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)

The effect of decreased hepatic energy state on xenobiotic conjugation was examined in vivo. The pharmacokinetics of acetaminophen, a drug that is conjugated with glucuronic acid, sulfate and glutathione, was analyzed in rats when the hepatic energy state had been decreased by ethionine or fructose. Treatment with ethionine or fructose reduced the hepatic adenosine triphosphate/diphosphate ratio by 30 to 65% and 43 to 54% and the phosphorylation potential by 50 to 80 and 43%, respectively. Ethionine treatment increased uridine triphosphate (UTP) and other UTP-derived nucleotides. However, uridine diphosphoglucuronic acid levels were decreased by 44% whereas uridine diphosphoglucose concentration was increased by 20%. This effect may be due to a decrease in redox state. Fructose treatment reduced the concentrations of UTP and UTP-derived nucleotides. Uridine diphosphoglucose was reduced by 50% and uridine diphosphoglucuronic acid by about 40%. Ethionine and fructose also decreased glutathione and adenosine 3'-phosphate 5'-phosphosulfate concentrations in the liver by 30 to 50%. During the period of decreased energy state, biliary and urinary excretion of acetaminophen (2 mmol/kg i.v.) and its metabolites was reduced 57% by ethionine and 66% by fructose. This was caused by decreased synthesis and excretion of the conjugates. Synthesis of the conjugates was impaired because of decreased hepatic cosubstrate levels. The present data suggest that energy state must be severely compromised before decreases in conjugation are observed in vivo. Thus, it is unlikely that energy state is often a limitation in the conjugation and excretion of xenobiotics.
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PMID:Effect of reduced hepatic energy state on acetaminophen conjugation in rats. 373 28

A 58-year-old man was initially seen with fatigue and weight loss. Laboratory examination detected hypercalcemia, elevated 1,25-dihydroxycholecalciferol levels, low parathyroid hormone (PTH) concentrations, and subperiosteal bone resorption. The patient underwent subtotal parathyroidectomy for presumed hyperparathyroidism, but serum calcium and 1,25-dihydroxycholecalciferol levels remained elevated following surgery. Search for another cause of the hypercalcemia disclosed enlarged para-aortic lymph nodes, biopsy specimens of which demonstrated Hodgkin's disease. After treatment of the patient with two cycles of chemotherapy with mechlorethamine hydrochloride, vincristine sulfate, procarbazine hydrochloride, and prednisone, serum calcium, 1,25-dihydroxycholecalciferol, and PTH levels normalized. We speculate that the humoral hypercalcemia in this patient resulted from tumor production of 1,25-dihydroxycholecalciferol.
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PMID:Humoral hypercalcemia in Hodgkin's disease. Association with elevated 1,25-dihydroxycholecalciferol levels and subperiosteal bone resorption. 383 28

We have measured mitochondrial ATP synthesis during passive anion influx and find that influx of phosphate leads to diminished efficiency (as reflected in the ATP:0 ratio) whereas influx of acetate produced enhanced efficiency. The anions, sulfate, propionate, and thiocyanate, are without influence on the ATP:0 ratio. It is likely that the opposite effects of phosphate and acetate on the ATP:0 ratio reflect phosphate-acetate exchange, and that acetate influx produces its positive effect on ATP synthesis by promoting phosphate efflux. Thus, phosphate efflux may be associated with increased, and phosphate influx, with decreased energy conservation.
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PMID:Influence of anion flux upon mitochondrial oxidative phosphorylation. 397 33

Mesocestoides tapeworm is a common cestode in carnivorous mammals, but human infection with the tapeworm of this genus have been infrequent. We have recently observed the 13th case of human infection with Mesocestoides lineatus in Japan. A 35-year-old man living in Gifu prefecture was admitted to our University Hospital with chief complaints of general fatigue and discharge of cestode segments in his stool. The patient gave a history of drinking blood and eating the raw liver of a snake Agkistrodon halys for medicinal purposes as same as the previous cases of all reported in Japan. The segments were identified as those of M. lineatus. He was treated orally 3 g of paromomycin sulfate. Stool examination after treatment with paromomycin sulfate revealed no evidence of parasitism. The present case may be the 2nd to have been successfully treated with paramomycin sulfate and the 21st case of Mesocestoides tapeworm infection in man described in the literature.
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PMID:[Therapeutic effect of paromomycin sulfate on the 13th case of Mesocestoides lineatus infection found in Japan]. 687 72

Mitochondrial cytopathies are due to genetic anomalies in the oxidative phosphorylation enzymes (excepting Krebs cycle, pyruvate and certain other mitochondrial enzymes). Recently discovered, these diseases have a characteristic heterogeneous clinical expression because of the ubiquitous nature of this intracellular organelle. We observed a case in a 16-year-old girl who had cytochrome C oxidase deficiency. The child was born to non-consanguinous parents and had a healthy brother. The first manifestation of the disease was a systolic murmur heard at the age of 4 years. Progressively, exertion dyspnoea, lipothymia with cyanose led to the first echocardiography at 8 years revealing non-obstructive cardiomyopathy. Functional inadaptation of cardiac performance worsened requiring various symptomatic treatments. At the age of 16, the symptomatology included lower limb fatigue and the diagnosis of a metabolic disease was entertained. Phosphorylase A and B activity and phosphokinase activity were normal. High lactic acid levels after exertion suggested a mitochondrial enzyme deficiency. The diagnosis of cytochrome C oxidase deficiency was confirmed by spectrophotometric and polarographic assay of mitochondria from a peripheral muscle biopsy. Treatment with riboflavin, ascorbic acid, factor P, menadione, carnitine and iron sulfate has currently provided some symptomatic improvement. In patients with unexplained cardiomyopathy, the diagnosis of mitochondrial cytopathy should be entertained if oxidoreduction potentials (lactate/pyruvate ratio) are perturbed. The diagnosis is confirmed by enzyme studies of fresh muscle mitochondria. Currently therapeutic prospects are at best very poor. Genetic counselling may be advisable.
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PMID:[Hypertrophic cardiomyopathy caused by cytochrome-oxidase deficiency]. 782 67

The efficacy and safety of an extended-release combination of loratadine plus pseudoephedrine sulfate (SCH 434) was compared with that of a tablet containing chlorpheniramine maleate plus pseudoephedrine sulfate (CTM-D) in 131 patients with symptomatic seasonal allergic rhinitis. Patients were randomly assigned to receive either SCH 434 (loratadine 5 mg and pseudoephedrine sulfate 120 mg) or CTM-D (chlorpheniramine maleate 12 mg and pseudoephedrine sulfate 120 mg) twice daily for 2 weeks. Evaluations were made after 3, 7, and 14 days of treatment. Demographics (age, race, sex, and duration of seasonal allergic rhinitis) and baseline total symptom scores were comparable between groups. Both combination products were effective in relieving the symptoms of allergic rhinitis. Improvement in total symptom scores was 54% on day 3 and 65% on day 14 in the SCH 434 group versus 57% on day 3 and 64% on day 14 in the CTM-D group. Individual symptom scores (nasal discharge, stuffiness, nasal itching, sneezing, and ocular symptoms) responded similarly. A smaller proportion of patients in the SCH 434 group reported side effects, especially dry mouth (7% vs 19%, P = 0.07), fatigue (6% vs 25%, P < 0.01), and sedation (7% vs 22%, P < 0.03). In conclusion, the combination of loratadine plus pseudoephedrine sulfate was equally as effective as a classic antihistamine (chlorpheniramine maleate) plus pseudoephedrine sulfate but had a lower incidence of side effects.
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PMID:Comparative study of SCH 434 and CTM-D in the treatment of seasonal allergic rhinitis. 791 2

Taste perception depends not only on the chemical and physical properties of tastants, but may also depend on the physiological and psychological conditions of those who do the tasting. In this study, the effects of mood state on taste sensitivity was evaluated in humans who were exposed to conditions of mental or physical fatigue and tension. Taste responses to quinine sulfate (bitter), citric acid (sour) and sucrose (sweet) were tested. The intensity of the taste sensations were recorded by a computerized time-intensity (Tl) on-line system. Subjects performed mental tasks by personal computer or physical tasks by ergometer for 10-40 min. Before and after these sessions, the duration of the after-taste and the intensity of the sensation of taste were recorded by the Tl system, and in addition, psychological mood states were evaluated with POMS (Profile of Mood State). Tl evaluation showed that after the mental tasks, the perceived duration of bitter, sour and sweet taste sensations was shortened relative to the control. Total amount of bitterness, sourness and sweetness was also significantly reduced. Furthermore, the maximum intensity of bitterness was significantly reduced. There were no significant differences in bitterness and sweetness sensations following physical tasks. However, relative to before the physical task, the duration of the after-taste of sourness was significantly shortened by the physical task. After the physical task, the buffering capacity of saliva was significantly increased. Thus mental and physical tasks alter taste perception in different ways; the mechanisms underlying these changes remain to be determined.
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PMID:Changes in taste perception following mental or physical stress. 867 Jun 98

In a controlled study of 100 patients, mean age 65 years old, suffering from chronic peripheral obliterative arterial disease, Leriche's stage II, were randomised in two groups treated respectively with defibrotide (400 mg bid) or heparan-sulfate (40 mg bid) by the oral route for a period of 6 months. At basal and after 30, 90 and 180 treatment days, patients were assessed for pain, paresthesias, rigidity and or tiredness in the leg, Winsor index (WI) relative and absolute walking distance (RWD, AWD), and time of recovery from pain. In order to evaluate microcirculation the following parameters were tested: resting flow (RF), standing flow (SF), veno-arteriolar reflex (VAR) and a capillaroscopy study was conducted. All patients showed an improvement in the clinical and instrumental parameters but more pronounced in the defibrotide group; the difference between the beginning and the end of the therapy was significantly better for defibrotide (p < 0.01). The tolerability observed was good, no side-effects were reported during the study.
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PMID:[Clinical experience in patients with chronic peripheral obliterating arteriopathy: defibrotide versus definite molecular weight heparan sulfate (MW 7500-15000 dalton)]. 876 20

The impact of hypothyroidism (Hyp) on myosin heavy chain (MHC) isoform expression, maximum specific force (P0), fatigability, and maximum unloaded shortening velocity (V0) was determined in the rat diaphragm muscle (Dia) at 0, 7, 14, 21, and 28 days of age. Hyp was induced by treating pregnant rats with 6-n-propyl-2-thiouracil (0.05% in drinking water) beginning at gestational day 10 and was confirmed by reduced plasma levels of 3,5,3'-triiodothyronine and thyroxine. MHC isoforms were separated on sodium dodecyl sulfate-polyacrylamide gel electrophoresis gels and analyzed by densitometry. Isometric P0 and fatigue resistance of the Dia were measured in vitro at 26 degrees C, and V0 was determined at 15 degrees C with the slack test. Compared with control muscles, expression of MHC-slow was higher and expression of adult fast MHC isoforms was lower in Hyp Dia at all ages. The neonatal isoform of MHC continued to be expressed in the Hyp Dia until day 28. At each age, P0 and fatigability were reduced and V0 was slower in the Hyp Dia. We conclude that Hyp-induced alterations in MHC isoform expression do not fully predict the changes in Dia contractile properties.
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PMID:Hypothyroidism alters diaphragm muscle development. 894 17

Patients reporting sensitivity to multiple chemicals at levels usually tolerated by the healthy population were administered standardized questionnaires to evaluate their symptoms and the exposures that aggravated these symptoms. Many patients were referred for medical tests. It is thought that patients with chemical sensitivity have organ abnormalities involving the liver, nervous system (brain, including limbic, peripheral, autonomic), immune system, and porphyrin metabolism, probably reflecting chemical injury to these systems. Laboratory results are not consistent with a psychologic origin of chemical sensitivity. Substantial overlap between chemical sensitivity, fibromyalgia, and chronic fatigue syndrome exists: the latter two conditions often involve chemical sensitivity and may even be the same disorder. Other disorders commonly seen in chemical sensitivity patients include headache (often migraine), chronic fatigue, musculoskeletal aching, chronic respiratory inflammation (rhinitis, sinusitis, laryngitis, asthma), attention deficit, and hyperactivity (affected younger children). Less common disorders include tremor, seizures, and mitral valve prolapse. Patients with these overlapping disorders should be evaluated for chemical sensitivity and excluded from control groups in future research. Agents whose exposures are associated with symptoms and suspected of causing onset of chemical sensitivity with chronic illness include gasoline, kerosene, natural gas, pesticides (especially chlordane and chlorpyrifos), solvents, new carpet and other renovation materials, adhesives/glues, fiberglass, carbonless copy paper, fabric softener, formaldehyde and glutaraldehyde, carpet shampoos (lauryl sulfate) and other cleaning agents, isocyanates, combustion products (poorly vented gas heaters, overheated batteries), and medications (dinitrochlorobenzene for warts, intranasally packed neosynephrine, prolonged antibiotics, and general anesthesia with petrochemicals). Multiple mechanisms of chemical injury that magnify response to exposures in chemically sensitive patients can include neurogenic inflammation (respiratory, gastrointestinal, genitourinary), kindling and time-dependent sensitization (neurologic), impaired porphyrin metabolism (multiple organs), and immune activation.
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PMID:Profile of patients with chemical injury and sensitivity. 916 75


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