scholarly journals Oxford-AstraZeneca Coronavirus Disease-2019 Vaccine-Induced Immune Thrombocytopenia on Day Two

2021 ◽  
Vol 2021 ◽  
pp. 1-3
Author(s):  
Azhar Kareem Razzaq ◽  
Ameer Al-Jasim
Keyword(s):  
Platelet Count ◽  
Immune Modulation ◽  
Clinical Manifestations ◽  
Resistance Pattern ◽  
Severe Thrombocytopenia ◽  
Close Monitoring ◽  
Severe Haemorrhage ◽  
Life Threatening ◽  
History Of ◽  
Complete Blood Counts

Introduction. Vaccines have been one of the most impactful human discoveries that have significantly changed life expectancy. Immune thrombocytopenic purpura (ITP) is an autoimmune disease characterized by platelet damage, life-threatening thrombocytopenia, and haemorrhage when the platelet count reaches below 20 × 109/mcL. Its pathogenesis involves viral mimicry or T-cell-induced immune destruction in antibody-negative cases. The clinical manifestations of thrombocytopenia vary according to the severity (level of platelets) and range from being asymptomatic to severe haemorrhage. ITP is treated with immunosuppression. Case Presentation. A 26-year-old Iraqi male laboratory analyst with an unremarkable medical history presented with severe thrombocytopenia 2 days after receiving the Oxford-AstraZeneca coronavirus disease-2019 vaccine. The patient was asymptomatic with unremarkable examination findings. However, his low platelet count was discovered accidentally, and the patient did not exhibit the resistance pattern of ITP and recovered successfully with regular immunosuppressant treatment. Conclusion. Patients with a history of thrombocytopenia can develop vaccine-induced thrombocytopenia earlier than the expected onset. Close monitoring, through regular complete blood counts, is highly recommended for patients with previous thrombocytopenia because the immune modulation process of the vaccine can worsen preexisting thrombocytopenia.

Recurrent hypoglycaemia and dilated cardiomyopathy: delayed presentation of Sheehan’s syndrome

2021 ◽  
Vol 14 (6) ◽  
pp. e242747
Author(s):  
Archita Makharia ◽  
Manoj Lakhotia ◽  
Vineet Tiwari ◽  
Kishan Gopal
Keyword(s):  
Dilated Cardiomyopathy ◽  
Clinical Manifestations ◽  
Diabetic Woman ◽  
Delayed Presentation ◽  
Sheehan’S Syndrome ◽  
Life Threatening ◽  
History Of ◽  
Sheehan's Syndrome ◽  
Ischaemic Necrosis ◽  
Recurrent Hypoglycaemia

Sheehan’s syndrome (SS) is ischaemic necrosis of the pituitary gland due to massive postpartum haemorrhage. The clinical manifestations may vary from subtle to life-threatening and may present immediately after delivery or many years later. We present a case history of a 58-year-old non-diabetic woman who had undetected SS and presented with two unusual manifestations, including recurrent hypoglycaemia and dilated cardiomyopathy 34 years after delivery. The dilated cardiomyopathy reversed partially after treatment.

scholarly journals Familial pneumothorax: towards precision medicine

Thorax ◽  
2017 ◽  
Vol 73 (3) ◽  
pp. 270-276 ◽  
Author(s):  
Rachel M Scott ◽  
Elizabeth P Henske ◽  
Benjamin Raby ◽  
Philip M Boone ◽  
Rosemary A Rusk ◽  
...  
Keyword(s):  
Family History ◽  
Precision Medicine ◽  
Genetic Disorders ◽  
Clinical Manifestations ◽  
Genetic Causes ◽  
Life Threatening ◽  
History Of

One in 10 patients suffering from primary spontaneous pneumothoraces has a family history of the disorder. Such familial pneumothoraces can occur in isolation, but can also be the presentation of serious genetic disorders with life-threatening vascular or cancerous complications. As the pneumothorax frequently precedes the more dangerous complications by many years, it provides an opportunity to intervene in a focused manner, permitting the practice of precision medicine. In this review, we will discuss the clinical manifestations and underlying biology of the genetic causes of familial pneumothorax.

Possible Severe Thrombocytopenia Associated with a Single Dose of Plicamycin

1992 ◽  
Vol 26 (11) ◽  
pp. 1369-1373 ◽  
Author(s):  
Weeranuj Yamreudeewong ◽  
Neil E. Henann ◽  
Anthony Fazio ◽  
Uma Rangaraj
Keyword(s):  
Platelet Count ◽  
Single Dose ◽  
Time Course ◽  
Clinical Status ◽  
Total Serum ◽  
Severe Thrombocytopenia ◽  
Close Monitoring ◽  
Contributing Factors ◽  
Baseline Platelet Count ◽  
Total Serum Calcium

OBJECTIVE: To report a case of possible severe thrombocytopenia associated with administration of a single dose of plicamycin. CASE SUMMARY: A 73-year-old man with prostate cancer was admitted to the hospital with hypercalcemia (total serum calcium concentration 4.02 mmol/L) and a low baseline platelet count (152 × 109/L). Because of his symptomatic hypercalcemia, he was treated with NaCl 0.9%, furosemide, oral inorganic phosphate, and a single dose of plicamycin (15 μg/kg). Five days after plicamycin administration his platelet count decreased to 52 × 109/L, and continued to decrease further even after the transfusion of four units of platelets to a nadir of 7 × 109/L (hospital day 20). A second transfusion produced a small increase in his platelet count. The patient's clinical status continued to deteriorate, however, and he subsequently died. DISCUSSION: Plicamycin and other drugs that may induce thrombocytopenia are reviewed. The time course between plicamycin administration and the development of thrombocytopenia in our patient is assessed. Other contributing factors such as a low baseline platelet count and advanced age are also addressed. CONCLUSIONS: It is likely that the severe thrombocytopenia experienced by our patient was caused by a single dose of plicamycin. Adjusting the dosage for a patient's renal function as well as close monitoring of the platelet count are necessary when administering this drug. We report this case to remind clinicians of the potential for the development of severe thrombocytopenia following administration of a single dose of plicamycin.

scholarly journals A Sudden Onset of Severe Thrombocytopenia While Using Evolocumab

2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Ikuo Inoue ◽  
Yasuhiro Takenaka ◽  
Yoshitora Kin ◽  
Satoshi Yamazaki ◽  
Yuichi Ikegami ◽  
...  
Keyword(s):  
Platelet Count ◽  
Immunoglobulin Therapy ◽  
Sudden Onset ◽  
High Dose ◽  
Severe Thrombocytopenia ◽  
First Line Therapy ◽  
Thrombopoietin Receptor ◽  
Thrombopoietin Receptor Agonist ◽  
History Of ◽  
Coa Reductase

A 72-year-old man with a 10-year history of coronary heart disease started evolocumab treatment once a month after developing excess myalgia due to therapy with a 3-hydroxy-methylglutaryl CoA reductase inhibitor. No side effects such as myalgia symptoms had been reported during the first 14 months of evolocumab treatment; however, he suddenly presented with acute severe thrombocytopenia following the 14th treatment. His platelet count continued to decrease to a nadir of 1,000/μL. His platelet-associated immunoglobulin G level had elevated to 790 ng/107 cells. He started receiving a combination of steroid therapy, high-dose immunoglobulin therapy, and platelet transfusions, but the first-line therapy was ineffective. He was subsequently treated with a thrombopoietin receptor agonist, and his platelet count recovered to 250,000/μL.

Patient with a History of Active Substance Abuse Requesting Opioids for Chronic Pain

2021 ◽  
Author(s):  
Alan D. Kaye ◽  
Martin J Carney ◽  
Mark R. Jones ◽  
Harold J. Campbell ◽  
Burton R. Beakley
Keyword(s):  
Substance Abuse ◽  
Chronic Pain ◽  
Health Care Providers ◽  
Active Substance ◽  
Ethical Issues ◽  
Clinical Manifestations ◽  
Prescription Opioid ◽  
Close Monitoring ◽  
Care Providers ◽  
History Of

Health care providers face a considerable challenge when treating chronic pain patients with prescription opioid medications. Although indications exist for the use of these drugs, their addictive nature and street value render them high-risk targets for abuse, misuse, and diversion. All patients receiving opioids should, therefore, be screened for abuse potential before beginning opioid therapy, be required to sign an opioid agreement, and receive close monitoring throughout the course of their treatment. Patients who present with a history of active substance abuse are at higher risk for iatrogenic dependence and necessitate more frequent monitoring. Herein arise several ethical issues, such as the principle of justice, which mediates equitable treatment for all patients. This review discusses the disease underlying substance abuse and clinical manifestations thereof, as well as relevant pathophysiology, ethical issues, and guidelines for the safe treatment with opioids. This review contains 3 tables and 43 references. Key Words: addiction, ethics, opioids, safety, substance abuse 

An Unusual Form of Immune Thrombocytopenic Purpura Characertized by a Platelet Activating IgG Antibody.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1086-1086
Author(s):  
Soames Boyle ◽  
Tamas Alexy ◽  
Leanne Rhochanda ◽  
Howard A. Liebman
Keyword(s):  
Platelet Count ◽  
Arterial Thrombosis ◽  
Heparin Therapy ◽  
Platelet Membrane ◽  
Laboratory Evaluation ◽  
Severe Thrombocytopenia ◽  
Membrane Glycoproteins ◽  
Igg Antibody ◽  
Potent Inducer ◽  
History Of

Abstract Autoimmune thrombocytopenia (ITP) is classically a disorder of accelerated platelet clearance and ineffective platelet production due to antibodies directed against common platelet membrane glycoproteins. The most common clinical manifestation of severe thrombocytopenia is bleeding. We report an unusual case of ITP in a 49 y.o. female with a 4 year history of thrombocytopenia, venous and arterial thrombosis secondary to a platelet activating IgG antibody. The patient was referred to one of the authors (HAL) for a second opinion with a diagnosis of ITP and a history of venous and arterial thrombosis. On presentation the patient was noted to have a platelet count of 34 × 109/L, a decreased fibrinogen of 128 mg/dL and D-dimers of greater than 4000 ng/ml. A diagnosis of chronic DIC was made and the patient was treated with therapeutic doses of LMW heparin resulting in an increase in her fibrinogen to 260 mg/dL, reduction in her D-dimers to <500 ng/ml and an increase in her platelet count to 118 × 109/L. An extensive clinical and laboratory evaluation, included screening for occult malignancy, cavernous hemangioma, antiphospholipid antibodies, dysfibrinogenemia, inhibitory antibodies against protein C and S, failed to disclose an etiology for her chronic consumptive coagulopathy. After 2 months of LMWH therapy the patient had a progressive drop in her platelet count to <30 × 109/L without evidence of recurrent coagulopathy. The patient’s thrombocytopenia was refractory to corticosteroids, Rituxan, azathioprine, cyclosporine, but responsive to IVIG. When the patients LMW heparin was stopped, the patient had evidence of a recurrence of her DIC as defined by an increase in her D-dimer and decreased fibrinogen. The patient underwent an open splenectomy which was complicated by portal vein and superior mesenteric vein thrombosis requiring catheter directed fibrinolysis and reinstitution of LMW heparin therapy. Repeated ELISA and functional assays for heparin induced thrombocytopenia were negative. However, the patient’s heat inactivated plasma and serum were shown to induce spontaneous aggregation. Patient IgG was subsequently isolated by staph A chromatography and found to be a potent inducer of platelet aggregation. Platelet specific IgG was further isolated from the patient’s IgG by affinity chromatography on a column of solubilized platelet membrane proteins. The affinity isolated antibody was then analyzed by the Western blotting using solubilized platelet membranes. Patient antibody was found to react with a 50 kD platelet membrane protein which has yet to be fully characterized. At the present time the patient remains on LMW heparin, but requires frequent infusions of IVIG to maintain platelet counts above 30 × 109/L. We are aware of only one other reported case of a spontaneous platelet activating antibody and no other case characterized by chronic DIC.

scholarly journals A New Look into Childhood Acute ITP: The Relationship Between Thrombin Generation and Thrombocytopenia

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 1058-1058
Author(s):  
Aimee Foord ◽  
Janet Hoang ◽  
Loan Hsieh ◽  
Diane J. Nugent
Keyword(s):  
Platelet Count ◽  
Thrombin Generation ◽  
Conflicts Of Interest ◽  
Acute Onset ◽  
Severe Thrombocytopenia ◽  
Test Analysis ◽  
Life Threatening ◽  
Bleeding Score ◽  
Acute Itp ◽  
Bleeding Severity

Abstract Introduction: Immune thrombocytopenic purpura (ITP) is the most common cause of primary isolated thrombocytopenia of childhood. Although ITP results in profound thrombocytopenia, the severity of bleeding in this disease does not correlate well with the platelet count suggesting a compensatory procoagulant state. The primary aim of this study is to evaluate thrombin generation in childhood acute ITP patients compared to age-matched controls and examine procoagulant activity in relation to bleeding severity in childhood acute ITP. Methods: After IRB consent was approved, platelet poor plasma was isolated from acute ITP patients at the time of initial diagnosis and serially for up to 6 months post-diagnosis. A single sample was obtained from age-matched controls. Thrombin generation assays were run via the Calibrated Automated Thrombogram (CAT) using reagent containing 1pM tissue factor and 4uM phospholipid. Peak thrombin levels were measured and compared to control samples using paired t-test analysis. Clinical bleeding severity was assessed using a modified overall Buchanan bleeding score at each time point (0=no bleeding, 1=minor, 2=mild, 3=moderate, 4=severe, 5=life threatening bleeding). Results: Samples from 19 childhood acute ITP patients, mean age 7 years, and 8 controls, mean age 5 years, were assessed. The figure below demonstrates that despite profound thrombocytopenia, the peak thrombin values of acute ITP patients were higher than controls throughout the first 3-4 months following diagnosis. ITP assays were significantly different from controls at the following time-points: 1-2 weeks (p =0.001), 3-4 weeks (p =0.022), 5-8 weeks (p =0.0009), 9-12 weeks (p =0.004), and 13-16 weeks (p =0.006) post-diagnosis. Peak thrombin values returned to values similar to controls 17 weeks from diagnosis. With the onset of acute ITP, higher bleeding scores were related to more severe thrombocytopenia. In ITP patients, thrombin peak values remained elevated regardless of resolving thrombocytopenia and improved bleeding scores (see figure). Conclusion: To our knowledge, this is the first study to assess longitudinal thrombin generation using the CAT in childhood ITP patients. In a highly significant pattern, acute ITP patients demonstrated sustained elevated peak thrombin levels compared to controls, even at acute onset of disease. Certainly, thrombin release, and subsequent thrombin generation play a compensatory role to decrease bleeding among childhood ITP patients when the platelet count remains in the 10-50,000 range. But, based on bleeding scores, this elevated thrombin may not be able to overcome the bleeding phenotype at presentation when platelets are most profoundly decreased or absent. Greater understanding of the etiology of this thrombin potential in childhood acute ITP is critical, as the thrombocytopenia in this disorder may be triggered or linked to a larger post infectious or inflammatory coagulopathy. Figure 1. Figure 1. Disclosures No relevant conflicts of interest to declare.

Severe pre-eclampsia: it’s recognition and management

2016 ◽  
Vol 1 (4) ◽  
Author(s):  
Barry NJ Walters ◽  
Theresa Mittermeier
Keyword(s):  
Clinical Manifestations ◽  
Close Monitoring ◽  
Life Threatening Illness ◽  
Life Threatening

<p>This article deals with certain aspects of the disorder that have not been as well covered in the literature as other elements. The clinical manifestations are manifold, variable and sometimes, if unrecognised, can have unfortunate results. The first truism to accept is that there is no such entity as ‘mild’ pre-eclampsia. All cases have the potential to undergo a transition to a life-threatening illness for mother and baby and, therefore, close monitoring as an inpatient is essential. </p>

Immune Thrombocytopenic Purpura Due to Passenger Donor Lymphocytes in Liver Transplantation

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4558-4558
Author(s):  
Imran Mirza ◽  
Areej Almugairi ◽  
Susan Nahirniak
Keyword(s):  
Liver Transplantation ◽  
Platelet Count ◽  
Organ Donor ◽  
Severe Thrombocytopenia ◽  
Antiplatelet Antibody ◽  
Thrombocytopenic Purpura ◽  
Post Transplant ◽  
Antiplatelet Antibodies ◽  
History Of ◽  
Donor Lymphocytes

Abstract Introduction: Thrombocytopenia is a frequent complication following solid organ transplant but previous reports suggest that the incidence of immune mediated thrombocytopenic purpura (ITP) following liver transplantation is low (0.7%). Although the mechanisms involved in post transplant thrombocytopenia are complex, the presence of alloantibody derived from passenger donor lymphocytes should be considered when severe thrombocytopenia is identified. Case presentation: Our case is a 58-year-old gentleman who underwent liver transplantation for end stage cirrhosis and hepatocellular carcinoma. His baseline pre-transplant platelet count was low at 83 ×109/L, but he postoperatively worsened to a platelet count of 5×109/L with bleeding sequelae. The liver donor was a 71-year-old previously healthy man who presented with severe thrombocytopenia (platelet count of 3 ×109/L) and hemorrhagic stroke, but no evidence of hematological pathology on bone marrow examination. As the donor history of presumptive ITP was known to the service, antiplatelet antibody assays on both the donor and recipient were performed using the ELISA based GTI-PAK12 kit (GTI Diagnostics, Waukesha, WI). Although there were no detectable antiplatelet antibodies in the organ recipient’s pre-transplant specimens, the immediate post-transplant specimen demonstrated reactivity in all three GPIIb/IIIa wells, corresponding to a stronger but identical reaction pattern in the organ donor. This suggested that the reactivity and subsequent worsening of the thrombocytopenia were secondary to antibodies produced by passenger donor lymphocytes in the transplanted liver. The transplant recipient was treated with corticosteroids, intravenous immune globulin and platelet transfusion with a return to his baseline platelet count and cessation of bleeding symptomatology five days later. Repeat platelet antibody testing in the organ recipient five weeks post-transplant revealed no detectable antiplatelet antibody reactivity, indicating lack of engraftment of the passenger donor lymphocytes. Conclusion: Passenger donor lymphocytes producing antiplatelet antibodies may be a contributing factor in post-transplant thrombocytopenia. Close monitoring and high clinical suspicion should be present when there is a history of immune/idiopathic thrombocytopenia in the organ donor.

scholarly journals Peripartum Cardiomyopathy: The Hidden Enemy

2021 ◽  
Author(s):  
Fatima Zahra Merzouk ◽  
Sara Oualim ◽  
Mohammed Sabry
Keyword(s):  
Heart Failure ◽  
Left Ventricular ◽  
Peripartum Cardiomyopathy ◽  
Lv Function ◽  
Close Monitoring ◽  
Mortality And Morbidity ◽  
Life Threatening ◽  
History Of ◽  
The Brain ◽  
In Pregnancy

Peripartum cardiomyopathy (PPCM) is the most common cardiomyopathy in pregnancy. It is potentially life-threatening. It is, diagnosed in women without a history of heart disease 1 month before delivery or within 5 months. It is marked by heart failure and left ventricular dyshfunction. The evolution is favorable. LV function improves within 6 months in the majority of patients, but long-lasting mortality and morbidity are not infrequent. Recent work suggests the critical toxic role for late-gestational hormones on the maternal vasculature and the genetic underpinnings of PPCM. Complications include different types of supraventricular and ventricular arrhythmias, heart failure and ischemic stroke. The brain natriuretic peptide (BNP) can be used to risk stratify women for adverse events. Management of peripartum cardiomyopathy is based on treatment of heart failure. The addition of bromocriptine seemed to improve LVEF. Close monitoring of pregnant women with cardiomyopathy by multidisciplinary team is recommended.

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