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)

We report a case of bone pain associated with primary hyperparathyroidism in a patient with sickle cell disease. A 17-year-old girl with sickle cell disease (SS phenotype) was seen for bilateral knee and back pain. She had had recurrent severe vaso-occlusive crises and acute chest syndrome in the course of her disease. In the last 2 years, she had frequent visits to the emergency department for severe bone pain. She complained of long-standing fatigue and lethargy. Her physical examination was normal. Hydroxyurea treatment, as well as and long- and short-acting narcotics were given, with little improvement in symptoms. Poor compliance with medication, family dysfunction, and potential narcotic addiction were felt to be significant contributors to the patient's symptoms. She was incidentally found to have an extremely elevated total calcium level of 3.19 mmol/L (range: 2.25-2.76) with an ionized calcium level of 1.9 mmol/L (range: 1.15-1.35). Phosphorus level was 0.82 mmol/L (range: 0.90-1.50), alkaline phosphatase level was elevated at 519 U/L (range: 10-170), and parathyroid hormone level was extremely high at 1645 pg/mL (range: 10-60). Her renal function was normal. Ultrasonography of the neck and a Sestamibi scan revealed a single left inferior parathyroid adenoma adjacent to the thyroid lobe. There was no evidence of an underlying multiple endocrine neoplasia. The patient was diagnosed with primary hyperparathyroidism. Fluid hydration, hydrocortisone, calcitonin, and bisphosphonates were initiated for acute hypercalcemia management before surgical excision of the left parathyroid adenoma. On review of previous blood work, a borderline calcium level of 2.72 was present 18 months before this admission. Two years postsurgery, she has normal renal function, calcium, and parathyroid hormone levels. The weekly visits to the emergency department for pain episodes decreased to 1 every 2 months within the first few months after her surgery. The decrease in pain episodes, even if it coincided with the treatment of primary hyperparathyroidism, may still reflect the natural evolution of sickle cell disease in this patient. However, the high morbidity associated with primary hyperparathyroidism was successfully prevented in this patient. Primary hyperparathyroidism is rare in childhood. In a recent study, it occurred more commonly in female adolescents and was because of a single adenoma, as in our patient. Significant morbidity, mainly secondary to renal dysfunction, was because of the delay in diagnosis after the onset of symptoms (2.0-4.2 years), emphasizing the need for a rapid diagnosis. Sickle cell disease affects approximately 1 of every 600 blacks in North America. Acute episodes of severe vaso-occlusive crisis account for > 90% of sickle cell-related hospitalizations and are a significant cause of morbidity in patients. There is no known association between sickle cell disease and primary hyperparathyroidism, and this case is most probably a random occurrence. However, as emphasized by this case report, pain may also be a harbinger of other disease processes in sickle cell disease. Because management may vary, we suggest that care providers consider the diagnosis of vaso-occlusive crisis as the diagnosis of exclusion and that other etiologies for pain be envisaged in this patient population, especially in the presence of prolonged pain or unusual clinical, radiologic, or biological findings.
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PMID:Primary hyperparathyroidism mimicking vaso-occlusive crises in sickle cell disease. 1688 90

The muscle metabolism of at-rest patients with varying degrees of postpolio residual paralysis (PPRP) was studied and compared with that of controls using in vivo phosphorus magnetic resonance spectroscopy. The phosphocreatine (PCr)/inorganic phosphate (Pi) and PCr/adenosine triphosphate ratios were lower in patients than in controls. Reduction in PCr/Pi suggests abnormalities in oxidative phosphorylation. A significant increase was observed in the phosphomonoester/PCr ratio in patients, indicating the accumulation of intermediary compounds of the glycolytic pathway. Furthermore, the phosphodiester/PCr ratio was also significantly increased in patients. In general, the observed changes in metabolite ratios were found to be related to the degree of residual paralysis, suggesting that metabolic changes are secondary to chronic neurogenic processes. These metabolic alterations appear to be the possible cause of energy deficit and underlying muscle fatigue in PPRP patients. The present results provide an insight into the metabolic impairment and degree of muscle damage in patients with PPRP.
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PMID:In vivo (31)P MRS study of skeletal muscle metabolism in patients with postpolio residual paralysis. 1727 21

Mesalazine is a first-line drug in pediatric inflammatory bowel disease, and is effective as primary treatment and maintenance therapy. It's usually well tolerated, but various side effects have been described. A 15-year-old female with ulcerative colitis developed polyuria, polydipsia, vomiting, and fatigue. She was receiving mesalazine (500 mg, thrice daily, p.o.) and prednisolone for 4 months. She was detected as acute tubular injury as she had dehydration, acidosis, hypostenuria, hematuria, proteinuria, low levels of potassium, uric acid and bicarbonate. These findings were attributed to interstitial nephritis as a side effect of mesalazine, however as renal biopsy was disapproved by the parents, it was not confirmed. After discontinuation of mesalazine her renal tubular functions improved. Potassium and phosphorus supplements were stopped after 7 months, although she had to continue bicarbonate supplementation. We conclude that regular renal screening is important in patients receiving 5-ASA therapy to prevent rare but serious complications, such as interstitial nephritis sometimes leading to chronic renal failure.
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PMID:Acute tubular injury associated with mesalazine therapy in an adolescent girl with inflammatory bowel disease. 1740 67

Rhodiola rosea is an herbal supplement purported to improve resistance to stressors and to enhance physical performance, potentially by improving adenosine triphosphate (ATP) turnover. Phosphocreatine (PCr) kinetics serves as a reflection of ATP turnover. The purpose of this investigation was to examine the effect of R rosea ingestion on human skeletal muscle PCr recovery after exhaustive exercise. Twelve resistance-trained men, aged 19 to 39 years, completed incremental forearm wrist flexion exercise to volitional fatigue, once after ingesting 1500 mg R rosea per day for 4 days, and once after ingesting an equivalent placebo dose. During exercise and recovery from exercise, muscle phosphates were examined using phosphorus 31 nuclear magnetic resonance spectroscopy. [PCr] during recovery was fit with a monoexponential function, and the resulting rate constants (k) were compared between groups. Rating of perceived exertion per stage and time to exhaustion were also compared between groups. For R rosea, k=0.3744+/-0.1532, whereas for placebo, k=0.3956+/-0.2238. Although rating of perceived exertion significantly increased within groups as workload increased, it did not differ between conditions, nor did time to exhaustion (R rosea, 10.71+/-0.54 minutes; placebo, 10.48+/-0.68 minutes). Estimates of [PCr] at time 0, 5, 10, 15, and 20 minutes of recovery were nearly identical between groups. In summary, there were no significant differences between groups for any of theparameters measured. Based on these results, we conclude that R rosea ingestion does not improve ATP turnover during or immediately after exercise.
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PMID:Failure of Rhodiola rosea to alter skeletal muscle phosphate kinetics in trained men. 1761 58

This investigation was designed to examine whether short-term administration of sex hormones could produce changes in contractile properties and the sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) function in genioglossal muscle (GG) of aged male rats. Twenty-four aged male rats were randomly divided into three groups to receive an intramuscular injection of either 0.1mg/kg oestrogen (group A), 2.5 mg/kg testosterone (group B), or 0.2 ml sterile peanut oil (group C, control), twice a week, during 4 weeks. After hormone treatment, in vivo isometric contractile properties were determined using surgically prepared GG muscles with platinum electrodes for stimulation of the medial branch of the hypoglossus nerve. Sarcoplasmic reticulum Ca(2+)-ATPase activity was measured in muscle homogenates by detecting the amount of inorganic phosphorus ion released in a standard coupled enzyme assay. SERCA1 mRNA level was observed using a real-time quantitative reverse transcription-polymerase chain reaction (Q-RT-PCR). It was found that, compared with group C, testosterone treatment decreased the fatigue resistance in GG muscles (p<.05), whereas no change was observed in the isometric twitch (P(t)) and tetanic tension (P(0)) (p>.05). By contrast, in oestrogen treated GG muscles, no significant modification was found either in the contractile or in endurance properties (p>.05). The change in GG fatigue resistance of group B was associated with a marked decrease in SR Ca(2+)-ATPase activity when compared with that of the control group (p<.01). Furthermore, SERCA1 mRNA level was also down regulated in group B (p<.05). No prominent differences in SR Ca(2+)-ATPase activity and SERCA1 mRNA expression existed between group A and group C (p>.05). The present results show that exogenous testosterone produces more pronounced changes in GG muscle fatigue resistance than oestrogen does by acting at SR Ca(2+)-ATPase activity and SERCA gene expression.
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PMID:Effects of sex hormones on genioglossal muscle contractility and SR Ca2+-ATPase activity in aged rat. 1807 Jun 14

Long-distance flights can cause a number of clinical problems in both passengers and crewmembers. Jet lag as well as mild hypoxia resulting from incomplete cabin pressurization could contribute to these problems. The objective of this study was to assess, using a chronobiological approach, the clinical impact of diurnal hypobaric, hypoxic exposure on fatigue and other common symptoms encountered during high-altitude exposure and to measure changes in blood chemistry (i.e., plasma creatinine, urea, uric acid, sodium, calcium, phosphorus, glycemia, and lipids). Fourteen healthy, diurnally active (from 07:00 to 23:00 h) male volunteers, aged 23 to 39 yrs, spent 8.5 h in a hypobaric chamber (08:00 to 16:30 h), at a simulated altitude of 8,000 ft (2,438 m). This was followed by an additional 8.5 h of study four weeks later at a simulated altitude of 12,000 ft (3,658 m). Clinical data were collected every 2 h between 08:00 and 18:00 h, and biological variables were assayed every 2 h over two (control and hypoxic-exposure) 24 h cycles. Clinical symptoms were more frequent with the 12,000 ft exposure. Wide interindividual variability was observed in the clinical tolerance to prolonged hypobaric hypoxia. The 24 h profiles of most biochemical variables were significantly altered at each altitude, with changes in mean plasma levels and a tendency toward phase delay, except for uric acid, which showed a phase advance. Changes in appetite mainly occurred with the simulated 12,000 ft exposure and may have been associated with changes in the postprandial glycemia profile. Finally, though the observed biochemical changes were significant, their clinical relevance must be clarified in studies involving actual long-distance flights.
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PMID:Impact of hypobaric hypoxia in pressurized cabins of simulated long-distance flights on the 24 h patterns of biological variables, fatigue, and clinical status. 1807 4

Tumor-induced osteomalacia is a rare acquired metabolic disorder characterized by hypophosphatemia and inappropriately low serum levels of 1,25-dihydroxyvitamin D. Symptoms include chronic muscle and bone pain, weakness, and fatigue in association with a high risk of fragility fractures due to osteomalacia. The diagnosis is commonly delayed for years due to the nonspecific nature of the presenting symptoms, failure to include determination of serum phosphorus levels in blood chemistry testing, and difficulty in identifying the responsible tumor. The pathogenesis of tumor-induced osteomalacia involves tumor expression of fibroblast growth factor 23, a hormone that inhibits proximal renal tubular reabsorption of phosphate and down-regulates renal conversion of 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D. The metabolic abnormalities may be partially or completely corrected with phosphate supplementation and calcitriol. A definitive diagnosis and treatment require excision of the responsible tumor.
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PMID:Tumor-induced osteomalacia: lessons learned. 1831 10

The aim of the present study was to compare the oxidative capacity of the forearm flexor muscles in vivo between children and adults using 31-phosphorus magnetic resonance spectroscopy. Seven boys (11.7 +/- 0.6 y) and 10 men (35.6 +/- 7.8 year) volunteered to perform a 3 min dynamic finger flexions exercise against a standardized weight (15% of the maximal voluntary contraction). Muscle oxidative capacity was quantified on the basis of phosphocreatine (PCr) post-exercise recovery kinetics analysis. End-of-exercise pH was not significantly different between children and adults (6.6 +/- 0.2 vs. 6.5 +/- 0.2), indicating that indices of PCr recovery kinetics can be reliably compared. The rate constant of PCr recovery (kPCr) and the maximum rate of aerobic ATP production were about 2-fold higher in young boys than in men (kPCr: 1.7 +/- 1.2 vs. 0.7 +/- 0.2 min(-1); Vmax: 49.7 +/- 24.6 vs. 29.4 +/- 7.9 mmol.L(-1).min(-1), p < 0.05). Our results clearly illustrate a greater mitochondrial oxidative capacity in the forearm flexor muscles of young children. This larger ATP regeneration capacity through aerobic mechanisms in children could be one of the factors accounting for their greater resistance to fatigue during high-intensity intermittent exercise.
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PMID:Comparative analysis of skeletal muscle oxidative capacity in children and adults: a 31P-MRS study. 1864 15

Although citrulline malate (CM; CAS 54940-97-5, Stimol) is used against fatigue states, its anti-asthenic effect remains poorly documented. The objective of this double-blind study was to evaluate the effect of oral ingestion of CM on a rat model of asthenia, using in situ (31)Phosphorus magnetic resonance spectroscopy ((31)P-MRS). Muscle weakness was induced by intraperitoneal injections of Klebsiella pneumoniae endotoxin (lipopolysaccharides at 3 mg/kg) at t(0) and t(0)+24 h. For each animal, muscle function was investigated strictly non-invasively before (t(0)-24 h) and during (t(0)+48 h) endotoxemia, through a standardized rest-stimulation-recovery protocol. The transcutaneous electrical stimulation protocol consisted of 5.7 min of repeated isometric contractions at a frequency of 3.3 Hz, and force production was measured with an ergometer. CM supplementation in endotoxemic animals prevented the basal phosphocreatine/ATP ratio reduction and normalized the intracellular pH (pH(i)) time-course during muscular activity as a sign of an effect at the muscle energetics level. In addition, CM treatment avoided the endotoxemia-induced decline in developed force. These results demonstrate the efficiency of CM for limiting skeletal muscle dysfunction in rats treated with bacterial endotoxin.
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PMID:Beneficial effects of citrulline malate on skeletal muscle function in endotoxemic rat. 1903 44

This report describes the clinical and biologic data and bone density measurements in 19 adults seen in a rheumatology department, with phosphate diabetes defined by low serum phosphate levels and decreased tubular reabsorption of phosphate in the absence of known etiology. There were 14 males and 5 females with a mean age at disease onset of 36.7 years (20-68 years) and at diagnosis of 43.9 years (24-70 years). Axial pain was present in 17 patients (90%), radicular pain in 13 patients (68%), pain at night in 14 patients (74%), fatigue in 7 patients (37%), myalgia in 6 patients (32%), fracture in 6 patients (32%), renal colic in 4 patients (21%) and depression 10 patients (53%). Mean serum phosphorus was 2.25 mg/dL (1.08-2.76); maximum tubular reabsorption of phosphate/glomerular filtration rate was 0.58 (0.4-0.76) (n > 0.77). Calcium/creatinine > 0.48 was seen in 9 patients (47%), indicating an associated hypercalciuria. Serum calcium, sodium, magnesium, creatinine, cortisol, T3, T4, thyroid-stimulating hormone (TSH), 25 and 1,25 OH2 vitamin D3 were normal. Glucose and amino acid were absent from urine. Bone mineral density at L2-L4 level (Z-score) was -2.13 (-0.9 to -4.25), and at the femoral neck was -1.34(-1.5 to -3.2). Bone biopsy in 5 patients showed osteoporosis with minor osteoid deposition.Idiopathic phosphorus diabetes (IPD) is a rheumatic disease with chronic axial pain at night, radiculitis-like symptoms, fatigue and depression. In half of the patients, IPD is associated with hypercalciuria. Bone mineral density at L2-L4 and femoral neck level is low. Bone biopsies show osteoporosis. Chronic pain, fatigue and depression resulting from IPD may be improved by treatment with oral calcitriol and phosphorus. There might be a delay in improvement of a few months, even if the blood phosphate level is normalized. A 3% increase in bone mineral density could be measured at 6-month intervals when blood phosphate was maintained. This disease is often misdiagnosed when the maximal reabsorption rate of phosphorus is not calculated.
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PMID:Adult onset idiopathic phosphate diabetes. 1907 33


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