Practical approach to thrombocytopenia in patients with sepsis: a narrative review.

Thrombocytopenia frequently occurs in patients with sepsis. Disseminated intravascular coagulation (DIC) may be a possible cause of thrombocytopenia owing to its high prevalence and association with poor outcomes; however, it is important to keep the presence of other diseases in mind in sepsis practice. Thrombotic microangiopathy (TMA), which is characterized by thrombotic thrombocytopenic purpura, Shiga toxin-producing Escherichia coli hemolytic uremic syndrome (HUS), and complement-mediated HUS, is characterized by thrombocytopenia, microangiopathic hemolytic anemia, and organ damage. TMA has become widely recognized in recent years because of the development of specific treatments. Previous studies have reported a remarkably lower prevalence of TMA than DIC; however, its epidemiology is not well defined, and there may be cases in which TMA is not correctly diagnosed, resulting in poor outcomes. Therefore, it is important to differentiate DIC from TMA. Nevertheless, differentiating between DIC and TMA remains a challenge as indicated by previous reports that most patients with TMA can be diagnosed as DIC using the universal coagulation scoring system. Several algorithms to differentiate sepsis-related DIC from TMA have been suggested, contributing to improving the care of septic patients with thrombocytopenia; however, it may be difficult to apply these algorithms to patients with coexisting DIC and TMA, which has recently been reported. This review describes the disease characteristics, including epidemiology, pathophysiology, and treatment, of DIC, TMA, and other diseases with thrombocytopenia and proposes a novel practical approach flow, which is characterized by the initiation of the diagnosis of TMA in parallel with the diagnosis of DIC. This practical flow also refers to the longitudinal diagnosis and treatment flow with TMA in mind and real clinical timeframes. In conclusion, we aim to widely disseminate the results of this review that emphasize the importance of incorporating consideration of TMA in the management of septic DIC. We anticipate that this practical new approach for the diagnostic and treatment flow will lead to the appropriate diagnosis and treatment of complex cases, improve patient outcomes, and generate new epidemiological evidence regarding TMA.

The history of thrombotic thrombocytopenic purpura research: a narrative review.

Background and Objective: Thrombotic thrombocytopenic purpura (TTP) is a rare but debilitating thrombotic microangiopathy that results from severe deficiency of the enzyme ADAMTS13. The disorder was first described in the early 20th century, but the pathophysiology of the disease has only been elucidated in the past three decades. In this narrative review, we will summarize the milestone moments in the history of TTP research and discovery. Methods: We searched literature using PubMed from 1924 to 2023 using the following free text searches: "thrombotic thrombocytopenic purpura", "Moschcowitz disease", and "thrombotic microangiopathy". We found 6,917 peer-reviewed articles and sorted through these for relevant literature pertinent to the review. A total of 46 articles were included for review and the remainder were excluded. Key Content and Findings: The history of TTP research was reviewed, with a sampling of major events in the evolution of the understanding of the pathophysiology and treatment of the disease discussed here. There remains much to be learned about the nature of the disease in order to develop more specific and less harmful treatments. Conclusions: An overview of the major discoveries that have led to our current understanding of TTP reveals the results of collaboration of multiple groups of physicians and scientists through the past century, with additional breakthroughs likely to occur in the future because of that same collaborative spirit.

A Complicated Case of Thrombotic Thrombocytopenic Purpura in Pregnancy with Superimposed Preeclampsia.

A 32-year-old woman at 26 weeks gestation presented with severe unexplained thrombocytopenia with signs and symptoms of severe pregnancy-induced hypertension and what appeared to be hemolysis, elevated liver enzymes, and low platelet count syndrome, leading to a severe diagnostic challenge. The multidisciplinary team identified her condition as thrombotic thrombocytopenic purpura. Timely management decisions and multidisciplinary care ensured a safe delivery.

Hypermethylation of the FOXP3 gene regulates Tregs immunodysregulation in chronic idiopathic thrombocytopenic purpura.

BACKGROUND: Chronic idiopathic thrombocytopenic purpura (ITP) is an autoimmune disease characterized by a breakdown of immune tolerance; in ITP, the body's immune system mistakenly attacks and destroys platelets. This study aims to investigate the role and underlying mechanisms of FOXP3 in chronic ITP. METHODS: Flow cytometry was used to detect the proportion of CD4+CD25+FOXP3+ regulatory T cells (Tregs) in CD4+CD25+ T lymphocytes from 20 patients with chronic ITP (CITP), 20 acute ITP (AITP) controls, and 20 healthy individuals.CD4+CD25+ Treg cells were isolated from peripheral blood of patients with CITP using magnetic beads and then treated with phosphate-buffered saline solution or decitabine (a methylation inhibitor) for 48 h. The levels of interleukin-2 (IL-2), IL-10, and transforming growth factor-beta1 (TGF-ß1) in the plasma and CD4+CD25+ Treg cells were assessed by Enzyme-linked-immunosorbent serologic assay and quantitative real-time polymerase chain reaction (qRT-PCR). FOXP3 level was measured by qRT-PCR and Western blot analysis. Methylation-specific PCR (MS-PCR) was adopted to detect the status of FOXP3 methylation. RESULTS: The number of Treg cells and the contents of IL-2, IL-10, and TGF-ß1 decreased in patients with CITP, compared to the AITP control group and normal group. FOXP3 expression was reduced and FOXP3 methylation increased in patients with CITP, compared to the AITP control group and normal group. Hypermethylation of FOXP3 promoter led to decrease in FOXP3 level in Treg cells. Inhibition of FOXP3 promoter hypermethylation promoted the secretion of IL-2, IL-10, and TGF-ß1 in Treg cells. CONCLUSION: The number of Treg cells in CITP patients decreased, and the hypermethylation of FOXP3 promoter led to reduction of its expression in Treg cells, thus affecting the immune functioning of Treg cells.

Large-scale bidirectional Mendelian randomization study identifies new gut microbiome significantly associated with immune thrombocytopenic purpura.

Introduction: A variety of studies have shown a link between the gut microbiota and autoimmune diseases, but the causal relationship with Henoch-Schönlein purpura (HSP) and immune thrombocytopenic purpura (ITP) is unknown. Methods: This study investigated the bidirectional causality between gut microbiota and HSP and ITP using Mendelian randomization (MR). Large-scale genetic data of gut microbiota at phylum to species level from the MiBioGen consortium and the Dutch Microbiome Project were utilized. Genome-wide association studies (GWAS) summary statistics for HSP and ITP came from FinnGen R10. Various MR methods were applied to infer causal relationships, including inverse variance weighted (IVW), maximum likelihood (ML), cML-MA, MR-Egger, weighted median, weighted model, and MR-PRESSO. Multiple sensitivity analyses and Bonferroni correction were conducted to enhance robustness and reliability. Results: Based on the IVW estimates, 23 bacterial taxa were identified to have suggestive associations with HSP and ITP. Remarkably, after Bonferroni correction, family Alcaligenaceae (OR = 2.86, 95% CI = 1.52-5.37; IVW, p = 1.10 × 10-3, ML, p = 1.40 × 10-3) was significantly associated with ITP as a risk factor, while family Bacteroidales S24 7group (OR = 0.46, 95% CI = 0.29-0.74; IVW, p = 1.40 × 10-3) was significantly associated with ITP as a protective factor. No significant associations between HSP and ITP and gut microbiota were found in reverse analyses. Conclusion: Our study provides evidence of causal effects of gut microbiota on HSP and ITP, highlighting the importance of further research to clarify the underlying mechanisms and develop targeted therapeutic interventions for these autoimmune diseases.

Role of plasma exchange in a post-partum case of severe thrombotic thrombocytopenic purpura with acute kidney injury.

Thrombotic thrombocytopenic purpura (TTP) is a life-threatening disease present with the classic pentad of microangiopathic hemolytic anemia (MAHA), fever, neurologic changes, thrombocytopenia, and renal dysfunction. In a diagnostic dilemma, therapeutic plasma exchange (TPE) is a choice of life-saving intervention. In this, we assess the efficacy of TPE in a suspected case of post-partum TTP. A 27 years old female was admitted in an emergency on day 8 after a lower segment cesarian section (LSCS) with unresponsive behavior for 3 days and with TTP. She was normal 32 days back with her second, 7-month pregnancy. Ultrasonography (USG) showed an umbilical cord around the neck of the baby. On the fifth post-operative day, she was shifted to emergency with fever, generalized anasarca, gastrointestinal tract (GI) bleeding, low platelet count, and low Hb, with a poor Glasgow coma scale (GCS) of 6. On the bases of serum urea and serum creatinine, she presented acute kidney injury with encephalopathy. At emergency, she was unresponsive to mechanical ventilation and supportive treatment; hence, therapeutic plasma exchange was performed. After eight TPE cycles, the patient presented with an improved hematological and renal profile with good GCS. TPE is helpful and life-saving for suspected TTP patients with AKI.

Immune Thrombotic Thrombocytopenic Purpura: Pathophysiology, Diagnosis, Therapy and Open Issues.

Immune thrombotic thrombocytopenic purpura (iTTP) is a life-threatening thrombotic microangiopathy characterized by microangiopathic hemolytic anemia, thrombocytopenia, and ischemic end-organ injury due to microvascular platelet-rich thrombi. iTTP pathophysiology is based on a severe ADAMTS13 deficiency, the specific von Willebrand factor (vWF)-cleaving protease, due to anti-ADAMTS13 autoantibodies. Early diagnosis and treatment reduce the mortality. Frontline therapy includes daily plasma exchange (PEX) with fresh frozen plasma replacement and immunosuppression with corticosteroids. Caplacizumab has recently been added to frontline therapy. Caplacizumab is a nanobody that binds to the A1 domain of vWF, blocking the interaction of ultra-large vWF multimers with the platelet and thereby preventing the formation of platelet-rich thrombi. Caplacizumab reduces mortality due to ischemic events, refractoriness, and exacerbations after PEX discontinuation. Until now, the criteria for response to treatment mainly took into account the normalization of platelet count and discontinuation of PEX; with the use of caplacizumab leading to rapid normalization of platelet count, it has been necessary to redefine the response criteria, taking into account also the underlying autoimmune disease. Monitoring of ADAMTS13 activity is important to identify cases with a low value of activity (<10IU/L), requiring the optimization of immunosuppressive therapy with the addition of Rituximab. Rituximab is effective in patients with refractory disease or relapsing disease. Currently, the use of Rituximab has expanded, both in frontline treatment and during follow-up, as a pre-emptive approach. Some patients do not achieve ADAMTS13 remission following the acute phase despite steroids and rituximab treatment, requiring an individualized immunosuppressive approach to prevent clinical relapse. In iTTP, there is an increased risk of venous thrombotic events (VTEs) as well as arterial thrombotic events, and most occur after platelet normalization. Until now, there has been no consensus on the use of pharmacological thromboprophylaxis in patients on caplacizumab because the drug is known to increase bleeding risk.

Microangiopathic thrombocytopenia caused by vitamin B12 deficiency responding to plasma exchange.

A young adult African American female presented with normocytic microangiopathic haemolytic anaemia, elevated lactate dehydrogenase and thrombocytopenia. The patient responded to therapeutic plasma exchanges (TPE) for presumed thrombotic microangiopathy caused by thrombotic thrombocytopenic purpura (TTP). After relapsing, the patient was found to have pancytopenia, megaloblastic bone marrow and low vitamin B12 consistent with pernicious anaemia, which improved with intramuscular B12 and discontinuation of TPE. B12-deficient macrocytosis was not seen at presentation due to concomitant alpha-thalassaemia. Initial clinical/laboratory improvement is attributed to B12 present in TPE plasma. B12 deficiency can mimic TTP. Vigilance is needed regarding atypical presentations of pernicious anaemia.

Double-territory STEMI with cardiogenic shock in immune thrombocytopenic purpura with severe thrombocytopenia-a case report.

Background: Myocardial infarction (MI) in a patient with immune thrombocytopenia is a rare scenario which is very challenging to manage. Case summary: We present a rare case of a patient with immune thrombocytopenic purpura who developed double territory segment-elevation MI with cardiogenic shock. She had an extremely rare presentation with a fresh mobile thrombus in the aortic root which was trap-dooring the right coronary artery ostium and extending into the artery with an embolism into the distal left anterior descending artery. We managed this patient conservatively with excellent recovery owing to the dangerous location of the hanging thrombus, and severe thrombocytopenia. Conclusions: Multidisciplinary approach is required for the management of MI in patients with pre-existing blood disorders, with therapy tailored to the patient's presentation and treatment requirements.

Acquired Thrombotic Thrombocytopenic Purpura (TTP) Presenting With Synthetic Cannabinoid Use.

Synthetic cannabinoids (SCs) have become commercially available throughout the United States as manufacturers circumvent regulations with labels stating "not for human consumption" with misleading advertisements, resulting in the consumption of products that are not safe or regulated. We present a case report of a middle-aged woman exhibiting altered mental status secondary to SC use who was found to have severe thrombocytopenia and hemolytic anemia. She was later confirmed to have thrombotic thrombocytopenic purpura (TTP) through ADAMTS13 testing. TTP is one of several platelet-related disorders presenting with findings of hemolytic anemia and thrombocytopenia. The presence of altered mental status is typically used as a symptomatic differentiator between hemolytic uremic syndrome, immune thrombocytopenic purpura, and TTP. SCs can cause superimposed altered mental status, which, in the setting of a concomitant platelet disorder, can complicate the standard workup and prolong the time to a final diagnosis. This case serves as an essential reminder that collecting detailed social history and promptly recognizing laboratory abnormalities is critical for early recognition of TTP, as the diagnosis is time-sensitive and delays in recognition can lead to significant morbidity and mortality.

Safety and efficacy of danazol in immune thrombocytopenia: a systematic review.

Background: The treatment landscape for relapsed or refractory immune thrombocytopenia (ITP) after corticosteroids is complex. Objectives: We aimed to assess the efficacy of danazol in treating ITP and evaluate the safety and adverse events following its administration. Methods: We searched the databases PubMed, EMBASE, and ClinicalTrials.gov for all published studies assessing danazol's efficacy and safety in treating ITP. The retrieved studies were screened by title and abstract, followed by full-text screening based on the eligibility requirements. The quality assessment was performed using a set of questionnaires. The data were extracted on the descriptive characteristics of the studies and participants, drug dosage, efficacy measures, and adverse effects, and the data were synthesized. Results: A total of 17 studies consisting of 901 participants were included. The overall response rate is around 61% in this analysis. Among the participants, 315 (34.9%) were men. The age of participants ranged from 16 to 86 years. Danazol combined with other pharmacologic interventions, including all-trans-retinoic acid or glucocorticoids, generated better results. The most common side effects appear to be liver injury and elevation of liver enzymes, weight gain, oligomenorrhea, amenorrhea, and myalgia. Conclusion: Danazol at low-to-medium doses was well tolerated and succeeded in improving ITP. Danazol therapy may be helpful in the treatment of chronic ITP that is corticosteroid refractory and when corticosteroids or splenectomy (or both) is contraindicated. Danazol can be considered for further research and development in treating primary immune thrombocytopenia.

Immune Thrombocytopenic Purpura and Ganglionic Tuberculosis: An Unlikely Link.

Tuberculosis (TB) is one of the leading infectious causes of morbidity and mortality worldwide. Either in its pulmonary (PTB) or extrapulmonary forms (EPTB), TB has a wide variety of manifestations, including hematological ones like thrombocytosis (especially in PTB) and thrombocytopenia (mainly with disseminated or miliary TB). Hematological manifestations are infrequently presenting features of TB, and within them, immune thrombocytopenic purpura (ITP)-associated TB is one of the rarest presenting features. We report a case of a 22-year-old woman with a diagnosis of ganglionic tuberculosis (GTB) presenting with ITP. The therapeutic approach was challenging and included the use, originally, of intravenous immunoglobulin 30 mg/day for five days and, posteriorly, of high-dose corticosteroids (dexamethasone 40 mg/day) and anti-tubercular therapy with satisfactory outcomes.

Clinical and economic burden of suspected thrombotic thrombocytopenic purpura in US hospitals.

DISCLAIMER: In an effort to expedite the publication of articles, AJHP is posting manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time. PURPOSE: Severe ADAMTS13 deficiency (activity <10%) is the diagnostic threshold for thrombotic thrombocytopenic purpura (TTP) and is associated with various clinical symptoms, abnormal laboratory results, and long-term complications. METHODS: This retrospective, noninterventional cohort study used the Premier Healthcare Database to identify patients with ADAMTS13 activity of <10% in US hospitals from January 1, 2016, through March 31, 2020. The objective was to describe patient characteristics, laboratory results, comorbidities (as measured by the Elixhauser comorbidity index), symptoms, length of stay, treatment patterns, mortality, inpatient costs, and readmission rates (summarized descriptively). Inpatient costs were calculated as total cost to the hospital. RESULTS: There were 211 patients with severe ADAMTS13 deficiency; 89% of patients had a TTP-related diagnosis, of whom 62% had a primary diagnosis of thrombotic microangiopathy. Over 80% of patients with available data had a decreased platelet count and elevated lactate dehydrogenase; schistocytes were detected in 99%. The most prevalent symptoms/complications were neurological, bleeding, and pain. Most patients (86%) had 2 or more Elixhauser comorbidities. Over 80% of patients received 1 or more TTP-related treatments, mostly plasma exchange. The mean length of stay was 11.5 days; 5% of patients died during their stay. Readmission rates at 30, 60, and 90 days were 20%, 26%, and 28%, respectively. The median (interquartile range) total inpatient cost to the hospital throughout the index admission was $33,221 ($19,431-$64,901). CONCLUSION: Patients with severe ADAMTS13 deficiency have substantial clinical burden, have high mortality and readmission rates, and generate high costs for hospitals. There is a high need for a therapy that replaces ADAMTS13, thus addressing the root cause of the symptoms and complications caused by this deficiency.

Primary immune thrombocytopenic purpura with exuberant oral manifestations in a patient with Turner syndrome.

BACKGROUND: Primary Immune Thrombocytopenic Purpura (ITP) is an autoimmune hematological condition characterized by isolated thrombocytopenia and frequently presents with oral manifestations. However, reports of primary ITP in patients with Turner Syndrome (TS) are exceptionally rare, with few cases documented in the literature. Herein, we describe an unusual case of primary ITP with exuberant oral manifestations in a patient with TS. CASE REPORT: A 29-year-old woman was referred to an oral diagnostic service with complaints of "blood blisters and gum bleeding" lasting 8 h. On extraoral physical examination, multiple petechiae were observed in the upper and lower limbs, in addition to hemorrhagic extravasation in the right ocular sclera (hyposphagma). On intraoral examination, multiple vesicles and blisters filled with blood were identified on the lower lip, back of the tongue, and buccal mucosa, along with spontaneous gingival bleeding and hemorrhagic petechiae on the palate. Laboratory tests revealed thrombocytopenia (5000/mm3), whereas the blood count showed normality in the red and white series. After excluding other etiological factors or associated diseases, the patient was diagnosed with severe ITP and began treatment with systemic corticosteroids in the intensive care unit, resulting in a successful increase in platelets. After a 2-year follow-up, the patient remains free of ITP recurrences. CONCLUSION: Oral manifestations may be one of the first signs of ITP. Therefore, it is essential that dentists are familiar with the condition and, when faced with unusual oral bleeding, consider the possibility of a hematological disorder such as ITP, ensuring a correct and early diagnosis. Moreover, the presence of ITP can further exacerbate complications associated with TS. Therefore, rigorous follow-up of these patients is crucial, considering the high incidence of cardiovascular and autoimmune diseases and the reduced life expectancy of these patients.

Rapid, Simple and Low-Cost Analytical Method Development for Quantification of Eltrombopag Olamine in Tablet Dosage by UV Spectroscopy Method.

BACKGROUND: Eltrombopag Olamine is a drug used to treat thrombocytopenia, a disorder where blood platelet counts get lower and severe aplastic anemia. It serves as a thrombopoietin receptor agonist, which give rise to platelet production in the bone marrow. OBJECTIVES: The objective of this study is to develop a simple, specific, accurate, precise and economical Ultraviolet spectroscopy method to estimate the amount of Eltrombopag Olamine in bulk and tablet dosage form. METHODS: The developed method was performed using methanol for identification and physicochemical characterization of the drug. The validation parameters like linearity, precision, accuracy, robustness limits of detection and quantitation, and specificity were assessed as per ICH Q2 (R2). RESULTS: The maximum absorbance wavelength (λmax) of the drug was found at 247 nm in methanol. The linearity was found in the concentration range of 2-14 µg/ml with regression equation y = 0.0619x - 0.0123 and r² = 0.999. The standard addition method was used to determine the accuracy of the developed method. The result was found in the % recovery range of 98-99%. The precision was done on λmax with respect to the parameters such as repeatability, intraday, and interday. The method was found to be precise as the % RSD value was found to be <2%. The detection limit value (LOD) and quantitation limit value (LOQ) were 0.0524 µg/ml and 0.1588 µg/ml, respectively. CONCLUSION: The developed method is simple, economical, accurate and selective. The developed method was adaptable for the estimation of Eltrombopag Olamine analysis in pharmaceutical dosage form and routine quality control laboratory.

Navigating the Nexus: Lenalidomide-Associated Thrombotic Thrombocytopenic Purpura.

Thrombotic thrombocytopenic purpura (TTP) is a life-threatening thrombotic microangiopathy (TMA) marked by thrombocytopenia, microangiopathic hemolytic anemia, and microvascular thrombosis leading to end-organ damage. While TTP commonly results from hereditary or acquired ADAMTS13 deficiency, its association with lenalidomide is notably rare. The link between lenalidomide and TMA is unclear and requires more studies, given the high mortality risk associated with TTP. The underlying mechanism may involve immunomodulatory effects leading to ADAMTS13 inhibitory antibody formation. Herein, we present a case of a 56-year-old male with a history of multiple myeloma status post autologous stem cell transplant, on lenalidomide maintenance therapy for over five years, who presented with progressive weakness, jaundice, palpitations, and paraesthesia in his extremities. On arrival, the patient was afebrile and was neurologically intact except for the subjective paraesthesia. He was found to have critically low ADAMTS13 activity at <0.03 IU/mL and detectable ADAMTS13 inhibitors, with other findings of TTP, requiring discontinuation of lenalidomide, in addition to receiving treatment for this life-threatening TMA.

VE-Cadherin is involved in endothelial cell detachment during Thrombotic Thrombocytopenic Purpura.

BACKGROUND AND OBJECTIVES: Immune Thrombotic thrombocytopenic purpura (i-TTP) is a life-threatening thrombotic microangiopathie linked to ADAMTS13 deficiency. It has long been assumed that the activation of endothelial cells is the triggering factor for the TTP crisis. Circulating endothelial cells (CEC) have been shown to be a biomarker of vascular damage and are associated with the clinical severity of i-TTP. However, the mechanisms leading to endothelial cell detachment remain unclear. OBJECTIVES: We have investigated junctional destabilization and the mechanisms underlying cell detachment in TTP. METHODS AND RESULTS: In plasma from i-TTP patients, we show that CEC count is associated with severity and correlated to intracellular calcium influx (p<0.01). In vitro, serum from i-TTP patients induced stronger detachment of human umbilical vein endothelial cells (HUVECs) than serum from control patients (p<0.001). Plasma from i-TTP patients induced a higher calcium-dependent phosphorylation (p<0.05) and internalization (p<0.05) of VE-cadherin compared to plasma from control patients. This effect could be reproduced by IgG fraction isolated from patient plasma and in particular by the F(ab)'2 fragments of the corresponding IgG. In addition, subcutaneous injection of i-TTP plasma into mice resulted in higher vascular permeability than plasma from control patients. An inhibitor of endothelial calcium influx, ITF1697, normalized this increase in permeability. CONCLUSIONS: Our results suggest that plasma-induced endothelial activation also leads to an increase in vascular permeability. They contribute to the understanding of the mechanisms behind the presence of elevated CECs in patients' blood by linking endothelial activation to endothelial injury.

COVID-19-induced immune thrombocytopenia management approach: A case report and literature review.

Key Clinical Message: Vincristine therapy can be effective in refractory Immune thrombocytopenia (ITP) following COVID-19 vaccination. Our case report highlights the need for further research to establish standard management guidelines for COVID-19-vaccine-associated ITP. Abstract: Adult immune thrombocytopenia (ITP) can occur as a rare complication following several viral infections or a rare adverse event or complication of vaccination. In this paper, we report a case of a 39-year-old male patient with severe refractory ITP that began 4-weeks after receiving his third (booster) dose of the COVID-19 vaccine (BNT162b2, Pfizer-BioNTech). He was given oral dexamethasone 40 mg daily for 4 days followed by prednisone at 1 mg/kg (85 mg daily) for 10 days. In the following weeks, we attempted several other lines of therapy to treat his ITP, including anti-RhD immunoglobulin, which, unfortunately, caused moderate hemolysis requiring packed red blood cell transfusion, intravenous immunoglobulin (given at a subtherapeutic dose of 0.4 g/kg for only 1 day since it was not available), rituximab, and eltrombopag. The patient, unfortunately, showed no response to any of these treatments. This was an indicator to initiate salvage therapy with vincristine 2 mg weekly for 3 weeks. The patient's platelet count started to increase remarkably during the third week of vincristine and normalized after 4 weeks. We review the findings, clinical characteristics, and management approaches that were reported in the literature regarding COVID-19-vaccine-induced ITP. More in-depth research is needed to delineate standard guidelines for the management of such cases. This report underscores the importance of resorting to vincristine and eltrombopag as great options for severe and refractory ITP related to the COVID-19 vaccine.

Cerebral venous sinus thrombosis in patient of immune thrombocytopenic purpura managed with mechanical thrombectomy: An anecdotal endovascular experience from lower middle income country.

Cerebral venous sinus thrombosis in itself is rarely encountered clinical entity and its association with immune thrombocytopenic purpura (ITP) makes it more unusual presentation. No any as such standard guidelines exist that guides the prompt evidence based management in such concurrent cases but neuroendovascular modality can play a pivotal role.