scholarly journals COVID-19—A Trigger Factor for Severe Immune-Mediated Thrombocytopenia in Active Rheumatoid Arthritis

Life ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 77
Author(s):  
Anca Bobircă ◽  
Florin Bobircă ◽  
Ioan Ancuța ◽  
Anca Florescu ◽  
Mihai Bojincă ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Platelet Count ◽  
Viral Infections ◽  
Molecular Mimicry ◽  
Rare Complication ◽  
Antigen Expression ◽  
Trigger Factor ◽  
Drug Induced ◽  
Immune Mediated ◽  
Prognosis Indicator

Thrombocytopenia is defined as a platelet count below 150,000/mm3 for adults. There is still controversy about whether individuals with platelet counts of 100,000/mm3 to 150,000/mm3 should be classified as having genuine thrombocytopenia or borderline thrombocytopenia. Thrombocytopenia is considered mild when the platelet count is between 70,000 and 150,000/mm3 and severe if the count is less than 20,000/mm3. Thrombocytopenia in rheumatoid arthritis is a rare complication, with an incidence estimated between 3 and 10%. The main etiological aspects include drug-induced thrombocytopenia and immune thrombocytopenic purpura. The most common hematological abnormalities in SARS-CoV-2 infection are lymphopenia and thrombocytopenia. It has been observed that the severity of thrombocytopenia correlates with the severity of the infection, being a poor prognosis indicator and a risk factor for mortality. COVID-19 can stimulate the immune system to destroy platelets by increasing the production of autoantibodies and immune complexes. Autoimmunity induced by viral infections can be related to molecular mimicry, cryptic antigen expression and also spreading of the epitope. During the COVID-19 pandemic, it is of great importance to include the SARS-CoV-2 infection in differential diagnoses, due to the increased variability in forms of presentation of this pathology. In this review, our aim is to present one of the most recently discovered causes of thrombocytopenia, which is the SARS-CoV-2 infection and the therapeutic challenges it poses in association with an autoimmune disease such as rheumatoid arthritis.

Heparin-induced thrombocytopenia: when a low platelet count is a mandate for anticoagulation

Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 225-232 ◽  
Author(s):  
Thomas L. Ortel
Keyword(s):  
Platelet Count ◽  
Heparin Therapy ◽  
Severe Thrombocytopenia ◽  
Drug Induced ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Immune Mediated ◽  
Number Of Patients ◽  
Increased Risk ◽  
Antibody Levels

Abstract Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder caused by the development of antibodies to platelet factor 4 (PF4) and heparin. The thrombocytopenia is typically moderate, with a median platelet count nadir of ~50 to 60 × 109 platelets/L. Severe thrombocytopenia has been described in patients with HIT, and in these patients antibody levels are high and severe clinical outcomes have been reported (eg, disseminated intravascular coagulation with microvascular thrombosis). The timing of the thrombocytopenia in relation to the initiation of heparin therapy is critically important, with the platelet count beginning to drop within 5 to 10 days of starting heparin. A more rapid drop in the platelet count can occur in patients who have been recently exposed to heparin (within the preceding 3 months), due to preformed anti-heparin/PF4 antibodies. A delayed form of HIT has also been described that develops within days or weeks after the heparin has been discontinued. In contrast to other drug-induced thrombocytopenias, HIT is characterized by an increased risk for thromboembolic complications, primarily venous thromboembolism. Heparin and all heparin-containing products should be discontinued and an alternative, non-heparin anticoagulant initiated. Alternative agents that have been used effectively in patients with HIT include lepirudin, argatroban, bivalirudin, and danaparoid, although the last agent is not available in North America. Fondaparinux has been used in a small number of patients with HIT and generally appears to be safe. Warfarin therapy should not be initiated until the platelet count has recovered and the patient is systemically anticoagulated, and vitamin K should be administered to patients receiving warfarin at the time of diagnosis of HIT.

scholarly journals Thrombocytopenia in children: a clinico-etiological profile in an urban tertiary care hospital

2018 ◽  
Vol 6 (1) ◽  
pp. 131
Author(s):  
Subramanian V. ◽  
Santosh Kumar K.
Keyword(s):  
Platelet Count ◽  
Viral Infections ◽  
Tertiary Care ◽  
Care Hospital ◽  
Drug Induced ◽  
Medical College ◽  
Clinical Complications ◽  
Paediatric Department ◽  
The Relationship ◽  
Haematological Finding

Background: Thrombocytopenia is a common haematological finding that we come across while managing a sick child. Etiological profile and presentation of thrombocytopenia varies among children. The objective of this study was to study the clinical and laboratory profile of children with thrombocytopenia, associated clinical complications and assess the relationship between platelet levels and severity of disease.Methods: The study was carried out in 644 children between 1 month and 12 years, admitted in Paediatric Department of Raja Rajeshwari medical college and hospital, Bangalore between August 2012 to August 2014.Results: The commonest causes of thrombocytopenia in our study were of infectious aetiology (86.6%). Among Infections Viral infections were the major cause in more than 78% of cases. Other causes included haematological problems, drug induced thrombocytopenia and connective tissue disorders. Bleeding manifestations were present in 33.07% of patients and the commonest bleeds were skin and mucous membranes. Bleeding manifestations were seen most commonly in children with a platelet count less than 50000/µl.Conclusions: Viral Infections were the commonest cause for thrombocytopenia in Children. Platelet count was neither predictive of bleeding manifestations nor predictive of need for platelet transfusion.

scholarly journals REFRACTORY THROMBOCYTOPENIA AND NEUTROPENIA: A DIAGNOSTIC CHALLENGE

2015 ◽  
Vol 7 ◽  
pp. e2015018 ◽  
Author(s):  
Emmanuel Gyan ◽  
François Dreyfus ◽  
Pierre Fenaux
Keyword(s):  
Who Classification ◽  
Viral Infections ◽  
Antigen Expression ◽  
Refractory Anemia ◽  
Diagnostic Challenge ◽  
Drug Induced ◽  
Unknown Significance ◽  
Concomitant Medications ◽  
Accurate Quantification ◽  
Who 2008

Background. The 2008 WHO classification identified refractory cytopenia with unilineage dysplasia (RCUD) as a composite entity encompassing refractory anemia, refractory thrombocytopenia (RT), and refractory neutropenia (RN), characterized by 10% or more dysplastic cells in the bone marrow respective lineage. The diagnosis of RT and RN is complicated by several factors.  Diagnosing RT first requires exclusion of familial thrombocytopenia, chronic auto-immune thrombocytopenia, concomitant medications, viral infections, or hypersplenism. Diagnosis of RN should also be made after ruling out differential diagnoses such as ethnic or familial neutropenia, as well as acquired, drug-induced, infection-related or malignancy-related neutropenia. An accurate quantification of dysplasia should be performed in order to distinguish RT or RN from the provisional entity named idiopathic cytopenia of unknown significance (ICUS). Cytogenetic analysis, and possibly in the future somatic mutation analysis (of genes most frequently mutated in MDS), and flow cytometry analysis aberrant antigen expression on myeloid cells may help in this differential diagnosis. Importantly, we and others found that, while isolated neutropenia and thrombocytopenia are not rare in MDS, those patients can generally be classified (according to WHO 2008 classification) as refractory cytopenia with multilineage dysplasia or refractory anemia with excess blasts, while RT and RN (according to WHO 2008) are quite rare.These results suggest in particular that identification of RT and RN as distinct entities could be reconsidered in future WHO classification updates.

Levofloxacin-Induced Acute Immune-Mediated Thrombocytopenia of Rapid-Onset

2017 ◽  
Vol 31 (2) ◽  
pp. 234-237 ◽  
Author(s):  
Andrew W. Shih ◽  
Andy S. Lam ◽  
Theodore E. Warkentin
Keyword(s):  
Platelet Count ◽  
Drug Exposure ◽  
Rapid Onset ◽  
Chronic Obstructive ◽  
Drug Induced ◽  
Obstructive Pulmonary Disease ◽  
Immune Mediated ◽  
Drug Dependent ◽  
Low Sensitivity ◽  
Count Recovery

Drug-induced immune thrombocytopenia (D-ITP) typically occurs after the patient has been receiving the implicated drug for at least 1 week, due to newly forming drug-dependent antibodies (“typical-onset” D-ITP). A “rapid-onset” form of D-ITP can occur when previous sensitization has occurred, where antibodies have thus already been formed, and a precipitous platelet count fall occurs upon reexposure. Typical-onset D-ITP has been reported after levofloxacin, but the rapid-onset form with a well-documented previous exposure has not been described. We report a 76-year-old male treated with levofloxacin for acute exacerbation of chronic obstructive pulmonary disease. After a single 750 mg oral dose of levofloxacin, his platelet count fell from 187 to 5 × 109/L (nadir) over 4 days. Other causes of thrombocytopenia were ruled out. He had received a previous course of levofloxacin 6 months earlier. Discontinuation of levofloxacin and treatment with intravenous immunoglobulin and dexamethasone resulted in platelet count recovery. Levofloxacin-dependent antibodies were not detectable, consistent with the known low sensitivity of laboratory tests for drug-dependent antibodies, presumably indicating antibodies against levofloxacin metabolites, as is indirectly supported by the abrupt but relatively slow platelet count decline observed. This case illustrates a rapid-onset presentation of levofloxacin-induced D-ITP in the setting of previous drug exposure.

Eptifibatide-induced profound thrombocytopaenia: a rare complication

2021 ◽  
Vol 14 (6) ◽  
pp. e241594
Author(s):  
Pranav Mahajan ◽  
Fatima Ayub ◽  
Roxana Azimi ◽  
Naveed Adoni
Keyword(s):  
Platelet Count ◽  
Intracranial Haemorrhage ◽  
Rare Complication ◽  
Antiplatelet Agent ◽  
Cardiac Catheterisation ◽  
Beta Lactam ◽  
Drug Induced ◽  
Beta Lactam Antibiotics ◽  
Common Causes ◽  
The Common

Drug-induced immune thrombocytopaenia (DITP) is a type of thrombocytopaenia caused by medications. It is one of the common causes of unexplained thrombocytopaenia. It is caused by the formation of autoantibodies against a particular drug and is commonly observed with medications like heparin and beta-lactam antibiotics. One of the rare causes of DITP is eptifibatide, a widely used antiplatelet agent for pretreatment in cardiac catheterisation. These patients can be asymptomatic or develop complications like skin bruising, epistaxis and even intracranial haemorrhage. We present a case of a 64-year-old man who developed eptifibatide-induced profound thrombocytopaenia leading to extensive skin bruising. He was treated with platelet transfusions followed by prompt improvement in platelet count.

scholarly journals P34 Early-onset neutropenia in rituximab treated rheumatoid arthritis patients: a case series

Rheumatology ◽  
2020 ◽  
Vol 59 (Supplement_2) ◽  
Author(s):  
Chung Mun Alice Lin ◽  
Alice R Lorenzi ◽  
Faye A. H Cooles
Keyword(s):  
Rheumatoid Arthritis ◽  
Early Onset ◽  
Bystander Effect ◽  
Case Reports ◽  
Rare Complication ◽  
Case Series ◽  
Acute Onset ◽  
Biliary Cirrhosis ◽  
Drug Induced ◽  
Cycle Number

Abstract Background Rituximab is a chimeric monoclonal anti-CD20 antibody, used in the management of autoimmunity. It is known to have a favourable safety profile, however, a rare complication includes early-onset neutropenia (EON), defined as neutropenia having occurred within four weeks of rituximab treatment. Only eight case reports have been published so far, the majority of which relate to its use in SLE and none in rheumatoid arthritis (RA). We report here the first dedicated case series of post-rituximab EON in RA. Methods We identified 4 RA patients with EON. All were anti-citrullinated protein antibody (ACPA) and rheumatoid factor (RF) positive. Demographics were female:male ratio 3:1, with mean age 58 (range 33-69). Our first patient (65F) had a past medical history (PMH) of asymptomatic primary biliary cirrhosis (ANA+ve, AMA+ve, M2+ve), the second (65F) had Sjogren’s syndrome (ANA+ve, dsDNA+ve, IgG+ve) and the third (69F) had diverticulosis, Raynaud’s phenomenon and subacute cutaneous lupus with no systemic manifestations (ANA+ve, Ro and La +ve). The fourth patient (33M) had no PMH. Three had previously reported intermittent neutropenia on prior disease modifying anti-rheumatic drug (DMARD) therapy, but none were on DMARDs/doses known to cause this at the time of Rituximab. Standard Rituximab regimens were administered (1g with 100mg IV methylprednisolone, two weeks apart) with two patients (33M, 69F) on concurrent methotrexate (15mg) and hydroxychloroquine (200mg) respectively. Results EON occurred at 4, 11 and 14 days (n = 2) (mean 10 days) post-infusion with mean nadir 0.57x109/L (range 0.05 - 1.17x109/L). It was the first treatment cycle for two patients (65F and 33M), whilst the others (65F and 69F) had received 2-3 previous cycles uneventfully. Patient 2, 65F and ANA+ve, subsequently developed neutropenic sepsis and was treated with standard protocol and G-CSF (granulocyte-colony stimulating factor). Cultures were negative and other investigations did not identify any infective source. The other three patients’ (33M, 69F) neutropenia resolved spontaneously without required intervention. Conclusion EON is a rare but serious complication of rituximab but to date no clear mechanism has been identified. It has been suggested that EON may be due to a bystander effect of lysozyme and granzyme release, secondary to B cell killing and that individuals with a high-affinity FcγRIIIa 158 V allele are more susceptible to this mechanism and therefore prone to a greater depth of neutropenia. Because of its relative acute onset, we may actually be under-recognising uncomplicated episodes of EON due to variability in routine blood monitoring post-treatment. We therefore want to highlight the need for vigilance in this patient cohort, particularly in those who are already susceptible to drug-induced neutropenia or are ANA+ve, in addition to vigilance irrespective of cycle number. Future monitoring of early neutrophil counts in Rituximab-treated RA patients may provide additional insight into this rare complication. Disclosures C. Lin None. A.R. Lorenzi None. F.A.H. Cooles None.

scholarly journals Myocarditis with COVID-19 mRNA Vaccines

Circulation ◽  
2021 ◽  
Author(s):  
Biykem Bozkurt ◽  
Ishan Kamat ◽  
Peter J. Hotez
Keyword(s):  
Immune Response ◽  
Viral Infections ◽  
Molecular Mimicry ◽  
Rare Complication ◽  
Male Predominance ◽  
Benefit Risk Assessment ◽  
Immune Pathways ◽  
Almost All ◽  
Symptoms And Signs ◽  
Self Antigens

Myocarditis has been recognized as a rare complication of coronavirus 2019 (COVID-19) mRNA vaccinations, especially in young adult and adolescent males. According to the U.S. Centers for Disease Control (CDC), myocarditis/pericarditis rates are approximately 12.6 cases per million doses of second dose mRNA vaccine among 12-39-year-olds. In reported cases, patients with myocarditis invariably presented with chest pain, usually 2-3 days after a second dose of mRNA vaccination and had elevated cardiac troponin levels. ECG was abnormal with ST elevations in most, and cardiac MRI was suggestive of myocarditis in all tested patients. There was no evidence of acute COVID-19 or other viral infections. In one case, a cardiomyopathy gene panel was negative, but autoantibody levels against certain self-antigens and frequency of natural killer cells were increased. Although the mechanisms for development of myocarditis are not clear, molecular mimicry between the spike protein of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and self-antigens, trigger of preexisting dysregulated immune pathways in certain individuals, immune response to mRNA and activation of immunological pathways, and dysregulated cytokine expression have been proposed. The reasons for male predominance in myocarditis cases are unknown, but possible explanations relate to sex hormone differences in immune response and myocarditis, and also under-diagnosis of cardiac disease in women. Almost all patients had resolution of symptoms and signs, and improvement in diagnostic markers and imaging with or without treatment. Despite rare cases of myocarditis, the benefit-risk assessment for COVID-19 vaccination shows a favorable balance for all age and sex groups; therefore COVID-19 vaccination is recommended for everyone 12 years of age and older.

Immuno-biological Assessments of Temporomandibular Joint Disease in Patients with Immune-mediated Rheumatic Conditions. A cross sectional study of 273 cases

2018 ◽  
Vol 68 (12) ◽  
pp. 2987-2991
Author(s):  
Cristina Iordache ◽  
Bogdan Vascu ◽  
Eugen Ancuta ◽  
Rodica Chirieac ◽  
Cristina Pomirleanu ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Psoriatic Arthritis ◽  
Temporomandibular Joint ◽  
Final Analysis ◽  
Cross Sectional Study ◽  
Joint Disease ◽  
Sectional Study ◽  
Cross Sectional ◽  
Immune Parameters ◽  
Immune Mediated

Temporomandibular joint (TMJ) is commonly involved in various immune-mediated rheumatic disorders accounting for significant disability and impaired quality of life. The aim of our study was to assess inflammatory and immune parameters in patients with TMJ arthritis related to rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) and to identify potential relation with severity and dysfunction of TMJ pathology. We performed a cross-sectional study in a cohort of 433 consecutive RA, 32 JIA, 258 AS, and 103 PsA. Only patients presenting with clinically significant TMJ involvement (273) related to their rheumatic condition were included in the final analysis. TMJ involvement is traditionally described in chronic inflammatory rheumatic disorders, particularly in patients with higher levels of inflammation as detected in rheumatoid arthritis and psoriatic arthritis. Disease activity and severity, as well as biological and positive serological assessments (rheumatoid factor, anti-cyclic citrullinated peptide, IL-1) remain significant determinants of the severity of TMJ arthritis.

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