Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A boy referred at the age of 4 years because of obesity and under observation for 16 years, was found to be suffering from a hypothalamic syndrome of unknown origin characterized by progressive obesity, polyphagia, deficiency of growth and thyroid hormone, hyperprolactinemia, hypodipsia, hypernatremia and hyperosmolality without diabetes insipidus. At ages 11 and 16 there were 3 day episodes of spontaneous muscular weakness, hypersomnolence and hypothermia associated with central sleep apnea and severe bradycardia. Subsequently, decreased ventilatory responsiveness to carbon dioxide (CO2) was found as a consequence of blunted neural drive. Therapy with clomipramine HCl (Anafranil Ciba-Geigy) for 6 months led to a normalization of serum sodium levels, pulse rate, ventilatory response to dioxide with no recurrence of the central apnea within 4 following years.
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PMID:Recurrent hypothermia, hypersomnolence, central sleep apnea, hypodipsia, hypernatremia, hypothyroidism, hyperprolactinemia and growth hormone deficiency in a boy--treatment with clomipramine. 346 79

A 57-year-old woman presented with palpitations, muscle weakness, bilateral proptosis, goiter, and tremor. The thyroxine (T4) level and the free T4 index were increased while the total triiodothyronine (T3) level was normal. Iodine 123 uptake was increased, and a scan revealed an enlarged gland with homogeneous uptake. Repeated studies again revealed an increased T4 level and free T4 index and normal total and free T3 levels. A protirelin test showed a blunted thyrotropin response. Treatment with propylthiouracil was associated with disappearance of symptoms and normal T4 levels, but after 20 months of therapy, hyperthyroidism recurred and the patient was treated with iodine 131. This was an unusual case of T4 toxicosis because the patient was not elderly and was not exposed to iodine-containing compounds or drugs that impair T4-to-T3 conversion. There was no evidence of abnormal thyroid hormone transport or antibodies.
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PMID:A case of thyroxine thyrotoxicosis. 357 39

A case of transient hypothyroidism in the course of hypokalemic myopathy is reported. A 69-year-old woman had severe muscle weakness and marked potassium deficiency associated with alkalosis during treatment with thiazide diuretics. The cause of muscle weakness proved to be hypokalemic myopathy confirmed by clinical findings and muscle biopsy. After the episode of hypokalemic myopathy, serum levels of thyroid hormone were lowered (T4; 3.8 micrograms/dl, T3; 54 ng/dl) and that of TSH was elevated (25.1 microU/ml). Antithyroid microsomal antibody was positive (1:25600) and anti-thyroglobulin antibody was negative. About one month after potassium supplement, her thyroid functions returned to normal, along with normalization of serum potassium level. This is the first documented case report of hypokalemic myopathy accompanied by transient hypothyroidism in a patient with autoimmune thyroiditis. We suggest that this transient hypothyroidism might be induced by hypokalemia during the course of autoimmune thyroiditis.
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PMID:A case of hypokalemic myopathy associated with transient hypothyroidism. 653 97

There is a spectrum of muscular abnormalities that occurs in patients with hypothyroidism. Alterations in deep tendon reflexes are commonly observed although more extensive muscle disease is less frequently seen. Two patients who demonstrated increased muscle mass, muscle stiffness with variable degrees of muscle weakness and low levels of serum thyroxine (Hoffmann's syndrome) are described. At the time of presentation, the serum creatinine phosphokinase level was more than 10 times greater than normal, and electromyography revealed repetitive positive waves. After therapy with thyroid hormone, there was complete resolution of the muscle abnormalities, and laboratory studies were performed. In this report, we review the clinical syndrome of muscle dysfunction that can be seen with the more severe forms of hypothyroid myopathy.
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PMID:Hypothyroidism presenting as muscle stiffness and pseudohypertrophy: Hoffmann's syndrome. 721 23

1. Body weight and total body potassium were measured in 23 hyperthyroid patients before and at various stages during treatment and in 19 athyreotic patients who were being treated with high-dose L-thyroxine. 2. In the hyperthyroid patients the total body potassium rose by 23 +/- 2.8% (SEM) within a few weeks of restoring the blood thyroid hormone levels to normal. The body potassium values after treatment were close to that expected in these individuals if they were healthy indicating that a considerable loss of body potassium is usual in hyperthyroidism. 3. The gain of total body potassium in hyperthyroidism averaged 71 +/- 8 mmol for each kg of body weight gained (compared with muscle potassium concentration of about 92 mmol/kg). In contrast, weight loss produced by dietary treatment of obesity caused very little change of body potassium (maximum averaged was 14 +/- 4 mmol/kg wt. loss). 4. Among the patients with hyperthyroidism, the greatest muscular weakness was present in those with the greatest body potassium loss and these patients regained a large amount of potassium relative to weight on recovery. 5. Total body potassium changes were closely related to total plasma tri-iodothyronine concentrations but unrelated to the thyroxine levels.
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PMID:Total body potassium in relation to thyroid hormones and hyperthyroidism. 723 44

Since experimental hyperthyroidism reduces skeletal muscle mass while simultaneously increasing cardiac muscle mass, the effect of hyperthyroidism on muscle protein degradation was compared in skeletal and cardiac muscle. Pulse-labeling studies using (3H) leucine and (14C) carboxyl labeled aspartate and glutamate were carried out. Hyperthyroidism caused a 25%-29% increase in protein breakdown in both sarcoplasmic and myofibrillar fractions of skeletal muscle. Increased muscle protein degradation may be a major factor in the development of skeletal muscle wasting and weakness in hyperthyroidism. In contrast, protein breakdown appeared to be reduced 22% in the sarcoplasmic fraction of hyperthyroid heart muscle and was unchanged in the myofibrillar fraction. Possible reasons for the contrasting effects of hyperthyroidism on skeletal and cardiac muscle include increased sensitivity of the hyperthyroid heart to catecholamines, increased cardiac work caused by the hemodynamic effects of hyperthyroidism, and a different direct effect of thyroid hormone at the nuclear level in cardiac as opposed to skeletal muscle.
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PMID:Effect of experimental hyperthyroidism on protein turnover in skeletal and cardiac muscle. 742 80

Common thyroid and parathyroid disorders present with reversible neurologic signs and symptoms affecting the central and peripheral nervous system, musculature, and mental function. Patients with thyrotoxicosis may have myopathy, spasticity, seizures, and multiple psychiatric symptoms. A deficiency of thyroid hormone also causes muscle weakness and may be accompanied by reversible muscle hypertrophy or movement disorders. The chronic hypercalcemia that develops secondary to hyperparathyroidism produces many psychiatric and cognitive symptoms, as well as a reversible myopathy. Calcium deficiency leads to neuromuscular irritability, paresthesias, and tetany. Psychiatric disorders are also common in this disorder.
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PMID:Neurologic complications of thyroid and parathyroid disease. 841 21

Pituitary tumors rarely metastasize outside the central nervous system. Of the more than 100 reported TSH-secreting adenomas, we now describe the first carcinoma. A 40-yr-old woman had transsphenoidal surgery for a large TSH-secreting pituitary adenoma in 1984. She had increased thyroid hormone levels with a TSH that varied from 16-31 microU/mL, and an unusually high alpha-subunit that ranged from 125-150 ng/mL. Because of residual tumor, she had a left craniotomy in 1985 followed by radiation. Despite these therapies, she had a residual tumor that remained stable until January 1989 when her tumor nearly doubled in size. She received radiation therapy and octreotide with marked diminution of the tumor and clinical improvement. In August 1989, she presented with leg weakness, and magnetic resonance imaging revealed a large sacral mass. A biopsy confirmed that the sacral mass was a metastasis from the pituitary tumor. Due to additional metastases in the lung, she received 5-fluorouracil, cytoxan, and adriamycin, with marked decrease in her lesions. Further substantiation of the metastatic pituitary tumor was made when the patient returned in December 1989 with a pleural effusion containing pituitary tumor cells. Of all the reported cases of TSH-secreting adenomas, this case had the highest alpha-subunit portending future metastases. Furthermore, the apparent response to octreotide and response to chemotherapy are encouraging and suggest that new therapies should be explored. Finally, since TSH-secreting adenomas tend to be more invasive than other pituitary tumors, this case underscores the need for early diagnosis and aggressive treatment of these tumors.
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PMID:Thyrotropin-secreting pituitary carcinoma. 843 99

Despite adequate adrenal, gonadal, and thyroid hormone replacement, many adults with hypopituitarism have a recognizable syndrome of weakness and diminished sense of well-being, accompanied by alterations in metabolism and body composition, as well as increased mortality. Short-term treatment with human growth hormone improves many of these abnormalities, but a clear improvement in functional status has yet to be demonstrated. Until such an effect is shown, the use of growth hormone replacement in adults with hypopituitarism remains investigational.
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PMID:Growth hormone deficiency in adults: characteristics and response to growth hormone replacement. 862 72

Hypothyroidism exerts a significant effect on several body systems, including the functioning of muscle and nerve. Described here is the case of a severely hypothyroid patient with weakness and numbness of the legs who showed marked clinical improvement with thyroid hormone treatment. Concurrently obtained phosphorus 31-nuclear magnetic resonance (NRM) spectra and nerve conduction studies showed changes in muscle phosphorus metabolism with increases in conduction velocities. Phosphorus 31-NMR spectroscopy is useful for evaluating metabolism in muscle in hypothyroid patients.
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PMID:Effects of thyroid hormone treatment on 31P-NMR spectroscopy of muscle and on nerve conduction studies in a patient with long-standing severe hypothyroidism. 875 77


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