Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six patients were admitted after erroneous massive intake of levothyroxine (70-1200 mg over an interval of 2-12 days). All patients developed classical symptoms of thyrotoxicosis within 3 days of the first dose; five patients presented grade II-III coma and one became stuporous (days 7-10). Two patients developed left ventricular failure and three had arrhythmias (days 8-11). Total thyroid hormone levels in serum on admission ranged 935-7728 nmol/l for T4 (TT4) and 23-399 nmol/l for T3 (TT3). All patients received treatment with hydrocortisone and Propranolol. Propylthiouracil was also given in 3 cases. Extractive techniques (charcoal haemoperfusion and/or plasmapheresis) were initiated 8-14 days after the first dose of L-T4. The plasma disappearance rate (K) of TT4 with plasmapheresis was 30 times higher, on average, than under standard medical treatment (M). Also, K of TT4 under haemoperfusion was about five times higher than K under M. K changes for TT3 were higher under haemoperfusion than under plasmapheresis. Furthermore, extractive procedures shortened the average half life of TT4, (from 106.5 +/- 44.6 to 59.7 +/- 20.2 h, p less than 0.05).
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PMID:Massive thyroxine intoxication: evaluation of plasma extraction. 355 34

Thyrotoxicosis may present with a hyperkinetic clinical picture typically associated with Graves' or Plummer's disease, or in an apathetic form characterized by lethargy, weakness, and withdrawal. Both the hyperkinetic and apathetic forms of thyrotoxicosis may be associated with or masked by predominantly extrathyroidal manifestations, occasionally referable primarily to the abdomen. We present two cases of apathetic thyrotoxicosis that suggested the need for urgent surgical intervention, and review the literature on apathetic thyrotoxicosis as an abdominal emergency, as well as laboratory studies and possible etiology.
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PMID:Apathetic thyrotoxicosis presenting as an abdominal emergency: a diagnostic pitfall. 705 58

L-Thyroxine (T4) is commonly prescribed medication for hypothyroidism in humans and animals. Overdose has generally resulted in limited symptomatology managed with sedatives and beta-adrenergic receptor antagonists. We describe the largest acute T4 ingestion ever reported, which resulted in a profound thyrotoxicosis, resistant to treatment. A 34-y-old man ingested 900 (0.8 mg) tablets of veterinary T4 (720 mg) and was given 60 g of activated charcoal. He became lethargic on post-ingestion days 2 and 3; had vomiting, diaphoresis and insomnia on day 4; on day 5 he "looked like he had too much coffee", began "using a lot of words" and became agitated, assaultive and stopped speaking intelligibly; and on day 6 returned to the hospital combative and confused. He was diaphoretic, mydriatic, hyperreflexic, tremulous, with clear lungs and active bowel sounds, and received activated charcoal, haloperidol, diazepam, and phenobarbital, and was tracheally intubated. During hospitalization he was rehydrated, treated with propranolol and diazepam, but remained continuously tachycardic. On day 12 he became afebrile and his tachycardia resolved. Free T4 levels ranged from > 13 mcg/dL on day 6 to 1.2 mcg/dL on day 12. By discharge (day 15) he had lost 20 kilograms of body weight, but was clinically euthyroid 2 w later. This case suggests that large intentional T4 ingestions should be managed differently than current T4 overdose protocol.
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PMID:Severe symptoms following a massive intentional L-thyroxine ingestion. 1050 39

We describe a case of thyroid storm due to thyrotoxicosis factitia, which was caused by the ingestion of excessive quantities of exogenous thyroid hormone for the purpose of reducing weight. An 18-year-old female was admitted to the hospital 24 hours after taking up to 50 tablets of synthyroid (1 tablet of synthyroid : levothyroxine 100 microg). Because of her stuporous mental state and acute respiratory failure, she was intubated and treated in the intensive care unit. After reviewing her history carefully and examining plasma thyroid hormone levels, we diagnosed this case as a thyroid storm due to thyrotoxicosis factitia. Her thyroid function test revealed that T3 was 305 ng/dL, T4 was 24.9 microg/dl, FT4 was 7.7 ng/dL, TSH was 0.05 micro IU/mL and TBG was 12.84 microg/mL (normal range: 11.3 - 28.9). TSH receptor antibody, antimicrosomal antibody, and antithyroglobulin antibody were negative. She was recovered by treatment, namely, steroid and propranolol, and was discharged 8 days after admission. Thyroid storm due to thyrotoxicosis factitia caused by the ingestion of excessive thyroid hormone is rarely reported worldwide. Therefore, we now report a case of thyroid storm that resulted from thyrotoxicosis factitia caused by the ingestion of a massive amount of thyroid hormone over a period of 6 months.
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PMID:A case of thyroid storm due to thyrotoxicosis factitia. 1272 81

A 65-year-old woman presented to the hospital with weight loss and diarrhea. A diagnosis of thyroid storm was established by the presence of fever, lethargy, tachycardia, heart failure (HF), and abnormal thyroid function tests. An acute coronary syndrome (ACS) was suspected because of anteroseptal ST-segment elevations on electrocardiogram and severe left ventricular (LV) dysfunction with apical dilation on echocardiogram. The ejection fraction (EF) was 25%. Treatment for ACS and HF was begun. Coronary arteriography revealed normal coronaries. Propylthiouracil and corticosteroids were added to treat thyrotoxicosis. On Day 4, repeat echocardiography confirmed an EF of 65% and complete resolution of LV dysfunction and cavity dilation. Reversible LV dysfunction and apical cavity dilation is consistent with Takotsubo cardiomyopathy. While commonly associated with psychological trauma, its association with thyroid storm has only been reported twice before. Knowledge of this possible association is of importance in establishing the diagnosis and instituting a proper treatment plan.
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PMID:An association between Takotsubo cardiomyopathy and thyroid storm. 1949 50

A 38-year-old gentleman presented with thyroid storm with multiorgan involvement in the form of heart failure (thyrotoxic cardiomyopathy), respiratory failure (respiratory muscle fatigue), hepatic dysfunction, fast atrial fibrillation, pulmonary embolism, and disseminated intravascular coagulation (DIC). His Graves' disease (GD) remained undiagnosed for nearly 8 months because apart from weight loss, he has not had any other symptoms of thyrotoxicosis. The presentation of thyroid storm was atypical (apathetic thyroid storm) with features of depression and extreme lethargy without any fever, anxiety, agitation, or seizure. There were no identifiable triggers for the thyroid storm. Apart from mechanical ventilation and continuous veno-venous renal replacement therapy in the intensive care unit, he received propylthiouracil (PTU), esmolol, and corticosteroids, which were later switched to carbimazole and propranolol with steroids being tapered down. He was diagnosed with thyrotoxic myopathy which, like GD, remained undiagnosed for long (fatigability). A high index of suspicion and a multidisciplinary care are essential for good outcome in these patients.
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PMID:Apathetic Thyroid Storm with Cardiorespiratory Failure, Pulmonary Embolism, and Coagulopathy in a Young Male with Graves' Disease and Myopathy. 3302 36