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Thyrotoxicosis and cerebral venous sinus thrombosis, causality or chance alone?
Tirotoxicosis y trombosis de senos venosos cerebrales, ¿causalidad o azar?
María Merinoa,
Corresponding author
marietta84@hotmail.com

Corresponding author.
, María Guadalupe Guijarroa, Paloma Iglesiasa, Yolanda Aladrob, Paloma Monterob
a Servicio de Endocrinología y Nutrición, Hospital Universitario de Getafe, Getafe, Madrid, Spain
b Servicio de Neurología, Hospital Universitario de Getafe, Getafe, Madrid, Spain
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He reported throbbing holocranial headache associated with photopsia&#44; as well as paresthesia in the right half of the face and right upper limb&#46; When questioned&#44; the patient reported both a loss of approximately 8&#8211;10<span class="elsevierStyleHsp" style=""></span>kg in weight and hyperhydrosis over the previous year&#46; A physical examination revealed bilateral grade II&#47;IV papilledema at eye fundus&#44; with no neurological focal signs&#46; The examination was otherwise normal&#44; with a heart rate of 80 beats per minute&#44; and no fine distal tremor&#44; exophthalmos&#44; or goiter&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">A supplemental complete blood count showed normal results&#44; except for elevated fibrinogen levels &#40;516&#46;9<span class="elsevierStyleHsp" style=""></span>mg&#47;dL&#59; normal range&#44; 200&#8211;400&#41;&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Thyroid function tests provided results consistent with hyperfunction&#58; FT4 4&#46;54<span class="elsevierStyleHsp" style=""></span>ng&#47;dL &#40;NR&#44; 0&#46;9&#8211;1&#46;7&#41;&#44; TSH 0&#46;01<span class="elsevierStyleHsp" style=""></span>&#956;U&#47;mL &#40;NR&#44; 0&#46;27&#8211;4&#46;5&#41;&#44; FT3 8&#46;61<span class="elsevierStyleHsp" style=""></span>pg&#47;mL &#40;NR&#44; 2&#8211;4&#46;4&#41;&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Tests for autoimmunity markers &#40;antinuclear&#44; ANCA&#44; anticardiolipin&#44; antimitochondrial&#44; antimicrosomal&#44; anti-TSH receptor&#44; and antithyroglobulin antibodies&#41; were only positive for the latter&#44; with values of 363<span class="elsevierStyleHsp" style=""></span>U&#47;mL &#40;NR&#44; &#60;280&#41;&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">A hypercoagulability study showed a chromogenic factor VIII level<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>120&#37; &#40;NR&#44; 80&#8211;110&#41; and a von Willebrand factor Ag level of 112&#37; &#40;NR&#44; 80&#8211;110&#41;&#46; No changes were found in any other proteins tested &#40;antithrombin III&#44; protein C&#44; protein S&#44; von Willebrand factor&#44; A2-antiplasmin antibodies&#44; plasminogen&#44; and protein C resistance test&#41;&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Because of the findings of hyperthyroidism&#44; thyroid gammagraphy was performed&#44; which showed diffuse hyperplasia with increased uptake&#46; MRI of the brain &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#44; performed because of clinical signs of paresthesia&#44; showed signal hyperintensity at the superior longitudinal sinus&#44; the confluence of sinuses&#44; the straight sinus&#44; and the proximal portion of the transverse sinuses consistent with subacute dural sinus thrombosis&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall">Cerebral sinus venous thrombosis secondary to hyperthyroidism was suspected&#44; and treatment was started with low molecular weight heparin and subsequently with coumarins&#44; tapering corticosteroids&#44; and low-dose thiamazole &#40;5<span class="elsevierStyleHsp" style=""></span>mg&#47;12<span class="elsevierStyleHsp" style=""></span>h&#41;&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">After two weeks of treatment with thiamazole &#40;10<span class="elsevierStyleHsp" style=""></span>mg&#47;24<span class="elsevierStyleHsp" style=""></span>h&#41;&#44; the patient was asymptomatic and showed subclinical hyperthyroidism&#58; FT4 0&#46;93<span class="elsevierStyleHsp" style=""></span>ng&#47;dL &#40;NR&#44; 0&#46;9&#8211;1&#46;7&#41;&#44; TSH 0&#46;02<span class="elsevierStyleHsp" style=""></span>&#956;U&#47;mL &#40;NR&#44; 0&#46;27&#8211;4&#46;5&#41;&#44; FT3 2&#46;15<span class="elsevierStyleHsp" style=""></span>pg&#47;mL &#40;NR&#44; 2&#8211;4&#46;4&#41;&#59; the dose was therefore decreased to 2&#46;5<span class="elsevierStyleHsp" style=""></span>mg&#47;24<span class="elsevierStyleHsp" style=""></span>h&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">One month later&#44; hormone values were within the normal range &#40;FT4 0&#46;98<span class="elsevierStyleHsp" style=""></span>ng&#47;dL &#40;NR&#44; 0&#46;9&#8211;1&#46;7&#41;&#44; TSH 0&#46;81<span class="elsevierStyleHsp" style=""></span>&#956;U&#47;mL &#40;NR&#44; 0&#46;27&#8211;4&#46;5&#41;&#44; FT3 2&#46;99<span class="elsevierStyleHsp" style=""></span>pg&#47;mL &#40;NR&#44; 2&#8211;4&#46;4&#41;&#41;&#44; and antithyroid treatment was therefore discontinued&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">The patient is currently asymptomatic and only receives oral anticoagulant therapy&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Although additional clinical trials are needed to confirm the association between coagulation&#47;fibrinolysis disorders and thyroid function changes&#44; the current evidence suggests that coagulation changes depend on the type of thyroid change&#46; Patients with hypothyroidism usually appear to have an increased risk of bleeding&#44; while hyperthyroid patients are more prone to arterial thrombosis&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Several pathogenetic mechanisms predisposing hyperthyroid patients to a hypercoagulability state have been proposed&#44; but the exact pathogenetic pathway is yet to be fully elucidated&#46; Some of the changes found by different authors include increased plasma von Willebrand factor levels&#44; improved platelet function&#44; and increased factor II&#44; VII&#44; VIII&#44; and X factors&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;6&#44;7</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">The evidence reported for an association of hyperthyroidism and venous thrombosis is limited to a few case reports&#46; According to a review by Franchini et al&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> documenting 34 cases of venous thrombosis in patients with hyperthyroidism&#44; thrombosis occurred in 80&#37; of these patients in uncommon locations such as the splanchnic and&#44; more frequently&#44; the cerebral venous systems&#44; which was the one involved in the reported patient&#46; Subacute and chronic venous thromboses were also more common than acute thrombosis&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">Squizzato et al&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> reported 13 cases of acute cerebral sinus venous thrombosis associated with thyroid disease&#46; The most common etiology of hyperthyroidism was Graves&#8211;Basedow disease&#44; and a hypercoagulability state and even vascular compression in the event of large goiter were suggested as a pathogenetic mechanism&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">In the reported case&#44; autoimmune hyperthyroidism could have been Hashimoto toxicosis instead of Graves&#8211;Basedow disease&#46; Both of them may show diffuse hyperuptake at gammagraphy&#44; but the absence of positive TSH receptor antibodies and the good response to antithyroid treatment suggest Hashimoto toxicosis as the first possibility&#44; despite the fact that 10&#37; of patients with Graves&#8211;Basedow disease test negative for these antibodies&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">Thus&#44; although there are many risk factors for the development of cerebral sinus venous thrombosis&#44; such as hereditary thrombophilia&#44; oral contraceptives&#44; pregnancy&#44; and postpartum&#44; hyperthyroidism should always be considered&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;6&#44;8</span></a> In patients with hyperthyroidism and neurological symptoms&#44; the diagnosis of cerebral sinus venous thrombosis should also be suspected and coagulation tests should be performed&#46;</p><p id="par0095" class="elsevierStylePara elsevierViewall">If this potential causal relationship is supported by larger observational studies&#44; this may have significant clinical implications&#44; particularly for prevention and treatment&#46;</p></span>"
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