ABSTRACT
Coronavirus disease has many systemic disease symptoms and has severe consequences for the cardiovascular system. Objective. To assess the role of clinical and laboratory indicators in determining the risk of chronic heart failure (CHF) in COV-ID-19 survivors. Material and methods. In total, 151 patients treated in a monoinfectious hospital from 03.11.20 to 10.02.21 with a confirmed diagnosis of COVID-19 were retrospectively selected. Medical history and laboratory data were collected by reviewing electronic medical records. The data included age, gender, body mass index, smoking status, and comorbidities. The laboratory data included the results of hematology and blood chemistry, coagulation, and the levels of acute-phase proteins. The CHF occurrence was used as the study endpoint. Results and discussion. The study patients were divided into two groups depending on the presence of CHF: group 1 included 46 patients with CHF, and group 2 included 105 patients without CHF. The median age was 66.2 (50-92) years;91 (60.3%) were females. Laboratory tests, such as levels of the hs-C-reactive protein, lactate dehydrogenase, procalcitonin, creatinine, and bilirubin, were statistically significantly different in patients of the study groups, and the median values were higher in patients with CHF. Neutrophil-lymphocyte ratio (NLR) showed statistically significant differences between groups: in patients with CHF, the median was 4.97% compared to 3.62% (p=0.011) in those without CHF. The most significant predictors of an increased risk of CHF were age >=66 years (OR=8.038, p<0.001), procalcitonin level >=0.09 ng/mL (increased the CHF risk by 3.8 times, p<0.001), thrombocy-topenia <=220x109/L (p=0.010), an NLR ratio >=4.11% (p=0.010), and a history of chronic kidney disease (p=0.018). Conclusion. A model has been developed to determine the factors closely associated with the risk of chronic heart failure in CO-VID-19 survivors.Copyright © 2023, Media Sphera Publishing Group. All rights reserved.
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Objective: Acute-phase proteins are a family of proteins synthesized by the liver. With this study, we aimed to investigate the effects of COVID-19 infection on acute phase reactants (AFR) and determine the usability of AFRs as prognostic factors in COVID-19 disease. Material(s) and Method(s): Serum samples taken for routine analysis of the patients admitted to the Emergency Department and diagnosed with COVID-19, were used. AFR levels of 30 patients who resulted in mortality and 30 recovered patients were evaluated. C-reactive protein (CRP), ferritin (FER), ceruloplasmin (Cp), albumin (Alb), prealbumin (Prealb), transferrin (Trf), lactate, Acute Physiology and Chronic Health Evaluation (APACHE), and Sequential Organ Failure Assessment (SOFA) assessment was performed. Result(s): The hazard ratio and 95% confidence interval for FER, CRP, lactate, Alb, Cp, Prealb, Trf, Age, SOFA, and APACHE were 1.001 (1.000-1.001), 1.005 (1.001- 1.008), 1.141 (1.016-1.243), 1.016 (0.740-1.399), 1.016 (0.740-1.399), 1.056 (1.017-1.100), 0.978 (0.917-1.035), 1.000 (0.995-1.006), 1.032 (1.004- 1.064), 1.104 (0.971-1.247), and 1.012 (0.974-1.051), respectively, in univariable model. Only CRP, lactate, and FER found significant in multivariable model. In addition, patients in the nonsurvivors group had significantly higher FER, CRP, lactate, APACHE, age, and SOFA. Nonsurvivors also had lower Alb, Prealb, and serum Trf level compared to survivors. Conclusion(s): CRP, lactate, and FER, which we have shown to be significantly higher in severe COVID-19 patients, will be valuable parameters that will contribute to clinical improvement if they are used in the follow-up of patients due to their easy measurement and predictive values.Copyright © 2023, Nobelmedicus. All rights reserved.
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Coronavirus disease has many systemic disease symptoms and has severe consequences for the cardiovascular system. Objective. To assess the role of clinical and laboratory indicators in determining the risk of chronic heart failure (CHF) in COV-ID-19 survivors. Material and methods. In total, 151 patients treated in a monoinfectious hospital from 03.11.20 to 10.02.21 with a confirmed diagnosis of COVID-19 were retrospectively selected. Medical history and laboratory data were collected by reviewing electronic medical records. The data included age, gender, body mass index, smoking status, and comorbidities. The laboratory data included the results of hematology and blood chemistry, coagulation, and the levels of acute-phase proteins. The CHF occurrence was used as the study endpoint. Results and discussion. The study patients were divided into two groups depending on the presence of CHF: group 1 included 46 patients with CHF, and group 2 included 105 patients without CHF. The median age was 66.2 (50-92) years;91 (60.3%) were females. Laboratory tests, such as levels of the hs-C-reactive protein, lactate dehydrogenase, procalcitonin, creatinine, and bilirubin, were statistically significantly different in patients of the study groups, and the median values were higher in patients with CHF. Neutrophil-lymphocyte ratio (NLR) showed statistically significant differences between groups: in patients with CHF, the median was 4.97% compared to 3.62% (p=0.011) in those without CHF. The most significant predictors of an increased risk of CHF were age >=66 years (OR=8.038, p<0.001), procalcitonin level >=0.09 ng/mL (increased the CHF risk by 3.8 times, p<0.001), thrombocy-topenia <=220x109/L (p=0.010), an NLR ratio >=4.11% (p=0.010), and a history of chronic kidney disease (p=0.018). Conclusion. A model has been developed to determine the factors closely associated with the risk of chronic heart failure in CO-VID-19 survivors.Copyright © 2023, Media Sphera Publishing Group. All rights reserved.
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Introduction: Subacute thyroiditis is a self-limiting post-viral inflammatory disorder occurring in 3 phases (hyper-, hypo-, and euthyroidism) Post-vaccine thyroiditis has also been reported, but is rare. Case Description: A 36-year-old Emirati female presented to our clinic with generalized fatigue, mild to moderate vague neck pain, intermittent palpitations, and loss of appetite 2 weeks after receiving her first dose of Pfizer-BioNTech mRNA vaccine against COVID-19. Clinical examination findings and laboratory test results were consistent with subacute thyroiditis. Patient is a mother of 5 healthy children, youngest is breast-fed infant (11 months old). There was no history suggestive of postpartum thyroiditis and no family history of thyroid dysfunction. Physical examination at initial visit showed mild tachycardia, and a normal blood pressure. She weighed 66 kg. Thyroid function tests revealed a suppressed TSH of 0.011 muIU/mL, high Free T4 of >100 pmol/l), and Free T3 FT3 of 29.6 pmol/L. Both TSH receptor antibodies, and Thyroid antibodies (TPO) were negative. Thyroid scintigraphy showed decreased uptake in both lobes. Thyroid ultrasound showed hypoechoic heterogeneous echotexture of the thyroid gland with vascular conglomerate and micro-calcification, along with normal sized reactive lymph nodes at sternal angle. Symptoms aggravated through the next week;patient dropped 3kg of her body weight and her palpitations increased, with a recorded resting heart rate between 120-130 beats/min. TSH decreased to 0.001muIU/mL while FT4 remained high, with an improvement to 90 pmol/L. Subsequently, the patient started to regain weight. Palpitations improved within a month. She developed a biochemically hypothyroid picture followed by clinical and biochemical euthyroidism after one more month. Second dose of the vaccine was uneventful. Last evaluation was 10 months later;TSH, FT3 and FT4 were all in normal range, acute-phase reactants were completely normal and in complete remission. Discussion(s): The exact mechanism for post-vaccination subacute thyroiditis remains unknown, vaccine adjuvants may induce diverse autoimmune and inflammatory reaction. Subacute thyroiditis has rarely been reported with other COVID-19 vaccines contains no Polyethylene glycol (PEG). A possible cross-reactivity between thyroid cell antigens and spike protein of the coronavirus produced by mRNA vaccines might be responsible. Further research is needed to investigate the incidence of subacute thyroiditis in COVID-19 pandemic days.Copyright © 2023
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Objectives: Identifying COVID-19 patients with risk of adverse outcomes at first admission to the intensive care unit has several diagnostic challenges. The concentration of acute phase proteins synthesized by the liver increases or decreases markedly in the serum following inflammation and infection. This study aimed to investigate the predictive value of acute phase proteins in critically ill COVID-19 patients and to evaluate the efficacy of inflammatory markers in predicting mortality risk in the intensive care unit. Material-Methods: A retrospective study was conducted in critically ill COVID-19 patients treated in the intensive care unit. Overall, 123 patients with ARDS and/or multi-organ dysfunction were included in the first 24 hours of admission to intensive care unit. After 28 days, groups of survived (n=54) and dead patient (n=69) or groups of patients with (n=83) and without (n=40) invasive mechanical ventilation were formed. Serum amyloid A, C-reactive protein, albumin, and prealbumin values considered as acute phase proteins within the first 24 hours of admission to the intensive care unit were compared between groups. Result(s): Albumin and prealbumin levels significantly decreased in dead patients (p=0.011, p<0.001, respectively) and were mechanically ventilated patients (p=0.010, p=0.006, respectively). The Serum amyloid A levels in mechanically ventilated patients significantly increased (p=0.022). Conclusion(s): Low prealbumin and albumin levels and high serum amyloid A levels during admission to ICU can be used as a prognostic marker of disease severity and mortality.
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SARS-CoV-2 infected patients show heterogeneous clinical presentations ranging from mild symptoms to severe respiratory failure and death. Consequently, various markers reflect certain disease presentations. Our cohort included moderate (n = 10) and severe (n = 10) COVID-19 patients, and 10 healthy controls. We determined plasma levels of nine acute phase proteins by nephelometry, full-length (M65), caspase-cleaved (M30) cytokeratin 18, and ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type-1 motif 13) by ELISA. In addition, we examined whole plasma N-glycosylation by capillary gel electrophoresis coupled to laser-induced fluorescence detection. When compared to healthy controls, COVID-19 patients had significantly lower concentrations of ADAMTS13 and albumin (ALB) but higher M30, M65, alpha-1-acid glycoprotein, alpha1-antitrypsin (AAT), ceruloplasmin, haptoglobin, and highsensitivity C-reactive protein. The concentrations of alpha1-antichymotrypsin, alpha2-macroglobulin and serum amyloid A proteins did not differ. We found significantly higher levels of AAT and M65 but lower ALB in severe compared to moderate COVID-19 patients. N-glycan analysis of the serum proteome revealed increased levels of oligomannose and sialylated di-antennary glycans, while the non-sialylated di-antennary glycan A2G2 significantly decreased in COVID-19 patients compared to controls. COVID-19-associated changes in levels and N-glycosylation of specific plasma proteins highlight involvement of different pathophysiological mechanisms and grant further investigations.
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Coronavirus disease 2019 is an infection caused by severe acute respiratory syndrome coronavirus-2. The clinical spectrum of this illness ranges from asymptomatic infection to acute respiratory distress syndrome (ARDS), circulatory shock, multiorgan failure, and ultimately death. The aims of this study are to assess of lymphocyte count, to study of acute phase proteins inflammatory biomarker which include ferritin, lactate dehydrogenase, and D-dimer, and to study of renal function markers which include blood urea nitrogen and serum creatinine. The data accumulated throughout this selective case control study which were extended from September 1st, 2020, to December 1st, 2020. A total of 176 human serum samples were collected, and subdivided into four groups moderate, sever, critical and control, each group comprised of 44 individuals. Results: The data was analyzed using the SPSS-20 statistical package that was available (Statistical Packages for Social Sciences-version 20). The results showed a highly significant decrease in the mean of Lymphocyte in Covid-19 patients when compared to the control group, p.value = 0.000. But Lymphocyte showed no significant differences among moderate, severe, and critical groups p.value = 0.580, p.value = 192, p.value = 456 respectively, where all of them had low lymphocyte count. The means of lactate dehydrogenase, ferritin, and D-dimer a showed a highly significant increase in Covid-19 patients when compared to the control group, p.value = 0.000, p.value = 0.000, p.value = 0.000 respectively. The results showed a highly significant increase in BUN in COVID-19 patient when compared with control group, p.value = 0.001, but the creatinine doesn't show any significant differences in COVID-19 patient when compared with control group, p.value = 0.405. Lactate dehydrogenase showed highly significant increase in critical group when compared with moderate group, p.value = 0.004, and showed significant differences in severe group when compared with moderate group, p.value = 0.031, but did not show significant differences between severe and critical groups, p.value = 0.690. Ferritin and D-dimer showed highly significant increase in critical group when compared with moderate group, p.value = 0.009, p.value = 0.000 respectively, and severe group, p.value = 0.002, p.value = 0.000 respectively. While, showed no nay significant differences between severe and moderate groups, p.value = 0.579, p.value = 0.075 respectively. Urea showed highly significant increase in critical group when compared with sever group and moderate group, p.value = 0.000. Creatinine showed significant increase in critical group when compared with sever group and moderate group, p.value = 0.031, p.value = 0.034 respectively. Both urea and creatinine showed no significant differences between severe and moderate groups p.value = 0.747, p.value = 0.958 respectively. Conclusions: In COVID- 19 patients, lymphopenia is a prognostic factor, increase levels of acute phase protein lactate dehydrogenase, D-dimer, and ferritin associated with disease severity, and the blood urea nitrogen and serum creatinine among critical group were associated with disease severity. © 2023 Author(s).
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Background: The emergence of autoinflammatory/autoimmune disorders in COVID-19 patients has necessitated the development of new strategies for the management of these phenomena. Several viruses have been shown to cause autoimmunity by boosting the production of autoreactive lymphocytes, resulting in a lack of tolerance in the host's immune response. The SARS-CoV- 2 virus and/or its proteins can cause autoimmunity by molecular mimicry, superantigen activity, and disruption of type I IFN production. Method(s): The data of three patients who applied to the outpatient clinics of pediatric immunology and rheumatology at Uludag University Hospital between March 2020 and December 2021 and were followed up with autoimmune/autoinflammatory disease following CCovid-19- 19 infection were analyzed retrospectively. Result(s): All patients were female and aged between 2-17 years. They had SARS-COV- 2 infection which was mild a few months ago. Before the Covid-19 infection, all of the patients were in good health. The patients had no history of frequent infections or familial predisposition to rheumatic diseases. Following the Covid-19- infection, all of our patients showed fever, rash, joint discomfort, and muscle soreness. Despite the fact that myalgia affects the whole body, arthralgia was present on the wrists and knees of patients. CRP, sedimentation rate, and acute phase reactants increased in all of them. According to the American College of Rheumatology's diagnostic criteria, our first patient was diagnosed with systemic lupus erythematosus (SLE) and was treated with hydroxychloroquine, intravenous immunoglobulin treatment and anakinra. Two of three were diagnosed with systemic juvenile idiopathic arthritis (sJIA) according to the League of Associations for Rheumatology (ILAR) criteria. Only one patient had low IgG and IgA levels (Table 1). Two patients showed a decrease in CD19+ naive cells percent and numbers. Conclusion(s): Following SARS-CoV- 2 infection, autoimmune and autoinflammatory disorders such as rheumatoid arthritis, psoriatic arthritis, type 1 diabetes and Still disease have been documented in adult cases. There are limited pediatric cases on this issue. It has been suggested that the persistence of the latent immune response after COVID-19 infection happens by sensitizing the immune system to viral particles long after they have been eliminated from organisms. Is the autoimmune process the effect of a viral infection or mis-targeted immune system? These questions need deep research and discussion.
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Neutrophils (Neu) play a pathogenic role in COVID19 by releasing Neutrophils Extracellular Traps (NETs) or HNE. Being HNE inhibited by a1AT, supplementation of this protein has been proposed. We aim to study a1AT/HNE balance in BALf from ICU admitted COVID19 patients. To assess HNE, a1AT and HNE/a1AT complexes, 33 COVID 19 BALf samples were analysed by means of ELISA or gel-Electrophoresis + Western Blot. Proteins bound to a1AT or HNE were identified by Liquid chromatography-mass spectrometry. NETs release (PMA stimulated Neu +/- a1AT) was analysed by confocal microscopy. Both HNE and a1AT were clearly detectable in BALf at high levels. Contrary to what previously observed in other settings (Bronchiolits obliterans) (Cagnone, M. et al. High Throughput 2019;8(1):5) we couldn't detect any HNE/ a1AT complex in COVID19 even when purified HNE was added to samples (Fig 1a). HNE was found to be bound to acute phase proteins, histones and C3. Due to the relevant role of NETs, we assessed the ability of free a1AT to bind to histones. Although this binding was confirmed, a1AT wasn't able to inhibit NETs formation (Fig 1b). Despite the finding of a high burden of free and bound HNE in COVID 19 BALf, the formation of HNE/ a1AT inhibitory complex is prevented. Furthermore, a1AT binds to histones but does not prevent NETs formation and their noxious activity.
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Aim. To establish risk factors for heart failure (HF) in patients with coronavirus disease 2019 (COVID-19). Material and methods. Medical records of 151 patients treated in an infectious disease hospital from November 3, 2020 to February 2, 2021 with a confirmed diagnosis of COVID-19 were retrospectively selected. The collection of clinical, history and laboratory data were carried out by analyzing electronic medical records. We analyzed information on age, sex, body mass index, smoking, and comorbidities. Following laboratory studies were analyzed: complete blood count, biochemical blood tests, coagulation profile, acute phase proteins (C-reactive protein (CRP), ferritin, lactate dehydrogenase (LDH)), procalcitonin. The diagnosis of HF was confirmed by clinical performance, echocardiography, and elevated levels of the N-terminal pro-brain natriuretic peptide (NT-proBNP). The risk of HF was taken as the endpoint of the study. Results. The studied sample of patients was divided into two groups depending on HF: the 1st group included 46 patients with HF, the 2nd group - 105 patients without HF. The median age was 66,2 (50-92) years (women, 91 (60,3%)). Laboratory indicators, such as the levels of CRP, LDH, procalcitonin, creatinine, bilirubin, differed significantly from each other, and the median values were higher in patients with HF. The neutrophil-to-lymphocyte ratio (NLR) showed significant intergroup differences: in the group of patients with HF, the median was 4,97% vs 3,62% (p=0,011) in the group of patients without HF. There were following most significant predictors increasing the HF risk: age >=66 years (odds ratio, 8,038, p<0,001), procalcitonin level, which increases the HF risk in patients by 3,8 times (p<0,001), NLR >=4,11% (p=0,010), thrombocytopenia <=220x109/l (p=0,010), history of chronic kidney disease (CKD) (p=0,018). Conclusion. The following predictors of HF were established: age >=66 years, procalcitonin >=0,09 ng/ml, NLR >=4,11%, thrombocytopenia <=220x109/l, history of CKD, LDH >=685 U/l and creatinine >=102 micromol/l, international normalized ratio >=1,19, QTc interval >=407,5 ms, bilirubin <=10,7 micromol/l. It is worth noting that the best accuracy values are demonstrated by the Random Forest algorithm (88,5% on the validation set), but the mathematical model of the neural network turned out to be the most sensitive (90,0% on the validation set).Copyright © 2023, Silicea-Poligraf. All rights reserved.
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Aim. To establish risk factors for heart failure (HF) in patients with coronavirus disease 2019 (COVID-19). Material and methods. Medical records of 151 patients treated in an infectious disease hospital from November 3, 2020 to February 2, 2021 with a confirmed diagnosis of COVID-19 were retrospectively selected. The collection of clinical, history and laboratory data were carried out by analyzing electronic medical records. We analyzed information on age, sex, body mass index, smoking, and comorbidities. Following laboratory studies were analyzed: complete blood count, biochemical blood tests, coagulation profile, acute phase proteins (C-reactive protein (CRP), ferritin, lactate dehydrogenase (LDH)), procalcitonin. The diagnosis of HF was confirmed by clinical performance, echocardiography, and elevated levels of the N-terminal pro-brain natriuretic peptide (NT-proBNP). The risk of HF was taken as the endpoint of the study. Results. The studied sample of patients was divided into two groups depending on HF: the 1st group included 46 patients with HF, the 2nd group - 105 patients without HF. The median age was 66,2 (50-92) years (women, 91 (60,3%)). Laboratory indicators, such as the levels of CRP, LDH, procalcitonin, creatinine, bilirubin, differed significantly from each other, and the median values were higher in patients with HF. The neutrophil-to-lymphocyte ratio (NLR) showed significant intergroup differences: in the group of patients with HF, the median was 4,97% vs 3,62% (p=0,011) in the group of patients without HF. There were following most significant predictors increasing the HF risk: age >=66 years (odds ratio, 8,038, p<0,001), procalcitonin level, which increases the HF risk in patients by 3,8 times (p<0,001), NLR >=4,11% (p=0,010), thrombocytopenia <=220x109/l (p=0,010), history of chronic kidney disease (CKD) (p=0,018). Conclusion. The following predictors of HF were established: age >=66 years, procalcitonin >=0,09 ng/ml, NLR >=4,11%, thrombocytopenia <=220x109/l, history of CKD, LDH >=685 U/l and creatinine >=102 micromol/l, international normalized ratio >=1,19, QTc interval >=407,5 ms, bilirubin <=10,7 micromol/l. It is worth noting that the best accuracy values are demonstrated by the Random Forest algorithm (88,5% on the validation set), but the mathematical model of the neural network turned out to be the most sensitive (90,0% on the validation set).Copyright © 2023, Silicea-Poligraf. All rights reserved.
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Aim. To establish risk factors for heart failure (HF) in patients with coronavirus disease 2019 (COVID-19). Material and methods. Medical records of 151 patients treated in an infectious disease hospital from November 3, 2020 to February 2, 2021 with a confirmed diagnosis of COVID-19 were retrospectively selected. The collection of clinical, history and laboratory data were carried out by analyzing electronic medical records. We analyzed information on age, sex, body mass index, smoking, and comorbidities. Following laboratory studies were analyzed: complete blood count, biochemical blood tests, coagulation profile, acute phase proteins (C-reactive protein (CRP), ferritin, lactate dehydrogenase (LDH)), procalcitonin. The diagnosis of HF was confirmed by clinical performance, echocardiography, and elevated levels of the N-terminal pro-brain natriuretic peptide (NT-proBNP). The risk of HF was taken as the endpoint of the study. Results. The studied sample of patients was divided into two groups depending on HF: the 1st group included 46 patients with HF, the 2nd group - 105 patients without HF. The median age was 66,2 (50-92) years (women, 91 (60,3%)). Laboratory indicators, such as the levels of CRP, LDH, procalcitonin, creatinine, bilirubin, differed significantly from each other, and the median values were higher in patients with HF. The neutrophil-to-lymphocyte ratio (NLR) showed significant intergroup differences: in the group of patients with HF, the median was 4,97% vs 3,62% (p=0,011) in the group of patients without HF. There were following most significant predictors increasing the HF risk: age >=66 years (odds ratio, 8,038, p<0,001), procalcitonin level, which increases the HF risk in patients by 3,8 times (p<0,001), NLR >=4,11% (p=0,010), thrombocytopenia <=220x109/l (p=0,010), history of chronic kidney disease (CKD) (p=0,018). Conclusion. The following predictors of HF were established: age >=66 years, procalcitonin >=0,09 ng/ml, NLR >=4,11%, thrombocytopenia <=220x109/l, history of CKD, LDH >=685 U/l and creatinine >=102 micromol/l, international normalized ratio >=1,19, QTc interval >=407,5 ms, bilirubin <=10,7 micromol/l. It is worth noting that the best accuracy values are demonstrated by the Random Forest algorithm (88,5% on the validation set), but the mathematical model of the neural network turned out to be the most sensitive (90,0% on the validation set).Copyright © 2023, Silicea-Poligraf. All rights reserved.
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Feline Infectious Peritonitis (FIP)is a fatal disease caused by Feline coronaviruses. The causative agent is Feline Infectious Peritonitis Virus, a mutation of Feline Enteric Coronavirus. Feline Corona Virusinfection is very common in the cat population.In Feline Corona Virus infected cats, the development of FIP depends on the cat's immune response. FIP disease is more common in young and old cats because young and old animals have a weaker immune system. The acute phase response is a complex systemic reaction that occurs as a response to acute or chronic inflammatory processes such as infection, neoplasia or immunological disorders, tissue damage, trauma, and surgery. The study material was composed of15 cats with FIP (study group) and 10 healthy cats (control group). Serum amyloid A (SAA), haptoglobin (Hp), alpha1-acid glycoprotein (AGP), albumin, interleukin-6 (IL-6), hepcidin, alanine-amino transferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), blood urea nitrogen(BUN), and creatinine levels were measured in the serum collected from both groups. There was no difference between the wet and dry FIP in albumin values (p<0.05).Haptoglobin, alpha1-acid glycoprotein, SAA, IL-6, and hepcidin values were significantly different between the two groups (P<0.001). It was also concluded that hepcidinhas a potential for use as a biomarker in Feline Infectious Peritonitis disease like other acute phase proteins.Copyright © 2023, Sima Sahinduran, Metin Koray Albay, Mehmet Karaca, Mehmet Cagri Karakurum, Reyda Kiyici
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This study aimed to evaluate the concentrations of α1-acid glycoprotein (AGP), haptoglobin (Hp), serum amyloid-A (SAA) and ceruloplasmin (Cp) in healthy and various diseased cats and establish reference intervals (RIs) for these acute phase proteins (APPs) in healthy cats. The animal material of the study consisted of 40 healthy cats and 152 cats with various diseases. The serum APPs in the diseased group were higher than those in the healthy group, and age affected Cp concentration in healthy cats. Also, the systemic inflammatory response syndrome (SIRS) positive (+) group had significantly higher AGP concentrations than the SIRS negative (-) group. In conclusion, this study contributes to the limited number of studies on RIs in serum APPs concentrations in healthy cats. The results of this study suggest that APPs are valuable diagnostic tools for identifying the inflammatory processes of various diseases, and AGP concentration could help determine the severity of the inflammatory condition.
Subject(s)
Acute-Phase Proteins , Cat Diseases , Cats , Animals , Serum Amyloid A Protein/analysis , Serum Amyloid A Protein/metabolism , Haptoglobins/metabolism , Orosomucoid/metabolism , Systemic Inflammatory Response Syndrome/veterinaryABSTRACT
Introduction/Background: Primary bone marrow oedema syndrome is an elusive and less well-defined entity. Whether Rheumatologists should consider it as a stand alone diagnosis, is debatable. It possibly would be best described as an MRI feature which could be a finding in a number of diseases which would include the initial phases of Osteonecrosis of the bone, Rheumatoid Arthritis, Spondyloarthritis, Enthesitis related, Post traumatic, OA, Infections and Cancers. The treatment options become constricted due to the paucity of evidence. Rheumatologists need to consider this as an area of unmet need with development of consensus classification criteria and treatment approaches. Description/Method: 27-year-old male, Height 174 cms Weight 90 Kgs BMI 29 Kg/m2, became symptomatic in Jan 2022 with complains of pain in the both hip joints & groin regions, pain became excruciating and he became bed-bound, with early morning stiffness lasting approximately 45 mins. Had received steroids for COVID infection in August 2020. Investigations Hb 13.5gm/dl TLC 7000/mm3 Platelet 400 x 103/mm3 Sr Bil 0.8mg/dl AST 16 IU/L. ALT 24 IU/L Sr Creatininine 1.1mg/dl Blood Sugar Levels, Fasting 89 mg/dl Post Prandial 102 mg/dl ESR 10mm in 1st hour by Wintrobes method CRP Quantitative 29.38mg/L HLA B27 by PCR Negative, RF Negative, ACCP Negative Serum, IgG, Beta2 Glycoprotein 1.44 SGU Serum, IgM, Beta2 Glycoprotein 3.44 SGU Serum, IgG, Cardiolipin antibody 8.4 GPL Serum, IgG, Cardiolipin antibody 17.45 GPL Lupus anticoagulant by DRVVT Negative Sr Cholesterol 211mg/dl HDL 29 mg/dl LDL 156mg/dl TGs 130 mg/dl MRI Hips & SI joints Transient bone marrow oedema/osteopenia of bilateral hip. PET CT Increased metabolic activity in both hip joints Bone Scan (99mTcMDP) Increased vascularity in perfusion phase, increased accumulation in soft tissue in blood pool phase and increased uptake in bilateral Hip joints in skeletal phase scan, suggestive of CRPS Type-I. Management Was initially managed with Tab Etoricoxib 90mg BD, also started on Tab Sulphaslazine and Tab Methotrexate. However, when he had no symptomatic relief he was administered Inj Infliximab on 12 May 2022 and a second dose on 9 June 2022. He had excellent pain relief after the 1st dose, however after 10 days of the administration, he again began experiencing pain especially after walking. He also had pain in the knees on this occasion. He was also administered Inj Zoledronic 4mg on 23 May 2022. He is at present not requiring any NSAIDs over the last 1 month. Discussion/Results: The patient having presented with excruciating and debilitating pain was worked up and evaluation revealed features of bone marrow oedema on MRI which was corroborated with bone scan and PET CT imaging. The acute phase reactant CRP was also significantly elevated. The patient also gave history of early morning stiffness lasting approximately 45 mins. Hence an underlying Inflammatory process such as Spondyloarthritis(Peripheral) with enthesitis was considered. The confounding factors were the pain which worsened on mobilization, HLA B27 negative status, Rheumatoid Factor and ACCP negative status and past history of having received IV Corticosteroids for COVID infection in August 2020. In view of the debilitating pain and aworking diagnosis of Spondyloarthritis, hewas started onNSAIDs alongwith rest, initially, followed by conventional synthetic disease modifying agents in Rheumatic disease followed by biologic synthetic diseasemodifying agent - Inj Infliximab. The thought process was to avoid prolonged NSAID use to prevent the associated side effects. However, since Avascular Necrosis of the Femoral head is a very likely possibility, the patient is planned to be kept under close follow up. Key learning points/Conclusion: Collaborative efforts between the Departments of Nuclear Medicine, Radiology, Orthopaedics and Rheumatology are crucial in the early detection and approach to cases of Bone Marrow oedema. Avascular necrosis of head of Femur is a far more common entity and must be kept in ind even when a diagnosis of Bone Marrow oedema syndrome is being entertained. Diagnosis of Bone Marrow oedema syndrome must be entertained only as a diagnosis of exclusion. Continued follow up and regular imaging must be pursued rigorously in patients diagnosed with Bone Marrow oedema syndromes. There is a requirement to document acute phase reactants such as CRP and ESR in patients diagnosed with Avascular necrosis of bone as this data could help us differentiate AVN from Primary Bone marrow oedema in the early stages.
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SESSION TITLE: Management of COVID-19-Induced Complications SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Therapeutic plasma exchange (TPE) in the management of COVID-19-induced cytokine storm syndrome (CSS) has remained unclear since the pandemic's emergence. A recent meta-analysis by Beraud et. al examined the use of TPE for treatment of CSS in COVID-19 patients. Although inconsistencies were noted, they demonstrated a general downtrend in cytokine markers and acute phase reactants following TPE administration. TPE was associated with improvements in clinical outcomes and appeared safe in critically ill patients. The analysis highlighted an ongoing need to establish clear criteria to identify a target population. This case series presents 3 critically ill adult COVID-19 patients with CSS and extreme hyperferritinemia (>10,000 ng/mL) who received TPE. We propose the use of ferritin as a sole biomarker for guiding therapy in this patient demographic. CASE PRESENTATION: Patient 1 presented with ferritin 16,060 and CRP 8.22. Despite receiving standard COVID-19 therapies, she decompensated and required intubation. Repeat labs revealed ferritin 92,488 and CRP 9.75. TPE was initiated. Ferritin decreased following each TPE session as shown in Graph 1. Patients 2 and 3 also presented with extreme hyperferritinemia and showed a similar downtrend following TPE therapy. All 3 patients made successful recoveries. DISCUSSION: Hyperferritinemia is present across a range of inflammation-mediated disorders and considered a validated biomarker in various disease states, including COVID-19. There are many hypothesized mechanisms of elevated ferritin in COVID-19;one of which is cytokine release. Severe-to-critical COVID-19 patients have shown higher ferritin levels compared to mild-to-moderately ill patients, and non-survivors have shown higher levels than survivors. Unlike those reported by Beraud et. al, our patients presented with extreme hyperferritinemia. All 3 showed a consistent downtrend in ferritin after TPE sessions, and resolution or near-resolution of hyperferritinemia. CRP levels were also obtained, however 2 of 3 cases showed only mild elevation, and levels trended inconsistently after individual sessions. As such, it was not used to gauge treatment duration or efficacy. CONCLUSIONS: Since biomarker selection and thresholds for therapy remain unclear, we propose further investigation into a ferritin-guided approach to TPE therapy in critically ill COVID-19 patients with CSS. Additionally, the marked ferritin elevation seen in extreme hyperferritinemia may aid in establishing upper thresholds above which TPE would no longer be considered safe or effective. Lastly, given that previous studies showed clinical improvements in patients with mild-to-moderate elevation, we consider that the rate of and/or percentage change in ferritin level may yield a reliable algorithm to direct therapy. Establishing selection criteria in this patient population may prove critical for reducing morbidity and mortality. Reference #1: Beraud, M., Hashami, S. A., Lozano, M., Bah, A., & Keith, P. (2022). Role of therapeutic plasma exchange in the management of COVID-19-induced cytokine storm syndrome. Transfus Apher Sci, 103433. https://doi.org/10.1016/j.transci.2022.103433 Reference #2: Kaushal, K., Kaur, H., Sarma, P., Bhattacharyya, A., Sharma, D. J., Prajapat, M., Pathak, M., Kothari, A., Kumar, S., Rana, S., Kaur, M., Prakash, A., Mirza, A. A., Panda, P. K., Vivekanandan, S., Omar, B. J., Medhi, B., & Naithani, M. (2022). Serum ferritin as a predictive biomarker in COVID-19. A systematic review, meta-analysis and meta-regression analysis. J Crit Care, 67, 172-181. https://doi.org/10.1016/j.jcrc.2021.09.023 Reference #3: Krzych, L. J., Putowski, Z., Czok, M., & Hofman, M. (2021). What Is the Role of Therapeutic Plasma Exchange as an Adjunctive Treatment in Severe COVID-19: A Systematic Review. Viruses, 13(8). https://doi.org/10.3390/v13081484 DISCLOSURES: No relevant relationships by Stefani Delvecchio No relevant relationships by Sean Masi No relevant relationships by Chris Recker-Herman
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Introduction and objectives: SARS-CoV 2 infection has spread throughout the world and affects patients of all ages. Until recently it was thought that children had a short course of the disease without complications;however, a group of children with severe multisystem disease known as pediatric inflammatory multisystem syndrome (PIMS or MIS-C), characterized by fever and multiple organ dysfunction were found to be associated with infection SARS-CoV 2 and development of COVID-19. An increase in the association of gastrointestinal symptoms and the presence of PIMS has been observed. The objective of this study was to analyze whether pediatric patients with COVID-19, who debut with gastrointestinal symptoms, have a higher risk of developing PIMS. Material(s) and Method(s): An observational, analytical and retrolective study was carried out with a review of the records of patients diagnosed with COVID-19 from April 27th, 2020, to May 9th, 2021. All pediatric patients who had a positive test for SARS-CoV 2 (RT- PCR test for SARS-CoV 2, by QUANT STUDIO 5 applied biosystems by Thermo Fisher equipment) were included, those patients who did not have laboratory results for acute phase reactants during their hospitalization were excluded. PIMS/MIS-C was defined according to the CDC criteria, which include patients under 21 years of age with fever greater than 38.0, with involvement of two or more organs or systems, with elevated acute phase reactants (ESR / CRP / Ferritin);which were determined as high according to the values established by the local hospital laboratory;as well as not having another disease that explains the patient's symptoms. In order to identify every patient with/without PIMS/MIS-C a thorough search through patient's files was conducted. With the objective of determining if every patient fulfilled the criteria established for PIMS/MIS-C and determine the cause of admission, as well as the presence of other factors that could influence or discard the diagnosis of PIMS/MISC as according to CDC criteria, excluding those patients with initial suspicion of PIMS/MIS-C that had other diseases that explained the symptoms at admission or during hospital stay. Normally distributed variables are summarized as the mean and standard deviation, data from skewed distributions are shown as the median (range), and categorical variables are summarized as frequency and percentages. A (two-tailed) P value<0.05 was considered to be significant. Odds ratios (ORs) with 95% confidence intervals (CIs) were computed for significant categorical variables. Given the retrospective nature of the study, informed consent was not required. Result(s): A total of 248 patients who met the selection criteria were included. Of Those 40% were female, with a mean age of 7 +/- 5.8 years. Although it wasn't possible to determine the strain of SARS-CoV 2 in our institution until after our study was finished (October 2021), based on epidemiological data we can assume our patients were infected with the Delta strain of the SARS-CoV 2 virus. Gastrointestinal symptoms were the initial presentation in 103 patients, with vomiting being the most frequent symptom, followed by abdominal pain and diarrhea. In total 52 patients developed PIMS, 30 of whom presented with gastrointestinal symptoms. The comparison of patient's characteristics, comorbidities and biometric laboratory results can be found in table 1. An OR of 2.35 (97% CI of 1.26-4.37) was found for the presentation of PIMS in patients positive for SARS-CoV 2 who present with gastrointestinal symptoms. Conclusion(s): There is an increased risk of developing pediatric multisystem inflammatory syndrome when there are gastrointestinal symptoms in pediatric patients with COVID-19. (Table Presented).
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Background: The treatment of COVID-19 caused by SARS-CoV-2 posed serious challenges to health care systems. In 8-10% of patients with severe COVID-19 have a cytokine storm syndrome, highlighting the importance of host immune response in pathogenesis. Objectives: Our aim was to evaluate the effect of tocilizumab treatment in COVID-19 patients with severe cytokine storm who were refractory to standard of care therapy. To determine the prognostic factors that indicate the success of treatment in these patients. Methods: Fifty-three patients were treated with tocilizumab during waves 2 and 3 of the pandemic due to a cytokine storm associated with SARS-CoV-2 infection. All patients underwent physical examination, saturation monitoring, laboratory examination, blood gas analysis and chest CT examination. Deteriorating clinical status, elevated IL-6 and other acute phase protein levels observed in patients treated with standard therapy suggest cytokine storm syndrome. The treatment of these patients was supplemented with 8 mg/kg (max. 800 mg) tocilizumab (1 or 2 times within 24 hours). We assessed the clinical and laboratory response of these patients to IL-6-R inhibitor therapy, the need for ventilation, the need for intensive care and mortality. Results: Immunological consultations were performed in 31 patients, of whom 21 (68%) were successfully treated. Eleven patients of them (22%) died. In the 22 non-consulted patients, this rate was reversed: 7 (22%) were successful and 15 (68%) were treatment failures. The success of the treatment was mainly influenced by the well-established indication, the recognition of contraindications, and the condition that did not require invasive ventilation method. The 29 tocilizumab therapies initiated in the non-intensive care unit avoided intensive care unit treatment in 18 patients. Eleven patients were admitted to the intensive care unit, but 7 patients required temporary respiratory support and recovered, 4 patients required invasive mechanical ventilation and later died (14%). In contrast, 24 treatments initiated in the intensive care unit saved the lives of only 3 patients, and 21 patients were lost (87.5%). The effectiveness of treatment was not affected by age, with survival rates of 40%, 44%, 57% and 55% for the 40-49, 50-59, 60-69, 70-79 age groups, respectively. Interestingly, the extent of lung involvement also did not show a signifcant difference. Although it was a prerequisite for initiating tocilizumab treatment to have fresh alveolitis on the CT image of the chest. Conclusion: Use of tocilizumab is most effective in patients with COVID-19 who have high levels of infammatory activity and IL-6, who are at an early stage of lung involvement and who do not respond to high-dose corticosteroid therapy, who have no bacterial superinfection and require not invasive mechanical ventilation. It is also important that specialist who has immunological approach and routine with biological treatment be also involved in the care of patients with severe COVID-19 disease.
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Background: In winter, you can usually see a picture of Perniosis and/or chilblains. Painful, often itchy, red-to-purple lesions that affect the acrid surfaces of the fngers and toes after contact with the cold, resembling vasculitis, characterize them. Chilblains can be idiopathic and self-limiting or associated with systemic diseases. The diagnosis is usually clinical, but in some circumstances, analytical and microscopic studies of a biopsy sample may be necessary. We present a series of 19 consecutive cases of Pseudoperniosis associated with probable past INFECTION by SARS-CoV-2. Methods: During the winter 2020-21, an unexpected number of cases referred as 'acute arthritis/vasculitis' have been received in our rheumatology section and associated consultations. In the pathochrony of patients, exposure to cold was referred to as the main triggering factor. Initially qualifed as PERNIOSIS. Given the appearance in the current situation of Pandemic by covid-19, we began to request the serology SARS2-COVID19 IgG/IgM. Appreciating an approximate rate of 70% of IgG+ positivity in which it was performed. Results: Characteristics of the clinical data collected evolutionarily in the 19 patients: These are preferably young people, without any other pathology, although there are also people of all ages, with a clinical picture of edema of soft parts preferably of the hands, but also in the feet, with pain and some hemorrhage infusions, including ulcerations in the areas of the knuckles or pressure (PHOTO1-2-3). Despite the overwhelming nature of the picture, they do not associate any other symptoms and the analyses are normal, including acute phase reactants (ESR and PCR), and serological markers of autoimmune disease. Approximately 1/4 of them reported having passed clinical compatible with the covid19 infection and/or having been isolated with some minor symptom, but they had not been performed PCR. The others did not report any symptoms associated with COD19 infection. From the initial diagnosis, about 40 days passed on average. Many of them were being treated with corticosteroids/NSAIDs without improvement. In the ultrasounds performed, only edema of periarticular and paratendinous tissue is appreciated, such as that which can occur after a momentary ischemic picture. All evolved favorably avoiding cold (probable triggering factor), and with antiplatelet agent (infant aspirin). Conclusion: This picture of Pseudoperniosis lacks the typical pruritus of perniosis and the main problem is pain along with edema of the tissues of the hand that leads to make it impossible to use. Similarly, asymmetric lesions similar to perniosis were observed in patients who presented skin manifestations of SARS-CoV-2 infection in a study conducted in Spain (1). We are following these patients to assess if there is any relationship with any other factor that facilitates this unusual incidence, and at the same time indicate the transience of the clinical picture that evolves favorably in a few weeks.
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Aim and background: SARS-CoV-2 pandemic questioned many basic concepts in medicine. COVID-19 affects many organ systems despite the lung being the primary affected organ. ARDS management is challenging and a new complication during the management adds to the burden. Macklin described a pathophysiological process by which air escaped through the ruptured alveolar basement membrane causing pneumomediastinum. The occurrence of air leak syndromes (ALS) in COVID-19 made us investigate the disease and its association with the complication. Objective: To observe the clinicopathological profile of patients who developed air leak syndrome during the second wave of the pandemic. Materials and methods: A retrospective analysis was conducted on SARSCoV- 2 patients admitted to ICU due to ARDS. The study included patients admitted from March to June 2021 with rTPCR positive test for SARS-CoV-2 illness and diagnosed to have ARDS as defined by the Berlin criteria. We analyzed 195 cases admitted in the ICU who met the above criteria and received protocolised care as per national and institutional guidelines. Cases who received ventilatory support either as HFNO (high flow nasal oxygenation), NIV (noninvasive ventilation), or invasive mechanical ventilation as per ARDS NET protocol and developed ALS were included. Demographic and clinical profiles of patients and laboratory parameters like acute phase reactants, haemogram, and serum creatinine were analysed. Results: 5.6% of patients were diagnosed to have air leak syndrome, which includes subcutaneous emphysema, pneumomediastinum, pneumopericardium, and pneumothorax. 81% of the cases were men. The average age was 44.8 years. 90% of the patients had no pre-existing lung pathology or respiratory comorbidity. 81.8% did not have a documented history of smoking. 63.33% of patients had other preexisting co-morbidities. 27.2% of patients had more than one comorbidity with diabetes mellitus being the most common. The average time to develop air leak syndrome was 6 days. 81% of the patients received mechanical ventilation, 2 patients were only on HFNO. 90% of the patients were prone in view of severe ARDS. From air leak syndromes mentioned above, 72.2% developed pneumothorax, 63.3% of the patients developed subcutaneous emphysema, 54.5% of the patients developed pneumomediastinum, and 9% developed pneumopericardium. 1 patient (9%) developed the complete spectrum of ALS. 63% of the patients developed 2 or more entities of the air leak, i.e., subcutaneous emphysema, pneumomediastinum, pneumopericardium, and pneumothorax. Acute phase reactants were elevated in all patients who developed ALS. There was neutrophil predominance in the haemogram. Only one patient developed AKI. Another compelling finding was the development of secondary infection, the majority was respiratory tract infections (81%) followed by urinary tract infections. Candiduria was observed in 36.6% of patients. The average duration of stay was 21.6 days. The mortality rate was 63%. 4 patients were discharged who had an average time to resolution of 8 days. Conclusion: COVID-19 is majorly a self-limiting disease. Secondary bacterial infection and poor oxygenation was major finding in our study. Development of ALS in a previously normal lung with no preexisting lung pathology points towards the need to conclude ALS and viral pneumonias.