Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Tiziana Ciarambino
 -- 2780 2023-06-23 13:38:44 |
2 format correction
Dean Liu
 -1 word(s) 2779 2023-06-25 04:38:38 |

Video Upload Options

Do you have a full video?
Send video materials Upload full video

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Ciarambino, T.; Crispino, P.; Minervini, G.; Giordano, M. Cerebral Sinus Vein Thrombosis and Gender. Encyclopedia. Available online: https://encyclopedia.pub/entry/45986 (accessed on 27 July 2024).
Ciarambino T, Crispino P, Minervini G, Giordano M. Cerebral Sinus Vein Thrombosis and Gender. Encyclopedia. Available at: https://encyclopedia.pub/entry/45986. Accessed July 27, 2024.
Ciarambino, Tiziana, Pietro Crispino, Giovanni Minervini, Mauro Giordano. "Cerebral Sinus Vein Thrombosis and Gender" Encyclopedia, https://encyclopedia.pub/entry/45986 (accessed July 27, 2024).
Ciarambino, T., Crispino, P., Minervini, G., & Giordano, M. (2023, June 23). Cerebral Sinus Vein Thrombosis and Gender. In Encyclopedia. https://encyclopedia.pub/entry/45986
Ciarambino, Tiziana, et al. "Cerebral Sinus Vein Thrombosis and Gender." Encyclopedia. Web. 23 June, 2023.
Cerebral Sinus Vein Thrombosis and Gender
Edit
This entry is adapted from the peer-reviewed paper 10.3390/biomedicines11051280

Cerebral sinus venous thrombosis (CSVT) is a relatively rare acute disorder of cerebral circulation, but it can potentially be associated with serious sequelae and a poor prognosis. The neurological manifestations associated with it are often not adequately taken into consideration given the extreme variability and nuances of its clinical presentation and given the need for radiological methods suitable for this type of diagnosis. CSVT is usually more common in women, but so far there are little data available in the literature on sex-specific characteristics regarding this pathology. CSVT is the result of multiple conditions and is therefore to be considered a multifactorial disease where at least one risk factor is present in over 80% of cases.

cerebral venous sinus thrombosis circulation risk factor

1. Introduction

Cerebral venous sinus thrombosis (CVST) is a rather rare thrombotic disease and its incidence can be considerably underestimated compared to the cases actually present in an emergency setting [1][2]. Acute venous occlusion can lead to increased pressure in small vessels, depending on the extent of thrombosis and the availability of collateral circles [1][2]. This leads to functional alteration of the blood–brain barrier, resulting in vasogenic edema and parenchymal tissue damage, a continuous increase in intracranial pressure results in an increase in capillary pressure which can cause cerebral hemorrhage. The symptomatologic picture of CSVT is extremely variable and is affected by the localization of the veno-occlusive process, the severity of the occlusion to the circulation, and the temporal latency. The most emblematic symptomatic parade is characterized by a headache associated with hemisensory loss, hemiplegia, or hemianopsia affecting one of the two hemispheres. Some more selective cases include the headache associated with visual symptoms such as those cases characterized by papilledema, and paralysis of the oculomotor nerve with a consequent decrease in visus. Other cases may manifest with a prolonged history of headaches preceding an acute event or sometimes the headache can also be associated with the presence of an altered mental state. Sporadically, especially in young patients without atherosclerotic risk factors, the development of acute symptomatology with an epileptic seizure is possible or convulsive crises that are often associated with neuroimaging characterized by infarcts in multiple vascular territories [3][4][5][6][7]. Novel biomarkers indicating the severe brain damage status [8][9] have been recently introduced in clinical practice, although there are difficulties in recognition of venous ischemic processes linked to the complexity of the etiology, and the polyfactorial which includes malignant hematological neoplasms, infectious diseases, pregnancy and the postpartum period, systemic autoimmune diseases, dehydration, intracranial tumors, oral contraceptives, hypercoagulable state, some drugs, trauma, and finally more recently COVID-19 infection and vaccination with adenovirus vaccines. In general, however, it must be said that about 30% of CVST cases still have an unknown etiology [10]. CVST caused by head injury is the rarest condition [10][11]. On the other hand, CVST is very insidious on the basis of underlying or unacknowledged, uncontrolled, or precipitated hyperthyroidism by some acute incidental factors, such as infections, traumas, and surgical interventions. In this case, thyroid storms occur leading to rapid deterioration, involving multiple organs and overall mortality of up to 20–30% [12][13]. Severe trauma is a rare cause of thyroid storms [14][15]. Thyroid storms among trauma patients are difficult to detect because usually, the focus is only on the management of significant post-traumatic injuries and their possible complications, while rarely, symptoms and manifestations such as tachycardia and loss of consciousness are related to an endocrine dysregulation triggered by the trauma. Even a rather frequently observed condition such as thyroid hyperfunction is associated with the genesis of CVST. This observation derives from the fact that at least 20% of patients with CVST have overt or silent manifestations of thyroid disease at diagnosis. This ratio stands at much higher levels if researchers take into consideration the rate reported by previous observations that have discussed the prevalence of risk factors underlying a CVST manifestation [16][17]. The link between thyroid hyperfunction and CVST, as highlighted for some time in previous studies, can be traced back to a state of aberrant hypercoagulability induced by the excessive increase of circulating thyroid hormones (thyrotoxicosis) [18][19][20][21]. Thyrotoxicosis is a cause of primary and secondary coagulation disorders ranging from an increase in plasma levels of tissue factor, factor VIII, and factor IX, up to an increase in fibrinogen, D-dimer, and activator inhibitor-1 of plasminogen. This set of factors promotes the activation of both the intrinsic and extrinsic pathways of coagulation and especially in the female subject or with other risk factors, it is correlated to a greater risk of acute events attributable to CVST [22][23]. With regard to chronic hematologic malignancies, it has been noted that thrombosis is the leading cause of death and disease in patients with chronic myeloproliferative Philadelphia chromosome-negative disease such as essential thrombocythemia (ET), polycythemia vera (PV), and idiopathic myelofibrosis (IM). Venous thrombosis in atypical sites is frequent and characteristic of these pathologies [24][25]. To date, only a few small studies have evaluated the presence of the JAK2 (V617T) mutation, the Karl gene, and the MPL gene in patients with cerebral venous thrombosis, and the prevalence of these mutations, omitting, however, the presence of gender differences in pathogenesis and therapies both in terms of prevention and treatment of events.

2. Myeloproliferative Neoplasms and CSVT

Myeloproliferative diseases (MPN) are associated with a greater risk of CSVT and are usually chronic but potentially life-threatening conditions, both for the related complications which include both the tendency to hypo- and hypercoagulable states caused by defective hematopoiesis which also affects the blood coagulation system and clot formation. For the purposes of the discussion, it is important to know that MPNs can be classified as positive or negative for BCR-ABL1, depending on the expression of this gene sequence [1]. In 2005, the somatic mutation in the Janus Kinase 2 (JAK2) gene was described; their replacement of the amino acid valine with the amino acid phenylalanine at codon 617 (V617T) involves increased activity of the JAK2 tyrosine kinase protein and is characteristic of pathological clone in myeloproliferative diseases. The JAK2 mutation (V617T), in fact, is found in 50–60% of patients with ET and IM, and in 95% of those with PV [10][11]. Since 2008, the search for the JAK2 mutation (V617T) has been included as a diagnostic criterion for myeloproliferative diseases in the guidelines of the world health Organization (WHO) and is commonly sought in patients with thrombosis splanchnic. The presence of mutation of the CALR gene is easily found in cases of PMF and ET and is even more evident in youth. It often manifests itself with leukopenia anemia and thrombocytosis [2]. ET is a fairly frequent subgroup of MPN and can be found in a quarter of patients with chronic myelodysplastic manifestations [12]. This clinical condition is characterized by an uncontrolled increase in platelets linked both to a prolongation of the life span of these cellular elements and to an aberrant proliferation of sometimes functionally immature and minimally mature megakaryocytes which introduce cellular elements with altered function into the circulation [13]. In fact, the excessive production of platelets of various levels of maturation and shape, a typical expression of ET, can lead to both thrombotic and hemorrhagic complications since an altered number is also associated with an altered function. The ET is characterized by one long average survival between 18 and 20 years, and it is important to underline that CSVT is more common in females than males and therefore with the concrete possibility of a link between the two conditions mediated by characteristics common to the female gender [14][15]. PV is the most common MPN, accounting for approximately 45% of all MPN cases [12]. It is characterized by an increase in the volume and cell mass of red blood cells and consequently by elevated hemoglobin [16]. In addition, hyperleukocytosis and platelet disease may also be present. These are cellular elements that, despite their excessive numbers, show structural or surface anomalies that affect and cause excessive destruction by the spleen with the consequent finding of splenomegaly [17]. PV is correlated to a very high risk of thrombosis precisely due to an absolute increase in cellular elements circulating in the blood which also tend to agglutinate with each other not only due to excessive concentration but also due to their altered morphology. It is known that the severity and genesis of all these diseases is strongly correlated to the mutation of the tyrosine kinase gene Janus Kinase 2 (JAK2), an important determinant in the estimation of hematopoietic stem cells of the bone marrow. The presence of a mutation in the JAK2 gene is found in almost all patients with PV and in over half of patients with suspected diagnostics of ET and MF [18][19][20][21]. Thus, JAK2 positivity is commonly associated with a more severe course and concurrently with more thrombotic sequelae in patients with MPN.

3. Cerebral Vein Thrombosis and COVID-19 Infection

In the case of COVID-19 infection, the greater the severity of the infection, the greater the risk and severity of thromboembolic manifestations, and this could be explained by some physio pathological alterations typical of this virosis, which provide for a direct effect of the virus on endothelial cells, triggering various cascade processes that provide for amplification of acute phase immune processes and inflammation, a decrease in the number of functioning angiotensin-converting enzyme 2 receptors, with consequent blood flow turbulence, and finally the activation of the intrinsic and extrinsic pathways of coagulation with the consequent establishment of a state of hypercoagulability [26][27]. If in the course of COVID-19 acute infection, the mechanisms that determine thromboembolism are quite recognized, and the degree of phenomenon knowledge is different in the post-infectious period since the various studies conducted on the subject show divergent opinions [27][28]. In this regard, a meta-analysis [29] highlighted a risk of venous thromboembolism of just over 10%, which can only be found in patients with an acute form of infection and moreover in the pre-vaccination period. Another case study that included a fair number of studies that compared patients in the post-COVID-19 period with unaffected control groups did not observe statistically significant differences as regards new cases of venous thromboembolism [30]. The increased risk of a first manifestation of thromboembolism was maximal up to three months post-COVID-19 in the case of a deep vein thrombosis and up to six months of acute pulmonary embolism [31]. Regarding the ongoing pulmonary embolism of acute infection with the COVID-19 virus and in the post-infectious period, a significant gender difference was found as regards the number of cases which was significantly higher in men, with a risk that remained high up to the first three months after acute infection and which involved a range of patients aged between 50 and 70 years [30]. In the general population, as regards cerebral venous thrombosis (CVT), cerebral venous sinus thrombosis (CVST) is more common in women than in men, probably due to the participation of specific risk factors in the pathological event of the female gender especially belonging to the younger age groups [31]. The most common risk factors for CSVT concerning young women are pregnancy, use of drugs (oral contraceptives), a pre-existing hereditary thrombophilia state perhaps already associated with previous thromboembolic events, the concomitance of malignant tumors, supervening serious infections, and finally in intra and post-operative period for neurological pathologies susceptible to invasive treatment [31]. Cases of CSVT in patients with COVID-19 have been described more commonly in individuals with severe forms and admitted to intensive care units. From the pathophysiological point of view, the role of any factors is not yet fully clarified—predisposing factors mentioned above or if the cerebrovascular manifestations are caused directly by the virus. It seems clear that pre-existing risk factors of infection act as deterrents of the cerebral embolic process, but there is also much debate about the possible mechanisms that COVID-19 uses to electively cause the involvement of the cerebral venous vessels [32]. At least four hypotheses have been advanced on the mechanism by which the thrombotic process is established:
  • Retrograde cerebral infection starting from the nasal mucosa colonized by the virus and subsequent inflammatory and neuropathic damage of the olfactory nerve [33].
  • Indirect action mediated by the inflammatory hyperactivity triggered by the virulence factors of COVID-19, which would be associated with a real storm of cytokines, dysregulation of the immune system up to the establishment of disseminated vascular coagulation [34].
  • The finding of some autoantibodies circulating during infection would lead to the suspicion of a mechanism of autoimmune genesis which is already the basis of cases of CSVT in the population affected by autoimmune pathologies [35].
  • Direct action of the virus against the vascular endothelium with evidence of histological signs of inflammation and radiological signs of microangiopathy [36][37].
In general, only fourteen cases of CVST have been reported in the literature in patients with COVID-19 which occurred in relatively young patients, with an equal division between the two sexes and in half of the cases, no known risk factors were documentable. As in the general population, most patients complained of headaches, sensory numbness, and confusion associated with focal neurological deficits. Interestingly, more than 60% of CSVT cases had a hemorrhagic transformation and about half of them died due to CVST complications and COVID-19 infection [32]. Ultimately, most probably, COVID-19 acts by means of a multifactorial process, which in conjunction with respiratory and cerebral manipulations is caused by a systemic hypercoagulable state [38]. The main manifestations of CSVTs directly linked to COVID-19 were recorded above all in the pre-vaccination era, and in the most catastrophic phases of the pandemic when it was still looking for the most effective drugs to counteract the manifestations of the disease and was looking for a serum capable of inactivating the virus. Precisely in the latter case, CVT linked to the use of vaccines with adenoviral vectors has been observed [39], among which one of the most devastating clinical manifestations was CVST (Figure 1) [39]. The mechanism of this phenomenon has been clarified and seems to be linked to the presence of a transitory thrombocytopenia vaccine induced by the development of autoantibodies against platelet factor 4 (PF4). The development of these antibodies would lead to a decrease in PF4, to a lower bond with heparin and heparan sulfate produced by the body with the consequent tendency of the platelets to agglutinate each other and to adhere to the endothelial cells. While specifically there were no gender differences in CSVT in patients infected with COVID-19, in this case, female sex and age < 60 years were identified as significant risk factors in subjects immunized with adenoviral vector vaccines [39].
Biomedicines 11 01280 g001 550
Figure 1. Characteristics and clinical features of CSVT.

4. CSVT during Subsequent Pregnancy and Puerperium

CSVT is largely a disease of young women and hormonal factors such as taking oral contraceptives or pregnancy are important risk factors in a large percentage of female patients. Hormonal changes during pregnancy and the puerperium led to an increased risk of venous thromboembolism (VTE), including cerebral venous and sinus thrombosis (CSVT) [40][41]. Furthermore, risk assessment of women with a history of CSVT regarding future pregnancies is due to the lack of reliable data on the usefulness of the prophylaxis associated with thrombotic risk. Since pregnancy and the puerperium are prothrombotic risk factors for VTE, often some women with the previous CSVT are discouraged to undertake new pregnancies. However, most studies [40][41] suggest that a history of CSVT is not a decisive factor in precluding a subsequent pregnancy. There is very weak evidence that risk of recurrent VTE for women with an extracerebral history of venous thrombotic events, thromboembolic prophylaxis is required unless there is persistent thrombophilia or if associated with a transient risk factor [40][41]. Conversely, the risk of recurrence increases if a persistent thrombophilia condition is present in these women or if the previous thrombotic episode was ascribed to idiopathic causes. For this reason, women with previous extracerebral or cerebral thrombotic events who are planning to become pregnant should be tested with a comprehensive thrombophilia screening in order to help reduce the individual risk of recurrence during the next pregnancies [40][41]. The decision for prophylactic anticoagulation during pregnancy in women without or without persistent thrombophilia prothrombotic risk factors may be based on the interval between the previous CSVT episode and the next pregnancy [41]. Preter et al. [42] reported an 11.7% recurrence rate of thromboembolic events within the first 12 months of the first episode over a mean follow-up time of over 5 years. From the available data, however, a real risk of recurrence during pregnancy within the first two years after the first event as well as the need for a prophylaxis anticoagulant cannot be estimated. As regards the puerperium period, it has been seen that the number of women treated with anticoagulants has increased considerably, suggesting that the risk of CSVT is also frequent during this phase and not only during pregnancy [43]. Anticoagulant prophylaxis is therefore recommended in women with previous thromboembolic events also in the postpartum period [44][45]. Although these data have been obtained by women with extracerebral thromboembolism, it would appear that similar management should also apply to women with CSVT history.

References

  1. Saadatnia, M.; Fatehi, F.; Basiri, K.; Mousavi, S.A.; Mehr, G.K. Cerebral Venous Sinus Thrombosis Risk Factors. Int. J. Stroke 2009, 4, 111–123.
  2. Rizk, J.G.; Gupta, A.; Sardar, P.; Henry, B.M.; Lewin, J.C.; Lippi, G.; Lavie, C.J. Clinical Characteristics and Pharmacological Management of COVID-19 Vaccine–Induced Immune Thrombotic Thrombocytopenia With Cerebral Venous Sinus Thrombosis: A Review. JAMA Cardiol. 2021, 6, 1451.
  3. Long, B.; Koyfman, A.; Runyon, M.S. Cerebral Venous Thrombosis: A Challenging Neurologic Diagnosis. Emerg. Med. Clin. N. Am. 2017, 35, 869–878.
  4. Kristoffersen, E.S.; Harper, C.E.; Vetvik, K.G.; Zarnovicky, S.; Hansen, J.M.; Faiz, K.W. Incidence and Mortality of Cerebral Venous Thrombosis in a Norwegian Population. Stroke 2020, 51, 3023–3029.
  5. Ferro, J.M.; de Sousa, D.A. Cerebral Venous Thrombosis: An Update. Curr. Neurol. Neurosci. Rep. 2019, 19, 74.
  6. Mehta, A.; Danesh, J.; Kuruvilla, D. Cerebral Venous Thrombosis Headache. Curr. Pain Headache Rep. 2019, 23, 47.
  7. Duman, T.; Uluduz, D.; Midi, I.; Bektas, H.; Kablan, Y.; Goksel, B.K.; Milanlioglu, A.; Orken, D.N.; Aluclu, U.; Colakoglu, S.; et al. A Multicenter Study of 1144 Patients with Cerebral Venous Thrombosis: The VENOST Study. J. Stroke Cerebrovasc. Dis. 2017, 26, 1848–1857.
  8. Giordano, M.; Trotta, M.C.; Ciarambino, T.; D’amico, M.; Schettini, F.; Di Sisto, A.; D’auria, V.; Voza, A.; Malatino, L.S.; Biolo, G.; et al. Circulating miRNA-195-5p and -451a in Patients with Acute Hemorrhagic Stroke in Emergency Department. Life 2022, 12, 763.
  9. Giordano, M.; Trotta, M.C.; Ciarambino, T.; D’amico, M.; Galdiero, M.; Schettini, F.; Paternosto, D.; Salzillo, M.; Alfano, R.; Andreone, V.; et al. Circulating MiRNA-195-5p and -451a in Diabetic Patients with Transient and Acute Ischemic Stroke in the Emergency Department. Int. J. Mol. Sci. 2020, 21, 7615.
  10. Sidhom, Y.; Mansour, M.; Messelmani, M.; Derbali, H.; Fekih-Mrissa, N.; Zaouali, J.; Mrissa, R. Cerebral Venous Thrombosis: Clinical Features, Risk Factors, and Long-term Outcome in a Tunisian Cohort. J. Stroke Cerebrovasc. Dis. 2014, 23, 1291–1295.
  11. Hersh, D.S.; Shimony, N.; Groves, M.L.; Tuite, G.F.; Jallo, G.I.; Liu, A.; Garzon-Muvdi, T.; Huisman, T.A.G.M.; Felling, R.J.; Kufera, J.A.; et al. Pediatric cerebral venous sinus thrombosis or compression in the setting of skull fractures from blunt head trauma. J. Neurosurg. Pediatr. 2018, 21, 258–269.
  12. Wilcher, J.; Pannell, M. Dural Sinus (Cerebral Venous) Thrombosis in a Pediatric Trauma Patient: A Rare Complication After Closed Head Injury. Pediatr. Emerg. Care 2016, 32, 872–874.
  13. Son, H.-M. Massive cerebral venous sinus thrombosis secondary to Graves’ disease. Yeungnam Univ. J. Med. 2019, 36, 273–280.
  14. Rehman, A.; Husnain, M.G.; Mushtaq, K.; Eledrisi, M.S. Cerebral venous sinus thrombosis precipitated by Graves’ disease. BMJ Case Rep. 2018, 2018, bcr-2017-224143.
  15. Wang, H.-I.; Yiang, G.-T.; Hsu, C.-W.; Wang, J.-C.; Lee, C.-H.; Chen, Y.-L. Thyroid Storm in a Patient with Trauma—A Challenging Diagnosis for the Emergency Physician: Case Report and Literature Review. J. Emerg. Med. 2017, 52, 292–298.
  16. Karaoren, G.Y.; Sahin, O.T.; Erbesler, Z.A.; Bakan, N. Thyroid Storm Due To Head Injury. Turk. J. Trauma Emerg. Surg. 2014, 20, 305–307.
  17. Strada, L.; Gandolfo, C.; Del Sette, M. Cerebral sinus venous thrombosis in a subject with thyrotoxicosis and MTHFR gene polymorphism. Neurol. Sci. 2008, 29, 343–345.
  18. Verberne, H.J.; Fliers, E.; Prummel, M.F.; Stam, J.; Brandjes, D.P.; Wiersinga, W.M. Thyrotoxicosis as a Predisposing Factor for Cerebral Venous Thrombosis. Thyroid 2000, 10, 607–610.
  19. Franchini, M.; Lippi, G.; Targher, G. Hyperthyroidism and Venous Thrombosis: A Casual or Causal Association? A Systematic Literature Review. Clin. Appl. Thromb. Hemost. 2010, 17, 387–392.
  20. Bensalah, M.; Squizzato, A.; Kablia, S.O.; Menia, H.; Kemali, Z. Cerebral vein and sinus thrombosis and hyperthyrodism: A case report and a systematic review of the literature. Thromb. Res. 2011, 128, 98–100.
  21. Stuijver, D.J.; van Zaane, B.; Romualdi, E.; Brandjes, D.P.M.; Gerdes, V.E.A.; Squizzato, A. The effect of hyperthyroidism on procoagulant, anticoagulant and fibrinolytic factors: A systematic review and meta-analysis. Thromb. Haemost. 2012, 108, 1077–1088.
  22. Mazur, P.; Sokołowski, G.; Hubalewska-Dydejczyk, A.; Płaczkiewicz-Jankowska, E.; Undas, A. Prothrombotic alterations in plasma fibrin clot properties in thyroid disorders and their post-treatment modifications. Thromb. Res. 2014, 134, 510–517.
  23. Arber, D.A.; Orazi, A.; Hasserjian, R.; Thiele, J.; Borowitz, M.J.; Le Beau, M.M.; Bloomfield, C.D.; Cazzola, M.; Vardiman, J.W. The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia. Blood 2016, 127, 2391–2405.
  24. Fowlkes, S.; Murray, C.; Fulford, A.; De Gelder, T.; Siddiq, N. Myeloproliferative neoplasms (MPNs)-Part 1: An overview of the diagnosis and treatment of the “classical” MPNs. Can. Oncol. Nurs. J. 2018, 28, 262–268.
  25. Kralovics, R.; Passamonti, F.; Buser, A.S.; Teo, S.-S.; Tiedt, R.; Passweg, J.R.; Tichelli, A.; Cazzola, M.; Skoda, R.C. A Gain-of-Function Mutation of JAK2 in Myeloproliferative Disorders. N. Engl. J. Med. 2005, 352, 1779–1790.
  26. Magadum, A.; Kishore, R. Cardiovascular Manifestations of COVID-19 Infection. Cells 2020, 9, 2508.
  27. McGonagle, D.; O’Donnell, J.S.; Sharif, K.; Emery, P.; Bridgewood, C. Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia. Lancet Rheumatol. 2020, 2, e437–e445.
  28. Varga, Z.; Flammer, A.J.; Steiger, P.; Haberecker, M.; Andermatt, R.; Zinkernagel, A.S.; Mehra, M.R.; Schuepbach, R.A.; Ruschitzka, F.; Moch, H. Endothelial cell infection and endotheliitis in COVID-19. Lancet 2020, 395, 1417–1418.
  29. Mai, V.; Tan, B.K.; Mainbourg, S.; Potus, F.; Cucherat, M.; Lega, J.-C.; Provencher, S. Venous thromboembolism in COVID-19 compared to non-COVID-19 cohorts: A systematic review with meta-analysis. Vasc. Pharmacol. 2021, 139, 106882.
  30. Katsoularis, I.; Fonseca-Rodríguez, O.; Farrington, P.; Jerndal, H.; Lundevaller, E.H.; Sund, M.; Lindmark, K.; Connolly, A.-M.F. Risks of deep vein thrombosis, pulmonary embolism, and bleeding after COVID-19: Nationwide self-controlled cases series and matched cohort study. BMJ 2022, 377, e069590.
  31. Kalita, J.; Misra, U.K.; Singh, V.K.; Kumar, S.; Jain, N. Does gender difference matter in cerebral venous thrombosis? J. Clin. Neurosci. 2022, 102, 114–119.
  32. Fraiman, P.; Junior, C.G.; Moro, E.; Cavallieri, F.; Zedde, M. COVID-19 and Cerebrovascular Diseases: A Systematic Review and Perspectives for Stroke Management. Front. Neurol. 2020, 11, 574694.
  33. Bohmwald, K.; Gálvez, N.M.S.; Ríos, M.; Kalergis, A.M. Neurologic Alterations Due to Respiratory Virus Infections. Front. Cell. Neurosci. 2018, 12, 386.
  34. Zhu, Q.; Xu, Y.; Wang, T.; Xie, F. Innate and adaptive immune response in SARS-CoV-2 infection-Current perspectives. Front. Immunol. 2022, 13, 1053437.
  35. Zhang, Y.; Xiao, M.; Zhang, S.; Xia, P.; Cao, W.; Jiang, W.; Chen, H.; Ding, X.; Zhao, H.; Zhang, H.; et al. Coagulopathy and Antiphospholipid Antibodies in Patients with COVID-19. N. Engl. J. Med. 2020, 382, e38.
  36. Hernández-Fernández, F.; Valencia, H.S.; Barbella-Aponte, R.A.; Collado-Jiménez, R.; Ayo-Martín, Ó.; Barrena, C.; Molina-Nuevo, J.D.; García-García, J.; Lozano-Setién, E.; Alcahut-Rodriguez, C.; et al. Cerebrovascular disease in patients with COVID-19: Neuroimaging, histological and clinical description. Brain 2020, 143, 3089–3103.
  37. Kremer, S.; Lersy, F.; Anheim, M.; Merdji, H.; Schenck, M.; Oesterlé, H.; Bolognini, F.; Messie, J.; Khalil, A.; Gaudemer, A.; et al. Neurologic and neuroimaging findings in COVID-19 patients: A retrospective multicenter study. Neurology 2020, 95, e1868–e1882.
  38. Weetman, A.P. Disease Graves’. N. Engl. J. Med. 2000, 343, 1236–1248.
  39. Squizzato, A.; Romualdi, E.; Büller, H.R.; Gerdes, V.E.A. Thyroid Dysfunction and Effects on Coagulation and Fibrinolysis: A Systematic Review. J. Clin. Endocrinol. Metab. 2007, 92, 2415–2420.
  40. Lamy, C.; Hamon, J.B.; Coste, J.; Mas, J.L. For the French Study Group on Stroke and Pregnancy. Neurology 2000, 55, 269–274.
  41. Ginsberg, J.S.; Greer, I.; Hirsh, J. Use of Antithrombotic Agents During Pregnancy. Chest 2001, 119, 122S–131S.
  42. Ray, J.G.; Chan, W.S. Deep Vein Thrombosis During Pregnancy and the Puerperium: A Meta-Analysis of the Period of Risk and the Leg of Presentation. Obstet. Gynecol. Surv. 1999, 54, 169–175.
  43. Taous, A.; Berri, M.A.; Lamsiah, T.; Zainoun, B.; Ziadi, T.; Rouimi, A. Cerebral venous thrombosis revealing an ulcerative colitis. Pan Afr. Med. J. 2016, 23, 120.
  44. Cohen, J.B.; Comer, D.M.; Yabes, J.G.; Ragni, M.V. Inflammatory Bowel Disease and Thrombosis: A National Inpatient Sample Study. TH Open 2020, 4, e51–e58.
  45. Ng, S.C.; Shi, H.Y.; Hamidi, N.; Underwood, F.E.; Tang, W.; Benchimol, E.I.; Panaccione, R.; Ghosh, S.; Wu, J.C.Y.; Chan, F.K.L.; et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: A systematic review of population-based studies. Lancet 2020, 56, 2769–2778.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Emergency Medicine
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Tiziana Ciarambino
,
Pietro Crispino
,
Giovanni Minervini
,
Mauro Giordano
View Times: 214
Revisions: 2 times (View History)
Update Date: 25 Jun 2023
Table of Contents
    1000/1000
    Hot Most Recent
    Video Production Service
    Feedback