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)

We identified 174 cases of chronic severe renal failure (blood creatinine > 650 mumol/l) and/or blood urea > 35 mmol/l) in a retrospective study of patients admitted to hospital between January 1989 and June 1996. Of these patients, 110 were men and 64 were women. The mean age was 36 +/- 15 years. Fifty three patients had a history of hypertension before admission, 3 patients had diabetes and 3 had gout. The most frequent clinical signs were dyspnea (55.2% of all patients), fatigue (78.2%), vomiting (63.2%) and edema (66.1%). The prevalence of hypertension was 64.9%. Glomerulonephritis was found in 42.5% of patients, chronic interstitial nephritis in 16.1%, polycystic kidney disease in 2 cases, congenital renal hypoplasia in 4 cases and unclassified kidney disease in 14.4% of cases. End-stage renal failure was complicated by heart failure in 40.2% of patients, pericarditis in 31.6%, hemorrhage of the gastrointestinal tract in 15% and infections in 22.4%. 47.7% of the patients died following admission.
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PMID:[Epidemiology of severe chronic renal insufficiency in Burkina Faso]. 950 95

Here, we report a 35-year-old man with non-fulminant acute non A, non B, non C hepatitis which developed into acute renal failure. The patient was admitted to hospital with the chief complaints of general fatigue, nausea and a high-grade fever of 40 degrees C. Laboratory examination revealed severe liver dysfunction and renal insufficiency on admission: his serum glutamic oxaloacetic transaminase was 3.203 IU/ml, serum glutamic pyruvic transaminase was 3.825 IU/ml, lactic dehydrogenase was 2.840 IU/ml, blood urea nitrogen was 65 mg/dl, and creatinine was 7.6 mg/dl. Hemodialysis was conducted during the initial 19-day period after admission because anuria was manifested on admission. On the 36th day after onset, renal functions returned to normal and the patient was negative for IgM-HA antibody. HBs antigen, IgM-HBC antibody, HCV antibody, cytomegalovirus antibody, and Epstein-Barr virus antibody. However, liver biopsy for histological examination on the 44th day after onset revealed no specific findings except the healing stage of acute hepatitis. Renal biopsy on the 49th day showed the healing stage of acute tubular necrosis without any glomerular change. It has been infrequently reported that acute renal failure develops following a non-fulminant acute state without hepatitis A, B or C virus infection. It is necessary to take acute renal failure into account in the clinical course of non-fulminant non A, non B, non C hepatitis.
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PMID:[Acute renal failure in non-fulminant acute hepatitis without hepatitis A, B or C virus infection]. 951 78

Well-trained subjects (n = 6) were studied before and after losing a mean 3.0%-4.3% of body mass to determine whether muscle performance could be maintained or even enhanced by dietary creatine supplementation. During a 5-day period of loss of mass the subjects were randomly assigned to a creatine or placebo supplemented diet. All the subjects were measured before and after loss of mass on both supplements for isokinetic peak torque (PT) and work at peak torque (W(PT)) of knee extensors, also for intermittent high intensity working capacity of the same muscle group. The latter test consisted of submaximal isokinetic knee extensions at an angular velocity of 1.57 rad x s(-1) for 45 s at the rate of 30 contractions each min (submaximal work, Ws max) followed by 15-s maximal effort (maximal work, Wmax). Total duration of the test was 3 min. Haematocrit was measured and haemoglobin, ammonia, lactate, glucose and urea concentrations were analysed in blood samples obtained at rest and after cessation of muscle performance tests. The results indicated that creatine supplementation in comparison with placebo treatment during rapid body mass reduction may help to maintain muscle PT and W(PT)1 at high angular velocities, not influencing Wmax and the rate of fatigue development during Wmax, but affecting adversely Ws max. Within the limitations of the present study the reasons for the partially detrimental effect of creatine administration remain obscure, but it is suggested that impaired creatine uptake in muscle during body mass loss as well as creatine induced changes in muscle glucose and glycogen metabolism may be involved.
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PMID:Effect of creatine supplementation during rapid body mass reduction on metabolism and isokinetic muscle performance capacity. 966 Jan 61

Oxygen free radicals have been implicated in exercise-induced cell and tissue injury, indicating an oxidative stress. Fatigue accompanied by a number of physiological and metabolic changes is in indication of overtraining. This study aimed to examine the influence of a continuous 24-h intermittent speed driving (1 h driving/1 h stop), on the response of hormones, antioxidative factors, lipid, and enzyme levels. Seven race car drivers of national level were examined before, during, and immediately after the trial of speed driving on a test designed to check endurance to stress. The parameters measured were: testosterone (Tes), cortisol (Cor), IgM, IgA, cholesterol, HDL, billirubin, ceruloplasmin, urea, uric acid, creatine kinase, and transaminases. Stress hormone Cor declined significantly (p < 0.05), while Tes did not change significantly. Fatigue enzyme, aspartate transaminase (GOT) increased significantly (p < 0.05), while alanine transaminase (GPT) did not change and urea declined. Muscle enzyme, creatine kinase (CK) increased to sixfold (p < 0.01). IgA, IgM and lipids did not change. The primary antioxidant ceruloplasmin increased significantly (p < 0.001), while antioxidants uric acid and glucose remained unchanged. Among the factors measured, ceruloplasmin, cortisol, urea, GOT, and CK seem to give a picture of the organism's alertness and defence capabilities in conditions of stress and fatigue.
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PMID:Stress hormonal factors, fatigue, and antioxidant responses to prolonged speed driving. 967 60

Abnormally low plasma cystine levels have been found in the late asymptomatic stage of HIV infection and several other diseases associated with progressive loss of skeletal muscle mass. The phenomenon is commonly associated with a low NK cell activity, skeletal muscle wasting or muscle fatigue and increased rates of urea production. In its extreme form, the negative nitrogen balance leads to overt cachexia and is associated with severe debilitation and psychological stress. The low NK cell activity is in most cases not life-threatening but may be disasterous in HIV infection, because it may compromise the initially stable balance between immune system and virus and trigger disease progression. This review summarizes briefly (i) the role of cysteine in the physiological regulation of body cell mass and the development of skeletal muscle wasting, and (ii) the role of glutathione in the immune system.
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PMID:Role of cysteine and glutathione in signal transduction, immunopathology and cachexia. 969 16

Cisplatin is a known cause of hemolytic uremic syndrome (HUS). The acute, fulminant form of cisplatin-induced HUS is almost always fatal. We present a 67-year-old Hispanic woman who was treated with cisplatin for squamous cell carcinoma of the tongue. Three days after receiving the treatment, she presented with increasing fatigue, decreased urine output, and confusion. Physical examination was remarkable for tachycardia of 130 beats/min, peripheral edema, and mental obtundation. Laboratory investigations showed a white cell count of 5,500/microL, hemoglobin level of 9.6 g/dL, hematocrit of 29.6%, and platelet count of 13,000/microL. Schistocytes were present on peripheral smear. Screening for disseminated intravascular coagulation was negative. Serum chemistry values included blood urea nitrogen 111 mg/dL, creatinine 3.8 mg/dL, and lactate dehydrogenase (LDH) 927 IU. The patient underwent hemodialysis and therapeutic plasma exchange (TPE), using fresh frozen plasma (FFP). Dialysis was no longer required after the fifth day. TPE was performed daily until the platelet count normalized on the 13th day, after which intertreatment intervals were extended until normalization of LDH levels on the 50th day. We conclude that the normally fatal, fulminant form of cisplatin-induced HUS can be successfully treated with standard TPE, using FFP replacement.
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PMID:Successful treatment of cisplatin-induced hemolytic uremic syndrome with therapeutic plasma exchange. 970 19

This study was carried out on 22 patients on maintenance hemodialysis. Among them, 20 patients were males and 2 were females, their age ranged from 12 to 50 years. Initially, the patients were assessed clinically and by laboratory investigations and their dialysis was assessed by studying their urea kinetic modeling following the nomographic approach for calculating their Kt/V values. Their nutrition was assessed by measuring skin folds, midarm circumference, laboratory parameters and by calculating the normalized protein catabolic rate (nPCR). Also their neuromuscular functions were assessed by clinical examination and neurophysiologic study. Dialysis dose was readjusted to achieve a target Kt/V value of 1.3 for patients on 3 times weekly dialysis and 1.6 for patients on twice weekly dialysis. Also, their nutrition was reviewed to achieve nPCR 1.2 g/kg/day and caloric intake 30-40 kcal/kg/day through diet manipulation and support. The patients were assessed finally after 3 months on targeted dialysis and nutrition by thorough clinical, laboratory and neuromuscular assessment. Analysis of neurophysiologic data showed significant improvement in electromyography. Furthermore, fatigue test showed significant (p = 0.002) decreases in muscle fatigue after optimization of dialysis dose and patients' nutrition. From this study, we may conclude that in dialysis patients, even when asymptomatic and clinically stable, neurologic deficits do exist and using area kinetic modeling to improve dialysis and patients' nutrition is valuable in improving their neuromuscular functions.
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PMID:Study of effect of optimization of dialysis and protein intake on neuromuscular function in patients under maintenance hemodialysis treatment. 973 May 63

Uncontrolled studies have reported that fatigue is a common symptom among patients with advanced cancer. It is also a frequent complaint among the general population. Simply asking cancer patients whether or not they feel fatigued does not distinguish between the 'background' level of this symptom in the community and any 'excess' arising as a result of illness. The aim of this study was to determine the prevalence of fatigue among palliative care inpatients in comparison with a control group of age and sex-matched volunteers without cancer. In addition, the correlates of fatigue were investigated. The prevalence of 'severe subjective fatigue' (defined as fatigue greater than that experienced by 95% of the control group) was found to be 75%. Patients were malnourished, had diminished muscle function and were suffering from a number of physical and mental symptoms. The severity of fatigue was unrelated to age, sex, diagnosis, presence or site of metastases, anaemia, dose of opioid or steroid, any of the haematological or biochemical indices (except urea), nutritional status, voluntary muscle function, or mood. A multivariate analysis found that fatigue severity was significantly associated with pain and dypnoea scores in the patients, and with the symptoms of anxiety and depression in the controls. The authors conclude that subjective fatigue is both prevalent and severe among patients with advanced cancer. The causes of this symptom remain obscure. Further work is required in order to determine if the associations reported between fatigue and pain and between fatigue and dyspnoea are causal or coincidental.
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PMID:Fatigue in advanced cancer: a prospective controlled cross-sectional study. 1018 94

Pseudo-hypoaldosteronism (PHA) is due to mineralocorticoid resistance and manifests as hyponatremia and hyperkalemia with increased plasma aldosterone levels. It may be familial or secondary to abnormal renal sodium handling. We report the case of a 54-year-old woman with multifocal cancer of the colon, who developed PHA after subtotal colectomy, ileal resection and jejunostomy. She was treated with 6 g of salt daily to prevent dehydration, which she stopped herself because of reduced fecal losses. One month later she was admitted with signs of acute adrenal failure, i.e. fatigue, severe nausea, blood pressure of 80/60 mmHg, extracellular dehydration, hyponatremia (118 mmol/l); hyperkalemia (7.6 mmol/l), increased blood urea nitrogen (BUN) (200 mg/dl) and creatininemia (2.5 mg/dl), and decreased plasma bicarbonates level (HCO3-: 16 mmol/l; N: 27-30). However, the plasma cortisol was high (66 microg/100 ml at 10:00 h; N: 8-15) and the ACTH was normal (13 pg/ml, N: 10-60); there was a marked increase in plasma renin activity (>37 ng/ml/h; N supine <3), active renin (869 pg/ml; N supine: 1.120), aldosterone (>2000 pg/ml; N supine <150) and plasma AVP (20 pmol/l; N: 0.5-2.5). The plasma ANH level was 38 pmol/l (N supine: 5-25). A urinary steroidogram resulted in highly elevated tetrahydrocortisol (THF: 13.3 mg/24h; N: 1.4+/-0.8) with no increase in tetrahydrocortisone (THE: 3.16 mg/24h; N: 2.7+/-2.0) excretion, and with low THE/THF (0.24; N: 1.87+/-0.36) and alpha THF/THF (0.35; N: 0.92+/-0.42) ratios. The number of mineralocorticoid receptors in mononuclear leukocytes was in the lower normal range for age, while the number of glucocorticoid receptors was reduced. Small-bowel resection in ileostomized patients causes excessive fecal sodium losses and results in chronic sodium depletion with contraction of the plasma volume and severe secondary hyperaldosteronism. Nevertheless, this hyperaldosteronism may be associated with hyponatremia and hyperkalemia suggesting PHA related to the major importance of the colon for the absorption of sodium. In conclusion, this case report emphasizes 1) the possibility of a syndrome of acquired PHA with severe hyperkalemia after resection of the ileum and colon responding to oral salt supplementation; 2) the major increase in AVP and the small increase in ANH; 3) the strong increase in urinary THF with low THE/THF and alpha THF/THF ratios; 4) the normal number of lymphocytic mineralocorticoid receptors outside the acute episode.
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PMID:Transient pseudo-hypoaldosteronism following resection of the ileum: normal level of lymphocytic aldosterone receptors outside the acute phase. 1019 79

We reported a case of adult-onset citrullinemia associated with hypertrigliceridemia and diabetes mellitus. A 24-year-old female was healthy until recently. She first felt intermittent headaches and nausea. Then she noticed memory loss and tiredness. Abnormal behavior such as getting lost on the way from her company sometimes occurred. She came to our hospital because these symptoms had been getting worse. Neurologically she had a very mild disturbed consciousness. An EEG recording showed diffuse slow wave with high amplitude. MR image of the brain showed hyper-intensity in globus pallidus with T1-weighted image. Plasma citrullin level was very high. Plasma ammonia and triglyceride showed a moderately high level. Using biopsied liver tissues, the enzymes of the urea cycle were analyzed. Argininosuccinate synthetase activity was extremely low. Because of clinical course and the result of liver biopsy, the patient was diagnosed as type 2 citrullinemia. A low protein diet was started, but intermittent nausea and consciousness disturbance did not improve. A partial liver transplantation was performed. The living donor was her father, a 50-year-old male, who had normal liver function. After the liver transplantation, all neurological signs soon disappeared. Plasma citrulline, ammonia and triglyceride normalized rapidly. An EEG recording became normal, and the hyper-intensity in globus pallidus with T1-weighted MR image disappeared two months after surgery. Liver transplantation should be planned as soon as possible in a type 2 citrullinemia patient.
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PMID:[Liver transplantation in type II citrullinemia]. 1065 68


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