ABSTRACT
Submission content Introduction: An unusual case of a very young patient without previously known cardiac disease presenting with severe left ventricular failure, detected by a point of care echocardiogram. Main Body: A 34 year old previously well man was brought to hospital after seeing his general practitioner with one month of progressive shortness of breath on exertion. This began around the time the patient received his second covid-19 vaccination. He was sleeping in a chair as he was unable to lie flat. Abnormal observations led the GP to call an ambulance. In the emergency department, the patient required oxygen 5L/min to maintain SpO2 >94%, but he was not in respiratory distress at rest. Blood pressure was 92/53mmHg, mean 67mmHg. Point of care testing for COVID-19 was negative. He was alert, with warm peripheries. Lactate was 1.0mmol/L and he was producing more than 0.5ml/kg/hr of urine. There was no ankle swelling. ECG showed sinus tachycardia. He underwent CT pulmonary angiography which demonstrated no pulmonary embolus, but there was bilateral pulmonary edema. Troponin was 17ng/l, BNP was 2700pg/ml. Furosemide 40mg was given intravenously by the general medical team. Critical care outreach asked for an urgent intensivist review given the highly unusual diagnosis of pulmonary edema in a man of this age. An immediate FUSIC Heart scan identified a dilated left ventricle with end diastolic diameter 7cm and severe global systolic impairment. The right ventricle was not severely impaired, with TAPSE 18mm. There was no significant pericardial effusion. Multiple B lines and trace pulmonary effusions were identified at the lung bases. The patient was urgently discussed with the regional cardiac unit in case of further deterioration, basic images were shared via a cloud system. A potential diagnosis of vaccination-associated myocarditis was considered,1 but in view of the low troponin, the presentation was felt most likely to represent decompensated chronic dilated cardiomyopathy. The patient disclosed a family history of early cardiac death in males. Aggressive diuresis was commenced. The patient was admitted to a monitored bed given the potential risk of arrhythmia or further haemodynamic deterioration. Advice was given that in the event of worsening hypotension, fluids should not be administered but the cardiac centre should be contacted immediately. Formal echocardiography confirmed the POCUS findings, with ejection fraction <35%. He was initiated on ACE inhibitors and beta adrenergic blockade. His symptoms improved and he was able to return home and to work, and is currently undergoing further investigations to establish the etiology of his condition. Conclusion(s): Early echocardiography provided early evidence of a cardiac cause for the patient's presentation and highlighted the severity of the underlying pathology. This directed early aggressive diuresis and safety-netting by virtue of discussion with a tertiary cardiac centre whilst it was established whether this was an acute or decompensated chronic pathology. Ultrasound findings: PLAX, PSAX and A4Ch views demonstrating a severely dilated (7cm end diastolic diameter) left ventricle with global severe systolic impairment.
ABSTRACT
Aim: People with type 1 or type 2 diabetes have a higher hospital admission rate following Covid-19 infection. This study aims to determine the degree to which the results of a previous study in Greater Manchester (GM) could be replicated in national-level data for England. Method(s): We focussed on the univariable regression analysis, which shows the association between admission and Covid-19 infection in people with diabetes. Modelling was conducted using logistic regression on data from the Covid-IMPACT database. Odds ratios were compared descriptively with the previous study. Result(s): In people with type 2 diabetes, factors associated with an increased risk of hospitalisation similar to the previous study were: older age, male sex, higher social deprivation, higher body mass index (BMI), higher cholesterol, lower eGFR, taking an ACE-inhibitor/ ARB, not taking metformin, and having asthma or hypertension. Patients with COPD, and those taking aspirin or clopidogrel also had increased risk, but the national data showed a greater risk (GM COPD odds ratio 1.89 [1.63-2.19] vs national 2.34 [2.28-2.40] / aspirin 1.49 [1.34-1.66] vs 1.66 [1.63-1.70] / clopidogrel 1.71 [1.47-1.98] vs 1.99 [1.94-2.04]). Similar results were observed in patients with type 1 diabetes. However, due to the increase in sample size, many factors which were previously not statistically significant have become significant, such as in type 2 diabetes BMI, low HDL-cholesterol. Conclusion(s): We have successfully replicated the methods, results and conclusions of our previous study in relation to factors associated with increased risk of hospital admission in diabetes individuals. Regional databases are suitable for large cohort studies, and in this instance produced similar results to a national database, validating our previous findings.
ABSTRACT
The coronavirus SARS-CoV-2 was detected in isolates of pneumonia patients in January 2020. The virus cannot multiply extracellularly but requires access to the cells of a host organism. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) as a receptor, to which it docks with its spikes. ACE2 belongs to the renin angiotensin system (RAS), whose inhibitors have been used for years against high blood pressure. Renin is an endopeptidase that is predominantly formed in the juxtaglomerular apparatus of the kidney and cleaves the decapeptide angiotensin I (Ang I) from angiotensinogen. Through the angiotensin-converting enzyme (ACE), another 2 C-terminal amino acids are removed from Ang I, so that finally the active octapeptide angiotensin II (Ang II) is formed. The biological effect of Ang II via the angiotensin II receptor subtype 1 (AT1-R) consists of vasoconstriction, fibrosis, proliferation, inflammation, and thrombosis formation. ACE2 is a peptidase that is a homolog of ACE. ACE2 is predominantly expressed by pulmonary alveolar epithelial cells in humans and has been detected in arterial and venous endothelial cells. In contrast to the dicarboxy-peptidase ACE, ACE2 is a monocarboxypeptidase that cleaves only one amino acid from the C-terminal end of the peptides. ACE2 can hydrolyze the nonapeptide Ang-(1-9) from the decapeptide Ang I and the heptapeptide Ang-(1-7) from the octapeptide Ang II. Ang-(1-7) acts predominantly antagonistically (vasodilatory, anti-fibrotic, anti-proliferative, anti-inflammatory, anti-thrombogenetically) via the G protein-coupled Mas receptor to the AT1-R-mediated effects of Ang II. In the pathogenesis of COVID-19 infection, it is therefore assumed that there is an imbalance due to overstimulation of the AT1 receptor in conjunction with a weakening of the biological effects of the Mas receptor.Copyright © 2022 Dustri-Verlag Dr. K. Feistle.
ABSTRACT
Objective: A new generation of vaccine technology platform has been developed to combat the COVID- 19 pandemic, the mRNA vaccine. The EMA granted the Pfizer- BioNTech COVID-19 vaccine an emergency use authorization in December 2020 with limited clinical experience, especially in the pediatric population. Method(s): Here, we present a case-report of a 17-yearold girl, who was vaccinated with the mRNA-COVID vaccine in October 2021, and developed a gross hematuria and proteinuria the day after the vaccination. Result(s): The patient presented at our outpatient clinic three days after the vaccination with new-onset hematuria and proteinuria. Up to this date, she had no former known medical conditions and the family history was negative regarding kidney diseases. We excluded nephrolithiasis, autoimmune glomerulonephritis and urinary tract infection as causes. The laboratory chemistry of the kidney was within normal range. The proteinuria dissolved spontaneously, and a microhematuria persisted. One day after the second dose of Cominarty in November 2021, the gross hematuria with proteinuria relapsed. A treatment with an ACE-inhibitor did not have any effect on the proteinuria. At this point, only a few casereports of patients with a comparable clinical course, especially from Japan, were published. In suspicion of a vaccine-triggered nephritis we started a prednisolon therapy which dissolved the proteinuria and induced a regression of the haematuria to a minimal stage. Conclusion(s): Within the last year, the medical community has gained more insights concerning mRNA vaccines. There is growing evidence, that mRNA vaccines can trigger de novo or relapse IgA nephropathy. But more systematic research and long-term evaluation is desirable to elucidate the underling pathophysiology as well as the influence on kidney survival of affected patients in the future. Furthermore, patient education should incorporate the risk of hematuria and proteinuria in children when applying mRNA vaccines.
ABSTRACT
Introduction In this study, we aimed to monitor anti-spike and anti-nucleocapsid antibodies positivity in healthcare workers (HCWs) vaccinated with two doses of inactivated CoronaVac (Sinovac, China) vaccine. Methods Overall, 242 volunteer HCWs were included. Of the participants, 193 were HCWs without history of prior documented COVID-19 (Group 1), while 49 had history of prior documented COVID-19 before vaccination (Group 2). The participants were followed up for SARS-CoV-2 antibodies positivity at four different blood sampling time points (immediately before the second vaccine dose and at the 1st, 3rd months and 141-150 days after the second dose). We investigated the serum IgG class antibodies against SARS-CoV-2 RBD region and IgG class antibodies against SARS-CoV-2 nucleocapsid antigen by chemiluminescent microparticle immunoassay (CMIA) method using commercial kits. Results We found positive serum anti-RBD IgG antibody in 76.4% of the participants (71% in Group 1;98% in Group 2) 28 days after the first dose. When the antibody levels of the groups were compared at the four blood sampling time points, Group 2 anti-RBD IgG levels were found to be significantly higher than those in Group 1 at all follow-up time points. Although anti-RBD IgG positivity persisted in 95.6% of all participants in the last blood sampling time point, a significant decrease was observed in antibody levels compared to the previous blood sampling time point. Anti-nucleocapsid IgG antibody was positive in 12 (6.2%) of participants in Group 1 and 32 (65.3%) in Group 2 at day 28 after the first dose. At the fourth blood sampling time point, anti-nucleocapsid antibodies were found to be positive in a total of 20 (9.7%) subjects, 10 (6.1%) in Group 1 and 10 (23.8%) in Group 2. Conclusions In this study, it was determined that serum antibody levels decreased in both groups after the third month after the second dose in HCWs vaccinated with CoronaVac vaccine.Copyright © GERMS 2022.
ABSTRACT
Background: Hepatocellular carcinoma (HCC) is the second leading cause of malignancy-related mortality and the fifth most common worldwide. Immuno-cancer microenvironment (ICME) was highlighted recently because scientists want to unlock the detailed mechanism in carcinogenesis pathway and find the novel interactions in ICME. Besides, single cell analysis could mitigate the interrupted signals between cells and tissues. On the other hand, COVID-19 angiotensin I converting enzyme (ACE) previously was reported associated with cancer. However, the robust association between COVID-19 and HCC ICME is still unaddressed. Aim(s): We plan to investigate the COVID-19 ACE relevant genes to HCC ICME regarding survival. Method(s): We used Reactome for COVID-19 ACE gene pathway mapping and explored the positive relevant gene expression. DISCO website was applied for single cell analyses using the above-collected genes from Reactome. Finally, we implanted the biomedical informatics into TIMER 2.0 for ICME survival analyses. Result(s): In Fig. 1, the gene-gene interaction mapping was shown. We collected 13 genes (CPB2, ACE2, AGT, MME, ANPEP, CPA3, ENPEP, GZMH, CTSZ, CTSD, CES1, ATP6AP2, and AOPEP) for further single cell relevant analyses, in Table 1, with detailed expression level (TPM). Among the above 13 genes, AGT, GZMH, CTSZ, CTSD, CES1, and ATP6AP2 were strongly expressed in liver tissue. We then applied the initial 13 genes to TIMER 2.0 for HCC ICME 2-year survival analyses. CPA3 and GZMH low expressions with high macrophage infiltration in HCC ICME showed significantly worse 2-year cumulative survival [hazard ratio (HR):CPA3 2.21, p-value 0.018;GZMH 2.07, p-value 0.0341]. ACE2, CPB2, AGT, MME, ANPEP, ENPEP, CTSZ, CTSD, CES1, and ATP6AP2 high expressions with high macrophage infiltration in HCC ICME revealed significantly worse 2-year cumulative survival. Conclusion(s): We demonstrate that ACE2 was strongly associated with HCC clinical survival with macrophage infiltration. However, the bidirectional translational roles about ACE2 relevant genes in HCC should be documented.
ABSTRACT
Intro: Coronaviruses infect humans and a wide range of wild and domestic animals. Some CoVs could be zoonotic, being able to mutate, crossing the species barrier and infecting humans (e.g. SARS-CoV and MERS-CoV). Since the emergence of SARS-CoV-2, several studies were carried out to ascertain the susceptibility of both domestic and wild animals to SARS-CoV-2. However, information on some species is lacking, and for others only RDB-ACE receptor affinity studies have been carried out. Considering the high densities of Marmota marmota in the alpine environment, where livestock and recreational activities are commonly present, this study aims to investigate the presence and characterization of CoVs in this species. Method(s): During provincial relocation plan carried out in 2021 and 2022, 170 alpine marmots were captured in municipality of Livigno in Sondrio province (North-Italy) for decreasing animal density and, after a quarantine period, they were released in other alpine places. Faecal samples were collected from each animal and then subjected to RNA extraction and nested RT-PCR pan-Coronavirus and real time RT-PCR for SARS-CoV-2. PCR positive samples for pan-CoV were then sequenced. Finding(s): The pan-Coronavirus RT-PCR detected CoVs in seven marmots. The CoV sequence originating from one marmot sampled in 2021 had 97% affinity to strains isolated in lagomorphs. The other six sequences from 2022 were highly correlate with Bovine Beta-CoVs. This could be explained by the fact that marmots share alpine pastures with these species;in fact, the trapping area in 2022 represented grazing and forage production areas. All samples tested for SARS-CoV-2 resulted negative. Conclusion(s): Despite the absence of zoonotic coronaviruses, marmots show high plasticity in harbouring CoVs of sympatric species. For this reason, and considering the affinity of their ACE-receptor demonstrated for SARS-CoV, it would be worthwhile to increase surveillance for CoVs in this species.Copyright © 2023
ABSTRACT
Background: Human monoclonal antibodies from convalescent individuals that target the SARS-CoV-2 spike protein have been deployed as therapeutics against SARS-CoV-2. However, nearly all of these antibodies have been rendered obsolete by SARS-CoV-2 variants that evolved to resist similar, naturally occurring antibodies. Moreover, Most SARS-CoV-2 specific antibodies are inactive against divergent sarbecoviruses Methods: By immunizing mice that carry human immunoglobulin variable gene segments we generated a suite of fully human monoclonal antibodies that bind the human ACE2 receptor (hACE2) rather than the viral spike protein and were engineered to lack effector functions such as ADCC. Result(s): These ACE2 binding antibodies block infection by all hACE2 binding sarbecoviruses, including emergent SARS-CoV-2 variants, with a potency that of the most potent spike binding therapeutic antibodies. Structural and biochemical analyses revealed that the antibodies target an hACE2 epitope that engages SARS-CoV-2 spike. Importantly, the antibodies do not inhibit hACE2 enzymatic activity, nor do they induce ACE depletion from cell surfaces. The antibodies exhibit favorable pharmacology in human ACE2 knock in mice and provide near complete protection of hACE2 knock-in mice against SARS-CoV-2 infection. Conclusion(s): ACE2 binding antibodies should be useful prophylactic and treatment agents against any current and future SARS-CoV-2 variants, as well as hACE2-binding sarbecoviruses that might emerge as future pandemic threats.
ABSTRACT
Acute pancreatic pseudocysts are increasingly recognized as complications in patients with coronavirus disease 2019 (COVID-19). There-fore, it is important for healthcare providers to be aware of this phenomenon to ensure proper diagnosis and treatment. Up to 17% of patients with severe acute respiratory syndrome corona-virus 2 (SARS-CoV-2) infection have been shown to develop pancreatic lesions. These pancreatic lesions can be caused directly by the cytopathic effects of the viral infection or indirectly by systemic responses to inflammation or respiratory failure. Several studies have shown that angio-tensin-converting enzyme 2 (ACE2) is the functional receptor used by SARS-CoV-2 to gain access to target cells, while ACE2 receptors are expressed in significant amounts in the pancreas. In this article, we present 2 cases of COVID-19. patients that presented with similar pancreatic lesions. The first case was a 47-year-old lady who presented to the emergency department (ED) with flu-like symptoms for ten days. Incidental findings on computed tomography (CT) scan showed a large, multiloculated cystic mass in the pancreatic tail. The second case was an 81-year-old Caucasian lady who presented to the outpatient clinic with multiple chronic complaints after an acute COVID-19 infection four months prior. Abdominal CT scan with oral contrast revealed multiple hypodense masses on the pancreas measuring 0.3 cm in diameter. The cases we reported in this article showed the degree of COVID-19's effect on the gastrointestinal system, with pancreatic injury occurring during the early phases of the acute phase of the infection and lasting up to 4 months post-resolution of the infection.Copyright © 2023, The Indonesian Foundation of Critical Care Medicine. All rights reserved.
ABSTRACT
BACKGROUND: The pathogenesis of angioedema induced by angiotensin-converting enzyme inhibitors is based on the accumulation of bradykinin as a result of angiotensin-converting enzyme blockade. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to the angiotensin-converting enzyme 2 receptor, which may inhibit its production and thereby lead to an increase in bradykinin levels. Thus, SARS-CoV-2 infection may be a likely trigger for the development of angioedema. AIMS: This study aimed to analyze cases of hospitalizations of patients with angioedema associated with the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers during the coronavirus disease 2019 (COVID-19) pandemic. MATERIALS AND METHODS: This study retrospectively analyzed medical records of patients admitted to the Vitebsk Regional Clinical Hospital between May 2020 and December 2020 with isolated (without urticaria) angioedema while receiving angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. In all patients, smears from the naso and oropharynx for COVID-19 were analyzed by polymerase chain reaction. RESULT(S): Fifteen inpatients (9 men and 6 women) aged 44-72 years were admitted because of emergent events, of which 53.6% had isolated angioedema. In two cases, a concomitant diagnosis of mild COVID-19 infection was established with predominant symptoms of angioedema, including edema localized in the face, tongue, sublingual area, and soft palate. All patients had favorable disease outcomes. CONCLUSION(S): Patients with angiotensin-converting enzyme inhibitor-induced angioedema may require hospitalization to monitor upper respiratory tract patency. There were cases of a combination of angiotensin-converting enzyme inhibitor-induced angioedema and mild COVID-19. Issues requiring additional research include the effect of SARS- CoV-2 infection on the levels of bradykinin and its metabolites, the triggering role of COVID-19 in the development of angioedema in patients receiving angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, recommendations for the management of patients with angiotensin-converting enzyme inhibitor-induced angioedema, and a positive result for COVID-19.Copyright © 2020 Pharmarus Print Media All rights reserved.
ABSTRACT
Purpose of study A 32-years old male with known multi-system sarcoidosis in remission for 5 years off treatment presented to the emergency room with complaints of generalized weakness, hematemesis, epistaxis, and bruises. Physical examination was notable for petechiae, ecchymosis along with papules and plaques suggestive of active sarcoid skin lesions on his extremities. Laboratory workup was significant for thrombocytopenia 3000/uL, acute kidney injury with sub-nephrotic proteinuria. Peripheral blood smear did not show evidence of hemolysis and direct Coombs test was negative. Infectious workup including COVID-19, HIV, and hepatitis serologies were negative. Computed Tomography (CT) of chest, abdomen, and pelvis showed mild splenomegaly and an increased number of sub-centimeter hilar and mediastinal lymph nodes. The patient was treated with dexamethasone 40 mg daily for 4 days and intravenousimmunoglobulins (IVIG-2 gm/kg) for possible Immune Thrombocytopenic Purpura (ITP) with improvement in platelet count to 42000/uL by day 3. His workup for AKI and sub-nephrotic proteinuria was negative apart from a positive ANA (1: 160) with low complements. The anti-phospholipid antibody panel was negative. The ACE level was markedly elevated (>80U/L). The patient could not get a renal biopsy due to severe thrombocytopenia. He was discharged but was re-admitted in 15 days for severe thrombocytopenia of 1000/uL, epistaxis, and bruising. We continued high dose steroids along with IVIG 1 gm/kg for refractory ITP with minimal response and started anti-CD20 agent (Rituximab) 375 mg/m2 weekly with thrombopoietin-receptor agonist (Eltrombopag). His platelets count improved in response to treatment and subsequent renal biopsy showed focal and segmental glomerulosclerosis along with mild interstitial fibrosis, tubular atrophy thought to be from long standing sarcoidosis. There was also evidence of focal arteriosclerosis with no evidence of granulomas, immune complex, complement, or IgG4 deposition. Given skin lesions, thrombocytopenia, extensive lymphadenopathy, and renal involvement with markedly elevated ACE levels the overall picture was consistent with active multi-system sarcoidosis. His platelet count increased to 177,000/uL at the time of discharge. Currently, the patient is on slow steroid taper along with Eltrombopag 25 mg every other day without any recurrence of his symptoms so far. Methods used We described one case of sarcoidosis with hematologic and renal involvement. Summary of results Our patient developed hematologic and renal complications approximately 6 years after being diagnosed with sarcoidosis. Initially, he did not demonstrate sufficient clinical response to IVIG and high dose steroids. However, after a course of anti-CD20 agent (Rituximab) and with the addition of thrombopoietin-receptor agonist (Eltrombopag) he showed improvement of platelet count and stabilization of the renal function. Currently, the patient is receiving maintenance therapy with Prednisone 7.5 mg daily along with Eltrombopag 25 mg twice weekly with no recurrence of ITP and stable renal function. A further decision on whether the patient needs another cycle of Rituximab will be determined by the patient's clinical course. Conclusions Highly variable manifestations of Sarcoidosis can pose a significant diagnostic and therapeutic challenge as can be seen from our case. ITP is a rare hematological manifestation of sarcoidosis and addition of anti-CD20 agents should be considered in refractory cases.
ABSTRACT
Background ACE is a potent pro-inflammatory modulator that controls chemokines and adhesion molecules, and elevated ACE activity associated with immunoinflammatory conditions, including cardiovascular diseases (CVD) and diabetes. The ACE inhibitors are recommended as primary treatment for these illnesses. ACE is a peptidyl-dipeptidase that catalyses Angiotensin I to Angiotensin II, whilst inactivating bradykinin during blood pressure regulation via the Renin-Angiotensin System. The purpose of this study is to establish a reference interval (RI) for ACE in the Irish population after COVID, and to examine if there is an underlying correlation between ACE concentrations and a range of biomarkers. Methods Serum samples of 200 randomly selected patients were obtained from several Irish hospitals in March 2022 (in compliance withGuidance on Anonymisation and Pseudonymisation, June 2019). We analysed for ACE (Buhlmann reagents), HBA1C, 25OHD and other biomarkers on the Abbott Architect ci8200. Full Blood Count was measured on Sysmex CS-2500. The statistical analysis used the EP Evaluator 11.3.0.23 and SPSS 22.0 software. Results The RI based on the central 95% of data was 8-78 U/L. This is higher than the RI proposed by the manufacturer (20-70 U/L) but is very close to our RI (5-79 U/L) from 2019. We found a significant positive correlation between ACE concentration and HBA1c, Urea, Creatinine, White Blood Cells (p<0.0001), Glucose (p=0.02), LDL (p=0.03), Neutrophils (p=0.003), Lymphocytes (p=0.001). A significant negative correlation was observed with 25OHD (p<0.0001). Conclusions This study did not show any notable change in the RI for ACE after COVID in Ireland. The significant positive correlations with HBA1c and other biomarkers may indicate the importance for ACE testing for diabetic management and progression, but further studies will be needed. Patients' overall health and medical history should always be considered when evaluating ACE results, including Vitamin D levels.
ABSTRACT
Background: The pathophysiology of viral-infections is highly complex and involves host immunocompetence, host genetics, and gene-environment interactions. We hypothesized that polymorphic variants in host genes, blood group and previous vaccination status against H1N1 may affect the clinical course of covid-19 infection. Method(s): A total of 202 subjects who were RT-PCR negative after Covid-19 infection were recruited. We investigated association between Covid-19 infection (Severity and recovery period) and multiple factors including ABO and Rh blood groups, H1N1 vaccination, polymorphism in Viral susceptibility genes (ACE2 G8790A), and polymorphism in host response genes (ACE I/D rs4646994, IL6- 174G/C, GSTT1/GSTM1 I/D and GSTP1 Ile 105 Val). Result(s): B-ve and O-ve ABO and Rh blood groups had significantly higher Covid-19 recovery period applied on one-vs.-all in a nonparametric t-test (p<0.05). Subjects who had vaccinated themselves against H1N1 presented with a lower recovery-period (p<0.05). Both variables (blood group and H1N1 vaccination) were not however associated with Covid-19 severity. Out of the studied polymorphisms, ACE2 G8790A and GSTT1/GSTM1 were significantly associated with covid-19 infection. Our results indicated that G/G genotype of ACE2 G8790A (OR 3.52, P 0.007) and GSTT1/ GSTM1 null (M1 - / - OR = 3.98, P = 0.0004;T1 - / - OR 3.84, P = 0.004) and double null (M1 - / - /T1 - / - OR = 9.66, P = 0.001) are likely to be associated with an increased risk for severe-critical outcomes in individuals with COVID-19. Other polymorphisms analyzed in this study were found to have no significant association with Covid-19 outcome. Conclusion(s): This study suggests that outcome of Covid-19 infection is affected by both clinical and genetic factors. Thus it seems plausible to utilize these factors as prediction and susceptibility markers in the prognosis of COVID-19, which may help to personalize the treatment.
ABSTRACT
Introduction: Hypertension is the most common co-morbidity associated with COVID-19 patients. Many patients take angiotensin-converting enzyme (ACE) inhibitors for the management of hypertension. The study aimed to compare the clinical and hematologic features in hypertensive and non-hypertensive patients suffering from COVID-19. Material(s) and Method(s): This observational study compared clinical and hematologic features in hypertensive and non-hypertensive patients suffering from COVID-19. The study enrolled patients from SMS Medical College, Jaipur (Rajasthan, India) after approval from the institutional Ethics Committee. The comparison of quantitative variables was performed using the Mann-Whitney test, and qualitative attributes were compared using the chi-squared test. The level of confidence is considered at 5%. Result(s): There were no significant differences found in clinical and hematologic features between hypertensives and non-hypertensives suffering from COVID-19. Conclusion(s): The present study concludes that there is no evidence that either use of ACE inhibitors is useful or harmful in patients with hypertension. Therefore, it is endorsed to use these agents in the management of hypertensives in patients suffering from COVID-19, till further evidence is found.Copyright © 2023, Dr Yashwant Research Labs Pvt Ltd. All rights reserved.
ABSTRACT
Although it has been almost three years since the World Health Organization (WHO) declared a pandemic, COVID-19 is still an unsolved problem, thereby attracting great scientific interest. The disease has a heterogeneous clinical picture with multiple manifestations from different organs and systems. Currently, COVID-19 is perceived as a polysyndromic inflammatory disease involving not only the respiratory system, but also the musculoskeletal system, the cardiovascular system, the skin, the excretory and the nervous system, and is accompanied by a number of hematological, gastrohepatoenterological and endocrine disorders. Various pain phenomena also appear in the clinical presentation of the disease, often as a single manifestation or in combination with symptoms from different organs and systems. The pathogenesis of pain is complex and there is still no consensus on the exact driving mechanisms. Several different signaling pathways play an important role in the generation of pain impulses and perception. They are different for different types of pain. At this stage, the role of angiotensin-converting enzyme 2 (ACE), the renin-angiotensin system (RAC), angiotensin 2 receptors (AT2R), direct neuronal invasion of the virus, the involvement of pro-inflammatory cytokines, hypoxia, the involvement of macrophages, is discussed. as well as the role of overactivity of the immune system, causing the so-called "cytokine storm". Pain is the result of complex biochemical processes influenced to varying degrees by biological, physiological and social factors. Our knowledge at this stage remains scarce and is the subject of many studies on the key pathogenic mechanisms. Therefore, the purpose of this review is to describe the known mechanisms for the occurrence and persistence of pain in patients with COVID-19, as well as to classify the pain phenomena and present its most common localizations. The diagnosis and treatment of COVID-19 and associated pain should be carried out by a multidisciplinary team of specialists, given the heterogeneous clinical presentation of the disease.Copyright © 2023 Medical Information Center. All rights reserved.
ABSTRACT
Background: Hymenoptera venom immunotherapy (VIT) is a safe and effective treatment for Hymenoptera venom allergy (HVA). Unexpected events, such as venom extracts shortage or COVID-19 pandemic, can impact HVA management, and a change in VIT supplier may became necessary. We aimed to evaluate the safety of switching VIT manufacturer without any dose adjustments. Method(s): A retrospective study of patients treated with VIT between 2013 and 2021, in the maintenance phase and without any previous systemic reactions was performed. All the patients switched to another manufacturer while keeping the same venom without any dose modification. All venom extracts were aqueous preparations. Demographic and clinical data were also analyzed. Result(s): A total of 40 patients were included (31 male, median age 44 years old);76% lived in a rural environment, 58% had apiaries <3km from home or work, and 18% were medicated with beta-blockers and/or angiotensin converting enzyme inhibitors. Most patients (68%) were treated with bee venom and the remaining wasp venom. The median time between the beginning of the maintenance phase and the switch to a different VIT supplier was 18 months [1-52 months]. A total of 42 changes between 4 suppliers were performed without any dose adjustments (39 Roxall to Leti;2 Stallergenes to Roxall;1 Inmunotek -> Roxall), with only local reaction reported. This healthy 50-year- old female patient treated with wasp VIT for 3-months in the maintenance phase, switched from Inmunotek to Roxall and presented a local reaction, similar to previous reactions with the former manufacturer. Two years later, she did not react when VIT was changed from Roxall to Leti. No systemic reactions occurred, and no one discontinued VIT. Conclusion(s): International recommendations regarding changing VIT supplier are scarce. Our results suggest that is safe to switch venom extracts from different manufacturers without the need for dose adjustment in patients on maintenance VIT without any previous systemic reactions.
ABSTRACT
Case report Erythema nodosum (EN) is considered a delayed type IV hypersensitivity reaction, triggered by exposure to an antigen, which diagnostic workout is usually challenging. Several conditions have been described as possible causes for EN, including infections, sarcoidosis, pregnancy, neoplasic and inflammatory diseases. Rarely, vaccines such as tetanus, diphtheria, BCG, hepatitis B, human papillomavirus, malaria, rabies, smallpox, typhoid, and cholera have been associated with subsequent EN. We present a 31-year- old leucodermic female with suppurative adenitis, who developed painful erythematous nodules on the pretibial area of the lower limbs. Ten days prior to presentation she had received the first dose of the COVID-19 mRNA-1273 vaccine. Fever, lymphadenopathy, fatigue, weight loss, arthritis, cough, diarrhoea, other organ-specifc symptoms and close contact with tuberculosis were excluded. She was under oral contraception for several years, that was not discontinued. Pregnancy was excluded. No positive signs were detected on physical examination besides the referred nodules. Laboratory tests revealed a normal complete blood count, erythrocyte sedimentation rate, C-reactive protein, antistreptolysin O titer, renal and hepatic tests. Interferon-gamma release assay was negative. Circulating rheumatoid factor was normal, anti-nuclear, anti-double stranded DNA and anti-neutrophil cytoplasmatic antibodies were negative. Angiotensin converting enzyme and protein electrophoresis were normal. Hepatitis B and C, HIV 1/2 and syphilis serologic profiles were negative. Urinalysis and fecal calprotectin were unremarkable. The patient was treated with naproxen and topic betamethasone dipropionate. Violaceous involution was reported, with complete resolution of the EN lesions over the following month. In the literature, there are rare reports of EN following SARS-COV2 infection and also after COVID-19 vaccination. To our knowledge this is the second report of EN after the COVID-19 mRNA-1273 vaccine. This case highlights the importance of clinical awareness for the possible association of COVID-19 vaccination and EN, adding to the already extensive list of causes included in the etiological investigation of these patients.
ABSTRACT
Background: The need for cardiac intensive care unit (ICU) beds remains high in order to monitor and treat emergency patients with severe cardiovascular diseases, particularly during the COVID-19 pandemic. Therefore, timely discharge strategies from the cardiac ICU to peripheral wards are crucial to meet the increasing demand for cardiac ICU beds. Early patient transfer from ICU to the peripheral ward may result in worsening of the patient's clinical condition and outcome with readmission to the ICU, while late transfer may require prolonged expert care and generate unwanted costs. Purpose(s): To investigate whether unplanned readmission of cardiac patients to the cardiac ICU within 72 hours after the index ICU stay is associated with increased mortality risk (primary outcome) and prolonged total hospital length of stay (LOS) (secondary outcome), as well as to identify predictors of ICU readmission in cardiac patients. Method(s): Adult patients who were admitted to the cardiac ICU due to a primary cardiac admission diagnosis at a tertiary care center between 2003 and 2021 were included. Outcomes were analysed with multivariable regression models adjusted for 26 a priori defined variables on patient demographics, underlying comorbidity levels, ICU procedures and administered ICU drugs. Result(s): 30,942 cardiac patients were included, out of whom 1,499 patients (4.84%) were readmitted to the cardiac ICU within 72 hours. 1,023 (68.2%) of readmitted patients were male. Compared to non-readmitted patients, readmitted patients were older, had more underlying comorbidities (Charlson Index), had more severe disease courses (SOFA score, TISS, APACHE II score and SAPS), as well as required more frequently vasopressor therapy, renal replacement therapy and coronary angiographies (Table 1). Readmission to the cardiac ICU was associated with higher in-hospital mortality risk (Odds Ratio 7.52, 95% Confidence Interval (CI) 4.15-12.27, P<0.001) and prolonged hospital LOS (Incidence Rate Ratio 1.56, 95% CI 1.15-1.58, P<0.001). Patients who were readmitted to the ICU had been discharged 18% earlier during the index ICU stay compared to non-readmitted patients (P<0.001). Of note, readmitted and nonreadmitted patients had similar vital parameters at time of ICU discharge after their index ICU stay. During the index ICU stay, non-readmitted patients were prescribed more beta blockers (65.3% vs. 45.8%), ACE inhibitors (37.0% vs. 27.2%) and blood transfusions (10.7% vs. 7.7%). Conclusion(s): Early readmission to the cardiac ICU was associated with increased in-hospital mortality and prolonged hospitalisation. Readmitted patients had been discharged earlier from their index ICU stay and required more comprehensive critical care. ICU discharge strategies should optimally be based on objective patient assessments to facilitate patient safety and shorten hospital length of stay. Artificial intelligence-based algorithms may support clinicians with safe ICU discharge. (Table Presented).