Anticardiolipin Research Articles

Post-COVID musculo-articular syndrome and COVID-19 association with rheumatoid arthritis

Introduction. Since the COVID-19 pandemic, there has been a great deal of evidence for a variety of post-COVID symptoms, including the presence of a musculo-articular syndrome. The aim of the study was to analyze the current literature data on the prevalence of musculo-articular syndrome and to study the association of coronavirus infection with the development of rheumatoid arthritis. Materials and methods. We searched PubMed, Medline, and Google Scholar (2020-2022) for articles using the following keywords: post-covid syndrome, muscular articular syndrome or muscle and joint pain, COVID-19, SARS-CoV-2, rheumatoid arthritis. We found 622 articles in which these words appeared in the text of the article. Further, 497 articles were excluded as irrelevant to the topic of the study. During the study of the remaining articles, special attention was paid to the occurrence of musculo-articular syndrome after COVID-19 infection and the association with rheumatoid arthritis. Results and discussion. There are studies describing musculo-articular pain syndrome and cases of antibodies to cyclic citrullinated peptide (ACCP) after COVID-19, which may indirectly indicate the development of rheumatoid arthritis in these patients. Studies reflect the increased autoreactivity of the immune system in COVID-19, consisting in increased titers of antinuclear antibodies, anti-cardiolipin antibodies, ACCP, and rheumatoid factor. A number of articles have presented results on the association between COVID-19 infection and the appearance, or exacerbation, of rheumatoid arthritis. Several mechanisms are discussed, presumably leading to the occurrence of post-COVID rheumatoid arthritis: induction by coronavirus of excess synthesis of angiotensin II, which increases the expression of inflammatory cytokines, chemokines and production of reactive oxygen species; activation of proinflammatory T-cell subpopulations; activation of Toll-like receptor-7 synovial membrane triggering the inflammatory response; "cytokine storm". Conclusion. A high percentage (from 15 to 47.7 %) of cases of musculo-articular lesions after COVID-19 infection has been identified. A number of articles have reported an association between COVID-19 infection and the onset, or exacerbation, of rheumatoid arthritis, but the issue is still under discussion, which necessitates large-scale studies specifically devoted to examining this association.

Antiphospholipid Syndrome and Pregnancy

Antiphospholipid syndrome is an autoimmune disease with a wide spectrum of manifestations from different organs, therefore it is challenging to diagnose. The disease presents antiphospholipid antibodies such as anticardiolipin antibodies (aCL), lupus anticoagulant (LA) and antiβ2-glycoprotein 1 antibodies (β2GPI). The most common symptoms include thrombosis in veins and arteries and obstretical complications such as early miscarriage, intrauterine fetal death, intrauterine growth restriction (IUGR), placental insufficiency, premature labor and eclampsia. To diagnose a patient with APS certain criteria have been chosen, where at least one clinical and one laboratory criterion must be present. In many cases it takes a lot of time before a proper diagnosis has been made, when a female patient presents obstretical complications. Adequate pharmacological treatment increases the odds of live birth rate from 20-30% to 70-80%. Scientific research shows correlation between antiphospholipid syndrome, infertility and premature ovarian insufficiency. Treatment mostly consists of heparin and low-dose aspirin, in certain cases hydrochloroquine is prescribed. Aside from pharamcological therapy, it is very important to minimize the effects of modifiable risk factors. The following article focuses on complications, diagnosing and therapy in pregnant women suffering from Antiphospholipid syndrome. All sources can be found in Pubmed’s website database.

Huge water-balloons in the belly: multiple pancreatic pseudocysts in systemic lupus erythematosus.

A 28-year-old woman presented with recurrent epigastric pain and abdominal distention for 6 months. Her symptoms first occurred on the first day of admission due to SLE flare (fever, polyarthritis, anaemia, leukocytopenia, proteinuria, low C3, positive tests on antinuclear, anti-double-stranded DNA, anti-Smith and anti-cardiolipin antibodies), when no treatment was initiated. Elevated blood amylase and CT (Fig. 1A) indicated acute pancreatitis and other common causes were excluded. Thrombotic microangiopathy (TMA) was then suspected because of renal, neuropsychiatric and haematological involvements. However, abdominal distention and peripancreatic effusions perpetuated though SLE, TMA and secondary infection remitted after using glucocorticoid, immunosuppressive agents, plasma exchange and supportive therapies. Therefore, drainage was performed a month before this presentation and CT (Fig. 1B) showed improvement. During this admission, emergency drainage was performed due to reappearing ascites. Analysis of chylous ascites identified extremely elevated amylase and lipase with Enterococcus faecium as pathogen. Massive ascites were encapsulated with a fistula connected to the newly emerged pseudocyst (Fig. 1C and D). Drainage was not removed until radiographic remission 7 months later (Fig. 1E). SLE flare and abdominal symptoms have not occurred up to the last follow-up 41 months after this admission. This case illustrates SLE-associated acute pancreatitis can present with atypical features [1, 2] and prolonged courses due to ‘add-on’ effects of SLE flare, infection, coagulopathy (thrombocytopenic purpura, antiphospholipid syndrome) and medication. Therefore, a tailored management strategy is required.

Risk factors for persistent positive anticardiolipin antibodies in women with recurrent pregnancy loss

Antiphospholipid syndrome (APS) is an established cause of recurrent pregnancy loss (RPL). It is necessary to detect persistently positive antiphospholipid antibodies to diagnose APS. This study aimed to explore risk factors for persistent anticardiolipin (aCL) positivity. Women with a history of RPL or with a history of one or more intrauterine fetal deaths after 10 weeks underwent examinations to determine the causes of RPL, including antiphospholipid antibodies. If aCL-IgG or aCL-IgM antibodies were positive, retests were performed at least 12 weeks apart. Risk factors for persistent aCL antibody positivity were retrospectively investigated. The number and percentage of cases above the 99th percentile were 74/2399 (3.1%) for aCL-IgG, and 81/2399 (3.5%) for aCL-IgM. Of the initially tested cases, 2.3% (56/2399) for aCL-IgG and 2.0% (46/2289) for aCL-IgM were ultimately positive above the 99th percentile in retests. Retest values after 12 weeks were significantly lower than the initial values for both IgG and IgM immunoglobulin classes. Initial aCL antibody titers were significantly higher in the persistent-positive group than in the transient-positive group for both IgG and IgM immunoglobulin classes. The cut-off values for predicting persistent positivity of aCL-IgG antibodies and aCL-IgM antibodies were 15 U/mL (99.1 percentile) and 11 U/mL (99.2 percentile), respectively. The only risk factor for persistently positive aCL antibodies is a high antibody titer during the initial test. When the aCL antibody titer in the initial test exceeds the cut-off value, therapeutic strategies can be defined in subsequent pregnancies without waiting for 12 weeks.

A rare presentation of primary apla and pulmonary thrombolism

Antiphospholipid syndrome (APS) is a state of hypercoagulation, causing thrombus in artery, vein and capillaries, with or without obstetrical events with the presence of autoantibodies, which includes lupus anticoagulant, anticardiolipin antibodies and anti-β2-glycoprotein 1 antibodies. It has variable clinical presentations such as vascular thrombosis and obstetrical complications, pulmonary thromboembolism (PTE), pulmonary hypertension, and acute respiratory distress syndrome. Hereby we presented a case of young male who came to our hospital with hemoptysis and isolated pulmonary embolism, with the background of APS which is rare. Hemoptysis and pulmonary thromboembolism both being fatal emergencies requiring completely different management methods.

Prediction model for missed abortion of patients treated with IVF-ET based on XGBoost: a retrospective study.

In this study, we established a model based on XGBoost to predict the risk of missed abortion in patients treated with in vitro fertilization-embryo transfer (IVF-ET), evaluated its prediction ability, and compared the model with the traditional logical regression model. We retrospectively collected the clinical data of 1,017 infertile women treated with IVF-ET. The independent risk factors were screened by performing a univariate analysis and binary logistic regression analysis, and then, all cases were randomly divided into the training set and the test set in a 7:3 ratio for constructing and validating the model. We then constructed the prediction models by the traditional logical regression method and the XGBoost method and tested the prediction performance of the two models by resampling. The results of the binary logistic regression analysis showed that several factors, including the age of men and women, abnormal ovarian structure, prolactin (PRL), anti-Müllerian hormone (AMH), activated partial thromboplastin time (APTT), anticardiolipin antibody (ACA), and thyroid peroxidase antibody (TPO-Ab), independently influenced missed abortion significantly (P<0.05). The area under the receiver operating characteristic curve (AUC) score and the F1 score with the training set of the XGBoost model (0.877 ± 0.014 and 0.730 ± 0.019, respectively) were significantly higher than those of the logistic model (0.713 ± 0.013 and 0.568 ± 0.026, respectively). In the test set, the AUC and F1 scores of the XGBoost model (0.759 ± 0.023 and 0.566 ± 0.042, respectively) were also higher than those of the logistic model (0.695 ± 0.030 and 0.550 ± 049, respectively). We established a prediction model based on the XGBoost algorithm, which can accurately predict the risk of missed abortion in patients with IVF-ET. This model performed better than the traditional logical regression model.

A combination of the HLA-DRB1*03 phenotype and low plasma mannose-binding lectin predisposes to autoantibody formation in women with recurrent pregnancy loss.

It is documented that a series of autoantibodies can be detected with increased frequency in women with recurrent pregnancy loss (RPL) and they may impact the pregnancy prognosis negatively. It is unknown whether the autoantibodies per se or the basic immune disturbances underlying autoantibody production, are the reason for this association. Our group has previously found that some genetically determined immunological biomarkers are associated with RPL and the same biomarkers are also in various degrees known to predispose to autoantibody production. The aim of this study was to clarify whether the RPL-associated immunogenetic biomarkers are associated with positivity for three major classes of autoantibodies associated with RPL. In 663 patients with RPL in whom we had results for HLA-DRB1 typing and plasma mannose-binding lectin (p-MBL) measurement, it was investigated whether there is a correlation between positivity for the autoantibodies: anticardiolipin antibodies, β2 glycoprotein I antibodies, and lupus anticoagulant (jointly called antiphospholipid antibodies), thyroid-peroxidase antibodies, and antinuclear antibodies and each of the HLA-DRB1 alleles HLA-DRB1*03 or HLA-DRB1*07 either alone or in combination with low p-MBL defined as ≤500 µg/l. Although slightly higher frequencies of positivity of two or more autoantibodies were seen in patients with either p-MBL ≤500 µg/l or being positive for HLA-DRB1*03, none were significantly associated. However, in patients with the combination of low p-MBL and HLA-DRB1*03, presence of at least one autoantibody was significantly more frequent than in patients with no such combination (OR= 2.4; 95% CI 1.2-5.0, p = 0.01). In an analysis of which autoantibodies were most strongly associated with the low p-MBL/HLA-DRB1*03 combination, antinuclear antibodies were significantly more frequent in these patients (OR 2.0; 95% CI 1.0-3.9, p=0.05) whereas the other autoantibodies were also positively but more weakly associated with this combination. In conclusion, to clarify the pathogenetic background, underlying immunogenetic factors should be examined in autoantibody positive RPL patients (as well as other patients with autoimmune diseases) but the genetic background may be complex.

Decreased protein C activity, lower ADAMTS13 antigen and free protein S levels accompanied by unchanged thrombin generation potential in hospitalized COVID-19 patients

IntroductionCOVID-19 is associated with an increased thromboembolic risk. However, the mechanisms triggering clot formation in those patients remain unknown. Patients and methodsIn 118 adult Caucasian severe but non-critically ill COVID-19 patients (median age 58 years; 73 % men) and 46 controls, we analyzed in vitro plasma thrombin generation profile (calibrated automated thrombogram [CAT assay]) and investigated thrombophilia-related factors, such as protein C and antithrombin activity, free protein S level, presence of antiphospholipid antibodies and factor V Leiden R506Q and prothrombin G20210A mutations. We also measured circulating von Willebrand factor (vWF) antigen and a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) antigen and activity. In patients, blood samples were collected on admission to the hospital before starting any therapy, including heparin. Finally, we examined the relationship between observed alterations and disease follow-up, such as thromboembolic complications. ResultsCOVID-19 patients showed 17 % lower protein C activity, 22 % decreased free protein S levels, and a higher prevalence of positive results for IgM anticardiolipin antibodies. They also had 151 % increased vWF, and 27 % decreased ADAMTS13 antigens compared with controls (p < 0.001, all). On the contrary, thrombin generation potential was similar to controls. In the follow-up, pulmonary embolism (PE) occurred in thirteen (11 %) patients. They were characterized by a 55 % elevated D-dimer (p = 0.04) and 2.7-fold higher troponin I (p = 0.002) during hospitalization and 29 % shorter time to thrombin peak in CAT assay (p = 0.009) compared to patients without PE. ConclusionsIn COVID-19, we documented prothrombotic abnormalities of peripheral blood. PE was characterized by more dynamic thrombin generation growth in CAT assay performed on admittance to the hospital.

Microstructural Changes in the Corpus Callosum in Systemic Lupus Erythematous.

Central nervous system (CNS) involvement in childhood-onset systemic lupus erythematosus (cSLE) occurs in more than 50% of patients. Structural magnetic resonance imaging (MRI) has identified global cerebral atrophy, as well as the involvement of the corpus callosum and hippocampus, which is associated with cognitive impairment. In this cross-sectional study we included 71 cSLE (mean age 24.7 years (SD 4.6) patients and a disease duration of 11.8 years (SD 4.8) and two control groups: (1) 49 adult-onset SLE (aSLE) patients (mean age of 33.2 (SD 3.7) with a similar disease duration and (2) 58 healthy control patients (mean age of 29.9 years (DP 4.1)) of a similar age. All of the individuals were evaluated on the day of the MRI scan (Phillips 3T scanner). We reviewed medical charts to obtain the clinical and immunological features and treatment history of the SLE patients. Segmentation of the corpus callosum was performed through an automated segmentation method. Patients with cSLE had a similar mid-sagittal area of the corpus callosum in comparison to the aSLE patients. When compared to the control groups, cSLE and aSLE had a significant reduction in the mid-sagittal area in the posterior region of the corpus callosum. We observed significantly lower FA values and significantly higher MD, RD, and AD values in the total area of the corpus callosum and in the parcels B, C, D, and E in cSLE patients when compared to the aSLE patients. Low complement, the presence of anticardiolipin antibodies, and cognitive impairment were associated with microstructural changes. In conclusion, we observed greater microstructural changes in the corpus callosum in adults with cSLE when compared to those with aSLE. Longitudinal studies are necessary to follow these changes, however they may explain the worse cognitive function and disability observed in adults with cSLE when compared to aSLE.

Mitral Valve Replacement for Enlarged Libman-Sacks Endocarditis in a Patient with Persistent Primary Antiphospholipid Syndrome and Recurrent Stroke: A Case Report.

BACKGROUND Anticardiolipin antibodies in patients with Libman-Sacks endocarditis (LS) are indicative of comorbid antiphospholipid syndrome (APS) and can result in cerebral infarctions. We describe a case of LS and primary APS with recurrent cerebral infarctions despite anticoagulation treatment. The patient underwent surgery for enlarged LS vegetation with high titers of antiphospholipid antibodies. CASE REPORT A 41-year-old Japanese man was admitted to hospital for small cerebral infarction recurrence in a left parietal lesion. At age 35, the patient had suffered multiple cerebral infarctions. He was found to have high serum titers of all 3 antiphospholipid antibodies. Transesophageal echocardiography (TEE) findings were normal. Differential diagnosis ruled out other autoimmune diseases and a clinical diagnosis of primary APS was made. Warfarin anticoagulation was started. When cerebral infarction recurred 6 years after the first episode, serum titers of antiphospholipid antibodies remained high, and TEE showed a 7×8 mm area of mitral vegetation. A TEE results from his first admission revealed a 5×6 mm area of mitral vegetation, which was believed to be related to the current vegetation. As anticoagulation produced no improvement, the mitral valve was replaced with a mechanical valve. Examination of the excised vegetation found it to be consistent with LS. The patient made good progress within 3 years after surgery. CONCLUSIONS LS size can increase despite anticoagulation in cases with high titers of all 3 antiphospholipid antibodies and cerebral infarction. Such patients require ongoing TEE follow-up and surgical treatment should be considered.

Long-term presence of autoantibodies in plasma of cured leprosy patients

Autoantibodies have been detected in leprosy patients, indicating that infection with M. leprae may lead to autoimmune disorders. However, whether autoimmune response last until patients are cured is unknown. Knowing the autoimmune response in cured leprosy patients is essential to identify whether symptoms are caused by leprosy itself or by other immune-related diseases. This knowledge is essential for the ongoing health management in cured leprosy patients where autoimmune disorders still exist. In our study, we selected six autoantibodies, including anticardiolipin antibody of IgG (ACA), anti-nuclear antibody (ANA), extractable nuclear antigen antibody (ENA), anti-streptolysin O (ASO), anti-double stranded DNA antibody (dsDNA), and rheumatoid factor (RF), that had been reported in leprosy patients as typical autoantibodies. We tested the six typical autoantibodies combined with LACC1, which encodes a protein associated with autoimmune disease such as Crohn’s disease and is also the susceptible gene conferring leprosy risk, in cured leprosy patients through ELISA to assess the cured patient’s immune status. We observed high positive rates of autoantibodies in cured leprosy patients, and the average plasma levels of five (ACA, ANA, ENA, ASO, and RF) out of the six autoantibodies were significantly higher in cured leprosy patients than in controls. The positive detection of autoantibodies is independent of the recovery period. Moreover, the level of these autoantibodies showed a strong positive correlation with the level of LACC1 in both controls and cured patients. This study showed that there is long-term autoimmunological activation in leprosy patients, even after decades of recovery. Autoimmune responses may influence the development and prognosis of leprosy. Special care should be given to posttreatment or cured leprosy patients regarding long-term autoimmunological activation.

Antiphospholipid Syndrome Complicated by Unilateral Pleural Effusion and Deep Vein Thrombosis: A Case Report

Antiphospholipid Antibodies (APLA) are autoantibodies directed against phospholipid-binding proteins. The development of thromboses in veins/arteries or the incidence of maternal morbidity, particularly miscarriages, in the presence of APLA constitutes Antiphospholipid Syndrome (APS). These Antiphospholipids (APLs) include antibodies against two glycoproteins, anticardiolipin antibodies, and Lupus Anticoagulant (LA). APLs are a diverse group of autoantibodies that have been linked to thrombus development, elevated maternal morbidity and mortality, and other symptoms that collectively constitute APS. Approximately half of APS cases are secondary disorders, while the remaining cases are autoimmune co-morbidities such as Systemic Lupus Erythematosus (SLE). This multisystem disorder mainly causes venous and arterial thrombosis and can also manifest as cutaneous, pulmonary, renal, and haematological involvement. APLA syndrome with pleural effusion is a rare complication. Patients with antiphospholipid syndrome can develop various types of pulmonary disease. The authors present the case of a 38-year-old male patient with a history of Deep Vein Thrombosis (DVT) and psoriasis, a known case of APLA syndrome, who presented with neck pain and breathlessness. Pulmonary embolism was ruled out, and the patient was discharged on oral anticoagulants. The present case highlights APLA as the culprit for the myriad presentations in the present case.

Antifosfolipidni sindrom kod dece

Antiphospholipid syndrome is a multisystemic autoimmune disease characterized by the appearance of arterial and/or venous thrombosis, often in multiple locations, thrombocytopenia and repeated spontaneous abortions in affected pregnant women, due to the permanent presence of antiphospholipid antibodies. It can also occur in children and manifest itself in any period of childhood, from infancy, due to transplacental transfer of maternal antibodies, or de novo production of autoantibodies, to adolescence. Clinical manifestations described in adults can also occur in children but are modified by age characteristics, such as the immaturity of the immune or other organ systems, greater exposure to viral and bacterial infections, implementation of routine immunization, absence of thrombogenic risk factors common to adults (hypertension, arteriosclerosis, consumption of cigarettes, alcohol and/or oral contraceptives), as well as the absence of pregnancy. Antiphospholipid antibodies most often used in daily clinical work are anticardiolipin antibodies, anti-b2 glycoprotein I antibodies, and lupus anticoagulants. Pathogenic mechanisms have not been investigated in detail - it is assumed that they are similar to the adult form of the disease. However, there is rare evidence of the existence of specific patterns of immune response to individual antigenic components, which may lead to specific production of antiphospholipid antibodies during childhood. It is also important to note that these antibodies can be found in about 25% of healthy children. The Sapporo criteria are used to diagnose antiphospholipid syndrome in adults. They include clinical (vascular thrombosis, repeated fetal losses) and laboratory parameters (persistent presence of one of the antiphospholipid antibodies) in the IgG and/or IgM class, in medium or high titer. The updated Sapporo criteria also apply to children. They include the same laboratory and clinical criteria, except for pregnancy pathology. The differential diagnosis is very broad and requires extensive diagnostics. Considering the specificity of the disease in childhood, the recommendations valid for adults, modified to a certain degree, apply to the treatment of diseases in children.

ANAESTHETIC CONSIDERATIONS OF ANTI-PHOSPHOLIPID ANTIBODY SYNDROME IN PREGNANCY

Anti-phospholipid syndrome (APS) is a systemic autoimmune acquired disease characterised by vascular thrombosis or pregnancy complications with the presence of antiphospholipid antibodies. It is a rare disease affecting 40-50/100,000 population and 10%-15% of recurrent abortions. Perioperative management in obstetric APS undergoing caesarean section stresses on the management of anticoagulation and prior choice of anaesthetic technique. We report the case of 26 year old multigravida ,37 weeks of gestation diagnosed with APS since 8 weeks of gestation. She had previous three miscarriages with lupus anticoagulant(LAC) value of 45.6 (normal – 36.8), IgM and IgG anticardiolipin antibody values were 8.5µ/ml and 3.8µ/ml, respectively. She was prophylactically put on Aspirin 75mg orally and Enoxaparin 0.4IU subcutaneously every 24 hours. She presented to the obstetric department and was planned for emergency caesarean section . She received her usual dose of enoxaparin on the day of surgery but aspirin was omitted. Surgery was conducted under subarachnoid blockade. Anticoagulation resumed 12 hours after surgery .No maternal and fetal complications were noted

A RARE CASE OF POST TUBERCULAR PLEURAL EFFUSION WITH SEROPOSITIVE SYSTEMIC LUPUS ERYTHEMATOSUS WITH NSIP PATTERN INTERSTITIAL LUNG DISEASE

Connective tissue disorders like systemic lupus erythematosus can have serious pulmonary complications like ILD. In this case report we had studied 25year male patient who came to OPD of Department of Respiratory Medicine NKPSIMS AND RC Nagpur Maharashtra, with complaint of breathlessness on exertion since 3-4 years and was on medication. Patient was case of post tubercular pleural effusion with Systemic Lupus Erythematosus(seropositive) with ILD. X ray chest showed prominent broncho-vascular markings in bilateral lung lobes. Pulmonary Function test showed Moderate Restriction with moderate obstruction with small airway disease. ANA &amp; Anti-cardiolipin antibody tests were positive. Patient got symptomatically relief after starting tab Deazacort (oral steroids) and inhaled corticosteroids formoterol and beclomethasone (Inhaler) with hydroxychloroquine tablet. Thus, concluding that early treatment of SLE leads to better remission of ILD.

Antiphospholipid Antibody Testing for Anti-cardiolipin and Anti-β2 Glycoprotein I Antibodies Using Chemiluminescence-Based Panels.

Antiphospholipid (antibody) syndrome (APS) is a prothrombotic condition with increased risk for thrombosis and pregnancy-related morbidity. In addition to clinical criteria related to these risks, APS is characterized by the persistent presence of antiphospholipid antibodies (aPL), as detected in the laboratory using a potentially wide variety of assays. The three APS criteria-related assays are lupus anticoagulant (LA), as detected using clot-based assays, and the solid-phase assays of anti-cardiolipin antibodies (aCL) and anti-β2 glycoprotein I antibodies (aβ2GPI), with immunoglobulin subclasses of IgG and/or IgM. These tests may also be used for the diagnosis of systemic lupus erythematosus (SLE). In particular, APS diagnosis/exclusion remains challenging for clinicians and laboratories because of the heterogeneity of clinical presentations in those being evaluated and the technical application and variety of the associated tests used in laboratories. Although LA testing is affected by a wide variety of anticoagulants, which are often given to APS patients to prevent any associated clinical morbidity, detection of solid-phase aPL is not influenced by these anticoagulants, and this thus represents a potential advantage to their application. On the other hand, various technical issues challenge accurate laboratory detection or exclusion of aPL. This report describes protocols for the assessment of solid-phase aPL, specifically aCL and aβ2GPI of IgG and IgM class by means of a chemiluminescence-based assay panel. These protocols reflect tests able to be performed on the AcuStar instrument (Werfen/Instrumentation Laboratory). Certain regional approvals may also allow this testing to be performed on a BIO-FLASH instrument (Werfen/Instrumentation Laboratory).

Lupus Anticoagulant and Anticardiolipin Antibody IgG are Associated with Increased Atherosclerosis at the Suprainguinal Elastic and Infrainguinal Muscular Arteries in the Abdomen and Lower Extremities

PurposeWhether antiphospholipid antibodies (aPLs) cause atherosclerosis in certain arteries with specific compositions and locations remains unknown. We investigated the relationship between aPLs and their association with locations of atherosclerosis in the arteries of the abdomen and lower extremities.MethodsOf 2273 patients, 697 who underwent computed tomography angiography of the abdomen and lower extremities and aPL evaluation were included. Atherosclerosis distribution score (ADS) was employed to quantify atherosclerosis severity. Multiple linear regression analysis was performed using the ADS of the suprainguinal elastic and infrainguinal muscular arteries as dependent variables and all aPLs, conventional risk factors of atherosclerosis, and coagulation-related factors as independent variables.ResultsIn the suprainguinal elastic and infrainguinal muscular arteries, common risk factors for higher ADS were age, smoking, hypertension, higher glycated hemoglobin, male sex, decreased protein S, and increased homocysteine. Lupus anticoagulant (LA) and increased triglyceride level in the suprainguinal elastic arteries and anticardiolipin antibody (aCL) immunoglobulin (Ig)G, longer alcohol consumption duration, and increased fibrinogen level in the infrainguinal muscular arteries were also risk factors for higher ADS.ConclusionLA and aCL IgG were associated with atherosclerosis in the suprainguinal elastic and infrainguinal muscular arteries, respectively. aPLs could predict the location of atherosclerosis.

A Comparative Analysis of Anticardiolipin, Anti-Β2-Glycoprotein-1, and Lupus Anticoagulants in Saudi Women with Recurrent Spontaneous Abortions.

Association and pathogenesis of antiphospholipid antibodies (APAs) in patients with Antiphospholipid syndrome (APS) as well as systemic lupus erythematosus (SLE) suffering from unexplained spontaneous abortions is controversial. Moreover, the majority of the published evidence is based on the patient histories rather than the study groups. The main objective of the present study is to do a comparative analysis of the high levels of antiphospholipid antibodies (APAs) including anticardiolipin (ACA), anti-β2-glycoprotein-1 (β2 GP1), and Lupus anticoagulants (LA) and their association with the gestational age of abortion and duration past abortion in Saudi women. In this study, 100 women living in Makkah city, located in the Western region of Saudi Arabia, with a mean age of 30.5 ± 12.60 years (mean ± standard deviation), having a previous history of recurrent spontaneous abortions were enrolled as case group and 100 healthy pregnant women previously having one or more successful pregnancies were selected as control group. Based on the gestational age of the patient’s miscarriages, our results revealed consistently and significantly high levels of ACA, β2 GP1, and LA, being greatest at more than 15 weeks when compared with 10 weeks and 11−15 weeks, respectively. Based on duration of past miscarriages, a slightly increased level was observed at ≤4 years after their first miscarriage. In addition, less or more equal levels of these antibodies were observed at 5−12 and more than 12 years in all the cases of miscarriages. We concluded an elevated pattern of APAs in these patients with an increase in the age of abortion. A comparison between the levels of ACA, β2 GP1, and LA further indicated a highly significant level of LA in all the cases of abortions (p < 0.0005).

Anticardiolipin and anti‐beta 2‐glycoprotein I antibodies in patients with unexplained articular manifestations

To determine the frequency of antiphospholipid antibodies (aPL) in patients with unexplained articular manifestations. Three hundred thirteen patients suffering from arthritis or arthralgia without evident cause and 266 healthy blood donors (HBD) were included in the study. Anticardiolipin antibodies (aCL) and anti-beta 2-glycoprotein I antibodies (aβ2GPI) were measured by ELISA. Out of the 313 patients, 250 were females and 63 were males. The mean age of patients was 49 ± 14 years (17-87 years). One hundred eleven patients have arthralgia and 202 have arthritis. The frequency of aCL and/or aβ2 GPI (24.9%) was significantly higher in patients than in HBD (10.9%). The frequency of aβ2GPI was 23.6% in patients and 9.4% in the control group (p < 10-3 ). aβ2GPI-IgA was significantly more frequent in patients than in the control group (20.4% vs. 7.5%, p < 10-3 ). aβ2GPI was most commonly observed than aCL in patients (23.6% vs. 6.4%, p < 10-6 ). IgA isotype of aβ2GPI was the most frequent in 20.4% of patients while IgG and IgM were detected in 5.4% and 2.9% respectively. This study showed that aPL were common in patients with articular manifestations and were mainly directed against β2 GPI. The role of these antibodies remains to be specified.

A Clinical Approach of Lupus Nephritis Associated with Catastrophic Antiphospholipid - Antibody Syndrome - Review and Case Report

Abstract Glomerulonephritis is a major cause of morbidity in systemic lupus erythematosus (SLE). In fact, immune complex formation and deposition in the kidney results in intraglomerular inflammation with recruitment of leukocytes and activation and proliferation of resident renal cells. Intense injury may destroy resident renal cells by necrosis or apoptosis resulting in fibrinoid necrosis. When injury is less intense, endocapillary cells respond by proliferating and production of extracellular matrix (proliferative lesions). Renal biopsy, examination of urine sediment and measurement of C3 levels (and to less anti-DNA titers) are essential for the management of lupus nephritis. Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by thrombotic episodes in the arterial or venous circulation, in the presence of antiphospholipid antibodies (aPL), namely lupus anticoagulant (LA), anticardiolipin antibodies, and anti-β2glycoprotein-I antibodies (anti-β2GPI). Catastrophic APS (CAPS) is a very rare (---lt---1%) and extremely severe variant of APS. It is characterized by multiple systems and thrombotic organ involvement that occurs in a very short period (days to weeks). Renal involvement is a common feature in CAPS, the most frequent finding is thrombotic microangiopathy (TMA), but other chronic lesions of APSN can also be found.