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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The hypotheses that defective platelet structure and function is the basis for migraines is presented, with evidence explaining the biochemical, clinical, pathological, and pharmacological aspects of migraine. Platelets undergo 2 types of reaction, a shape change and a granule release reaction, releasing adenosine diphosphate (ADP) serotonin 5-hydroxy-tryptamine (5-HT), and thromboglobulin in response to collagen and thrombin. Platelets from migraine suffers contain more ADP, have more dense granules, and show some qualitative differences in their release reaction. Their platelets aggregate more readily when exposed to 5-HT, their platelet fibrinogen receptors have greater affinity, and their platelet membranes show altered viscosity. Some drugs that inhibit platelet aggregation, such as methysergide, aspirin, and amitryptylline, are beneficial in cases of migraine. Some migraine triggers, such as tyramine and catecholamines, are known to be vasoactive. The release by platelets of 5-HT may account for the visual aura or prodrome that migraine patients experience. Some migraine precipitating factors, such as stress, fatigue, hunger, certain foods, and hormones, may stimulate 5-HT release by platelets. Alterations in hormones, notably puberty, menstruation, oral contraceptive use, and menopause, are characterized by altered platelet aggregation and by onset of migraine in previously healthy people. Other arguments in favor of the platelet hypothesis involve prostacyclin deficit during menstruation and migraine associated with sudden decline in platelet numbers in cases of thrombocytopenic purpura and essential thrombocythemia.
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PMID:Migraine: the platelet hypothesis after 10 years. 270 Dec 86

There is increasing evidence that platelets play an important role in the pathogenesis of acute ischemic heart disease. Therefore an understanding of factors that influence platelet performance is important. This study was undertaken (1) to characterize during evolving myocardial infarction platelet activity in the peripheral circulation and across the ischemic/infarcting myocardial compartment, the locus of presumed platelet hyperactivity, and (2) to evaluate the effects of prostacyclin (PGI2), a most potent antiplatelet agent and vasodilator. A total of 59 patients with evolving myocardial infarction were studied. Twenty-two patients were instrumented with arterial and coronary sinus catheters and received intravenous infusion of PGI2, 13 +/- 4.5 ng/kg/min (mean +/- SD), for 90 min. In 15 patients with anterior myocardial infarction, transcardiac platelet function and response to PGI2 were studied. Plasma levels of beta-thromboglobulin (beta-TG) and of thromboxane B2 (TxB2), in vivo measures of platelet activity, were elevated three- and 10-fold. 6-Keto-prostaglandin F 1 alpha, the stable end product of PGI2, was less than 10 pg/ml, reflecting a leftward shift of the TxB2/PGI2 ratio. Platelets circulating during evolving myocardial infarction ("ischemic platelets") were hyperaggregable in response to ADP and relatively resistant to PGI2, both in vivo and in vitro. Concentrations of platelet cyclic AMP and the cyclic AMP response to PGI2 were diminished. The platelet hyperreactivity, expressed by plasma beta-TG, platelet aggregation, and PGI2-induced inhibition of aggregation, was most intense early during infarct evolution and decreased with time. The increased platelet performance resulted in "platelet fatigue," indicated by decreased contents of beta-TG of the ischemic platelet and decreased TxA2 production in response to collagen. However, the ischemic platelet produced twice normal TxA2 in response to arachidonic acid (stimulus and substrate), demonstrating a heightened metabolic capacity. TxA2 was produced across the ischemic/infarcting compartment in 10 of 15 patients with anterior myocardial infarction. The antiplatelet effect of PGI2 was greatly diminished. In summary, the data define an abnormal pattern of platelet behavior during evolving myocardial infarction, characterized by a proaggregatory environment, heightened platelet reactivity in both the peripheral and coronary circulation, and relative resistance to PGI2. The clinical consequences of the data are that the patient in the acute phase of myocardial infarction may benefit from suppression of platelet function and requires significantly greater doses of PGI2 than normal subjects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Systemic and transcardiac platelet activity in acute myocardial infarction in man: resistance to prostacyclin. 293 81

In a single-blind trial 25 patients with progressive scleroderma and Raynaud's phenomenon intravenous infusions of iloprost, a prostacyclin derivative (carbaprostacyclin), were given daily for five hours during a six-day hospital stay, after a comparable initial single placebo infusion. Duration, frequency and intensity of Raynaud symptoms improved in more than 75% of the patients. This improvement was objectified by telethermometry which demonstrated acral hyperthermia and significantly briefer rewarming after standardized cooling of the hands. In addition, there was more rapid healing of ulcerations and necroses of the digital pulp. A significant inhibition of ADP- and collagen-dependent platelet aggregation was demonstrated during the iloprost infusion. Side effects, such as headache, nausea and tiredness occurred only transitorily during the infusion, were individually highly variable, and then only at higher concentrations. A dosage of 2 ng/kg X min was tolerated by all patients.
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PMID:[Treatment of Raynaud's phenomenon in scleroderma with a new stable prostacyclin derivative]. 638 60

Prostacyclin (or epoprostenol), an arachidonic acid metabolite, is an effective treatment for patients with primary pulmonary hypertension. Interruption of chronic prostacyclin infusion can result in recurrent symptoms of dyspnea and fatigue. The etiology of this phenomenon is unknown. We hypothesized that sympathoadrenal activation could lead to increased vascular tone after abrupt termination of the infusion. To evaluate this effect, we monitored six chronically instrumented, awake sheep during and after infusion of prostacyclin. Prostacyclin decreased mean arterial pressure (MAP) by 14% and increased cardiac output by 33%. After the infusion ceased, MAP rebounded 23% above baseline, and cardiac output decreased by 28% from peak values within 10 min. We were unable to demonstrate an increase in norepinephrine levels after cessation of prostacyclin, nor did alpha-adrenergic blockade affect postinfusion hemodynamics. However, plasma renin activity increased >10-fold at peak infusion and remained elevated for up to 2 h after discontinuation of prostacyclin. Coinfusion of the angiotensin II-receptor antagonist L-158,809 resulted in complete abrogation of the postcessation rise in MAP. We conclude that renin-angiotensin system activation is primarily responsible for systemic hypertension occurring after abrupt cessation of prostacyclin infusion in sheep and that angiotensin II receptor blockade prevents this response. Our data do not support a role for sympathetic nervous system activation in the systemic pressor response after prostacyclin infusion.
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PMID:Angiotensin II mediates systemic rebound hypertension after cessation of prostacyclin infusion in sheep. 968 53

Primary pulmonary hypertension (PPH) is a pulmonary vascular disease characterized by an elevation in mean pulmonary artery pressure and pulmonary vascular resistance. Recently, PPH gained national attention because of its association with appetite suppressants. PPH may also be associated with pregnancy, hypothyroidism, autoimmune disorders, human immunodeficiency virus infection, and the use of drugs such as oral contraceptives and cocaine. Patients with PPH may report dyspnea on exertion and fatigue. Early diagnosis is crucial. New therapeutic regimens have dramatically reduced mortality rates and improved quality of life by halting the progression of pulmonary vascular remodeling and averting right-sided heart failure. These therapies include high-dose calcium channel antagonists, anticoagulants, and continuous intravenous prostacyclin. Lung or heart-lung transplantation remains a viable therapeutic option for patients who are treated late in the disease process, who are not responsive to medical management, or who remain symptomatic and continue to deteriorate.
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PMID:Diagnosing and treating primary pulmonary hypertension. 1050 69

Primary pulmonary hypertension (PPH) is a condition characterized by sustained elevation of pulmonary artery pressure (PAP) without demonstrable cause. The most common symptom at presentation is dyspnea. Other complaints include fatigue, chest pain, syncope, leg edema, and palpitations. Right heart catheterization is diagnostic, showing a mean PAP >25 mmHg at rest and >30 mmHg during exercise, with a normal pulmonary capillary wedge pressure. In the National Institutes of Health-PPH registry, the median survival period was 2.8 years. Treatment is aimed at lowering PAP, increasing cardiac output, and decreasing in situ thrombosis. Vasodilators have been used with some success in the treatment of PPH. They include prostacyclin, calcium-channel blockers, nitric oxide and adenosine. Anticoagulation has also been advised for the prevention of deep vein thrombosis, pulmonary embolism, and in situ thromboses of the lungs. New drug treatments under investigation include L-arginine, plasma endothelin-I, and bosentan. Use of oxygen, digoxin, and diuretics for symptomatic relief have also been recommended. Patients with severe PPH refractory to medical management should be considered for surgery.
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PMID:Primary pulmonary hypertension. 1172 93

Congenital heart disease can increase or decrease pulmonary blood flow, pulmonary vascular resistance (PVR) or pulmonary artery pressure (PAP). PAP is the product of PVR and pulmonary minute volume (Qp), such that pulmonary hypertension (PHT) may develop as a result of an increase in either PVR or Qp or both. Given that the pulmonary vascular bed is a low pressure system with high flow, any increase in resistance would generate PHT. The normal value of PVR is 2 Woods units (mm Hg/l/min). Increased PAP is due to hypoxic lesions of the endothelium, which release proteolytic enzymes that alter the balance of metabolites of arachidonic acid, regulators of pulmonary vasomotor tone. Hypoxia and acidosis cause intense pulmonary vasoconstriction (hypoxic vasoconstrictor reflex). An increase of PVR is due to a combination of vasoconstrictive processes and remodeling, with hypertrophy of the pulmonary artery. Structural lesions are related to hypertrophy of the endothelium, the transformation of fibroblasts to myocytes and the decrease of the alveolar/arteriolar ratio with the formation of new vessels.PHT may be primary or secondary to another disease. Primary PHT is a rare genetic disease. The most common secondary forms of PHT in pediatrics are due to persistence of neonatal anatomy (neonatal PHT), to heart diseases with left-right shunt (CIV, DAP, etc.), to diseases of the pulmonary parenchyma (interstitial viral infection, mucoviscidosis), and complications of heart surgery. All congenital heart diseases can lead to PHT if not treated promptly. Clinical signs of PHT are highly non-specific: dyspnea, fatigue, syncopes, exercise intolerance, precordialgia, cyanosis and edema. The best approaches to diagnosis and prognosis are echocardiography and cardiac catheterization with vasodilators. Anesthetics that do not alter PVR should be used in such patients, who are sensitive to changes in pulmonary ventilation, to changes in cardiac output and to anesthetics. The treatment of PHT during intra and postoperative pediatric surgery is based on the use of high inspirated oxygen concentration (100%), an adequate sedation and the use of vasodilators (prostaglandin I2, nitric oxide, sodium nitroprusiate and milrinone).
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PMID:[Pulmonary hypertension in pediatric heart surgery]. 1179 1

Intermittent claudication (IC) is leg muscle pain, cramping and fatigue brought on by exercise and is the primary symptom of peripheral arterial disease. The goals of pharmacotherapy for IC are to increase the walking capacity/quality of life and to decrease rates of amputation. In 1988, pentoxifylline was the only drug that had reasonable supportive clinical trial evidence for being beneficial in IC. Since then a number of drugs have shown benefit or potential in IC. Cilostazol, a specific inhibitor of phosphodiesterase 3 and activator of lipoprotein lipase, clearly increases pain-free and absolute walking distances in claudicants. However, cilostazol does cause minor side effects including headache, diarrhoea, loose stools and flatulence. Naftidrofuryl, a serotonin (5-HT2) receptor antagonist and antiplatelet drug, is beneficial in claudicants. Inhibitors of platelet aggregation (including nitric oxide from L -arginine or glyceryl trinitrate) and anticoagulants (low molecular weight heparin, defibrotide) probably have both short and long-term benefits in IC. In addition, intravenous infusions of prostaglandins (PGs) PGE1 and PGI2 have an established role in severe peripheral arterial disease and the recent introduction of longer lasting and/or oral forms of the PGs makes them more likely to be useful in the IC associated with less severe forms of the disease. There are some exciting new approaches to the treatment of IC, including propionyl-L-carnitine and basic fibroblast growth factor (bFGF).
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PMID:Pharmacotherapy of intermittent claudication. 1182 12

Liver disease affects the lungs. The majority of patients exhibit mild to moderate arterial hypoxaemia essentially attributable to an alteration in ventilation/perfusion matching and limited by an increase in ventilation. A minority (some 10%) of patients exhibit a "hepatopulmonary syndrome" defined by severe hypoxaemia with arterial PO2 below 60 mm Hg, dyspnoea, cyanosis, digital clubbing, orthodeoxia, platypnoea and demonstrable pulmonary vascular dilatations causing a true pulmonary shunt and a diffusion/perfusion imbalance. The hepatopulmonary syndrome is incurable but resolves over time after liver transplantation. An even lower proportion of patients, approximately 1%, develop pulmonary hypertension. Clinically this "portopulmonary hypertension" resembles primary pulmonary hypertension, with dyspnoea and fatigue as the main symptoms, histopathology and response to prostacyclin therapy. Portopulmonary hypertension is irreversible. Liver transplantation mortality in patients with portopulmonary hypertension ranges from 50 to 100%. The common cause of the hepatopulmonary syndrome and portopulmonary hypertension is portal hypertension and portosystemic shunting, indicating that vasoactive and angiogenetic factors originating from the liver normally control the pulmonary circulation.
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PMID:Hepatopulmonary syndrome and portopulmonary hypertension. 1271 85


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