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      Progressive Ischemic Stroke due to Thyroid Storm-Associated Cerebral Venous Thrombosis

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          Abstract

          Patient: Female, 49

          Final Diagnosis: Cerebral venous thrombosis

          Symptoms: Altered mental state • weakness in limbs

          Medication: —

          Clinical Procedure: —

          Specialty: Endocrinology and Metabolic

          Objective:

          Rare co-existance of disease or pathology

          Background:

          Cerebral venous thrombosis (CVT) is a rare but fatal complication of hyperthyroidism that is induced by the hypercoagulable state of thyrotoxicosis. Although it is frequently difficult to diagnose CVT promptly, it is important to consider it in the differential diagnosis when a hyperthyroid patient presents with atypical neurologic symptoms.

          Care Report:

          A 49-year-old Japanese female with unremarkable medical history came in with thyroid storm and multiple progressive ischemic stroke identified at another hospital. Treatment for thyroid storm with beta-blocker, glucocorticoid, and potassium iodide-iodine was started and MR venography was performed on hospital day 3 for further evaluation of her progressive ischemic stroke. The MRI showed CVT, and anticoagulation therapy, in addition to the anti-thyroid agents, was initiated. The patient’s thyroid function was successfully stabilized by hospital day 10 and further progression of CVT was prevented.

          Conclusions:

          Physicians should consider CVT when a patient presents with atypical course of stroke or with atypical MRI findings such as high intensity area in apparent diffusion coefficient (ADC) mapping. Not only is an early diagnosis and initiation of anticoagulation important, but identifying and treating the underlying disease is essential to avoid the progression of CVT.

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          Most cited references25

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          Life-threatening thyrotoxicosis. Thyroid storm.

          Although important strides in recognition and therapy have significantly reduced the mortality in this disorder from the nearly 100% fatality rate noted by Lahey, survival is by no means guaranteed. More recent series have yielded fatality rates between 20% and 50%. Although some authors have attributed this improvement, in part, to a relaxation of the diagnostic criteria for thyroid storm, it more likely represents improvements in early recognition and the beneficial effects of the serial addition of antithyroid, corticosteroid, and antiadrenergic therapies to the treatment of this disorder. Thyroid storm is a dreaded, fortunately rare complication of a very common disorder. Most cases of thyroid storm occur following a precipitating event or intercurrent illness. Effective management is predicated on a prompt recognition of impending thyroid storm which is, in turn, dependent on a thorough knowledge of both the typical and atypical presentations of this disorder. An unwavering commitment to an aggressive, multifaceted therapeutic intervention as outlined herein is critical to the obtainment of a satisfactory outcome.
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            Thyroid diseases and cerebrovascular disease.

            Acute cerebral ischemia has been described in different diseases of the thyroid gland, and not only as a result of thyrotoxic atrial fibrillation and cardioembolic stroke. The purpose of this review is to summarize the studies on the relationship between thyroid diseases and cerebrovascular diseases, discussing the main findings for overt hyperthyroidism and hypothyroidism, as well as for subclinical thyroid dysfunction. In overt hyperthyroidism, cardioembolic stroke is clearly associated to thyrotoxic atrial fibrillation, and in subclinical hyperthyroidism with serum thyroid-stimulating hormone levels <0.1 mU/L, the incidence of atrial fibrillation is increased. Although in vitro and in vivo studies indicate a hypercoagulability state in hyperthyroidism, there is insufficient evidence to prove that this state leads to an increased risk of cardiac emboli. However, the hypothesis that overt hyperthyroidism may cause acute cerebral venous thrombosis is intriguing. Possible associations between hyperthyroidism and Moyamoya or Giant cell arteritis have only been described in case reports. There is enough evidence that overt hypothyroidism is associated with several traditional and newer atherosclerotic risk factors, especially hypertension, hyperlipidemia, and hyperhomocysteinemia. For subclinical hypothyroidism, these associations are less certain. Hypothyroidism has been associated with signs of aortic or coronary atherosclerosis, but no case-control or cohort studies have ever investigated hypothyroidism as a possible risk factor for atherothrombotic stroke. Hyperthyroidism is associated with atrial fibrillation and cardioembolic stroke. Hypothyroidism is associated with a worse cardiovascular risk factor profile and leads to progression of atherosclerosis. Associations between hyperthyroidism and acute cerebral venous thrombosis, Moyamoya, and Giant cell arteritis have been suggested, but sound evidence is lacking. Additional studies are needed to clarify these issues.
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              The effect of hyperthyroidism on procoagulant, anticoagulant and fibrinolytic factors: a systematic review and meta-analysis.

              Several coagulation and fibrinolytic parameters appear to be affected by thyroid hormone excess; however, the net effect on the haemostatic system remains unclear. We aimed to update our previous review and systematically summarise and meta-analyse the data by assessing the effects of thyrotoxicosis on the coagulation and fibrinolytic system in vivo . Data sources included MEDLINE (2006-2012), EMBASE (2006-2012), and reference lists. The sources were combined with our previous search containing studies from 1980-2006. Eligible studies were all observational or experimental studies. Two investigators independently extracted data and rated study quality. Weighted mean proportion and 95% confidence intervals were calculated and pooled using a fixed and a random-effects model. A total of 29 articles consisting of 51 studies were included, as in several articles more than one study was described. We included four intervention (before and after treatment in hyperthyroid patients), five cross-sectional (hyperthyroid subjects and euthyroid controls), and four experimental (before and after use of thyroid hormone in euthyroid subjects) medium/high quality studies for meta-analysis. We found that thyrotoxicosis shifts the haemostatic balance towards a hypercoagulable and hypofibrinolytic state with a rise in factors VIII and IX, fibrinogen, von Willebrand factor, and plasminogen activator inhibitor-1. This was observed in endogenous and exogenous thyrotoxicosis, and in subclinical as well as overt hyperthyroidism. We conclude that both subclinical and overt hyperthyroidism induce a prothrombotic state, which is therefore likely to be a risk factor for venous thrombosis.
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                Author and article information

                Journal
                Am J Case Rep
                Am J Case Rep
                amjcaserep
                The American Journal of Case Reports
                International Scientific Literature, Inc.
                1941-5923
                2017
                23 February 2017
                : 18
                : 194-197
                Affiliations
                [1 ]Department of Internal Medicine, Tokyo Bay Urayasu Ichikawa Medical Center, Urayasu, Chiba, Japan
                [2 ]Department of Internal Medicine, Funabashi General Hospital, Funabashi, Chiba, Japan
                [3 ]Department of Internal Medicine, University of Hawaii, Honolulu, HI, U.S.A.
                [4 ]Department of Neurosurgery, Tokyo Bay Urayasu Ichikawa Medical Center, Urayasu, Chiba, Japan
                [5 ]Department of Critical Care Medicine, Tokyo Bay Urayasu Ichikawa Medical Center, Urayasu, Chiba, Japan
                [6 ]Department of Nephrology, Endocrinology, and Diabetes, Tokyo Bay Urayasu Ichikawa Medical Center, Urayasu, Chiba, Japan
                Author notes

                Authors’ Contribution:

                [A]

                Study Design

                [B]

                Data Collection

                [C]

                Statistical Analysis

                [D]

                Data Interpretation

                [E]

                Manuscript Preparation

                [F]

                Literature Search

                [G]

                Funds Collection

                This case was previously presented at the Society of General Internal Medicine (SGIM) Annual Meeting 2016 and the abstract was published in the Journal of General Internal Medicine

                Conflict of interest: None declared

                Corresponding Author: Eiji Hiraoka, e-mail: eijih@ 123456jadecom.jp
                Article
                902297
                10.12659/AJCR.902297
                5333713
                28228636
                2945e698-b202-4e96-b765-283970e8a47e
                © Am J Case Rep, 2017

                This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)

                History
                : 09 November 2016
                : 07 December 2016
                Categories
                Articles

                early diagnosis,intracranial thrombosis,thrombophilia,thyroid crisis,venous thrombosis

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