Linked Life Data

6305250

Source:http://linkedlifedata.com/resource/pubmed/id/6305250

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1983-7-15
pubmed:abstractText
A 54-year-old woman, with no previously documented thyroid disease, treated with amiodarone (200 mg/day, five days a week for 33 months) for paroxysmal tachyarrhythmia complicating mitral stenosis, suddenly developed extremely severe thyrotoxicosis. After therapeutic failures with carbimazole and propylthyrouracil (PTU) associated with beta-blockers, she was transferred to intensive care for plasma exchange (PE). Two PE were performed, temporarily aggravating the cardiovascular status of the patient, with no secondary improvement. The quantity of T3 removed was very small, about 1,000 ng per exchange. On the 14th day PTU had to be discontinued (toxic thrombopenia) and only symptomatic treatment was maintained (assisted ventilation, digitalis, hyperalimentation). In the 4th month, while the patient had a high total serum iodine, hypothyroidism developed due to partial block of the organification of the iodine with high TSH and fixation; this state also lasted 4 months. Spontaneous recovery was observed after 8 months. In addition a severe peripheral neuropathy was observed during the hyperthyroid phase confirmed by electromyography, distinct from the signs of thyrotoxic myopathy. This gradually regressed over 7 months and may be attributed to amiodarone therapy. The association of these two successive types of thyroid disorder due to amiodarone is an exceptionally rare phenomenon. Severe thyrotoxicosis generally requires long-term symptomatic therapy, its natural course being towards spontaneous regression. PE are ineffective on the circulating hormonal levels and were dangerous because of the underlying cardiac disease. The development of hypothyroidism at the 4th month is explained by the persistent iodine overload, and therefore prolonged surveillance after withdrawal of therapy is advised. The neurological complication of amiodarone was quite distinct from the hyperthyroid myopathy.
pubmed:language
fre
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0003-410X
pubmed:author
pubmed:issnType
Print
pubmed:volume
134
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
31-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
[Thyrotoxicosis, then hypothyroidism caused by iodine overload (amiodarone) associated with neuropathy. Failure of plasma exchange].
pubmed:publicationType
Journal Article, English Abstract, Case Reports