Challenging Organizational Factors Associated With Admission Delay to Intensive Care Unit-A Novel Quality Indicator.

BACKGROUND: Delays in admitting patients to the intensive care unit (ICU) can defer the timely initiation of life-sustaining therapies and invasive monitoring, jeopardizing the success of the treatment. Nevertheless, the availability of research on interventions that reduce or minimize admission delays is limited. OBJECTIVES: The current study aimed to assess the factors related to delays in admission times of critically ill patients transferred to the ICU. METHODS: A software was designed to follow-up, compare and measure the defined intervals of the time to admission, implemented at the ICU for 6 months. Measurements included 5 time intervals, referral department, and work shift at admission. Data from 1004 patients admitted to the ICU between July 2017 and January 2020 were analyzed in a retrospective observational study. RESULTS: Precisely, 53.9% of total patients were referred from the hospital emergency department, and 44% were admitted during the evening shift. Significant differences were found in time intervals between shifts, showing the morning round had the longer total admission time (median: 67.8 min). Analysis showed that admission time was longer at times of full capacity compared to times of available bed (mean: 56.4 and 40.2 min, respectively; U = 68,722, p < .05). Findings demonstrated a significant shortening of time to admission after implementing a new time monitoring software by the Institutional Quality Control Commission (U = 5072, p < .001). CONCLUSIONS: Our study opens doors for potential studies on applying effective initiatives in critical care settings to improve patient care and outcomes. Additionally, it generates new insights regarding how clinicians and nursing teams can jointly develop and promote multidisciplinary interventions in intensive care work environments.

Assessment of Predictors for SARS-CoV-2 Antibodies Decline Rate in Health Care Workers after BNT162b2 Vaccination-Results from a Serological Survey.

Background: SARS-CoV-2 is a novel human pathogen causing Coronavirus Disease 2019 that has caused widespread global mortality and morbidity. Since health workers in Israel were among the first to be vaccinated, we had a unique opportunity to investigate the post-vaccination level of IgG anti-S levels antibodies (Abs) and their dynamics by demographic and professional factors. Methods: Prospective Serological Survey during December 2020−August 2021 at Barzilai Medical Center among 458 health care workers (HCW) followed for 6 months after the second BNT162b2 vaccine dose. Results: Antibody levels before the second dose, and 30, 90 and 180 days after were 57.1 ± 29.2, 223 ± 70.2, 172.8 ± 73.3 and 166.4 ± 100.7 AU/mL, respectively. From GEE analysis, females had higher Abs levels (ß = 26.37 AU/mL, p = 0.002). Age was negatively associated with Abs, with a 1.17 AU/mL decrease for each additional year (p < 0.001). Direct contact with patients was associated with lower Abs by 25.02 AU/mL (p = 0.009) compared to working with no such contact. The average decline rate overall for the study period was 3.0 ± 2.9 AU/mL per week without differences by demographic parameters and was faster during the first 3 months after vaccination than in the subsequent 3 months. Conclusions: All demographic groups experienced a decline in Abs over time, faster during the first 3 months. Findings of overall Abs lower in males, workers with direct contact with patients, and older workers, should be considered for policy-making about choosing priority populations for additional vaccine doses in hospital settings.

Impact in total ischemic time and ST-segment elevation myocardial infarction admissions during COVID-19.

BACKGROUND: Despite the COVID-19 pandemic, cardiovascular disease is still the main cause of death in developed countries. Of these deaths, acute coronary syndromes (ACS) account for a substantial percentage of deaths. Improvement in ACS outcomes, are achieved by reducing the time from symptom onset until reperfusion or total ischemic time (TIT). Nevertheless, due to the overwhelming reality at the beginning of the pandemic, acute coronary syndrome (ACS) care may have been compromised. OBJECTIVES: We evaluated delays in TIT based on the date and timing of admissions in patients with STEMI, by a timeline follow-up form, before and during the current COVID-19 pandemic. METHODS: Between July 2018 and June 2020, two hundred and twelve patients diagnosed with ST-segment elevation myocardial infarction (STEMI) were admitted to our medical center. Upon presentation, cases were assigned a timeline report sheet and each time interval, from onset of symptoms to the catheterization lab, was documented. The information was later evaluated to study potential excessive delays throughout ACS management. RESULTS: Our data evidenced that during the COVID-19 pandemic ACS admissions were reduced by 34.54%, in addition to several in-hospital delays in patient's ACS management including delays in door-to-ECG time (9.43 ± 18.21 vs. 18.41 ± 28.34, p = 0.029), ECG-to-balloon (58.25 ± 22.59 vs. 74.39 ± 50.30, p = 0.004) and door-to-balloon time (57.41 ± 27.52 vs. 69.31 ± 54.14, p = 0.04). CONCLUSIONS: During the pandemic a reduction in ACS admissions occurred in our hospital that accompanied with longer in-hospital TIT due to additional tests, triage, protocols to protect and prevent infection within hospital staff, and maintenance of adequate standards of care. However, door-to-balloon time was maintained under 90 min.

Prevalence of Classic and Non-Classic Antiphospholipid Antibodies in Multiple Sclerosis.

BACKGROUND: The association between antiphospholipid antibodies (aPL) and multiple sclerosis (MS) has been suggested previously, but prior studies provided contradicting findings. OBJECTIVES: To characterize the expression profile of eight classic and non-classic aPL in patients diagnosed with MS. METHODS: Using the BioPlex 2200 immunoassay, we measured the levels of serum immunoglobulin (Ig)M and IgG isotypes of three classic aPL and five non-classic aPL in 98 subjects with MS and 237 healthy controls. RESULTS: Three non-classic aPL were significantly more prevalent among MS patients in comparison to the control group. These antibodies included IgM and IgG against phosphatidylserine-ß2GPI (PS-B2), IgG prothrombin complex (PT-PT) and IgM prothrombin (PT). The positive results according to Bonferroni correction are PS-B2 IgG and PT-PT IgG. The remaining aPL profiles did not differ significantly between the two groups. CONCLUSIONS: An association between certain non-classic aPL and MS has been established. The specific role of these autoantibodies in the pathogenesis of the condition remains uncertain.

A volcanic explosion of autoantibodies in systemic lupus erythematosus: a diversity of 180 different antibodies found in SLE patients.

Recent research in systemic lupus erythematosus (SLE) yielded new antigens and antibodies in SLE patients. We describe the various autoantibodies that can be detected in patients with SLE. A literature review, using the terms "autoantibody" and "systemic lupus erythematosus", was conducted to search for articles on autoantibodies in SLE, their target antigens, association with disease activity and other clinical manifestations. One hundred and eighty autoantibodies were so far described in SLE patients. These include autoantibodies that target nuclear antigens, cytoplasmic antigens, cell membrane antigens, phospholipid-associated antigens, blood cells, endothelial cells, and nervous system antigens, plasma proteins, matrix proteins, and miscellaneous antigens. The target of an autoantibody, the autoantigen properties, autoantibody frequencies in SLE, as well as clinical associations, and correlation with disease activity are described for all 180 autoantibodies. SLE is so far the autoimmune disease with the largest number of detectable autoantibodies. Their production could be antigen-driven, the result of a polyclonal B cell activation, impaired apoptotic pathways, or the outcome of an idiotypic network dysregulation.

Early operative intervention is associated with better patient survival in patients with intracapsular femur fractures but not extracapsular fractures.

The purpose of this study was to determine patients' survival after undergoing an early or delayed operation. We retrospectively assessed 1849 files of patients operated for proximal femoral fracture, divided into two diagnostic groups: intracapsular (n = 640) and extracapsular (n = 1209). 1163 (63%) were treated within 48 h from hospital admission and 686 (37%) were treated >48 h afterwards. Delayed operation in patients with intracapsular fractures was associated with a 1.8-fold excess risk for 1-year mortality (HR = 1.83, P = 0.008), while no effect was observed for patients with extracapsular fractures. Males had a higher HR for mortality in both diagnostic groups. Early surgical intervention is beneficial for intra-capsular femoral fractures; male gender and a high ASA score are associated with an increased mortality hazard risk.

Novel antiphospholipid antibodies in autoimmune bullous diseases.

BACKGROUND: Pemphigus and bullous pemphigoid are two autoimmune diseases that have similar pathogenesis. Both have a genetic predisposition, which promotes the production of auto antibodies targeted against different components of the epidermal desmosome and hemidesmosome. Antiphospholipid antibodies (aPL) are heterogeneous group of antibodies found in patients with autoimmune diseases and inflammatory conditions and are associated with thrombotic events. OBJECTIVE: We sought to determine the expression profile of eight non classical aPLs in ABD patients. METHODS: A cohort of 266 serum samples of patients with pemphigus, bullous pemphigoid and controls was screened for the presence of eight aPL antibodies, using the Bio-Rad BioPlex™ 2200 system. RESULTS: Phosphatidylserine-beta-2-glycoprotein-I (aPS-ß2GPI) and anti prothrombin complex (aPT-PT) serum profiles were significantly more prevalent among ABD patients; 20.7% patients with ABD compared to 5.9% of control patients were positive for aPS-ß2GPI IgM. In addition, aPT-PT IgM was more prevalent among ABD patients (31% vs. 14.8%). CONCLUSION: aPL auto antibodies are more prevalent in ABD. Any clinical association should be further determined.

Scientific evidence of the therapeutic effects of dead sea treatments: a systematic review.

OBJECTIVES: The Dead Sea, the deepest and most saline lake on earth, has been known from biblical times for its healing properties. The aim of this systematic review was to present critically the level of evidence for the claims of therapeutic effects of Dead Sea treatments in several rheumatologic diseases and psoriasis as well as to review these treatments' safety. METHODS: All articles cited in MEDLINE under the query, "Dead Sea," were reviewed. RESULTS: We found bona fide evidence that Dead Sea treatments are especially effective in psoriasis due to both the special characteristics of solar ultraviolet radiation in the Dead Sea and the Dead Sea water balneotherapy. Dead Sea mud and Dead Sea balneotherapy have been found to be beneficial in rheumatologic diseases, including rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and knee osteoarthritis. In the safety analysis, we found no evidence for an increase in skin neoplasia, although skin actinic damage seems to be increased in patients treated in the Dead Sea. Dead Sea treatments do not lead to worsening of blood pressure. Substantial ingestion of Dead Sea water (generally in unusual near-drowning cases) is toxic and can result in cardiac rhythm disturbances because of electrolyte concentration abnormalities. Laboratory analysis of Dead Sea mud did not reveal mineral concentrations that could represent a health concern for their intended use. CONCLUSIONS: Dead Sea treatments are beneficial in several rheumatologic diseases and psoriasis and have a good safety profile.

Autoimmune bullous diseases the spectrum of infectious agent antibodies and review of the literature.

Pemphigus and bullous pemphigoid are two autoimmune diseases that have a similar pathogenesis. Both have a genetic predisposition which promotes the production of auto-antibodies targeted against different components of the epidermal desmosome and hemidesmosome. Environmental factors play an important role in the pathogenesis of this autoimmune disease. Among these, the role of infectious agents was debated as a causative factor. We sought to determine a possible connection between various infectious agents and autoimmune bullous disease (ABD). A cohort of 148 serum samples of patients with pemphigus, bullous pemphigoid and controls was screened for evidence of a prior infection with HBV, HCV, EBV, CMV, Helicobacter pylori, Toxoplasma gondii and Treponema pallidum, utilizing the Bio-Rad BioPlex 2200 system as well as ELISA assays to complete the panel. HBV, HCV, H. pylori, T. gondii and CMV were demonstrated to have significantly higher prevalence of antibodies in patients with pemphigus and bullous pemphigoid in comparison to controls. Among them, we found a novel association between H. pylori and ABD. Our study suggests a contributing role for HBV, HCV, H. pylori, T. gondii and CMV in inducing ABD in the genetically susceptible host.

Atherosclerosis in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease that has a late mortality phase owing mainly to cardiovascular manifestations. Atherosclerosis itself is characterized by inflammatory components, fulfilling the criteria of Witebsky and Rose for an autoimmune disease. SLE patients have increased risk for cardiovascular events, and these are the result of both atherosclerosis and thromboembolic events. Risk factors for atherosclerosis in SLE include "traditional" risk factors (mainly the Framingham risk factors), as well as disease-related factors including disease duration, steroid therapy, and renal disease, and inflammatory mechanisms that specifically contribute to enhanced atherosclerosis in SLE. These include specific antibodies to beta2GPI; anticardiolipin antibodies; anti-oxidized low-density lipoprotein; and antibodies to heat shock proteins, complement activation, impaired ability to activate TGF-beta1, and elevated levels of CRP. These findings stress the importance of surveillance and preventive strategies to control atherosclerosis in SLE.

Exposure to Epstein-Barr virus infection is associated with mild systemic lupus erythematosus disease.

Infections may act as environmental triggers for the induction of systemic lupus erythematosus (SLE). In this study, we determine the relationship between disease manifestations of SLE patients and the titers of five Epstein-Barr virus (EBV) Abs. We evaluated the titers of early antigen IgG (EAG), nuclear antigen IgG, viral capsid antigen (VCA) IgG and IgM, and heterophile IgM, using the BioPlex 2200 multiplexed immunoassay method in 260 sera (120 SLE patients and 140 controls). EAG titers were significantly elevated (P < 0.024) in patients with cutaneous symptoms and increased anti-Ro antibody titers (P < 0.005). VCA IgG titers were significantly elevated (P < 0.003) in patients with joint involvement. None of the titers differed by central nervous system or renal involvement or antiphospholipid syndrome. We conclude that exposure to EBV infection may predict a disease phenotype of mild SLE disease with cutaneous and joint manifestations and elevated titers of anti-Ro Abs.

Atherosclerosis in autoimmune rheumatic diseases-mechanisms and clinical findings.

Atherosclerosis is one of the major entities leading to morbidity and mortality in the western world. It is known now that atherosclerosis cannot be explained merely by the presence of the Framingham traditional risk factors and that autoimmunity takes a significant role in its pathogenesis. It is also known that individuals with autoimmune diseases demonstrate increased incidence of cardiovascular manifestations and subclinical atherosclerotic disease. The mechanisms for the assumed accelerated atherosclerosis in diseases such as systemic lupus erythematosus, rheumatoid arthritis, antiphospholipid syndrome, and systemic sclerosis include the classical risk factors, but may also be due to chronic inflammatory processes and immune dysregulation. Autoantibodies, autoantigens, pro-inflammatory cytokines, and infectious agents play a role in that process. Involvement of autoimmunity in the pathogenesis of accelerated atherosclerosis in rheumatic diseases and the common pathway that leads to this condition may lead to significant change in prevention of treatment.

Pemphigus and infectious agents.

Pemphigus is a group of autoimmune bullous diseases characterized by a loss of cell adhesion and blister formation within the epidermis in the skin and/or the mucosal surfaces. Pemphigus develops due to the interaction between predisposing genetic factors and environmental factors. Among the latter, infectious agents such as viruses and bacteria were reported as preceding or exacerbating pemphigus disease. In this article we review the literature concerning the relationship between pemphigus, viral and bacterial pathogens.

Anti-cardiolipin antibodies and endothelial function in patients with coronary artery disease.

Endothelial dysfunction is considered an important marker in atherosclerosis, having a prognostic value. Antiphospholipid antibodies are considered prothrombotic and have recently been reported to be associated also with atherosclerosis. This study was conducted to investigate a possible association of endothelial dysfunction with various antiphospholipid autoantibodies in healthy subjects and patients with cardiovascular disease. In a single-center, prospective study, 2 groups were included. The study group included patients with cardiovascular diseases (coronary disease and/or cerebrovascular disease) and healthy subjects without apparent heart disease who were referred to the endothelial function laboratory for the assessment of endothelial function. Flow-mediated dilatation, which indicates endothelial function, and nitroglycerin-mediated vasodilatation, which indicates smooth-muscle function, were measured. The 2 groups were evaluated for autoantibodies, including anticardiolipin (aCL; immunoglobulin G [IgG], immunoglobulin M [IgM], and immunoglobulin A [IgA]), antinuclear antibody, anti-beta2-glycoprotein I (IgG, IgM, and IgA), and oxidized low-density lipoprotein. One hundred seven subjects were included in the study: 45 patients (42%) and 62 healthy controls (58%). Flow-mediated dilatation was significantly lower in patients compared with healthy controls (8.0 +/- 9.5% vs 8.0 +/- 13.5%, p = 0.012). In addition, nitroglycerin-mediated vasodilatation was nonsignificantly lower in patients than in healthy controls (8.0 +/- 13.4% vs 11.0 +/- 16.7%, p = 0.084). The mean levels of anti-beta2-glycoprotein I (IgG, IgM, and IgA), aCL (IgM and IgA), antinuclear antibody, and oxidized low-density lipoprotein were not different between groups. However, the mean level of IgG aCL was significantly higher in patients than in healthy controls. In conclusion, in accordance with previous reports of an association between aCL and atherosclerosis, patients with cardiovascular disease had endothelial dysfunction and elevated levels of aCL.

Carotid artery intima-media thickness, heat shock proteins and oxidized LDL autoantibodies in systemic necrotizing vasculitis.

In this study we evaluate early atherosclerotic changes and determine whether anti-HSP-60, anti-HSP-65 and anti-oxLDL autoantibodies are elevated in systemic necrotizing vasculitis. Thirty-two patients having systemic necrotizing vasculitis were compared with normal controls and patients with systemic lupus erythematosus (SLE). The antibodies against human HSP-60, HSP-65 and oxLDL were measured by antihuman ELISA kit. All patients underwent non-invasive measurements of carotid artery intima-media thickness (IMT). In a comparison between carotid IMT extent between vasculitis patients and SLE, no significant differences were noted. Levels of anti-HSP-60, anti-HSP-65 IgG and anti-oxLDL autoantibodies were similar among patients compared to controls. IgM anti-HSP-60 antibody levels were significantly lower in patients compared to controls and a similar trend was found regarding IgM anti-HSP-65. As a group, patients having various necrotizing vasculitis have similar extent of early atherosclerotic changes regardless of the vasculitis type, and these levels are similar to those found in SLE.

Low dose intravenous immunoglobulin in systemic lupus erythematosus: analysis of 62 cases.

BACKGROUND: Systemic lupus erythematosus is an autoimmune disease with diverse clinical manifestations that cannot always be regulated by steroids and immunosuppressive therapy. Intravenous immunoglobulin is an optional immunomodulatory agent for the treatment of SLE, but the appropriate indications for its use, duration of therapy and recommended dosage are yet to be established. In SLE patients, most publications report the utilization of a high dose (2 g/kg body weight) protocol. OBJECTIVES: To investigate whether lower doses of IVIg are beneficial for SLE patients. METHODS: We retrospectively analyzed the medical records of 62 patients who received low dose IVIg (approximately 0.5 g/kg body weight). RESULTS: The treatment was associated with clinical improvement in many specific disease manifestations, along with a continuous decrease in SLEDAI scores (SLE Disease Activity Index). However, thrombocytopenia, alopecia and vasculitis did not improve following IVIg therapy. CONCLUSIONS: Low dose IVIg is a possible therapeutic option in SLE and is associated with lower cost than the high dose regimen and possibly fewer adverse effects.