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)

A 26-year-old female with Bartter's syndrome associated with Graves' disease is reported. This patient had a history of Graves' disease from the age of 22 and anti-thyroid drug (Methimazole) had been administered for 2 years. Thyroid function returned to normal but general fatigue and polyuria continued. Hypokalemia was diagnosed at 25 years of age and she was referred to our hospital for evaluation. Blood pressure was normal and laboratory data revealed normal thyroid function, hypokalemic alkalosis, high plasma renin activity and high plasma aldosterone concentration. She showed normal pressor sensitivity to norepinephrine infusion, grossly diminished pressor sensitivity to exogenous angiotensin II infusion compared with the normal. A renal biopsy specimen showed juxtaglomerular cell hyperplasia. Electron microscopy confirmed lacis cell (agranular cell) proliferation.
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PMID:Bartter's syndrome--case report. 15 51

After prolonged (8 hrs) swimming, the level of corticosteroids was reduced and the contents of aldosterone and DOC in the blood was increased in the rats. At incubation of these rats' adrenals in the L-thyrosine substratum the synthesis of adrenaline was reduced. Addition of hydrocortisone, prednisolone and corticosterone into the medium as well as in vivo administration of these increased the adrenaline synthesis in swimming rats and did not alter it in intact rats. Neither in vitro addition of aldosterone nor in vivo administration of ACTH activated the process. The activating effect of glucocorticoids was absent at incubation of the adrenals with L-DOPA and L-noradrenaline. Synthesis of cathecholamines in the heart of swimming rats in the presence of L-thyrosine and L-DOPA as precnrsors was suppressed; neither was it restored by administration of corticosteroids both in vitro and in vivo. This suggests that one of the reasons for suppression of the catecholamine synthesis in adrenals at obvious physical fatigue is the decrease of the glucocorticoid activity.
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PMID:[Interaction of catecholamines and corticosteroids during the process of muscle fatigue]. 20 48

Hyperaldosteronism due to aldosteronoma is a rare but potentially curable form of pediatric hypertension. We have presented a patient who had symptoms of enuresis and fatigue, and in whom the diagnosis was suggested by low serum potassium and persistent hypertension. Diagnosis was confirmed by increased plasma and urinary aldosterone and decreased plasma renin. The tumor was localized with the aid of adrenal venography and catheterization, which showed greatly increased plasma aldosterone levels in the right adrenal vein. The pathologic findings were totally reversed by right adrenalectomy. The clinical picture and results following surgical removal of aldosterone-producing tumors in six children are reviewed.
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PMID:Aldosteronoma in a child with localization by adrenal vein aldosterone: collective review of the literature. 120 77

In seven patients who presented with lightheadedness, fatigue, "weakness," and sometimes syncope, blood pressure was found not to fall after standing for 3 to 4 minutes but to fall severely, frequently with syncope or presyncopal symptoms, after 13 to 30 minutes when measured every minute with an automatic device. This delayed orthostatic hypotension could be corrected with inflation of a pressure suit to 45 mm Hg. Its mechanism was further investigated with measurements of plasma catecholamines, plasma cortisol and aldosterone responses to corticotropin, and the effects of norepinephrine infusions on blood pressure and venous contractility. There was normal or excessive orthostatic norepinephrine release in all patients, evidence of impaired venous innervation in the legs in some, and various disorders in the other patients. Since therapeutic improvement in the orthostatic hypotension greatly reduced the symptoms, we concluded that orthostatic hypotension occurring after more than 10 minutes of standing is a potentially debilitating and often correctable disorder.
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PMID:Delayed orthostatic intolerance. 158 Jul 14

A 76-year-old man was admitted because of general fatigue and lumbago. Two years before admission, hyponatremia and hyperkalemia were pointed out, subsequently hydrocortisone (20 mg/day) was given under the diagnosis of panhypopituitarism. The marked improvement was found in the electrolytes abnormality. On examination at admission, there was no abnormality of anterior pituitary function. In addition to the extremely low level of plasma renin activity and aldosterone concentration, the persistent microhematuria and hyperuricemia were found, however, renal histology only showed the benign arteriosclerosis but no significant alteration in juxtaglomerular apparatus and glomeruli. The urinary prostacyclin metabolite output was rather increased compared to that of normal subject, suggesting that prostaglandins may not be responsible for the defect of renin secretion. Although, the cause was still unknown, small dose of dexamethasone was extremely effective to resolve electrolytes abnormality and hematuria.
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PMID:[A case of hyporeninemic hypoaldosteronism improved by dexamethasone treatment]. 160 44

Knowledge of the basic alterations of central hemodynamics in congestive heart failure has failed to explain many aspects of this important syndrome. Increasing attention has recently been paid to compensatory and adaptive mechanisms occurring after the initial insult. Thus, new insights have been gained into the pathophysiology of contraction of hypertrophied myocardium and changes of adrenergic receptors in the myocardium due to chronically increased cardiac sympathetic tone. The role of the renin-angiotensin-aldosterone system in early and advanced congestive heart failure has been further elucidated, and the role of the vasodilating atrial natriuretic peptide is undergoing further definition. New results further clarify the mechanisms leading to breathlessness and muscular fatigue in congestive heart failure, with emphasis shifting from the traditional concept of the importance of increased filling pressures to changes to the peripheral circulation and exercising muscles. Although progress has been made in understanding of the pathophysiology of congestive heart failure, many aspects are still poorly understood and await clarification.
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PMID:Circulatory abnormalities and compensatory mechanisms in heart failure. 204 68

To investigate the adrenostatic potential of a nonhypnotic low dose etomidate infusion, we administered 0.03 mg/kg etomidate in a bolus injection, followed by constant infusion of 0.3 mg/kg.h for 24 h to 6 patients with severe Cushing's syndrome. The dose-response relationship also was determined in 15 normal subjects. Three groups of 5 received, respectively, doses of 0.03, 0.1, and 0.3 mg/kg.h etomidate for 5 h after an initial bolus dose of 0.03 mg/kg. The response to exogenously administered ACTH [0.25 mg ACTH-(1-24)], injected after the etomidate or control infusion, was determined in all normal subjects. In the six hypercortisolemic patients, serum cortisol concentrations decreased from 1374 +/- 436 nmol/L (mean +/- SEM) to 188 +/- 91 nmol/L after 11 h of etomidate infusion and remained low until the end of the infusion. Cortisol levels returned to pretreatment concentrations by 24 h. Excretion of urinary free cortisol decreased from 1180 +/- 196 to 185 +/- 66 nmol/day. In the normal subjects, administration of etomidate led to a dose-dependent decrease in serum cortisol from about 550 to 83 nmol/L, while 11-deoxycortisol rose from low or undetectable levels up to 346 nmol/L. In response to ACTH, cortisol levels rose in inverse proportion to the etomidate dose. It was, however, significantly reduced compared to normal saline infusion even after the lowest dose. Changes in aldosterone and corticosterone concentrations were similar to those in cortisol, and 11-deoxycorticosterone changed in a pattern similar to that of 11-deoxycortisol. Two of five normal subjects reported tiredness during the highest etomidate infusion. No other side-effects were noted. We conclude that iv administered etomidate in a low nonhypnotic dose reduces serum cortisol concentrations in a dose-dependent manner in both hyper- and eucortisolemic subjects. This study suggests that etomidate at a dose of 0.1 mg/kg.h or lower may be an effective strategy for the control of severe hypercortisolemia.
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PMID:Infusion of low dose etomidate: correction of hypercortisolemia in patients with Cushing's syndrome and dose-response relationship in normal subjects. 215 85

We report a case of 47-year-old woman with an isolated deficiency of adrenocorticotropic hormone. She was admitted complaining of fatigue and frequent loss of consciousness. The patient developed severe hyponatremia (100 mEq/l) after five days of the admission. Her plasma renin activity and plasma aldosterone concentration were low though she was dehydrated. After the treatment of dehydration, plasma osmolality was low but high plasma antidiuretic hormone (ADH) level sustained. Both high urinary sodium excretion and low urinary aldosterone excretion still remained after one month of replacement therapy with prednisolone. But, glomerular filtration rate and a response of urinary volume to acute water loading were normalized. These results suggested that severe hyponatremia of the patient was caused by an inappropriate secretion of ADH and suppression of renin-aldosterone system. We consider the suppression of renin-aldosterone system was partially independent of an inappropriate secretion of ADH.
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PMID:[Hyponatremia in isolated deficiency of adrenocorticotropic hormone: role of a decrease in aldosterone secretion independent of antidiuretic hormone excess]. 217 15

Knowledge of the basic alterations of central hemodynamics in congestive heart failure (CHF) has failed to explain many aspects of this important syndrome. Increasing attention has recently been paid to compensatory and adaptive mechanisms occurring after the initiating insult. Thus, new insights have been gained into the pathophysiology of contraction of hypertrophied myocardium and changes of adrenergic receptors in the myocardium due to chronically increased cardiac sympathetic tone. The role of the renin-angiotensin-aldosterone system in early and advanced CHF has been further elucidated and the role of the vasodilating and natriuretic atrial natriuretic peptide is undergoing further definition. New results further clarify the mechanisms leading to breathlessness and muscular fatigue in chronic CHF with emphasis shifting from the traditional concept of the importance of increased filling pressures to changes to the peripheral circulation and the exercising muscles. Although progress has been made in the understanding of the pathophysiology of CHF, many aspects are still poorly understood and await clarification.
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PMID:Compensatory and adaptive mechanisms in congestive heart failure. 248 Apr 83

The renin-angiotensin-aldosterone system plays an important role in the development of congestive heart failure (CHF). In patients with chronic heart failure, angiotensin-converting enzyme (ACE) inhibitors, such as captopril, enalapril, and quinapril, have been shown to improve hemodynamics, reduce symptoms of fatigue and dyspnea, increase exercise capacity, correct hyponatremia, reduce diuretic requirements and ventricular arrhythmias, and conserve potassium and magnesium. ACE inhibitors reduce circulating levels of angiotensin II and aldosterone and may reduce plasma norepinephrine and vasopressin levels. They are equally effective in patients with mild to moderate heart failure and in patients with severe cardiac impairment. ACE inhibitors are at least as beneficial as digitalis in patients with mild heart failure, and they may even be considered as first-line therapy. Promising results have also been obtained in patients with myocardial infarction, in whom long-term therapy with ACE inhibitors has prevented an increase in heart size. ACE inhibitors improve prognosis in patients with severe heart failure and in patients with hyponatremia; the question of effect on survival in mild to moderate heart failure has yet to be answered.
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PMID:ACE inhibitors in congestive heart failure. 267 Feb 20


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