Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Is well being in the elderly be improved by hormone replacement therapy which compensate deficits accounting for generalized weakness, poor endurance, loss of muscle strength, impaired mobility and balance and decreased cognitive functions? Hormone replacement therapy of menopause has favorable effects on bone loss and decreased cognitive functions but also on several unpleasant symptoms--vasomotor instability, skin atrophy, mucosal dryness, anxiety and fatigue--but at the prize of increased incidence of cancer and cardiovascular morbidity. Decreased testosterone levels in elderly men are associated with increased fatigability, decreased muscle strength and bone mass and increased risks of accelerated atheromatosis. Testosterone substitution seems to be helpful but with side effects, particularly development of prostate cancer. Aging also affects adrenal function. The consequences of decreased DHEA production are still matter of debate. DHEA administration in elderly women seems to be associated with favorable effects on physical and psychological well being. Somatopause is characterized by a progressive decrease of growth hormone production starting as soon as the third decade. Growth hormone therapy has favorable effects on lean body mass, skin atrophy as well on body fat reduction. However, numerous side effects and the theoretical increased risk of cancer limit the use of growth hormone therapy in the elderly.
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PMID:[Hormone therapy of ageing: myths and realities]. 1551 74

The purpose of the study was to investigate whether severe fatigue, possibly leading to overreaching, could be diagnosed at an early stage by a combination of parameters. Seven well-trained male subjects (age [mean +/- SD]: 25.3 +/- 4.7 yr; body mass: 76 +/- 6.6 kg; VO2max: 61.1 +/- 7 ml.kg(-1).min(-1)) increased their training load by doubling their training volume and increasing the intensity by 15 % over a period of two weeks. Before and after this intensified training period subjects underwent a series of tests including a maximal incremental cycle ergometer test (Wmax) with continuous ventilatory measurements and blood lactate values, time trial, basal blood parameter tests (red and white blood profile), hormones [growth hormone (GH), insulin-like growth factor 1(IGF-1), adreno-corticotropic hormone (ACTH), cortisol], neuro-endocrine stress test [short insulin tolerance test (SITT), combined anterior pituitary test (CAPT) and exercise], a shortened Profile of Mood State (POMS), the estimated rate of perceived exertion (RPE) and a cognitive reaction time test. The intensified training period resulted in a significant increase of the training load (p <0.01), training monotony (p <0.01) and training strain (p <0.01). The RPE during training increased significantly (p <0.01) during the intensified training period. Total mood score obtained from the POMS tended to increase (p=0.06), reflecting an increase in worse mood state. A novel finding was that reaction times increased significantly, indicating that overreaching might adversely affect speed of information processing by the brain, especially for the most difficult conditions. After the intensified training period, neither changes in exercise-induced plasma hormone values, nor SITT values were observed. During the CAPT only cortisol showed a significant decrease after the intensified training period. Hemoglobin showed a significant decrease after the intensified training period whereas hematocrit, red blood cell count (RBC) and MCV tended to decrease. The intensified training had no effect on physical performance (Wmax or time trial), maximal blood lactate, maximal heart rate and white blood cell profile. The most sensitive parameters for detecting overreaching are reaction time performance (indicative for cognitive brain functioning), RPE and to a lesser extend the shortened POMS. This strongly suggests, that central fatigue precedes peripheral fatigue. All other systems,including the neuro-endocrine, are more robust and react most likely at a later stage in exhaustive training periods.
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PMID:Physiological, biochemical and psychological markers of strenuous training-induced fatigue. 1564 30

Dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) age-related withdrawal is very likely to be involved in the aging process and the onset of age-related diseases, giving rise to the question of whether preventing or compensating the decline of these steroids may have endocrine and clinical benefits. The aim of the present trial was to evaluate the endocrine, neuroendocrine and clinical consequences of a long-term (1 year), low-dose (25 mg/day) replacement therapy in a group of aging men who presented the clinical characteristics of partial androgen deficiency (PADAM). Circulating DHEA, DHEAS, androstenedione, total testosterone and free testosterone, dihydrotestosterone (DHT), progesterone, 17-hydroxyprogesterone, allopregnanolone, estrone, estradiol, sex hormone binding globulin (SHBG), cortisol, follicle stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH) and insulin-like growth factor 1 (IGF-1) levels were evaluated monthly to assess the endocrine effects of the therapy, while beta-endorphin values were used as a marker of the neuroendocrine effects. A Kupperman questionnaire was performed to evaluate the subjective symptoms before and after treatment. The results showed a great modification of the endocrine profile; with the exception of cortisol levels, which remained unchanged, DHEA, DHEAS, androstenedione, total and free testosterone, DHT, progesterone, 17-hydroxyprogesterone, estrone, estradiol, GH, IGF-1 and beta-endorphin levels increased significantly with respect to baseline values, while FSH, LH and SHBG levels showed a significant decrease. The Kupperman score indicated a progressive improvement in mood, fatigue and joint pain. In conclusion, the present study demonstrates that 25 mg/day of DHEA is able to cause significant changes in the hormonal profile and clinical symptoms and can counteract the age-related decline of endocrine and neuroendocrine functions. Restoring DHEA levels to young adult values seems to benefit the age-related decline in physiological functions but, however promising, placebo-controlled trials are required to confirm these preliminary results.
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PMID:Long-term low-dose dehydroepiandrosterone replacement therapy in aging males with partial androgen deficiency. 1567 38

Recent studies have demonstrated that hypopituitarism, and in particular growth hormone (GH) deficiency, is common among survivors of traumatic brain injury (TBI) tested several months or years following head trauma. In addition, it has been shown that post-traumatic neuroendocrine abnormalities occur early and with high frequency. These findings may have significant implications for the recovery and rehabilitation of patients with TBI. Although data emerging after 2000 demonstrate the relevance of the problem, in general there is a lack of awareness in the medical community about the incidence and clinical repercussions of the pathology. Most, but not all, head trauma associated with hypopituitarism is the result of motor accidents. The subjects at risk are those who have suffered moderate-to severe head trauma although mild intensity trauma may precede hypopituitarism also. Particular attention should be paid to this problem in children and adolescents. Onset of pituitary deficits can evolve over years following injury. For the assessment of the GH-IGF axis in TBI patients, plasma IGF-I concentrations, plus dynamic GH testing is indicated. Some degree of hypopituitarism is found in 35-40% of TBI patients. Among multiple pituitary deficits, the most common ones were GHD and gonadotrophin deficiency. In most series 10-15% presented with severe GHD and 15% with partial GHD after stimulating GH secretion confirming that the most common isolated deficit is GHD. Psychometric evaluation together with neurocognitive testing shows variability of disability and the possibility that untreated TBI induced hypopituitarism contributes to the chronic neurobehavioral problems seen in many head-injured patients warrants consideration. Preliminary data, from small pilot, open-label studies show that subjects treated with GH experience significant improvements in concentration, memory, depression, anxiety and fatigue. In conclusion, pituitary failure can occur even in minor head injuries and is poorly recognized.
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PMID:Hypopituitarism following traumatic brain injury. 1593 80

To investigate the impact of acute salbutamol intake on performance and selected hormonal and metabolic variables during supramaximal exercise, 13 recreational male athletes performed two 30-second Wingate tests after either placebo (PLA, lactose) or salbutamol (SAL, 4 mg) oral administration, according to a double-blind and randomized protocol. Blood samples collected at rest, end of the Wingate test, recovery (5, 10, 15 min) were tested for growth hormone (GH), insulin (INS), blood glucose (GLU), and lactate determination. We found the peak and mean power performed significantly increased after SAL vs. PLA (PPSAL: 896 +/- 46; PPPLA: 819 +/- 57 W; MPSAL: 585 +/- 27; MPPLA: 534 +/- 35 W, p < 0.05), whereas no change was observed in the fatigue index. Blood glucose and INS were significantly increased by SAL at rest, at the end of the Wingate test, and during the 5 first minutes of recovery (p < 0.05). Plasma GH was significantly decreased by SAL (p < 0.05) during the recovery whereas end-exercise and recovery blood lactate tended but were not significantly increased after SAL vs. PLA. From these data, acute salbutamol intake at therapeutical dosage did appear to improve peak power and mean power during a supramaximal exercise, but the mechanisms involved need further investigation.
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PMID:Effects of acute salbutamol intake during a Wingate test. 1619 82

Cognitive functioning, especially memory performance, is known to be impaired in patients with childhood-onset growth hormone deficiency (CO-GHD), and growth hormone substitution has been found to counteract this memory impairment. Neuropsychological and functional magnetic resonance imagining (fMRI) data acquired during a working memory task in 13 childhood-onset GH-deficient patients were compared with 13 age, sex and education level matched healthy controls. Results demonstrated that there is no difference in the quality of the performance in the working memory task between GH-deficient patients and control subjects. However, memory speed was found to be subnormal in patients. Concerning mood, patients reported more complaints of fatigue, and less vigor. Imaging data showed that patients had increased activity in dorsolateral/ventrolateral prefrontal cortex, anterior cingulate cortex, parietal cortex, supplementary motor and motor cortex, as well as in the thalamus and precuneus area. Increasing task load was also associated with an increase in brain activity in similar areas in patients compared to control subjects. In conclusion, this fMRI study shows that GH-deficient patients have a subnormal memory speed, but no impaired quality of memory performance, which may be due to compensatory recruitment of dorsal prefrontal brain regions. These findings indicate that the GH-IGF-1 axis contributes to prefrontal functioning in patients with CO-GHD.
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PMID:Growth hormone deficiency and memory functioning in adults visualized by functional magnetic resonance imaging. 1633 Aug 84

A syndrome of growth hormone deficiency in adults (GHDA) is a syndrome characterised by metabolic deviations, body composition abnormalities, fatigue, decreased quality of life and some cardiovascular changes. The aim of the study was to assess the influence of the growth hormone (GH) replacement therapy on body composition, bone changes, serum lipids levels and some parameters of sugar metabolism in the course of 7-year monitoring. We followed 34 individuals of mean age of 41.73 +/- 2.49 years (mean +/- SE). Severe deficiency of GH was demonstrated by performing stimulation insulin tolerance test. Duration of treatment was 4.13 +/- 0.36 years (mean +/- SE). Patients were examined before the initiation of replacement therapy, after 6 months and further in yearly visits. To determine a statistical level of significance in individual parameters we compared initial baseline status (before drug administration) with the status in individual time intervals. The body composition was examined by anthropometric methods, bioelectric impedance and by densitometry, bone changes were examined by means of DEXA. There were no statistically significant changes of weight, but the waist circumference significantly decreased (p < 0.05), as well as the sum of skinfold thickness (p < 0.05) within the whole treatment period. The percentage of body fat mass measured by the BIA method was significantly changed after the period of 3 years (p < 0.05). Upon the densitometrical measurement of the body composition a significant decrease in kilograms of body fat mass (FM) occurred in the first year of the treatment (p < 0.05) and an increase in lean body mass (LBM) in kilograms during our complete monitoring (p < 0.05). A statistically significant increase in bone density was found in the whole-body BMD and BMC after the first year of the treatment. In the examination of peripheral bone changes a statistically significant increase in BMD occurred (expressed as a Z score) in the area of proximal femur after the first year and collum femoris after three years (p < 0.05), there was a significant increase in BMD of the lumbar spine already after one year of the treatment (p < 0.05) and changes were significant also in further four years. There were found no statistically significant changes related to the sugar metabolism. In the field of lipid metabolism a decrease of total and LDL cholesterol occurred already after a half of the year of the treatment (p < 0.05), changes were significant also in further four years. HDL cholesterol levels have had a progressive tendency, but they were not statistically significant. Positive changes of body composition, an increase in bone density and a decrease of total and LDL cholesterol were demonstrated in the course of the growth hormone replacement therapy.
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PMID:[The influence of long-term growth hormone replacement therapy on body composition, bone tissue and some metabolic parameters in adults with growth hormone deficiency]. 1643 Jan 2

Albright hereditary osteodystrophy (AHO) is a genetic disorder caused by heterozygous inactivating mutations in GNAS, the gene that encodes the alpha-chain of Gs (G alpha s). This syndrome is associated with short stature, obesity, brachydactyly, and subcutaneous ossifications. Patients with GNAS mutations on maternally-inherited alleles are resistant to multiple G-protein-coupled hormones, including parathyroid hormone (PTH), thyroid-stimulating hormone (TSH), luteinizing hormone/follicle-stimulating hormone (LH/FSH), and glucagon. This variant of AHO, termed pseudohypoparathyroidism (PHP) type 1a, is due to tissue-specific paternal imprinting of G alpha s. We investigated whether patients with PHP type 1a exhibited evidence of resistance to growth hormone releasing hormone (GHRH) (1), another hormone requiring G alpha s function. In addition, G alpha s transcripts are imprinted in the pituitary somatotrophs responsible for growth hormone (GH) secretion which could thereby influence GHRH-dependent stimulation of somatotrophs. We therefore hypothesized that patients with PHP type 1a may be GH deficient which could contribute to the obesity and short stature in this condition. We found that GH deficiency is common in PHP type 1a (69%) with a prevalence that is much greater than in the general population (0.03%). We propose that GH status be evaluated in all patients with this condition. Treatment with recombinant GH could lead to improvements in height in children, as well as other physical (eg, obesity, hyperlipidemia, osteoporosis, reduced renal function) and psychological (fatigue and diminished sense of well-being) parameters in GH-deficient PHP type 1a patients of all ages.
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PMID:Short stature, obesity, and growth hormone deficiency in pseudohypoparathyroidism type 1a. 1667 31

Fatigue is frequent and disabling in patients with traumatic brain injury (TBI). Its mechanisms are complex and multifactorial. We performed a literature review of reports of the condition using the following key words: brain injury, depression, neuroendocrine dysfunction, and treatment. Five scales have been used to evaluate fatigue in TBI patients: the Fatigue Severity Scale, the visual analog scale (VAS) for fatigue, the Fatigue Impact Scale, the Barrow Neurological Institute (BNI) Fatigue Scale and the Cause of Fatigue (COF) Questionnaire. The BNI Fatigue Scale and the COF Questionnaire have been designed specifically for brain-injured patients. Fatigue is present in 43-73% of patients and is one of the first symptoms for 7% of them. Fatigue does not seem to be significantly related to injury severity not to time since injury. It can be related to mental effort necessary to overcome attention deficit and slowed processing ("coping hypothesis"). It can also be related to sleeping disorders and depression, although the relation between fatigue and depression are debated. Finally, fatigue can also be related to infraclinical pituitary insufficiency (growth hormone insufficiency, hypocorticism). To date, no published study of treatment of fatigue after TBI exists.
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PMID:Fatigue and traumatic brain injury. 1671 38

The use of sustained release tri-iodothyronine (SR-T3) in clinical practice, has gained popularity in the complementary and alternative medical community in the treatment of chronic fatigue with a protocol (WT3) pioneered by Dr. Denis Wilson. The WT3 protocol involves the use of SR-T3 taken orally by the patient every 12 hours according to a cyclic dose schedule determined by patient response. The patient is then weaned once a body temperature of 98.6 degrees F has been maintained for 3 consecutive weeks. The symptoms associated with this protocol have been given the name Wilson's Temperature Syndrome (WTS). There have been clinical studies using T3 in patients who are euthyroid based on normal TSH values. However, this treatment has created a controversy in the conventional medical community, especially with the American Thyroid Association, because it is not based on a measured deficiency of thyroid hormone. However, just as estrogen and progesterone are prescribed to regulate menstrual cycles in patients who have normal serum hormone levels, the WT3 therapy can be used to regulate metabolism despite normal serum thyroid hormone levels. SR-T3 prescription is based exclusively on low body temperature and presentation of symptoms. Decreased T3 function exerts widespread effects throughout the body. It can decrease serotonin and growth hormone levels and increase the number of adrenal hormone receptor sites. These effects may explain some of the symptoms observed in WTS. The dysregulation of neuroendocrine function may begin to explain such symptoms as alpha intrusion into slow wave sleep, decrease in blood flow to the brain, alterations in carbohydrate metabolism, fatigue, myalgia and arthralgia, depression and cognitive dysfunction. Despite all thermoregulatory control mechanisms of the body and the complex metabolic processes involved, WT3 therapy seems a valuable tool to re-establish normal body functions. We report the results of 11 patients who underwent the WT3 protocol for the treatment of CFS. All the patients improved in the five symptoms measured. All patients increased their basal temperature. The recovery time varied from 3 weeks to 12 months.
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PMID:Supraphysiological cyclic dosing of sustained release T3 in order to reset low basal body temperature. 1688 75


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