surgical site infection, reoperation for bleeding, blood transfusion and length of stay in the intensive care unit. The analysis of this multicenter registry will allow our better knowledge of the prognostic importance of preoperative inflammation and different anti-inflammatory strategies in adverse events after surgery for AAS. This registry is expected to provide insights into novel different inflammatory resolutions in management of AAS beyond conventional surgical repair. ClinicalTrials.gov Identifier:NCT04398992 (Initial Release: 05/19/2020).

Risk Factors and Electromyographic Characteristics of Acquired Weakness in Critically Ill Patients: A Retrospective Study.

This retrospective study examines risk factors and electromyographic (EMG) characteristics associated with acquired weakness in critically ill patients and assesses their impact on patient prognosis. Ninety-seven critically ill patients, ventilated for over 48 hours, were included. Patient data, encompassing general condition, medical history, Medical Research Council (MRC) scores, serum markers (c-reactive protein, calcitonin gene, albumin, brain natriuretic peptide, urea nitrogen, creatinine), EMG characteristics, respiratory treatment modalities, and parameters, were recorded. Mechanical ventilation duration, ICU stay duration, hospitalization duration, and patient prognosis were documented. Based on MRC scores, patients were categorized into the ICU-acquired weakness (ICU-AW) group (MRC <48 points) and the non-ICU-AW group (MRC ≥48 points). The study comprised 47 ICU-AW and 50 non-ICU-AW patients. Significant differences (p <0.05) were observed in age, MRC scores, albumin levels, c-reactive protein, calcitonin gene, brain natriuretic peptide, urea nitrogen, creatinine, mechanical ventilation duration, ICU stay duration, and hospitalization duration between groups. In the ICU-AW group, nerve conduction examinations revealed slow conduction velocity, reduced wave amplitude, and in severe cases, a complete loss of motor and sensory potentials. Multivariate logistic analysis identified low serum albumin levels and MRC scores as potential ICU-AW risk factors. This study suggests that low serum albumin levels and MRC scores may contribute to ICU-AW risk. The ICU-AW group exhibited varied peripheral nerve damage and slow conduction velocities on EMG. Additionally, severe systemic inflammatory responses, renal function, brain natriuretic peptide levels, prolonged mechanical ventilation, and peripheral nerve damage may be associated with ICU-AW. Follow-up studies are essential for further understanding these complex interactions.

Desenlace fatal en paciente con coinfección entre SARS-CoV-2 y dengue

COVID-19, a result of SARS-CoV-2 infection, is characterized by a primary impact on the alveolar cells of the respiratory system. However, the possibility of co-infection with dengue virus (DENV) has been documented, triggering a severe systemic inflammatory response. This heightened inflammatory response leads to a substantial release of viral RNA into the cellular cytoplasm, which amplifies the viral load and aggravates lung damage, causing multiple organ dysfunction. In the case of DENV, the infection induces a cytokine storm that increases capillary permeability, resulting in plasma leakage. The present report aims to describe a case of an adult male patient with COVID-19 and dengue co-infection who had a fatal outcome.

Serotonin Signaling and the Hyperpermeable Endothelial Barrier in Sepsis: Clues to a Molecular Mechanism.

Sepsis is characterized by a severe systemic inflammatory response caused by hyperpermeability of the endothelial barrier resulting microvascular leakage, which is a leading factor to multiorgan failure. In sepsis, the hyperpermeable endothelial cells contribute to the activation of platelets, which release numerous mediators that affect coagulation, inflammatory response and are believed to directly or indirectly affect the integrity of the endothelial barrier. One such mediator is serotonin (5-hydroxytryptamine, 5-HT), a signaling molecule which mediates a number of cellular functions including regulation of cytoskeletal dynamics associated with barrier function of endothelial cells. The actions of 5-HT are mediated by different types of receptors and terminated via an uptake mechanism of a 5-HT transporter (SERT) on the platelet and endothelial cell. Earlier studies revealed unexpected discoveries concerning the impact of 5-HT signaling on the permeability of the endothelial barrier. These findings have been supported by the clinical reports on the anti-inflammatory property of 5-HT reuptake inhibitor, SSRIs in treating sepsis-related morbidity and mortality. This review focuses on a wide-range of literature to pinpoint cellular and molecular mechanisms that mediate 5-HT-induced microvascular injury in sepsis pathogenesis.

Effects of combustible cigarettes and electronic nicotine delivery systems on the development and progression of chronic lung inflammation in mice.

Although detrimental effects of combustible cigarettes (CCs) on the progression of lung inflammatory diseases are well known, changes in electronic nicotine delivery systems (ENDS)-exposed lung-infiltrated immune cells are still unrevealed. The analysis of blood gas parameters, descriptive and quantitative histology of lung tissues, determination of serum cytokines, intracellular staining and flow cytometry analysis of lung-infiltrated immune cells were used to determine the differences in the extent of lung injury and inflammation between mice from experimental (CC and ENDS-exposed animals) and control group (Air-exposed mice). Continuous exposition to either CCs or ENDS induced severe systemic inflammatory response, increased activation of NLRP3 inflammasome in neutrophils and macrophages and enhanced dendritic cell-dependent activation of Th1 and Th17 cells in the lungs. ENDS induced less severe immune response than CCs. Serum concentrations of inflammatory cytokines were significantly lower in the samples of ENDS-exposed mice. Compared to CCs, ENDS recruited lower number of circulating leukocytes in injured lungs and had less capacity to induce CD14/TLR-2-dependent activation of NLRP3 inflammasome in lung-infiltrated neutrophils and macrophages. ENDS-primed dendritic cells had reduced capacity for the generation of Th1 and Th17 cell-driven lung inflammation. Accordingly, extensive immune cell-driven lung injury resulted in severe respiratory dysfunction in CCs-exposed mice, while ENDS caused moderate respiratory dysfunction in experimental animals. Continuous exposition to either CCs or ENDS induced immune cell-driven lung damage in mice. ENDS triggered immune response which was less potent than inflammatory response elicited by CCs and, therefore, caused less severe lung injury and inflammation. This is the first study that compared the effects of CCs and ENDS on lung-infiltrated immune cells. Although both CCs and ENDS elicited systemic inflammatory response, immune cell-driven lung injury and inflammation were less severe in ENDS-exposed than in CC-exposed animals. Continuous exposition to ENDS-sourced aerosols was less harmful for respiratory function of experimental animals than CC-derived smoke.

Cytokine storm and severe hepatitis in pregnancy due to herpes simplex virus 2

Case presentationA pregnant woman developed hepatitis due to a herpes simplex virus 2 primary infection with a severe systemic inflammatory response. Treatment with acyclovir and human immunoglobulin was given and both mother and baby survived.PurposeWe provide the first description of the inflammatory response associated with herpetic hepatitis in pregnancy.

IRAK3-mediated suppression of pro-inflammatory MyD88/IRAK signaling affects disease severity in acute pancreatitis

Acute pancreatitis (AP), which is characterized by self-digestion of the pancreas by its own prematurely activated digestive proteases, is a major reason for hospitalization. The autodigestive process causes necrotic cell death of pancreatic acinar cells and the release of damage associated molecular pattern which activate macrophages and drive the secretion of pro-inflammatory cytokines. The MYD88/IRAK signaling pathway plays an important role for the induction of inflammatory responses. Interleukin-1 receptor associated kinase-3 (IRAK3) is a counter-regulator of this pathway. In this study, we investigated the role of MYD88/IRAK using Irak3−/− mice in two experimental animal models of mild and severe AP. IRAK3 is expressed in macrophages as well as pancreatic acinar cells where it restrains NFκB activation. Deletion of IRAK3 enhanced the migration of CCR2+ monocytes into the pancreas and triggered a pro-inflammatory type 1 immune response characterized by significantly increased serum levels of TNFα, IL-6, and IL-12p70. Unexpectedly, in a mild AP model this enhanced pro-inflammatory response resulted in decreased pancreatic damage, whereas in a severe AP model, induced by partial pancreatic duct ligation, the increased pro-inflammatory response drives a severe systemic inflammatory response syndrome (SIRS) and is associated with an increased local and systemic damage. Our results indicate that complex immune regulation mechanism control the course of AP, where moderate pro-inflammation not necessarily associates with increased disease severity but also drives tissue regenerative processes through a more effective clearance of necrotic acinar cells. Only when the pro-inflammation exceeds a certain systemic level, it fuels SIRS and increases disease severity.

Anti-inflammatory Effect of Low-Intensity Ultrasound in Septic Rats.

Sepsis is a severe systemic inflammatory response caused by infection. Here, the spleen region of Sprague-Dawley (SD) rats with sepsis was irradiated with low-intensity ultrasound (LIUS) to explore the regulation of inflammation and its mechanism by LIUS. In this study, 30 rats used for survival analysis were randomly divided into the sham-operated group (Sham, n=10), the group in which sepsis was induced by cecal ligation and puncture (CLP, n=10) and the group treated with LIUS immediately after CLP (LIUS, n=10). The other 120 rats were randomly divided into the aforementioned three groups for detection at each time point. The parameters used in the LIUS group were 200 mW/cm2, 0.37 MHz, 20% duty cycle and 20 min, and no ultrasonic energy was produced in the Sham and CLP groups. Seven-day survival rate, histopathology and expression of inflammatory factors and proteins were evaluated in the three groups. LIUS was able to improve the survival rate of septic SD rats (p < 0.05), significantly inhibit the expression of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), interleukin 6 (IL-6) and nuclear factor-κB p65 (NF-κB p65) (p < 0.05) and restore the ultrastructure of the spleen. Our study determined that LIUS can relieve spleen damage and alleviate severe cytokine storm to improve survival outcomes in septic SD rats, and its mechanism may be related to the inhibition of the NF-κB signaling pathway by downregulation of IL-1β.

Bone mesenchymal stromal cell-derived small extracellular vesicles inhibit inflammation and ameliorate sepsis via delivery of microRNA-21a-5p

Background aimsSepsis is a potentially life-threatening disease that results from a severe systemic inflammatory response due to infection. Mesenchymal stromal cell-derived small extracellular vesicles (MSC sEVs) are able to transfer bioactive molecules and have been demonstrated to play an important role in the pathophysiological process of sepsis. Herein the authors aimed to investigate the potential role and downstream molecular mechanism of MSC sEVs in sepsis. MethodsMSC sEVs were acquired by ultracentrifugation and then injected into a cecal ligation and puncture mouse model. The efficacy of MSC sEVs in both in vitro and in vivo models of sepsis was evaluated. ResultsMSC sEV therapy improved survival, reduced sepsis-induced inflammation, attenuated pulmonary capillary permeability and improved liver and kidney function in septic mice. In addition, the authors found that microRNA-21a-5p (miR-21a-5p) was highly enriched in MSC sEVs, could be transferred to recipient cells, inhibited inflammation and increased survival in septic mice. Furthermore, the authors demonstrated that MSC sEV miR-21a-5p suppressed inflammation by targeting toll-like receptor 4 and programmed cell death 4. The therapeutic efficacy of MSC sEVs was partially abrogated by transfection with miR-21a-5p inhibitors. ConclusionsCollectively, the authors’ data suggest that miR-21a-5p-bearing MSC sEVs may be a prospective and effective sepsis therapeutic strategy.

Vitronectin promotes immunothrombotic dysregulation in the venular microvasculature.

Microvascular immunothrombotic dysregulation is a critical process in the pathogenesis of severe systemic inflammatory diseases. The mechanisms controlling immunothrombosis in inflamed microvessels, however, remain poorly understood. Here, we report that under systemic inflammatory conditions the matricellular glycoproteinvitronectin (VN) establishes an intravascular scaffold, supporting interactions of aggregating platelets with immune cells and the venular endothelium. Blockade of the VN receptor glycoprotein (GP)IIb/IIIa interfered with this multicellular interplay and effectively prevented microvascular clot formation. In line with these experimental data, particularly VN was found to be enriched in the pulmonary microvasculature of patients with non-infectious (pancreatitis-associated) or infectious (coronavirus disease 2019 (COVID-19)-associated) severe systemic inflammatory responses. Targeting the VN-GPIIb/IIIa axis hence appears as a promising, already feasible strategy to counteract microvascular immunothrombotic dysregulation in systemic inflammatory pathologies.

Effect of Anticoagulant Versus Non-Anticoagulant Therapy on Mortality of Sepsis-Induced Disseminated Intravascular Coagulation: A Systematic Review and Meta-Analysis.

Sepsis is a syndrome of severe systemic inflammatory response. When combined with disseminated intravascular coagulation, mortality is increased. The need for anticoagulant therapy is still the focus of debate. PubMed, Embase, Cochrane Library, and Web of Science were searched. Adult patients with sepsis-induced disseminated intravascular coagulation were included in this study. All-cause mortality as efficacy and serious bleeding complications as adverse effect were measured as primary outcomes. Methodological quality of included studies were assessed using the Methodological Index for Non-randomized Studies (MINORS). Meta-analysis was performed using R software (version 3.5.1) and Review Manager (version 5.3.5). There were nine eligible studies with 17,968 patients included. There were no significant reductions in mortality between the anticoagulant group and the non-anticoagulant group (RR, 0.89; 95% CI, 0.72-1.10; P = 0.27). The DIC resolution rate in the anticoagulation group has a statistically significant increase compared with the control group [OR: 2.62, 95% CI (1.54-4.45), P < 0.05]. And there was no significant difference in bleeding complications between the two groups (RR, 1.27; 95% CI, 0.77-2.09; P = 0.69). SOFA score reduction did not change significantly between the two groups (P = 0.13). Our study observed no significant benefit of anticoagulant therapy on mortality of sepsis-induced DIC. Anticoagulation therapy can promote DIC resolution in sepsis-induced DIC. In addition, anticoagulant therapy does not increase the risk of bleeding in these patients.

Rapid genome sequencing identifies novel variants in complement factor I.

Complement factor I deficiency (CFID; OMIM #610984) is a rare immunodeficiency caused by deficiencies in the serine protease complement factor I (CFI). CFID is characterized by predisposition to severe pneumococcal infection, often in infancy. We report a previously healthy adolescent male who presented with respiratory failure secondary to pneumococcal pneumonia and severe systemic inflammatory response. Rapid genome sequencing (rGS) identified compound heterozygous variants in CFI in the proband, with a novel maternally inherited likely pathogenic variant, a single nucleotide deletion resulting in premature stop (c.1646del; p.Asn549ThrfsTer25) and a paternally inherited novel likely pathogenic deletion (Chr 4:110685580-110692197del).

A genome-wide association study of survival in patients with sepsis

BackgroundSepsis is a severe systemic inflammatory response to infections that is accompanied by organ dysfunction and has a high mortality rate in adult intensive care units. Most genetic studies have identified gene variants associated with development and outcomes of sepsis focusing on biological candidates. We conducted the first genome-wide association study (GWAS) of 28-day survival in adult patients with sepsis.MethodsThis study was conducted in two stages. The first stage was performed on 687 European sepsis patients from the GEN-SEP network and 7.5 million imputed variants. Association testing was conducted with Cox regression models, adjusting by sex, age, and the main principal components of genetic variation. A second stage focusing on the prioritized genetic variants was performed on 2,063 ICU sepsis patients (1362 European Americans and 701 African-Americans) from the MESSI study. A meta-analysis of results from the two stages was conducted and significance was established at p < 5.0 × 10−8. Whole-blood transcriptomic, functional annotations, and sensitivity analyses were evaluated on the identified genes and variants.FindingsWe identified three independent low-frequency variants associated with reduced 28-day sepsis survival, including a missense variant in SAMD9 (hazard ratio [95% confidence interval] = 1.64 [1.37–6.78], p = 4.92 × 10−8). SAMD9 encodes a possible mediator of the inflammatory response to tissue injury.InterpretationWe performed the first GWAS of 28-day sepsis survival and identified novel variants associated with reduced survival. Larger sample size studies are needed to better assess the genetic effects in sepsis survival and to validate the findings.

Can endoscopic retrograde cholangiopancreatography-related procedures for resolving acute cholangitis be effectively and safely performed in patients with surgically altered anatomy? Comparison study to evaluate the timing of short-type single-balloon enteroscopy-assisted endoscopic retrograde cholangiopancreatography.

Balloon enteroscopy (BE)-assisted endoscopic retrograde cholangiopancreatography (ERCP)-related procedures to resolve acute cholangitis (AC) in patients with surgically altered anatomy (SAA) are limited. There is a lack of evidence on whether the timing of BE-assisted ERCP affects clinical outcomes in patients with AC. This study aimed to evaluate the clinical outcomes of short-type single-balloon enteroscopy (short SBE)-assisted ERCP in patients with SAA and AC. Patients with AC who underwent short SBE-assisted ERCP procedures between September 2011 and April 2022 were retrospectively reviewed. The outcomes of procedures undergone at ≤24 h and >24 h were compared. The primary outcome was the length of stay (LOS). Overall, 56 patients underwent procedures at ≤24 h, and 58 patients at >24 h. The procedural success and adverse event rates of short SBE-assisted ERCP were 87.7% (95% confidence interval [CI] 80.3-93.1%) and 4.4% (95% CI 1.4-9.9%), respectively. Patients with severe (Grade III) AC and systemic inflammatory response syndrome were more in early (at ≤24 h) ERCP groups. LOS and median time from ERCP procedures to discharge were shorter in the early group. Procedural success and adverse event rates between both groups had no significant differences. Multivariable linear regression analysis showed that ERCP performed at ≤24 h was associated with shorter LOS, while severe cholangitis and malignant biliary obstruction were associated with longer LOS. Short SBE-assisted ERCP is effective and safe in patients with SAA and AC. Early procedures seemed to attribute early improvement of general condition, thus shortening the LOS.

Bifidobacterium spp. and their metabolite lactate protect against acute pancreatitis via inhibition of pancreatic and systemic inflammatory responses

ABSTRACT Severe acute pancreatitis (SAP) is a critical illness characterized by a severe systemic inflammatory response resulting in persistent multiple organ failure and sepsis. The intestinal microbiome is increasingly appreciated to play a crucial role in modulation of AP disease outcome, but limited information is available about the identity and mechanism of action for specific commensal bacteria involved in AP-associated inflammation. Here we show that Bifidobacteria, particularly B. animalis, can protect against AP by regulating pancreatic and systemic inflammation in germ-free (GF) and oral antibiotic-treated (Abx) mouse models. Colonization by B. animalis and administration of its metabolite lactate protected Abx and GF mice from AP by reducing serum amylase concentration, ameliorating pancreatic lesions and improving survival rate after retrograde injection of sodium taurocholate. B. animalis relieved macrophage-associated local and systemic inflammation of AP in a TLR4/MyD88- and NLRP3/Caspase1-dependent manner through its metabolite lactate. Supporting our findings from the mouse study, clinical AP patients exhibited a decreased fecal abundance of Bifidobacteria that was inversely correlated with the severity of systemic inflammatory responses. These results may shed light on the heterogeneity of clinical outcomes and drive the development of more efficacious therapeutic interventions for AP, and potentially for other inflammatory disorders.

The COVID-19 Pandemic and Post-Infection Irritable Bowel Syndrome: What Lies Ahead for Gastroenterologists

The COVID-19 Pandemic and Post-Infection Irritable Bowel Syndrome: What Lies Ahead for Gastroenterologists

Rationale and Initiative of the Impella in Cardiac Surgery (ImCarS) Register Platform.

Cardiac support systems are being used increasingly more due to the growing prevalence of heart failure and cardiogenic shock. Reducing cardiac afterload, intracardiac pressure, and flow support are important factors. Extracorporeal membrane oxygenation (ECMO) and intracardiac microaxial pump systems (Impella) as non-permanent MCS (mechanical circulatory support) are being used increasingly. We reviewed the recent literature and developed an international European registry for non-permanent MCS. Life-threatening conditions that are observed preoperatively often include reduced left ventricular function, systemic hypoperfusion, myocardial infarction, acute and chronic heart failure, myocarditis, and valve vitia. Postoperative complications that are commonly observed include severe systemic inflammatory response, ischemia-reperfusion injury, trauma-related disorders, which ultimately may lead to low cardiac output (CO) syndrome and organ dysfunctions, which necessitates a prolonged ICU stay. Choosing the appropriate device for support is critical. The management strategies and complications differ by system. The "heart-team" approach is inevitably needed.However despite previous efforts to elucidate these topics, it remains largely unclear which patients benefit from certain systems, when is the right time to initiate (MCS), which support system is appropriate, what is the optimal level and type of support, which therapeutic additive and supportive strategies should be considered and ultimately, what are the future prospects and therapeutic developments. The European cardiac surgical register ImCarS has been established as an IIT with the overall aim to evaluate data received from the daily clinical practice in cardiac surgery. Interested colleagues are cordially invited to join the register. DRKS00024560. AZ 246/20 Faculty of Medicine, Justus-Liebig-University-Gießen.

Progress in the clinical treatment of alcoholic hepatitis

Alcoholic hepatitis is a severe and life-threatening systemic inflammatory response syndrome, which has a high incidence and mortality rate worldwide. The severity ranges from asymptomatic liver biochemical disturbances to fulminant liver failure or death; however, there are few effective therapeutic interventions. Maddrey discriminant function not only predicts short-term mortality, but it also guides clinicians to choose appropriate alcoholic hepatitis-specific treatments. Alcohol abstinence, nutritional support, psychological counseling, and infection prevention remain the cornerstones for alcoholic hepatitis treatment. Corticosteroids remain the mainstay of treatment when patients have a good appetite and normal serum creatinine levels, but early liver transplantation is the only life-saving option for steroid-unresponsive patients. New studies have found that gut microbiota is an important therapeutic targets in patients with alcohol hepatitis, and N-acetylcysteine, granulocyte colony-stimulating factor, and metadoxine as adjunctive therapy have a positive effect on patient survival.

PLATELET AGGREGATION IN PATIENTS WITH PULMONARY TUBERCULOSIS AND SYSTEMIC INFLAMMATORY RESPONSE SYNDROME

Platelets play a special role in the systemic inflammatory response syndrome, as they acquire the ability to become activated and aggregate. Literature has no direct evidence of a link between platelet aggregation activity and the severity of the systemic inflammatory response syndrome in patients with pulmonary tuberculosis.&#x0D; The aim of the paper is to study platelet aggregation in patients with pulmonary tuberculosis with severe systemic inflammatory response syndrome.&#x0D; Materials and Methods. Spontaneous and induced by ADP (0.1, 1.0 and 5.0 ml) platelet aggregation was determined by Born turbodynamic method. The study enrolled 27 patients with severe and 33 patients with indolent systemic inflammatory response syndrome Spontaneous and induced by ADP (0.1 and 1.0 ml) platelet aggregation was evaluated in absorbance units (a.u.); platelet aggregation induced by 5.0 ml of ADP was measured in percentage terms. Statistica 10 was used to process the results. Discrepancy tests were used to determine the significance of differences of mean values; McNemar’s test and Fisher’s exact test were used to estimate event rate, p&lt;0.05.&#x0D; Results. In Group 1 spontaneous and induced by ADP (0.1, 1.0 and 5 ml) platelet aggregation was 0.85–2.65 (1.210.1) a.u., 0.81–3.67 (3.030.38) a.u., 1.06–6.25 (6.50.51) a.u., 5–66 % (39.53.6); in Group 2 – 0.84–1.36 (1.10.04) a.u., 0.77–2.49 (2.10.26) a.u., 0.64–5.49 (2.200.08) a.u., 8–66 (35.74.14) %, respectively. Frequency of spontaneous and induced by ADP (0.1, 1.0 and 5 ml) platelet hypoaggregation in Groups 1 and 2 was 33.3 % and 27.3 %; 14.8 % and 24.2 %; 0 % and 39.4 %; 14.8 % and 24.2 %, respectively; frequency of hyperaggregation was 14.8 % and 0 %; 11.1 % and 9.1 %; 29.6 % and 0 %; 0 % and 0 %, respectively.&#x0D; Conclusion. Platelet aggregation activity in patients with pulmonary tuberculosis is determined by the severity of the systemic inflammatory response syndrome. A pronounced systemic inflammatory response syndrome is associated with increased spontaneous and induced by ADP (1.0 ml) platelet aggregation in 14.8 % and 29.6 % of cases, respectively.

Case reports: spondylodiscitis and epiduritis after suffering COVID-19

Background: The study analyzes a possible rare complication of COVID-19 in the form of spondylodiscitis, including that followed by epiduritis, in patients who survived COVID-19 characterized by severe pneumonia, respiratory failure and systemic inflammatory response syndrome (SIRS).&#x0D; Clinical case description: Three clinical cases of patients are presented, each of whom had high fever, SIRS with a significant increase in the laboratory markers of inflammation (C-reactive protein (CRP), leukocytosis, erythrocyte sedimentation rate (ESR), fibrinogen, procalcitonin, ferritin), bacterial pneumonia, and severe hemostasis disorders. Despite an antibiotic therapy with broad-spectrum drugs, the development of spondylodiscitis was observed, manifested as acute pain syndrome in the lumbar spine. In the first patient, against the background of a massive antibacterial therapy, revisions of purulent foci, therapy with glucocorticosteroids (GCS), and a surgical treatment, there was significant positive dynamics in the form of the pain syndrome relief. The second patient showed positive dynamics against the background of a conservative antibacterial therapy. The third patient, with a paravertebral abscess at the level of developed spondylodiscitis, received a massive antibiotic therapy combined with GCS, and was operated for the spinal cord decompression.&#x0D; Conclusion: Spondylodiscitis and epiduritis may be possible complications of COVID-19, including those resulting from the immunosuppressive therapy, which is actively used to stop the cytokine storm.