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Thromboembolism after COVID-19 vaccine in patients with preexisting thrombocytopenia.
Mauriello, A, Scimeca, M, Amelio, I, Massoud, R, Novelli, A, Di Lorenzo, F, Finocchiaro, S, Cimino, C, Telesca, R, Chiocchi, M, et al
Cell death & disease. 2021;(8):762
Abstract
While vaccination is the single most effective intervention to drastically reduce severe disease and death following SARS-CoV-2 infection, as shown in UK and Israel, some serious concerns have been raised for an unusual adverse drug reaction (ADR), including vaccine-induced immune thrombotic thrombocytopenia (VITT) with concurrent low platelets as well as capillary leak syndrome. In fact, the overall safety of the vaccine is highlighted by the low frequency of ADR considering that in UK, by the early June, 40 million first doses and 29 million second doses have been injected; nonetheless, 390 thrombotic events, including 71 fatal events have been reported. Interestingly, the cases reported low platelet counts with the presence of anti-platelet factor-4 (PF4) antibodies, indicating an abnormal clotting reaction. Here, out of three referred cases, we report a post-vaccine clinical case of fatal thrombosis with postmortem examination and whole exome sequencing (WES) analysis, whose pathogenesis appeared associated to a preexisting condition of thrombocytopenia due to myelodysplasia.
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2.
Non-Vitamin K-Dependent Oral Anticoagulants for Nonvalvular Atrial Fibrillation in Patients With CKD: Pragmatic Considerations for the Clinician.
Shroff, GR, Stoecker, R, Hart, A
American journal of kidney diseases : the official journal of the National Kidney Foundation. 2018;(5):717-727
Abstract
Management of atrial fibrillation (AF) in patients with advanced chronic kidney disease (CKD) poses a complex conundrum because of higher risks for both thromboembolic and bleeding complications compared to the general population. This makes it particularly important for clinicians to carefully weigh the risks versus benefits of anticoagulation therapy to determine the individualized net clinical benefit for every patient. During the past few years, 4 non-vitamin K-dependent oral anticoagulant (NOAC) agents have supplemented warfarin in the therapeutic armamentarium for the prevention of systemic thromboembolism in nonvalvular AF. However, the use of NOACs in CKD specifically mandates a nuanced understanding due to their varying dependence on renal clearance, with resultant safety implications related to either underdosing (thromboembolism) or excessive drug exposure (bleeding). This pragmatic review highlights unique considerations pertaining to accurate estimation and temporal monitoring of kidney function in the context of NOAC use with specific clinical deliberations and variables when determining whether an NOAC is appropriate for a patient with CKD. The dependence of NOACs on renal clearance and several troubling safety signals in the published literature suggest that it is vital for nephrologists to be active members of a multidisciplinary team caring for these high-risk patients with CKD and AF.
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3.
Native valve endocarditis and femoral embolism due to Granulicatella adiacens: a rare case report.
Vandana, KE, Mukhopadhyay, C, Rau, NR, Ajith, V, Rajath, P
The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases. 2010;(6):634-6
Abstract
The fastidious Gram-positive cocci Granulicatella adiacens, previously known as nutritionally variant streptococci (NVS) are unusual but significant cause of endocarditis due to increased mortality and morbidity. Difficulties in reaching correct bacteriological identification, increased resistance to beta-lactam antibiotics and macrolides and complicated clinical course have contributed to problems in management of cases of infective endocarditis caused by this bacterium. We present the first Indian case of endocarditis with arterial embolus by G. adiacens in an elderly male with no preexisting cardiac abnormality.
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4.
Potential association of thyrotoxicosis with vitamin B and folate deficiencies, resulting in risk for hyperhomocysteinemia and subsequent thromboembolic events.
Colleran, KM, Ratliff, DM, Burge, MR
Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2003;(4):290-5
Abstract
OBJECTIVE To describe a patient with severe thyrotoxicosis attributable to Graves' disease who had a thrombotic cerebrovascular accident and hyperhomocysteinuria, which resolved on correction of the thyrotoxicosis, and to present findings in a pilot study undertaken to investigate the relationship among thyrotoxicosis, homocysteine, folate, and vitamin B(12). METHODS We present a case report of the index case, with clinical and laboratory details. For the investigative analysis, 21 patients who were 18 to 50 years old and had newly diagnosed, untreated Graves' disease and 10 age-and sex-matched euthyroid control subjects were studied. Of the patients with Graves' disease, 11 underwent studies both at diagnosis and after treatment. Fasting blood tests were performed for thyrotropin, free thyroxine, homocys-teine, vitamin B(12), folate, and methylmalonic acid, a marker of vitamin B(12) deficiency. RESULTS Vitamin B(12), folate, homocysteine, and methylmalonic acid levels were not significantly different between the thyrotoxic and control or posttreatment groups. In patients with thyrotoxicosis, however, free thyroxine was positively correlated with both homocysteine (r = 0.67; P = 0.03) and methylmalonic acid (r = 0.89; P = 0.003). CONCLUSION The positive correlation between free thyroxine levels and both homocysteine and methylmalonic acid suggests that thyrotoxicosis may be associated with functional vitamin B(12) deficiency. Such a deficiency may result in clinically important hyperhomocysteine-mia.
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Homozygous antithrombin deficiency type II (99 Leu to Phe mutation) and childhood thromboembolism.
Kuhle, S, Lane, DA, Jochmanns, K, Male, C, Quehenberger, P, Lechner, K, Pabinger, I
Thrombosis and haemostasis. 2001;(4):1007-11
Abstract
We report 5 children from 3 families with homozygous antithrombin deficiency type II affecting the heparin binding site (99 Leu to Phe mutation). Four children had severe spontaneous thromboembolic events (deep leg or caval vein thrombosis, ischaemic stroke) at one week, 3 months, 13 and 14 years of age. The fifth patient, a 17 year-old boy was asymptomatic. Early manifestation of homozygous deficiency calls for prompt and accurate diagnosis. In doubtful cases genetic analysis is required. Long-term oral anticoagulation should be considered in affected individuals.