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 68-year-old woman with clinical, electromyographic, and pharmacologic evidence of myasthenia gravis experienced increasing proximal and bulbar muscular weakness. The diagnosis of pernicious anemia was established by typical abnormalities in the peripheral blood and bone marrow aspirate, the serum B12 level, by results of the Schilling test, and by the presence of serum parietal cell antibody. The diagnosis of Hashimoto's thyroiditis was established by the presence of diffuse thyroid enlargement, microsomal thyroid antibodies, an increased thyroid stimulating hormone level, and depressed T2 and T4 levels.
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PMID:Myasthenia gravis, pernicious anemia, and Hashimoto's thyroiditis. 58 4

We treated a 32-year-old man with hearing loss in the right ear followed by severe muscle weakness of the extremities. When admitted to hospital by ambulance, the serum potassium level was 1.5 mEq/L. The muscle weakness was improved following administration of potassium chloride but the hearing impairment continued. Hearing level of the right ear was extremely impaired at the level of 60-105 dB, while hearing in the left ear was fairly normal. Spontaneous nystagmus was also present. The triiodothyronine level was 290 ng/dl, thyroxine 14.4 micrograms/dl, thyroid stimulating hormone (TSH) 0.84 microU/ml, and the anti-TSH-receptor antibody was positive. Attaining an enthyroid state, the patient was discharged on 80th hospital day with the continuous medication of Methimazole. This is a very rare case of sudden deafness complicated by hypokalemic paralytic attacks. Circulatory insufficiency and electrolytes imbalance in the right inner ear was assumed to have caused the deafness.
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PMID:Sudden deafness in a man with thyrotoxic hypokalemic periodic paralysis. 319 64

Two Scottish Deerhound puppies had clinical and pathological features consistent with the diagnosis of congenital non-goitrous hypothyroidism. They were from separate litters, but were the progeny of the same sire and dam. The puppies were smaller, had shorter limbs and shorter, broader heads than their littermates. They also had histories of weakness, difficulty in walking and somnolence. A characteristic radiographic feature was the absence of epiphyseal growth centres. Both had depressed serum thyroxine (T4) levels and one did not respond to exogenous thyroid stimulating hormone. On necropsy, the thyroid glands were small, the follicles varied in size and contained little or no colloid. The adenohypophysis contained many cells with markedly vacuolated cytoplasm. It is suggested that the clinicopathological pattern is the result of a primary thyroid abnormality. Possible mechanisms include either primary thyroid hypoplasia or an unresponsiveness to thyroid stimulating hormone.
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PMID:Congenital hypothyroidism in Scottish Deerhound puppies. 322 52

Ten patients with varying degrees of hypothroid myopathy were studied clinically and by serial percutaneous needle muscle biopsies before and during treatment with L-thyroxine. The biochemical evidence of hypothyroidism was related to the severity of the myopathic and signs before treatment. The severity of myopathic symptoms before and during treatment correlated with the biochemical evidence of hypothyrodism, a type II fibre atrophy and increased central nuclear counts. Likewise, the clinical evidence of a myopathy before and during treatment was correlated with both a type II fibre atrophy and loss and increased central nuclear counts but was not related to the biochemical parameters of hypothyroidism, except the level of thyroid stimulating hormone. In the muscle, before and during treatment, of the two most severely affected patients, intracellular glycogen inclusions were seen in scattered muscle fibres. On light microscopy and on electronmicroscopy, numerous mitochondria were seen responding to L-thyroxine with accumulations of subsarcolemmal honey-combing. Vesicular abnormalities, an electron dense matrix or occasional crystalline deposits were seen in muscle mitochondria from less severely azffected patients. Severely myopathic muscle contained excessive glycogen, membrane bound glycogen and excess lipid in a mainly perinuclear distribution. Occasional myelin and membranous bodies were seen and satellite cells during the recovery phase. A group of patients with hypothyroid myopathy who are likely to have a delayed recovery of full muscle strength on L-thyroxine may be recognised by the presence of severe proximal muscle weakness and characteristic changes on histochemical and electronmicroscopic examination of muscle. The spectrum of histochemical and electronmicroscopic abnormalities of muscle revealed with increasing degree of hypothyrodism, suggests that a generally reversible acquired glycogen storage and mictochondrial disorder is an important feature in the pathogenesis of this condition.
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PMID:Hypothyroid myopathy. A clinical and pathologaical study. 743 Nov 56

Thyroid diseases affect up to 10% of women, but most respond well to treatment. During pregnancy, however, normal metabolic changes may obscure pathology, and improper management may harm the fetus. Tests for levels of thyroid stimulating hormone (TSH), free thyroxine, and free triiodothyronine are essential. Generally, high TSH values suggest primary hypothyroidism, while suppressed levels indicate hyperthyroidism. Hyperthyroidism is commonly manifested by goiter, ophthalmopathy, proximal muscle weakness, tachycardia, and weight loss or inability to gain weight. Among women, the most common etiology of thyroid disease is thyroid autoimmunity (Graves' disease or Hashimoto's thyroiditis); affected women are at an increased risk of postpartum thyroid dysfunction. Women who have Graves' disease diagnosed during pregnancy typically have a history of hyperthyroidism symptoms antedating conception, and occasionally thyroid stimulating immunoglobulins may be elevated enough to induce fetal hyperthyroidism. Women with Hashimoto's thyroiditis typically are euthyroid but may be hypothyroid with diffuse goiter; diagnosis is confirmed by elevated levels of antithyroid peroxidase antibodies or antimicrosomal antibodies. Other forms of thyroid dysfunction include benign or malignant nodules and hyperemesis gravidarum. Hypothyroidism typically is treated with levothyroxine. Hyperthyroidism is treated with antithyroid drugs. The goal is to avoid overdosage of medication, which could cause goiter and/or hypothyroidism in the fetus.
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PMID:Perinatal Thyroid Dysfunction: Prenatal Diagnosis and Treatment. 974 98

Prior to presentation, two physically fit adults, a 39-year-old male and 40-year-old female, began supplementation with an over-the-counter thyroid preparation marketed as a metabolic accelerator and fat loss aid, tiratricol. Both participants took the supplement for 5 weeks (3000-4000 mcg/d) and 3 weeks (6000 mcg/d), respectively. At presentation, both complained of lethargy, loss of appetite, and muscle weakness. Upon initial laboratory evaluation, results revealed low thyroid stimulating hormone with profoundly elevated T3 values in both patients. After an extensive review of the literature, the cause of the problem was found to be the nutritional supplement they consumed contained tiratricol. After discontinuation of the supplement, thyroid levels slowly returned to baseline 40 days and 5 months later, respectively.
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PMID:A report of hypothyroidism induced by an over-the-counter fat loss supplement (Tiratricol). 1266 Apr 10

We report a 66-year-old woman with Hashimoto's encephalopathy who showed rapidly developing cognitive deficits, inactivity, and gait disturbance without involuntary movements or convulsions. She had had right-sided hemiparesis and dysarthria caused by a lacunar infarction and had been admitted to our hospital for 2 weeks. Although the dysarthria and hemiparesis gradually improved, difficulty in walking, disorientation, and drowsiness developed 2 months after discharge. Upon readmission, the patient was alert but apathetic and sometimes sleepy. The right upper and lower limbs showed mild weakness, which was considered to be due to the previous infarction. Cerebrospinal fluid showed mild elevation of protein without pleocytosis. An electroencephalogram was normal, and a magnetic resonance imaging of the brain showed only the old lacunar infarction. Titers of antithyroglobulin antibodies and levels of thyroid stimulating hormone in serum were elevated. We made a diagnosis of Hashimoto's encephalopathy and treated the patient with high-dose corticosteroids. Within 1 week, her mental status improved and she was able to walk. Generalized seizure, myoclonus, and tremor, which are characteristic of Hashimoto's encephalopathy, never developed. The findings in this patient suggest that Hashimoto's encephalopathy, a treatable condition, should be included in the differential diagnosis of dementia.
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PMID:[A patient with Hashimoto's encephalopathy showing subacute global cognitive dysfunction]. 1450 57

An eight-year-old, male boxer dog was presented with a one-month history of hindlimb weakness followed by compulsive ineffective drinking, dysphagia, regurgitation and nasal reflux during drinking. A neurological examination revealed weakness and conscious proprioception deficits in both hindlimbs with normal spinal reflexes. The dog's swallowing function was examined by fluoroscopy. This showed normal prehension of the barium paste, bolus formation and contraction of the pharyngeal muscle, but no opening of the upper oesophageal sphincter was detected. A serum thyroid stimulating hormone level of 0.402 ng/dl and serum total T4 of 0-01 microg/dl were determined. The dog fully recovered one month after L-thyroxine therapy. The association found between cricopharyngeal achalasia and hypothyroidism suggests that hypothyroidism should be included in the list of differential diagnoses for dogs with cricopharyngeal achalasia.
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PMID:L-thyroxine responsive cricopharyngeal achalasia associated with hypothyroidism in a dog. 1630 Jan 18

Despite enormous medical progress during the past few decades, the last years of life are still accompanied by increasing ill health and disability. The ability to maintain active and independent living for as long as possible is a crucial factor for ageing healthily and with dignity. The most important and drastic gender differences in aging are related to the reproductive organs. In distinction to the course of reproductive ageing in women, with the rapid decline in sex hormones expressed by the cessation of menses, men experience a slow and continuous decline. This decline in endocrine function involves: a decrease of testosterone, dehydro epiandrosterone (DHEA), oestrogens, thyroid stimulating hormone (TSH), growth hormone (GH), IGF1, and melatonin. The decrease of sex hormones is concomitant with a temporary increase of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In addition sex hormone binding globulins (SHBG) increase with age resulting in further lowering the concentrations of free biologically active androgens. These hormonal changes are directly or indirectly associated with changes in body constitution, fat distribution (visceral obesity), muscle weakness, osteopenia, osteoporosis, urinary incontinence, loss of cognitive functioning, reduction in well being, depression, as well as sexual dysfunction. The laboratory and clinical findings of partial endocrine deficiencies in the aging male will be described and discussed in detail. With the prolongation of life expectancy both women and men today live 1/3 of their life with endocrine deficiencies. Interventions such as hormone replacement therapy may alleviate the debilitating conditions of secondary partial endocrine deficiencies by preventing the preventable and delaying the inevitable.
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PMID:Endocrinology of the aging male. 1658 70

We report the case of a 28-year-old woman who presented simultaneously with superior sagittal sinus thrombosis and thyroid crisis, and was subsequently found to have protein C deficiency. February 3, 2003, she admitted complaining of abdominal pain. The diagnosis of appendicitis was made, and she was operated on under lumbar anaesthesia. Day 7, she developed acute headache and distal weakness of the left lower limb. On examination she was alert, with a temperature of 38 degrees C, a sinus tachycardia of 124/min and blood pressure 164/84 mmHg. Neurological examination revealed neck stiffness and left hemiparesis, predominantly in her lower limb. Gadlinium-enhanced brain MRI revealed extensive superior sagittal sinus thrombosis. CT scan demonstrated infarction in the right frontal cortex, and subarachnoid hemorrhage adjacent to the right cerebellar tentorium. The patient was treated with a free radical scavenger edarabon, and glycerin. No anticoagulant therapy was instituted. Over the next 24 hours, her condition worsened. She became comatose, as well as developing a generalized tonic-clonic seizure. Day 12, laboratory examinations revealed an undetectable TSH-level CTSH (thyroid stimulating hormone) <0.005 mcIU/ml), with a level of free thyroxin 7.77 ng/dl (0.9-1.7), free triiodothyronin 29.6 pg/ml (2.3-4.3), and positive anti-TSH receptor antibodies determined subsequently. Coagulation factor VIII activity was 155% (normal range 60-150). Protein C deficiency (antigen 59%, activity 49%) was also present, suggesting a congenital type I heterozygous deficiency. A diagnosis of thyroid crisis on the basis of Graves' disease was made. The patient remained comatose and died on Day 16, with renal failure. The patient had protein C deficiency, a well-established risk factor for cerebral venous thrombosis (CVT). However, additional risk factors are required in most cases to precipitate CVT. In our case, this trigger was most likely thyroid crisis, suggesting that thyrotoxicosis, probably through hypercoagulability, may be a predisposing factor for the development of CVT.
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PMID:[Thyroid crisis and protein C deficiency in a case of superior sagittal sinus thrombosis]. 1737 Jun 53


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