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)

The Northwest Regional Screening Program to detect congenital hypothyroidism in infants born in Oregon, Montana, Alaska, and Idaho (combined birthrate of 69,000/ yr) was added to our ongoing screening program in 1975. The program utilizes dried blood filter paper specimens collected routinely in the first few days of life in all four states and again at about 6 weeks of age in Oregon only. The screening test consist of an initial thyroxine (T4) measurement; a thyroid-stimulating hormore (TSH) determination is performed on those specimens with T4 concentrations in the lowest 3% group. Serum samples obtained by venipuncture are requested for confirmation of the diagnosis. In the first two years of the program, 25 infants with primary hypothyroidism were detected amont 110,667 infants screened, a frequency of 1:4,430. Fourteen cases of thyroxine-binding globulin deficiency were also detected, a frequency of 1:7,900. Using the T4 followed by TSH testing approach, the frequency of request for repeat specimens was 0.4% in Oregon and 0.05% in the other states. The cost per specimen was $1.96. The majority of infants lacked clinical signs or symptoms of hypothyroidism; only one infant was clinically suspected of having hypothyroidism prior to detection. The most common neonatal symptoms were constipation, lethargy, and prolonged jaundice, while the most common physical signs were hypotonia, umbilical hernia, and large fontanels. Thyroid scans showed the most common etiology to be thyroid aplasia, followed by an ectopic gland, hypoplasia, and goiter. Serum T4 concentrations were lowest in those infants with aplasia, intermediate in infants with an ectopic gland or hypoplasia, and normal in the infant with the goiter. Neonatal hypothyroidism varies in degree and has several different causes; the capacity to secrete thyroid hormone, the duration before hypothyroidism becomes clinically manifest, and possibly the eventual prognosis for intellectual function depend on the nature of the underlying cause. While the mean age at treatment was 59 days, the goal of diagnosing congenital hypothyroidism and treating affected infants by 1 month of age seems realistic.
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PMID:Neonatal hypothyroidism detected by the Northwest Regional Screening Program. 10 59

An overdose of up to 850 levothyroxine sodium tablets (0.2 mg) in a healthy 6-year-old 16.8-kg dog induced an episode of vomiting and hippus within 9 hours of ingestion. The dog was treated with activated charcoal and saline (magnesium sulfate) cathartic. Initially the serum concentration of thyroxine (T4) 4,900.9 nmol/L. On the second day, serum concentration of triiodothyronine (T3) was 5.3 nmol/L. Serum T4 concentration decreased slowly and was not determined to be normal until day 36. Serum T3 concentration was found to be normal on day 6. Serum alanine transaminase activity peaked on day 6 at 345 U/L. Significant abnormalities were not found during the following 36 days. Clinical signs of thyroid hormone toxicosis in dogs and cats include hyperactivity, lethargy, tachycardia, tachypnea, dyspnea, abnormal pupillary light reflexes, vomiting, and diarrhea. High overdoses of levothyroxine sodium in dogs should be managed by initial decontamination and administration of activated charcoal with a cathartic followed by supportive care.
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PMID:Acute overdose of levothyroxine in a dog. 161 89

Congenital hypothyroid dwarfism was diagnosed in a family of Giant Schnauzers. Three female and two male puppies from different litters were evaluated for dwarfism, lethargy, somnolence, gait abnormalities, and constipation. On physical examination, disproportionate dwarfism (n = 5), macroglossia (n = 3), hypothermia (n = 3), delayed dental eruption (n = 3), ataxia (n = 2), and abdominal distension (n = 1) were identified. Results of initial laboratory tests showed anemia (n = 4), hypercholesterolemia (n = 4), hypercalcemia (n = 2), and transudative abdominal effusion (n = 1). Radiographic skeletal surveys disclosed epiphyseal dysgenesis and delayed skeletal maturation (n = 5). A diagnosis of hypothyroidism was established on the basis of low basal serum thyroxine concentrations that failed to increase following the administration of TSH (n = 5) and markedly reduced to absent thyroid image when evaluated with gamma camera imaging of the thyroid gland (n = 4). In the two dogs that were most thoroughly evaluated, the results of thyroid histology, prolonged TSH testing, and repeat thyroid imaging, after three daily injections of TSH, were all consistent with secondary or tertiary, rather than primary, hypothyroidism. When TSH was administered over a period of 3 consecutive days (5 IU/day, subcutaneously), serum thyroid hormone response became normal and resulted in a normal thyroid image in the two dogs re-evaluated with gamma camera imaging. Daily treatment with oral levothyroxine (20 micrograms/kg) resulted in complete remission in puppies (n = 4) treated prior to 4 months of age. The other puppy failed to attain normal breed standards for height.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Congenital hypothyroid dwarfism in a family of giant schnauzers. 174 85

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

A 52-year-old man with myxedema was evaluated for anterior chest pain that was considered to be compatible with myocardial ischemia. The night after admission he developed extreme bradycardia, hypotension, and apneic episodes lasting up to 25 s. Continuous positive airway pressure and administration of medroxyprogesterone acetate prevented further episodes and relieved much of the somnolence and lethargy that had contributed to the evidence for myxedema. Alveolar hypoventilation caused by decreased sensitivity to carbon dioxide, inadequate central neural drive, peripheral muscle force, and obesity all may have contributed to the apnea. Chest pain has not recurred, and results of electrocardiography have remained normal following full thyroid hormone replacement. The early recognition of myxedema causing sleep apnea will allow specific treatment to avoid the cardiovascular risks related to prolonged apnea and will help avoid confusion with other etiologies of cardiovascular abnormalities.
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PMID:Extreme bradycardia during sleep apnea caused by myxedema. 363 55

Hypothyroidism in the foal occurs as two entities because of the separate actions of thyroid hormones in regulation of metabolic rate and in cell differentiation. The hypometabolic state which results in inadequate thermogenesis and lethargy, occurs concurrently with a period when thyroid hormone secretion is inadequate. Also the severity of the concurrent symptoms is related to the degree of hormone inadequacy as measured by plasma concentrations of free T4 and T3. By contrast, the developmental lesions caused by hypothyroidism are often observed during periods when plasma thyroid hormone concentrations are normal. This is because during the development of most tissues there is a period during which deprivation of thyroid hormones leads to developmental defects which may first appear weeks or months later, by which time thyroid hormone levels may have returned to normal. In the foal the critical period for some developmental processes, eg, myelination, is before birth so it is difficult to confirm a pre-natal hypothyroid state as the cause of neonatal neuromuscular incompetence. Post natal developmental lesions of the epiphyses or ossification centres, for example, may also manifest themselves some weeks subsequent to the period during which hypothyroidism existed. Because confirmation of diagnosis using plasma hormone measurements is very difficult in the foal, and because the symptoms of hypothyroidism are not specific, the incidence of confirmed hypothyroidism in foals is low. However there is suggestive evidence that where awareness of the condition exists it is diagnosed frequently. The aetiology is obscure although diet has been implicated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothyroidism in the foal. 638 12

We examined the thyroid status of 58 patients with primary biliary cirrhosis (PBC) using total serum thyroxin, thyroid hormone binding ratio, free thyroxin index, serum TSH, antithyroglobulin, and antimicrosomal antibodies. Seven patients were known to be hypothyroid prior to the diagnosis of PBC. Six additional patients were found to have biochemical evidence of hypothyroidism. The prevalence of hypothyroidism was 12% if we include only those six PBC patients with newly diagnosed hypothyroidism or 22% if we include all 13 patients. Five of the 58 patients had evidence for an elevation of thyroid hormone binding capacity. Three hypothyroid patients had normal total thyroxins with low thyroid hormone binding ratios. Two euthyroid patients had elevated total T4s with low thyroid hormone binding ratio and normal FTI. The prevalence of positive antimicrosomal antibodies was 34%, including 11 euthyroid PBC patients. The prevalence of positive antithyroglobulin antibodies was 20% including five euthyroid patients. There was no association between HLA DR3 or DR5 and the patients with hypothyroidism and/or antithyroid antibodies. Because fatigue, lethargy, and anorexia as well as hypercholesterolemia are common features of both hypothyroidism and PBC, patients with PBC should be screened for evidence of thyroid dysfunction. Thyroid disease may precede the diagnosis of PBC by several years. Therefore, the development of cholestatic liver disease in a patient with known autoimmune thyroiditis should arouse suspicion of PBC.
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PMID:Increased incidence of hypothyroidism in primary biliary cirrhosis. 662 57

Hypothyroidism is commonly thought to cause decreased gastric emptying and secretion, but these may be related to associated autoimmune disease or chronic changes. Therefore, we measured gastric emptying and secretion in 11 healthy controls and in nine patients (19-54 years old; five females and 4 males) rendered athyreotic by surgery and/or 131I for thyroid cancer. Replacement T4 was stopped 47-65 days and subsequent replacement T3 was stopped 33-40 days before the study. All patients were symptomatic with complaints including weight gain, lethargy, and constipation. Deep tendon reflexes had delayed relaxation phase. Serum cholesterol and creatine phosphokinase levels were elevated. Thyroid hormone levels were markedly decreased (means +/- SE; T4: 0.7 +/- 0.3 micrograms/dl; free T4: 0.2 +/- 0.1 ng/dl; T3: 28 +/- 6 ng/dl) and TSH was markedly increased (88 +/- 16 microU/ml). Gastric fractional emptying rate (%/min) and hydrogen ion (H+) output (meq/hr) were determined before and following two sequential stimulations: a 250-ml water load and an intravenous infusion of pentagastrin (6 micrograms/kg/hr). There were no significant differences between controls and athyreotic patients. Our data demonstrated that short-term, profound, thyroid hormone deficiency does not modify gastric emptying or acid output.
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PMID:Gastric secretion and emptying in hypothyroidism. 671 56

In an attempt to study "manic-depressive" affairs associated with endocrine and mental disorders, our clinical data are analyzed before and after appropriate treatment in Cushing's disease, Cushing's syndrome, hyperthyroid Graves' disease and primary hypothyroidism. Although our data do not provide definite findings on manic-depressive affairs associated with Cushing's disease and syndrome, review data by others indicated a high incidence of depression under untreated condition and its disappearance after appropriate treatment. In contrast, patients with adrenocortical insufficiency did have a depression but this was cleared after supplemental therapy. In hyperthyroid Graves' disease, a number of emotional and mental instability and irritability were noticed before the treatment, but these abnormalities all disappeared after appropriate treatment for 3-6 months. In contrast, patients with primary hypothyroidism did show lethargy and apathy, and these abnormalities disappeared after appropriate treatment. From the data accumulated, it is concluded that adrenal steroid and thyroid hormone do affect the functions of nervous system and, as a result, cause a number of clinical symptoms. The exact biochemical processes underlying these abnormalities are not known and remains for further investigations.
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PMID:[Manic-depressive symptom associated with endocrine and metabolic disorders]. 800 7

Hypothyroidism is a commonly diagnosed endocrine disorder. Typical signs and symptoms of hypothyroidism include lethargy, cold intolerance, hoarseness, dry skin, constipation, delayed relaxation phase of deep tendon reflexes, and bradycardia. Hypothyroidism, presenting with such classic manifestations, usually is readily recognized and, therefore, easy to diagnose. Occasionally patients have less commonly emphasized symptoms, making the diagnosis less apparent. Such atypical presentations may suggest other diseases as the primary problem and, therefore, the initial focus of attention is on a diagnosis other than hypothyroidism. We have observed patients with hypothyroidism with rare manifestations. The diagnosis of primary hypothyroidism was established in all patients by thyroid function tests, and initiation of thyroid hormone therapy resulted in significant improvement of the presenting symptom. We considered it instructive to report about these patients because it shows the need to be aware of the unusual presentations of hypothyroidism and to consider hypothyroidism when confronted with atypical clinical manifestations.
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PMID:Unusual presentations of hypothyroidism. 936 36


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