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

A 59-year-old man with a 30-year history of type 2 diabetes mellitus presented with fatigue, confusion, and weight loss over a 3-month period. He was found to be hypercalcemic (11.8 mg/dL) and dehydrated, and his hypercalcemia improved with intravenous fluids. While in the hospital, he developed hyponatremia, hypoglycemia, and hypotension. He was found to have a subnormal cortisol level of 2.3 microg/dL at baseline, which increased to only 5.6 microg/dL 60 minutes after a 250-microg corticotropin intravenous stimulation test. The patient developed pneumonia and adult respiratory distress syndrome and died of an acute myocardial infarction. During the autopsy, he was found to have lymphocytic hypophysitis with a severe reduction in corticotropin-producing anterior pituitary cells. No malignancy was identified at autopsy. He is the first male patient to be described in the literature who presented with hypercalcemia caused by lymphocytic hypophysitis.
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PMID:Lymphocytic hypophysitis in a man presenting with hypercalcemia. 1126

Cold exposure facilitates body heat loss which can reduce body temperature, unless mitigated by enhanced heat conservation or increased heat production. When behavioral strategies inadequately defend body temperature, vasomotor and thermogenic responses are elicited, both of which are modulated if not mediated by sympathetic nervous activation. Both exercise and shivering increase metabolic heat production which helps offset body heat losses in the cold. However, exercise also increases peripheral blood flow, in turn facilitating heat loss, an effect that can persist for some time after exercise ceases. Whether exercise alleviates or exacerbates heat debt during cold exposure depends on the heat transfer coefficient of the environment, mode of activity and exercise intensity. Prolonged exhaustive exercise leading to energy substrate depletion could compromise maintenance of thermal balance in the cold simply by precluding continuation of further exercise and the associated thermogenesis. Hypoglycemia impairs shivering, but this appears to be centrally mediated, rather than a limitation to peripheral energy metabolism. Research is equivocal regarding the importance of muscle glycogen depletion in explaining shivering impairments. Recent research suggests that when acute exercise leads to fatigue without depleting energy stores, vasoconstrictor responses to cold are impaired, thus body heat conservation becomes degraded. Fatigue that was induced by chronic overexertion sustained over many weeks, appeared to delay the onset of shivering until body temperature fell lower than when subjects were rested, as well as impair vasoconstrictor responses. When heavy physical activity is coupled with underfeeding for prolonged periods, the resulting negative energy balance leads to loss of body mass, and the corresponding reduction in tissue insulation, in turn, compromises thermal balance by facilitating conductive transfer of body heat from core to shell. The possibility that impairments in thermoregulatory responses to cold associated with exertional fatigue are mediated by blunted sympathetic nervous responsiveness to cold is suggested by some experimental observations and merits further study.
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PMID:Exertion-induced fatigue and thermoregulation in the cold. 1128 20

Hypoglycemia during exercise is a common event due to an unbalance between training volume, nutrition, and external influences such as chronobiology, temperature or altitude, in subjects characterized by an acute and chronic increase in glucose effectiveness and insulin sensitivity. While it is preventable by adequate pre-exercise feeding with carbohydrates, it can also be induced by a prior carbohydrate meal with high glycemic index. Adequate training induces resistance to hypoglycemia via a shift in the balance of oxidized substrates and marked hormonal adaptations, but overtraining, by partially reversing this adaptation, favorizes hypoglycemia. Exercise hypoglycemia is a cause of fatigue or exercise cessation, but also impairs thermoregulatory adaptation and is assumed to fragilize muscles and tendons for traumatic events.
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PMID:Exercise hypoglycemia in nondiabetic subjects. 1135 74

Carnitine palmityl transferase I is the key enzyme in the carnitine dependent transport of long chain fatty acids across the mitochondrial inner membrane and its deficiency results in a decrease rate of fatty acids beta-oxidation with decreased energy production. We reported a family of 3 affected siblings who are the product of a first degree cousin marriage. The first 2 presented with typical Reye-like syndrome with unconsciousness, hepatomegaly, hypoglycemia, hyperammonemia and very high liver enzymes. Liver biopsy showed steatosis. On screening of the complete family, the 3rd sibling was found to have hepatomegaly. The 3 siblings showed an acyl carnitine profile with very high free carnitine with almost absent long chain acyl carnitines, suggestive of carnitine palmityl transferase I deficiency. This was confirmed by enzyme analyses in fibroblast cultures. These patients were effectively treated with a diet high in carbohydrate, low in long chain fatty acids with medium chain triglycerides. In conclusion, carnitine palmityl transferase I deficiency is an important cause of Reye-like syndrome, which may be treated easily with very good results if detected early in life.
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PMID:Carnitine palmityl transferase I deficiency. 1174 80

Four cases of asthma (one adult, three children) developing acute adrenal crisis after introduction of high-dose inhaled fluticasone proprionate are presented. The three children, aged 7-9 yrs, had been prescribed inhaled fluticasone, dosage 500-2,000 microg x day(-1) and duration 5 months-5 yrs. All presented with convulsions due to hypoglycaemia (blood glucose 1.3-1.8 mM). The fourth case was a male of 33 yrs with difficult-to-control asthma and had been taking fluticasone propionate 1,000-2,000 microg x day(-1) for 3 yrs. He presented with fatigue, lethargy, nausea and postural hypotension. Acute adrenal crisis in each case was confirmed by investigations which included measurement of acute phase cortisol levels, short and long Synacthen stimulation tests and glucagon stimulation tests. Other cases of hypthoalamic-pituitary-adrenal axis suppression were excluded.
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PMID:Acute adrenal crisis in asthmatics treated with high-dose fluticasone propionate. 1210 82

Advanced renal cell carcinoma is a chemoresistant disease. Immunotherapy with alpha interferon or interleukin (IL)-2 has produced response rates of approximately 15%, but better treatments are needed. IL-4 is a cytokine produced by activated CD4+ lymphocytes and has pluripotent activities including inhibiting the in vitro proliferation of human renal cell carcinoma cell lines. In this trial, patients were required to have a histologic diagnosis of renal cell adenocarcinoma with measurable disease and performance status (SWOG) of 0-1. Patients had to have adequate bone marrow, renal, and hepatic function as well as no clinically significant pulmonary or cardiac dysfunction. IL-4 was given by subcutaneous injection at a dose of 5 micorg/kg/d, daily for 28 days followed by a 7-day rest period. Fifty-eight patients were registered with seven patients ineligible and two patients not analyzable because they did not receive treatment. In the 49 eligible and analyzable patients, there were no confirmed complete or partial responses. There was one unconfirmed partial response in retro-caval lymph nodes, but no verifying measurement was done. There were seven patients with stable disease, no response, 25 with increasing disease/progression, and 16 patients whose assessment was inadequate to determine response. The median time to progression was 3 months, and the median survival was 13 months. Toxicity was significant with the most common side effects nausea, vomiting, or diarrhea, followed by headache/pain and malaise/fatigue/lethargy. There were 13 instances of grade 4 toxicity that occurred in nine different patients. Unique toxicities included Bell's palsy in three patients and hypoglycemia in a previously well-controlled diabetic. Despite promising growth inhibitory and immunologic effects, IL-4 in this dose and schedule is not useful for the treatment of patients with disseminated renal cell carcinoma.
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PMID:Phase II trial of recombinant human interleukin-4 in patients with advanced renal cell carcinoma: a southwest oncology group study. 1214 58

Energy for muscular exercise is derived initially from the breakdown of muscle glycogen, and later from circulating glucose released by the liver and from non-esterified fatty acids. Muscle glucose uptake may increase 20-fold. In normal subjects, insulin secretion declines and release of counter-regulatory hormones increases. In type 1 diabetes, glycaemic changes during exercise depend largely on blood insulin levels. In the young diabetic, during insulin deficiency, and therefore in a poor degree of metabolic control, i.e. hyperglycaemic and ketotic, exercise accentuates hyperglycaemia and ketosis, leading to extreme fatigue. If the insulin dosage is too high, the increase in muscular assimilation, combined with the shutdown of liver glucose production, may result in a severe hypoglycaemia. During the recovery period, the repletion of muscular and hepatic glycogen stores may also provoke an hypoglycaemia during hours after the cessation of muscular work. The recommendations for physical activity in type 1 diabetes include: 1) obtain good metabolic control; 2) in the few hours preceding the exercise, ingest complex carbohydrates; 3) in the case of unforeseen physical activity, increase glucose consumption immediately before, during, and after the activity; 4) in the case of foreseen activity, decrease the insulin dose (from 10 to 50%) acting during and even after intense muscular work; 5) do not inject the insulin at a site that will be heavily involved in the muscular activity.
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PMID:[Sports and type I diabetes: personal experience]. 1242 37

Two cases of alcoholics associated with rhabdomyolysis and acute renal failure were reported. Case 1 was a 67-year-old male who had complained of general fatigue and generalized muscle pain. He had drunken and slept outdoor in winter until he was found. Laboratory data on admission showed remarkable elevation of muscle enzymes (AST, LDH, CPK) and serum levels of myoglobin, BUN, and Cr. He was treated with hemodialysis because of acute renal failure caused by rhabdomyolysis and recovered from renal failure. Case 2 was a 50-year-old male who had been unconscious and suffered from muscle weakness. He had drunken and slept in the bed for several days without eating any food until he was found by his sister. Laboratory data on admission showed remarkable elevation of muscle enzymes and serum levels of myoglobin, BUN, and Cr. It also showed hypoglycemia and hyponatremia. He developed into acute renal failure caused by rhabdomyolysis, but had a good clinical course without hemodialysis. The rhabdomyolysis of case 1 might have been caused by alcohol and sleeping outdoor in winter. That of case 2 might have been caused by alcohol and pressure necrosis due to immobility for several days in his bed.
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PMID:[Two cases of alcoholics associated with rhabdomyolysis and acute renal failure]. 1246 66

The aim of the present study was to clarify the effect of carbohydrate (CHO) supplementation on moderate and high-intensity endurance exercise in the heat. Eight endurance-trained men [maximal oxygen uptake ( VO(2max)) 59.5+/-1.6 ml kg(-1) bw(-1), mean+/-SE] cycled to exhaustion twice at 60% VO(2max) and twice at 73% VO(2max) at an ambient temperature of 35 degrees C. Subjects ingested either a 6.4% maltodextrin solution (CHO) or an artificially flavoured and coloured placebo (PLA). Time to fatigue was significantly greater with CHO in both the 60% and 73% VO(2max) trials (14.5% and 13.5% improvement, respectively). Heart rate and oxygen uptake ( VO(2)) did not differ at any point between PLA and CHO. Hypoglycaemia was not seen in any condition but plasma glucose concentrations tended to be higher at both intensities when CHO was fed. CHO oxidation rates were similar at 60% VO(2max) between CHO and PLA. There were no differences between PLA and CHO in the rate of rise of rectal temperatures ( T(rec)) at either intensity but there was a trend for subjects to fatigue at a high temperature when taking CHO. Ratings of perceived exertion (RPE) tended to be lower throughout both CHO trials; this was significant at 80 min and at fatigue at 60% VO(2max). It is concluded that supplementation with CHO improves exercise performance in the heat at both moderate and high endurance intensities. In the absence of a clear metabolic explanation, a central effect involving an increased tolerance of rising deep body temperature merits further investigation.
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PMID:Carbohydrate supplementation improves moderate and high-intensity exercise in the heat. 1273 59

A 56-year-old black woman with diabetes mellitus was admitted for hypoglycemia and confusion. Her past medical history included breast cancer, for which she had undergone a left lumpectomy and then mastectomy for in-breast recurrence. Her oral intake had decreased during the past month because of increasing discomfort from left-sided chest pain. During this period, she continued to take pioglitazone for diabetes at her originally prescribed dose. The patient's mental status improved quickly after taking orange juice and intravenous glucose, but the chest pain persisted. The pain, which was described as an ache along the left costal margin, increased with palpation, deep inspiration, or coughing. She had recently presented with similar complaints at another hospital where she had been prescribed a muscle relaxant that provided no relief from the pain. She also reported a 14-lb weight loss during the previous 3 months, as well as fatigue, weakness, and aches in her legs and arms. She denied fevers, chills, sweats, abdominal pain, nausea, or recent trauma. Laboratory values at the time of admission were: calcium, 11.8 mg/dL; total protein, 11.1 mg/dL; albumin, 3.2 g/dL; creatinine, 1.0 mg/dL; and hematocrit, 29.3%, with a mean corpuscular volume of 89.3. Chest radiography revealed a lytic lesion in the left lateral fourth rib and left humerus (). Serum and urine protein electrophoresis revealed a monoclonal spike in the gamma region consistent with monoclonal gammopathy. The serum spike was quantified at 3.78 g/dL. A skeletal survey showed many small well-defined lytic lesions in the skull (with one 1.5-cm lytic lesion in the upper posterior parietal bone), arms, and legs. A bone scan showed multiple foci of increased uptake in the right and left ribs as well as the proximal portion of the left femur. The peripheral blood smear revealed rouleaux formation () and plasma cells (). What is the diagnosis?
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PMID:Cases from the Osler medical service at Johns Hopkins University. 1275 89


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