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)

To determine the maximum tolerated dose (MTD) of escalating doses of interferon-alpha-2b (IFN, Intron A) with 5-fluorouracil (5-FU) and cisplatin (DDP) in patients with advanced cancer, 15 patients were accrued between May 1990 and July 1991. Primary sites were unknown (3), colorectal (3), head and neck (2), lung (2), gynecologic (1), gallbladder (1), sarcoma (1), anal canal (1) and pancreas (1). IFN was given s.c. on days 1-5 and then three times weekly with DDP (75 mg/m2, day 1) and 5-FU [750 mg/m2, days 1-5, continuous infusion (CI) on a 28-day cycle. The first two patients treated at level I (3 x 10(6) U/m2 s.c.) experienced possible neurotoxic deaths [massive cerebrovascular accident (CVA) and metabolic encephalopathy], and patient 3 had a grade 4 toxicity of performance status decline. Analysis of these events led us to exclude the enrollment of patients on i.v. morphine and of those with prior exposure to DDP. This resulted in grade 3 toxicity in terms of nausea, vomiting, fatigue and leukopenia but in no further CNS event. All patients were evaluable for toxicity but only ten were evaluable for response. Only two partial responses were seen, one in a patient with an unknown primary tumour and one in a patient with head and neck cancer. The combination of IFN is possible with 5-FU and DDP. The recommended dose of IFN is 2 x 10(6) U/m2 s.c. in patients with no prior exposure to DDP or i.v. morphine, given together with 5-FU (750 mg/m2, days 1-5, CI) and DDP (75 mg/m2, day 1) on a 28-day cycle.
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PMID:A phase I study of recombinant human interferon alpha-2b combined with 5-fluorouracil and cisplatin in patients with advanced cancer. 788 58

Alternative surgical treatments to orthotopic cardiac transplantation are needed for patients with heart failure. We hypothesized that descending thoracic aortomyoplasty with conditioned (fatigue-resistant) latissimus dorsi muscle could provide diastolic augmentation that would improve left ventricular function. Six mongrel dogs were studied. The left latissimus dorsi muscle was wrapped clockwise around the descending thoracic aorta. Left ventricular volume was measured with a conductance catheter. Aortic and left ventricular pressures were measured with a micromanometer. The following were measured after descending thoracic aortomyoplasty at baseline and with the descending thoracic aortomyoplasty stimulated 1:1 with the heart rate: stroke work, stroke volume, left ventricular peak pressure, maximum rate of increase of left ventricular pressure, diastolic relaxation time constant, peak rate of pressure decay, left ventricular end-diastolic pressure, endocardial viability ratio, mean diastolic aortic pressure, peak diastolic aortic pressure, and time-averaged aortic diastolic velocity. Before data collection, the latissimus dorsi was stimulated (5 pulses delivered at 33 Hz at a rate of 28 per minute for 4 weeks) with burst stimulation to induce fatigue resistance. Results (expressed as the mean +/- the standard error of the mean) showed significant improvement in the indices of ventricular contractility (maximum rate of increase of left ventricular pressure, 1,217 +/- 83 to 1,414 +/- 91 mm Hg/s) and diastolic relaxation mechanics (peak rate of pressure decay, 1,152 +/- 92 to 1,282 +/- 79 mm Hg/s; diastolic relaxation time constant, 43 +/- 2 to 38 +/- 2 ms). Significant differences were noted with stimulation at 1:1 in the endocardial viability ratio (0.90 +/- 0.05 to 1.14 +/- 0.04), an index of myocardial oxygen supply. Systemic diastolic pressures (peak diastolic aortic pressure, 95 +/- 6 to 107 +/- 5 mm Hg; mean diastolic aortic pressure, 92 +/- 6 to 102 +/- 6 mm Hg) and the time-averaged aortic diastolic velocity (1.5 +/- 0.6 to 3.3 +/- 1.0 m/s) increased significantly. We conclude that descending thoracic aortomyoplasty stimulation with conditioned latissimus dorsi muscle can improve indices of ventricular contractility, diastolic relaxation mechanics, diastolic pressures, and diastolic aortic velocity in the nonfailed canine heart. Further studies with the chronic failed heart model are required.
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PMID:Autogenous cardiac assist with chronic descending thoracic aortomyoplasty. 801 Jul 99

Moxonidine is an imidazoline receptor modulator, specific for the I1-imidazoline receptor. The stimulation of imidazoline receptors represents a new mode of antihypertensive action to inhibit peripheral alpha-adrenergic tone by a central mechanism. Acute hemodynamic studies reveal moxonidine produces an acute fall of blood pressure and systemic vascular resistance. Heart rate, cardiac output, stroke volume, and pulmonary artery pressures are not affected. Left ventricular end-systolic and diastolic volumes are reduced. Ejection fraction is not significantly affected but 6-month studies showed a regression of left ventricular hypertrophy. After oral administration the maximum concentration of moxonidine is reached in about 1 hour, and elimination half-life is 2.5 hours, prolonged by renal insufficiency. The antihypertensive effect lasts longer than would be expected from the half-life. Open studies with moxonidine have revealed falls between 20 and 29 mmHg systolic, and between 10 and 19 mmHg diastolic blood pressure. In the largest study, over 12 months in 141 patients, most patients were controlled by 0.2 mg daily (58%) or 0.2 mg b.i.d. (38%). Moxonidine has been compared with representatives from each important class of antihypertensive drugs. In a crossover trial of clonidine in 20 patients, blood pressure control was similar, but the incidence of tiredness and dry mouth was less on moxonidine, as was the total number of patients experiencing side effects, 85% versus 30% (p < 0.01). In a larger parallel group study of moxonidine (n = 122) and clonidine (n = 30), blood pressure control was similar, but the overall incidence of side effects was less on moxonidine. In comparative studies of moxonidine with atenolol, ACE inhibitors, dihydropyridine calcium antagonists, hydrochlorothiazide, and alpha 1 blockade, the blood pressure control with representatives of these various classes of drugs was similar to moxonidine.
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PMID:Clinical experience with moxonidine. 806 79

A case of systemic lupus erythematosus (SLE) complicated with hypopituitarism after steroid pulse therapy is reported. A 46-years-old-female with a history of SLE starting in 1975 was admitted to our hospital in February 1991 for lupus nephritis. Steroid pulse therapy, 1000 mg methyl-prednisolone for 3 successive days as one therapy unit, was administered. Proteinuria improved remarkably, however, general fatigue and headache appeared 2 weeks after initiation of therapy. Endocrinological examination revealed hypopituitarism including the levels of TSH, FSH, GH and ACTH. The secretion of FSH and LH gradually improved after replacement therapy of dried thyroid. MRI examination of the brain revealed an empty sella. It is known that pituitary tumor, cerebrovascular accident and autoimmune lymphocytic hypophysitis cause hypopituitarism. In this case, it is unlikely that the pulse therapy may be responsible for the infarction of the anterior pituitary artery furthermore, there has been no articles describing such incidence after steroid pulse therapy. This case may be indicative of a very rare case in which the empty sella might have been exacerbated by the pulse therapy in the causation of hypopituitarism.
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PMID:[Hypopituitarism associated with empty sella after steroid pulse therapy in a patient with SLE]. 814 29

The objective of this study was to determine the pumping capability of dynamic cardiomyoplasty during induced ventricular fibrillation. In this acute study of 6 dogs, the pumping capability of the unconditioned left latissimus dorsi (LD) muscle (141 to 292 gm), wrapped around both ventricles, was investigated during induced ventricular fibrillation. Left-ventricular and femoral artery pressure, the ECG and aortic root flow velocity were monitored. Prior to inducing ventricular fibrillation, the ability of the unconditioned LD muscle to augment stroke volume (SV), was quantified as the area under the aortic flow-velocity record. The ventricles were then fibrillated and, after 10 sec, rhythmic 250 msec trains (1/sec) of stimuli (40/sec) were delivered to the thoracodorsal nerve to contract the LD muscle tetanically. In no case could dynamic cardiomyoplasty produce the same SV as when the ventricles were beating normally. In one animal, the SV attained two percent of the normal SV by 5 contractions; in another, the SV reached one percent by 25 contractions. In the remaining animals, the SV varied around 20% of the prefibrillation SV. By 90 contractions, the stroke volume was 10% of the prefibrillation value. The progressive decrease in SV was likely a consequence of LD muscle ischemia and fatigue, since the latissimus dorsi muscle provided low blood flow during the period of fibrillation.
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PMID:Stroke volume with dynamic cardiomyoplasty during ventricular fibrillation in the acute dog. 820 83

The nature of association between depression and disabling illness, whether as an organic symptom or emotional consequence, has been the source of interest and controversy. Depression in three groups of medically ill, disabled patients (Parkinson's disease, right hemisphere stroke, and amputation) was studied. Mean depression severity and frequency of depression were equal for all groups. Severity of neurologic symptomatology was not consistently related to depression. Type of prosthesis, but not amputation type, was related to depression for amputees. Patterns of depression on discriminant analysis did differentiate the groups. A depression symptom conglomerate suggesting guilt and body image change with fatigue characterized the Parkinson patients most and the amputees least. A second depression conglomerate suggesting indecisiveness and thoughts of death or self-harm characterized amputees most and stroke patients least. Depression as an emotional response may not be a singular, specific feature of disabling illness in general, given uniformity of prevalence and severity, but differential etiology in specific instances should be considered.
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PMID:Depression in disabling illness: severity and patterns of self-reported symptoms in three groups. 820 89

When the latissimus dorsi is used for ventricular augmentation in cardiomyoplasty, a delay of several weeks occurs before the muscle revascularizes, adheres to the heart, and is transformed to fatigue-resistant status. This study analyzes the effect of static (unstimulated) cardiomyoplasty on left ventricular function. Four mongrel dogs underwent staged left latissimus dorsi cardiomyoplasty. Left ventricular pressure was measured with a micromanometer catheter. Left ventricular volume was measured by sonomicrometry. Cardiac output, heart rate, preload recruitable stroke work, maximum elastance, left ventricular end-diastolic volume, left ventricular end-diastolic pressure, stroke work, and the diastolic relaxation constant were measured before and immediately after cardiomyoplasty with the myoplasty static. Results, expressed as mean +/- standard error of the mean, showed no significant differences in indexes of systolic function (stroke work, 1017 +/- 223 gm.cm to 984 +/- 403 gm.cm; preload recruitable stroke work, 110 +/- 13 gm.cm/cm3 to 115 +/- 19.8 gm.cm/cm3; maximum elastance, 10.38 +/- 5.6 mm Hg/ml to 13.59 +/- 6.5 mm Hg/ml; cardiac output 4.51 +/- 0.43 L/min to 4.21 +/- 0.34 L/min) or diastolic function (left ventricular end-diastolic volume, 21 +/- 5.2 ml to 20 +/- 5.3 ml; left ventricular end-diastolic pressure, 13 +/- 3.5 mm Hg to 15 +/- 3 mm Hg; diastolic relaxation constant 42.8 +/- 5.2 msec to 42.5 +/- 4.5 msec). Heart rate also remained unchanged (131 +/- 8.9 beats/min to 140 +/- 9.8 beats/min). The static (unstimulated) left latissimus dorsi cardioplasty can be done with little effect on left ventricular systolic or diastolic function in the normal canine heart.
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PMID:Static left latissimus dorsi cardiomyoplasty: effect on left ventricular function. 831 3

We previously found that double cardiomyoplasty using both acutely raised, unconditioned latissimus dorsi muscles increased cardiac output by 9.6% (1,547 +/- 154 versus 1,695 +/- 166 mL/min), stroke volume by 18.2% (12.1 +/- 0.6 versus 14.3 +/- 0.7 mL), peak left ventricular pressure by 18.4% (98 +/- 3 versus 116 +/- 5 mm Hg), and peak right ventricular pressure by 62.5% (24 +/- 2 versus 39 +/- 4 mm Hg) (p < 0.05 for all differences). In this study 10 dogs underwent double cardiomyoplasty: 3 died perioperatively, and 7 underwent 8 weeks of muscle conditioning. After the conditioning period, the muscle flaps did not contract in 2 of the 7 dogs. Hemodynamics were measured in the remaining 5 dogs. Using fatigue-resistant muscle, cardiac output decreased by 3.7% (1,279 +/- 262 versus 1,233 +/- 274 mL/min), stroke volume decreased by 9.0% (9.5 +/- 1.2 versus 8.8 +/- 1.2 mL), and peak left ventricular pressure increased by 10.6% (82.1 +/- 6.5 versus 90.8 +/- 3.2 mm Hg), but not significantly. Peak right ventricular pressure increased significantly by 31.3% (24.3 +/- 2.1 versus 31.9 +/- 3.6 mm Hg; p < 0.05). Hemodynamic effects of individual left or right muscle contractions versus bilateral muscle stimulation were not significantly different except for a greater percentage increase in peak right ventricular pressure (right, 24.9 +/- 2.1 mm Hg unstimulated versus 28.0 +/- 2.1 stimulated; left, 26.3 +/- 0.9 mm Hg unstimulated versus 30.7 +/- 2.4 mm Hg stimulated; bilateral, 24.3 +/- 2.1 mm Hg unstimulated versus 31.9 +/- 3.4 mm Hg stimulated; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Double cardiomyoplasty: acute versus chronic results. 832 73

The dependence of power on aerobic and anaerobic energy metabolism and on force production was studied in maximal leg exercise. National and international level male rowers (n = 9) performed four modified (legs-only) rowing ergometer exercises: a progressive test, 2-min (T2), 12-min (T12) and 6-min (T6) all-out tests. In T2, significant correlations were observed between power in T2 (PT2) and oxygen debt (r = 0.83, P < 0.05) and between PT2 and average force production (Fav) during the last 30 s (r = 0.85, P < 0.05). These parameters explained 93% of the variation in PT2. The highest correlations between power in T6 (PT6) and physiological parameters were as follows: maximal oxygen uptake (VO2 max: r = 0.87, P < 0.01), blood bicarbonate concentration before the test ([HCO3-before]: r = 0.85, P < 0.05) and blood lactate concentration on anaerobic threshold (BLaAnT: r = -0.82, P < 0.05). Together, these parameters explained 92% of the variation in PT6. In T12, the total power (PT12) correlated with power of anaerobic threshold (PAnT: r = 0.95, P < 0.001) and with the highest VO2 value in this test (VO2 peak: r = 0.92, P < 0.001). These two parameters explained 96% of the variation in PT12. The decrease of at least one of the force parameters during each test was taken as a sign of fatigue. The decline in force was compensated for by an increase in stroke rate at the end of T6 and T12 (P < 0.01, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interrelations between power, force production and energy metabolism in maximal leg work using a modified rowing ergometer. 833 55

This report describes an unusual case of secondary nocturnal enuresis presumptively secondary to progressive bradycardia from complete heart block. Congenital complete heart block occurs in approximately 1 of 22,000 livebirths and is typically associated with structural congenital heart disease or maternal collagen vascular diseases. It can be entirely asymptomatic during infancy and childhood, depending in part on the escape rate and rhythm and other hemodynamic variables. The case described above was not diagnosed until the patient coincidentally underwent cardiac monitoring. The picture was confusing initially, as a tricyclic antidepressant medication had been ingested. Heart block is one of the known cardiovascular effects of tricyclic antidepressant overdose. However, the conduction disturbance should have resolved as the drug was excreted from the body. As children with congenital complete heart block get older, the ventricular escape rate typically decreases. In addition, as activity increases with age, more demand is placed for cardiac output. The resting end-diastolic volume is increased to elevate stroke volume in compensation for lower heart rate. As the escape rate decreases and the metabolic demand increases, patients with congenital complete heart block then may begin to develop symptoms. Typical symptoms in children include dizziness, Stokes-Adams syncopal attacks, fatigue, daytime somnolence, and other somatic complaints. Bedwetting has not been reported as an initial symptom, but in this case is likely secondary to the excessive somnolence and difficulty with arousal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nocturnal enuresis secondary to heart block: report of cure by cardiac pacemaker implantation. 833 31


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