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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperthyroidism is a common endocrinologic disorder affecting many organ systems. Musculoskeletal and neurological involvement present themselves as fatigue, muscle weakness and paralysis. Electromyography (EMG) is essential for differential diagnosis of muscle weakness. Well defined neuropathy and myopathy have been described in these patients. In the present study 17 hyperthyroid patients were evaluated with electrophysiological tests in addition to physical and neurological examinations and biochemical laboratory studies. Needle EMG, motor and sensory conduction velocities, median and tibial somatosensory evoked potentials (SEP) were studied. For assessment of the activity of disease clinical status, neurological symptom and disability scores and serum T3, T4 and TSH levels were examined. Statistical analysis of neuroelectrophysiological findings of the patient and the control groups yielded meaningful difference in the needle EMG, sensory conduction velocity and evoked potential findings. Abnormalities were observed in 80% of the proximal muscles besides polyphasic potentials that were seen in 20% of the extensor digitorum brevis muscle. Median, ulnar and sural nerve sensory action potential amplitudes were found to be lower than that of the control group. Sural sensory nerve conduction velocity of patients was decreased in 35.5%, prolongation of median SEP latencies and increase in the amplitudes were not however statistically significant. Prolongation of Tibial SEP N1, P2 latencies were seen in 47%, amplitudes of N1 were increased in 88.2%, P2 in 58.8%, N2 in 47%. The thyroid clinical status score was correlated with Tibial SEPs amplitude. These findings suggest the presence of an initial axonal type of mild polyneuropathy. As a conclusion electrophysiological studies can be useful in the diagnosis of asymptomatic polyneuropathy in hyperthyroid patients.
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PMID:Neuroelectrophysiological evaluation of untreated hyperthyroid patients. 753 51

TSH-secreting pituitary adenoma with calcification and proliferation of the collagen fibers was presented. A 42-year-old man had shown general fatigue and thyroid hypertrophy caused by hyperthyroidism for 3 years. CT and MRI revealed pituitary adenoma with calcification extending into the cavernous sinus and sphenoid sinus. The patient was operated on using the transsphenoidal route twice, but the tumor was not able to be removed totally, partly due to the hardness of the tumor. The tumor in- and around the left cavernous sinus as well as the hardest part of the tumor itself due to the calcification could not be removed. Histopathological examination revealed chromophobe adenoma with proliferation of the collagen fibers. Immunohistological and electronmicroscopic examination demonstrated TSH-secreting adenoma. Postoperatively, thyroid function improved and the patient's symptoms due to hyperthyroidism disappeared.
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PMID:[TSH-secreting fibrous pituitary adenoma showing calcification: a case report]. 770 Apr 96

A 16-year-old depressed adolescent, who had received sertraline treatment for the previous 18 months, developed insomnia, daytime somnolence and lack of energy. His thyroid function tests revealed low levels of total T4 with normal levels of free T4 and TSH, and a normal thyrotropin-releasing hormone (TRH) stimulation test. Discontinuing sertraline resulted in improved sleep and disappearance of daytime somnolence. Although daytime somnolence and low levels of total T4 can mimic hypothyroidism, in this case sertraline only displaced the bound-fraction of total T4 and was not associated with true hypothyroidism.
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PMID:Effects of long term treatment with sertraline (Zoloft) simulating hypothyroidism in an adolescent. 777 34

In the present paper we described the first case report of silent thyroiditis following alpha-interferon (IFN-alpha) treatment for chronic type C hepatitis in Japan. A 51-year-old woman with chronic type C hepatitis was treated with 6 million units of IFN-alpha three times a week for 24 weeks. Thyroid function was within normal limits and thyroid autoantibodies were negative before IFN therapy. Sixteen weeks after initiation of the treatment, she complained of increasing fatigue, palpitation and losing 7 kg in weight. Thyroid function tests at that time revealed an increase in serum T3, T4, free T3 and free T4 and a markedly suppressed TSH concentration. Both antithyroglobulin antibody (TgAb) and antimicrosomal antibody (McAb) were positive in a dilution of 1: 400. The computed tomographic (CT) scan of the thyroid showed a decrease in the CT number (Hounsfield unit; H.U.) to 58 H.U. (normal, 95-167 H.U.). The 24-h thyroid uptake of 123I was 0.75%. Aspiration biopsy specimens from a nodule in the right lobe and the remaining struma disclosed papillary adenocarcinoma and Hashimoto thyroiditis, respectively. Thyroid function spontaneously returned to normal two months after the onset of thyrotoxicosis through the subclinical hypothyroid stage. After recovery of thyroid function, patient had an operation of papillary cancer without any complications. These clinical features and laboratory findings led to the diagnosis of silent thyroiditis developing in the course of the long-term IFN therapy, which, to our knowledge, has not been reported before in Japan.
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PMID:An episode of silent thyroiditis in a patient with chronic thyroiditis and papillary adenocarcinoma following alpha interferon treatment for hepatitis C. 792 Aug 83

A case of systemic lupus erythematosus (SLE) complicated with hypopituitarism after steroid pulse therapy is reported. A 46-years-old-female with a history of SLE starting in 1975 was admitted to our hospital in February 1991 for lupus nephritis. Steroid pulse therapy, 1000 mg methyl-prednisolone for 3 successive days as one therapy unit, was administered. Proteinuria improved remarkably, however, general fatigue and headache appeared 2 weeks after initiation of therapy. Endocrinological examination revealed hypopituitarism including the levels of TSH, FSH, GH and ACTH. The secretion of FSH and LH gradually improved after replacement therapy of dried thyroid. MRI examination of the brain revealed an empty sella. It is known that pituitary tumor, cerebrovascular accident and autoimmune lymphocytic hypophysitis cause hypopituitarism. In this case, it is unlikely that the pulse therapy may be responsible for the infarction of the anterior pituitary artery furthermore, there has been no articles describing such incidence after steroid pulse therapy. This case may be indicative of a very rare case in which the empty sella might have been exacerbated by the pulse therapy in the causation of hypopituitarism.
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PMID:[Hypopituitarism associated with empty sella after steroid pulse therapy in a patient with SLE]. 814 29

Various diseases often occur after delivery but the systemic examinations have not been studied before. Thyroid dysfunction frequently (4.4%) occurs after delivery through an immune rebound mechanism. If postpartum women complain of the symptoms caused by thyrotoxicosis (palpitation, weight loss, increased sweating, finger tremor, fatigue) or hypothyroidism (edema, cold intolerance, hoarseness, sleepiness, fatigue), it is essential to examine thyroid hormones, thyroid stimulating hormone, anti-thyroid microsomal antibody (MCHA) and anti-TSH receptor antibody. To predict who will develop postpartum thyroid dysfunction, the measurement of MCHA during pregnancy is useful because 62% of the subjects with positive MCHA show thyroid dysfunction after delivery. The individuals at high risk of postpartum onset of Graves' thyrotoxicosis can be found early in their pregnancy by the detection of thyroid stimulating antibody (TSAb). Other autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, autoimmune hypophysitis and so on, also could develop after delivery. These findings indicate that laboratory tests in the postpartum period are essential to diagnose postpartum onset of autoimmune diseases and the measurement of autoantibodies in early pregnancy is useful for prediction of their onset in the postpartum period.
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PMID:[Postgravid health care and laboratory tests]. 855 72

Patients who have undergone thyroidectomy for thyroid carcinoma are frequently subjected to periods of induced severe hypothyroidism in preparation for 131I whole body scanning and measurement of serum TG. These two tests are crucial in evaluating the patient's clinical status and determining administration of 131I or other necessary treatment. Severe hypothyroidism produces fatigue, weight gain, depression, inability to carry out usual activities, and occasionally significant illness. We compared the efficacy of inducing moderate hypothyroidism by cutting replacement therapy in half, to a standard method. In the standard preparation, patients substituted triiodothyronine for thyroxine replacement over a 3-week period, and then omitted hormone therapy for 3 weeks. For the subsequent scan, 6 to 12 months later, the thyroxine dosage was cut in half. TSH levels were assessed 4 weeks later, and if adequately elevated, whole body scanning was conducted at the end of the fifth week. Pulse, weight, clinical symptoms, thyroid hormone levels, and some clinical chemistries were evaluated prior to each scan, and some of the tests were also carried out during the interval between scans. Moderate hypothyroidism induced by the half-dose protocol induced TSH elevations above the target level (25-30 microU/mL) at 5 weeks in most patients. Typically TSH of 15 microU/mL in the previous week predicted adequate elevation of TSH at the time of scan. Half dose therapy can be prolonged, if necessary, especially in patients who begin with extreme suppression of TSH, or if a higher TSH is desired. Pulse, weight gain, and cholesterol were significantly different in the two protocols, and the patient's subjective evaluation of hypothyroid symptoms was significantly reduced. Reduction of thyroxine replacement dosage to half the usual amount, in patients with thyroid cancer, allows after 5 weeks in most patients sufficient elevation of TSH for whole body scanning and measurement of TG levels. This simple and economical procedure drastically reduces symptomatology of hypothyroidism and makes this key procedure much more tolerable to patients.
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PMID:Moderate hypothyroidism in preparation for whole body 131I scintiscans and thyroglobulin testing. 1566 27

In order to test the possibility for rapid responses of blood hormone levels in short-term supramaximal exercises, serum concentrations of corticotropin (ACTH), cortisol (C), total testosterone (tT), free testosterone (fT), growth hormone (GH), thyrotropin (TSH), free thyroxine (fT4), free triiodothyronine (fT3), prolactin (PRL), insulin-like growth factor (IGF-I), and sex hormone-binding globulin (SHBG) were determined by RIA procedures in blood samples obtained before and immediately after a 60-s period of consecutive vertical jumps (Bosco test). The study subjects were 16 Italian professional soccer players. Immediately after exercise, significant increases (p < 0.05) were found in the concentrations of ACTH (by 39%), C (by 14%), TSH (by 20%), fT3 (by 28%), fT4 (by 30%), tT (by 12%), fT (by 13%), and SHBG (by 21%). Significant changes were not detected in the blood levels of GH, IGF-I and PRL. Most pronounced testosterone responses were typical for persons of high jumping performance (the increase of serum tT correlated with average power output, r = 0.61 and jumping height, r = 0.66). The larger the drop in power output during 60-s jumping, the higher was the thyroid response: the difference in jumping height between the first and last 15-s period correlated with increases in TSH (r = 0.52) and in fT4, (r = 0.55). In conclusion, the obtained results indicate that in intense exercise, causing the rapid development of fatigue, rapid increases in serum levels of hormones of the pituitary-adrenocortical, pituitary-gonadal and pituitary-thyroid systems occur.
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PMID:Hormonal responses in strenuous jumping effort. 874 23

We have made a prospective study of 23 patients diagnosed of subclinical hypothyroidism and 45 of overt hypothyroidism, aged 68.3-70.3 years and with a mean illness of 4.5 and 6.5 years respectively. It has been proved a higher prevalence of females in both groups. The most frequent clinical symptoms, similar in both groups, were fatigue, constipation and dyspnea. The most repeated initial diagnosis at the entry were prymary hypothyroidism, heart failure, hypertensive urgencies and stroke. We have found differences of statistical significance between the Free Thyroxine (fT4), triiodothyronine (T3), total serum cholesterol (CT), triglycerides (TG), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C) and thyrotropin (TSH) initial and ending serum levels in patients with overt hypothyroidism (p < 0.05). We only have found significant differences in TSH serum levels in patients with subclinical hypothyroidism. The antithyroglobulin and antimicrobial antibodies, have been both positive in two and one patient respectively. Both are more useful as a predictor than their diagnostic value. The levothyroxine (L-T4) daily dose needed to normalize the TSH serum concentration, was lesser in subclinical hypothyroidism (71.8 micrograms opposite 107 micrograms-p < 0.001). We didn't find significant differences between the different groups in the time necessary for normalizing TSH. It seems that the L-T4 therapy should be started in all patients with subclinical hypothyroidism and TSH > or = 10 microU/ml or with TSH > 5 and goiter or with thyroid antibodies. The aim to reach is to normalize the TSH serum levels. The mean daily necessary L-T4 dose is 50-100 micrograms.
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PMID:[Clinical and subclinical hyperthyroidism: two faces of the coin?]. 892 46

We here present a family where three individuals in three generations had varying degrees of goiter, tachycardia, fatigue, hyperactivity, and learning disability. Serum T3 and free T4 were elevated, whereas TSH was normal or slightly increased. The clinical findings in combination with the hormone values led to several supplementary investigations and therapies being carried out, but they had no beneficial influence on the patients' symptoms. The commonest form of thyroid hormone resistance (RTH) is an autosomal dominantly inherited disorder with varying degrees of hypo- and hyperthyroidism, including the hormonal changes described above. Several mutations, particularly in exons 9 and 10 of the thyroid hormone receptor beta gene, have been described and shown to be responsible for RTH. Exons 7, 8, 9, and 10 in the thyroid hormone receptor beta gene were amplified by polymerase chain reaction and analyzed by DNA sequencing. A heterozygous point mutation in nucleotide 1244 in exon 9 was demonstrated in the two patients with RTH that were available for the study. The guanidine to thymidine point mutation changed the codon for arginine in position 320 in the receptor protein to leucine. This mutation has previously been shown to decrease receptor affinity for T3; it has been demonstrated in some patients with RTH, and it is probably the cause of RTH in the family described in this study.
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PMID:[Thyroid hormone resistance. Clinical, biochemical and genetic study of a family]. 952 May 78


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