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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid pathology is rarely involved in the pathogenesis of sudden death in young people, and usually, when this is the case, is associated with acute changes of thyroid hormone blood levels. Three main thyroid causes of sudden death are known and used in tanathologic chains: thyrotoxicosis, myxedematous coma and, as of recently, lymphocytic thyroid infiltration. Coagulation disorders associated with thyroid disease are usually mild and not associated with sudden death. There are some studies showing an increased risk for unprovoked deep venous thrombosis in patients with hypothyroidism but there is none, to our knowledge, showing a correlation between hypothyroidism, deep venous thrombosis and sudden death. Our article suggests that subclinical hypothyroidism can lead to coagulation disorders and deep venous thrombosis which can explain some cases of sudden death associated with pulmonary embolism without other significant risk factors.
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PMID:Can subclinical hypothyroidism explain some sudden deaths due to pulmonary embolism without evident risk factors? 2142 Jul 93

All available evidence today indicates that chronic thromboembolic pulmonary hypertension (CTEPH) is primarily caused by venous thromboembolism, as opposed to primary pulmonary vascular in situ thrombosis. Both the initial magnitude of clot and pulmonary embolism (PE) recurrence may contribute to the development of CTEPH. Only few specific thrombophilic factors, such as phospholipid antibodies, lupus anticoagulant and elevated factor VIII, are statistically associated with CTEPH. A mechanistic view of CTEPH as a disease caused by obliteration of central pulmonary arteries by pulmonary emboli is too simplistic. Based on available data one may speculate that PE may be followed by a pulmonary vascular remodelling process modified by infection, immune phenomena, inflammation, circulating and vascular-resident progenitor cells, thyroid hormone replacement or malignancy. Both plasmatic factors (hypercoagulation, "sticky" red blood cells, high platelet counts and uncleavable fibrinogens) and a misguided vascular remodelling process contribute to major vessel and small vessel obliteration. Endothelial dysfunction and endothelial-mesenchymal transition may be important, but their precise roles remain obscure. There exists no animal model for CTEPH; therefore, experimentation in the future must include human tissues and clinical data in parallel.
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PMID:Risk factors and basic mechanisms of chronic thromboembolic pulmonary hypertension: a current understanding. 2270 Aug 39

The administration of iodinated contrast medium may lead to excess free thyroid hormone release and cause thyroid storm. A woman presented to the emergency department with dyspnea, hemoptysis, and intermittent bilateral lower extremities edema. Physical examination revealed mildly enlarged thyroid. Patient underwent a computed tomography scan of the chest with intravenous iodinated contrast medium to rule out pulmonary embolism, the patient developed a thyroid storm second to iodinated contrast medium injection. Proper treatment was provided and the patient had a good outcome. We present this case of an unusual presentation of a thyroid storm with cardiac arrest. This case illustrates that evaluating thyroid function tests in patients with an enlarged thyroid prior to the administration of iodinated contrast medium could prevent the development of thyroid storm.
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PMID:In the eye of the storm: iodinated contrast medium induced thyroid storm presenting as cardiopulmonary arrest. 2371 92