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)

Klinefelter's syndrome affects 1 in 500 men across all ethnic groups but the diagnosis is often delayed because of substantial variations in clinical presentation. A 26 year-old male came to observation for chronic fatigue. His laboratory data and radiological examination were negative. Examination showed eunuchoidal body habitus with sparse facial hair, small and firm testes and no gynecomastia. The patient had heterosexual orientation with regular sexual intercourses but diminished libido. Serum gonadotropin concentrations were raised while serum testosterone concentration was low-normal level. Serum PRL concentration and thyroid function were normal. Seminal analysis revealed azoospermia and peripheral lymphocyte karyotyping showed a 47,XXY karyotype, confirming diagnostic suspicion. Patient was given testosterone enanthate 200 mg intramuscularly every 2 weeks. He noted improvements in fatigue and libido and increase of muscle mass. Since the true prevalence of Klinefelter's syndrome is very high, the diagnosis of this disease should be considered in every men with complaints related to hypogonadism (fatigue, weakness, gynecomastia, infertility, erectile dysfunction, small testis and osteoporosis). Testosterone replacement therapy should be started early to minimize the physical and psychological effects of androgen deficiency. There have been recent advances in the options for the treatment of infertility in patients with Klinefelter's syndrome: however findings that this syndrome may be transmitted by the new assisted reproductive techniques is cause for concern.
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PMID:[Klinefelter's syndrome: diagnosis and treatment. Case report]. 1167 82

A 56-year-old man with persistently elevated liver enzyme levels, fatigue, lethargy and a 9.0 kg weight loss over six months underwent a percutaneous liver biopsy that demonstrated multiple granulomas. Screening serologies were positive for histoplasmosis, and he was started on itraconazole treatment. He returned to hospital the same night with coffee-ground emesis and in Addisonian crisis requiring parenteral steroids and intensive care unit support. An abdominal computed tomography scan revealed bilaterally enlarged, nonenhancing adrenal glands suggestive of infarcts, presumed secondary to histoplasmosis. Treatment was initiated with amphotericin B, and Histoplasma capsulatum was cultured from his urine and cerebrospinal fluid. A serum immunodiffusion test was also positive for both H and M bands, indicating active infection with Histoplasmosis species. His serum and urine samples were also weakly positive for the antigen. Despite complications of renal failure, pneumonia and congestive heart failure, he recovered with medical therapy and was discharged home to complete a prolonged course of itraconazole therapy. While hepatic granulomas often reflect an occult disease process, the cause may remain undiscovered in 30% to 50% of patients despite exhaustive investigations. H capsulatum is an uncommon cause of granulomatous liver disease, and with its protean clinical presentation, a high index of suspicion is needed to make the diagnosis and avoid the potentially high fatality rate associated with disseminated infection.
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PMID:A case of Histoplasma capsulatum causing granulomatous liver disease and Addisonian crisis. 1169 4

In this short review of the literature and our own data the characteristics of structural organization of sarcoplasmic reticulum Ca-release channels (ryanodine receptors) in different types of muscles, the participation of other sarcoplasmic reticulum proteins in excitation-contraction coupling and Ca-release channel operation, and the regulation of the channel activity by endogenous low molecular weight compounds are analyzed. Special attention is given to changes that occur in muscle cells during exhausting work and to the role of sarcoplasmic reticulum Ca-release channels in the loss of muscle contractile activity during the development of fatigue. It is concluded that the protection of muscle fibers against fatigue in the presence of the histidine-containing dipeptide carnosine, called in the literature "Severin's phenomenon", is primarily connected with modulation of sarcoplasmic reticulum Ca-release channel activity by carnosine.
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PMID:Molecular mechanisms of regulation of the activity of sarcoplasmic reticulum Ca-release channels (ryanodine receptors), muscle fatigue, and Severin's phenomenon. 1173 34

A 69-year-old man was transferred to our hospital because of severe general fatigue and progressive systemic muscle weakness. He had taken 300 mg/day of cibenzoline for his sustained ventricular tachycardia (VT) for years. At the end of June 2001 he began to feel general fatigue, which slowly progressed to systemic muscle weakness and walking disturbance. On 2nd July 2001, he finally could not stand up by himself. He also felt dyspnea. He was transferred to our emergency room, where he developed severe respiratory depression. Acute myocardial infarction was ruled out based on his ECG and blood chemistry data. Serum BUN and creatinine were elevated to 32 and 2.2 mg/dl, respectively, which returned to normal range 2 weeks later. What we did in our ICU were basically a replacement of cibenzoline with mexiletine and mechanical support of ventilation. As his renal function gradually improved, his spontaneous respiration and muscle power were slowly restored. He was discharged on foot after 1 month of hospitalization. His blood cibenzoline content taken 2 days after the cessation of cibenzoline was 959.6 mg/ml that was abnormally elevated. Considering metabolism and excretion for the 2 days between the cibenzoline cessation and the blood sample drawing, his cibenzoline level on the day of admission must have been extraordinary high. We should be aware of the possibility of abrupt overdosage of cibenzoline even in patients with normal kidney function in the event of a transient or an acute renal dysfunction.
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PMID:A case of severe respiratory depression due to cibenzoline overdosage induced by a transient renal dysfunction. 1185 4

David is a 29-year-old Hispanic male who presents complaining of fatigue, headache, muscle aches, a sore throat, and nausea. Physical assessment demonstrates an erythematous maculopapular rash on the trunk and symmetric adenopathy. His temperature is 37.6 degrees C; other vital signs are within normal limits. Laboratory findings include a white blood cell count of 4.5/microL and a platelet count of 98,000/mm3. Blood chemistry is unremarkable. David states that his symptoms began one week ago.
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PMID:Nursing assessment of the patient with primary HIV infection: key to improving clinical recognition. 1196 24

An unusual cause of upper gastrointestinal bleeding is described in a previously healthy 45-year-old man who was admitted to hospital with weakness and fatigue, and had experienced an episode of melena two days before admission. His medical and surgical history was unremarkable. Upon admission to hospital, he showed evidence of iron-deficiency anemia, with a hemoglobin concentration of 61 g/L (normal range 135 to 175 g/L), a mean corpuscular volume of 73 fL (normal range 85.0 to 95.0 fL) and a ferritin concentration of 1.0 microg/L (normal range in males 15 to 400 microg/L). Upper gastrointestinal endoscopy revealed a 3.5 cm ulcerated submucosal mass in the third portion of the duodenum, for which mucosal biopsies were nondiagnostic. A subsequent endoscopic ultrasound revealed a 2.7 x 4.0 cm hyperechoic, cystic, submucosal tumour in the third portion of the duodenum. Endoscopic ultrasound-guided fine needle aspiration revealed no malignant cells. The patient eventually underwent a resection of the third portion of his duodenum. Surgical pathology revealed that this tumour was a Brunner's gland hamartoma, 4.5 cm in its greatest dimension.
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PMID:Brunner's gland hamartoma: a rare cause of gastrointestinal bleeding -- case report and review of the literature. 1204 80

A 77-year-old man was in good health until he complained of fatigue 3 weeks before presentation. Two weeks before admission, he developed gradually worsening shortness of breath. One week before admission, he developed a cough that initially was nonproductive but later was associated with hemoptysis.His past medical history was remarkable for a history of colon cancer (Dukes' stage III), for which he underwent a hemicolectomy and treatment with adjuvant chemotherapy in 1993. He had a myocardial infarction in 1986 and underwent coronary artery bypass surgery in 1999. He also had a history of hypertension, type 2 diabetes, and gout. He smoked in the past but had stopped more than 30 years ago.He was initially evaluated by his primary care physician, who noted that he complained of diaphoresis but denied fevers, chills, or contact with others who were ill. His physical examination was remarkable for bilateral crackles that were more pronounced on the right. A chest radiograph demonstrated bilateral pulmonary infiltrates (Figure 1). He was treated with amoxicillin. The next day, however, his physician noted that his dyspnea had worsened and that his oxygen saturation on room air was poor. He was therefore admitted for further evaluation. The amoxicillin was discontinued, and he was treated with levofloxacin, followed by ceftriaxone and azithromycin as his pulmonary status continued to deteriorate. He received intravenous diuretic agents, which failed to improve his respiratory status. During the initial phase of hospitalization, he was anemic, with a hematocrit of 21.3%. His serum creatinine level, which had been 1.0 mg/dL in 1999, was now 2.5 mg/dL. Urinalysis was remarkable for the presence of numerous red blood cells. His oxygen requirement increased, and he eventually required a 100% nonrebreather mask. A computed tomographic scan of the chest demonstrated prominent alveolar opacities throughout the right upper, middle, and lower lobes, with similar opacities in the left upper and left lower lobes (Figure 2). An echocardiogram showed an ejection fraction of 50%, as well as mild mitral regurgitation. Serologies were remarkable for an antinuclear antibody titer of 1:320 and a P-antineutrophil cytoplasmic antibody (P-ANCA) titer of greater than 1:320. C-ANCA was negative. Anti-glomerular basement membrane and anti-human immunodeficiency virus antibodies were undetectable.
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PMID:Cases from the medical grand rounds of the Osler Medical Service at Johns Hopkins University. 1207 15

Soshitsu Sen's keynote speech before a symposium on population and the environment is summarized unofficially by the editorial staff. The instability of human thinking is given as the cause for the present destruction of the environment. In a visit to the His Majesty King of Sweden, Sen remarked that stabilizing human minds can be achieved within the tea ceremony through "serving tea heartily, receiving it with gratitude, and offering it to another." In this way, the spirit of concern for others can be practiced in everyday life and tranquility of mind reached. News broadcasts of starving parents and children as victims of civil war are disheartening. The Japanese people are not suffering such hunger, even though the economy has not been as robust as desired. The analogy is provided in the story by Chuang Chou about King Hun Dun and King Xiu and man's good intentions, which nonetheless destroy the earth. Japan has experienced forest and environmental destruction on the road to economic prosperity and satisfaction of self-interests. The advice on living in accord with nature is to appreciate each season for its own changes. For example, when it is the winter season, the complaint is about the cold and the desire is for spring; but when spring comes, the desire is for the cooler weather of fall. the ordinary way is to appreciate all seasons and is the best way of sustaining a healthy environment. In the garden of the tea hut, humans enter without their worldly title, position, and means; at the water basin, hands and mouth are cleansed, and entrance is made through a small hole into the hut much the same as emerging from the womb. Worldly matters are dispensed with and purity of thought is shared in the sharing of the bowl of green tea, saying "after you" to one another. Christianity and the Way of Tea share the same symbols of purification. The black tea bowl is in harmony with the green tea. Fatigue is relieved when gazing upon the color green; examples are given. The spirit of the Way of Tea is described as based on the principles of harmony, respect, purity, and tranquility by Sen Rikyu.
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PMID:Sharing a bowl of tea. 1228 76

Amyloid beta-peptide [Abeta(1-42)] is central to the pathogenesis of Alzheimer's disease (AD), and the AD brain is under intense oxidative stress, including membrane lipid peroxidation. Abeta(1-42) causes oxidative stress in and neurotoxicity to neurons in mechanisms that are inhibited by Vitamin E and involve the single methionine residue of this peptide. In particular, Abeta induces lipid peroxidation in ways that are inhibited by free radical antioxidants. Two reactive products of lipid peroxidation are the alkenals, 4-hydroxynonenal (HNE) and 2-propenal (acrolein). These alkenals covalently bind to synaptosomal protein cysteine, histidine, and lysine residues by Michael addition to change protein conformation and function. HNE or acrolein binding to proteins introduces a carbonyl to the protein, making the protein oxidatively modified as a consequence of lipid peroxidation. Immunoprecipitation of proteins from AD and control brain, obtained no longer than 4h PMI, showed selective proteins are oxidatively modified in the AD brain. Creatine kinase (CK) and beta-actin have increased carbonyl groups, and Glt-1, a glutamate transporter, has increased binding of HNE in AD. Abeta(1-42) addition to synaptosomes also results in HNE binding to Glt-1, thereby coupling increased Abeta(1-42) in AD brain to increased lipid peroxidation and its sequelae and possibly explaining the mechanism of glutamate transport inhibition known in AD brain. Abeta also inhibits CK. Implications of these findings relate to decreased energy utilization, altered assembly of cytoskeletal proteins, and increased excitotoxicity to neurons by glutamate, all reported for AD. The epsilon-4 allele of the lipid carrier protein apolipoprotein E (APOE) allele is a risk factor for AD. Synaptosomes from APOE knock-out mice are more vulnerable to Abeta-induced oxidative stress (protein oxidation, lipid peroxidation, and ROS generation) than are those from wild-type mice. Further, synaptosomes from allele-specific APOE knock-in mice have tiered vulnerability to Abeta(1-42)-induced oxidative stress, with APOE4 more vulnerable to Abeta(1-42) than are those from APOE2 or APOE3 mice. These results are consistent with the notion of a coupling of the oxidative environment in AD brain and increased risk of developing this disorder. Taken together, the findings from in-vitro studies of lipid peroxidation induced by Abeta(1-42) and postmortem studies of lipid peroxidation (and its sequelae) in AD brain may help explain the APOE allele-related risk for AD, some of the functional and structural alterations in AD brain, and strongly support a causative role of Abeta(1-42)-induced oxidative stress in AD neurodegeneration.
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PMID:Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer's disease brain contribute to neuronal death. 1239 66

A case of a renal transplant recipient with colchicine-induced myopathy is presented. He was on colchicine therapy for 10 months. He was hospitalized for investigation of fatigue, severe myalgia in the lower extremities and elevated serum aminotransferase levels. His viral markers and other factors that may cause myalgia and that may increase the serum aminotransferase levels were either normal or negative. Creatine phosphokinase (CK) levels were normal. Electrophysiological findings indicated myopathy and muscle biopsy was consistent with vacuolar myopathy. After withdrawal of colchicine, the symptoms disappeared gradually and serum aminotransferase levels were normalized. We suggest that colchicine myopathy should be taken into account in patients who have been on colchicine therapy and had unexplained myalgia as well as elevated aminotransferase levels even with normal CK levels.
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PMID:Colchicine-induced myopathy with normal creatine phosphokinase level in a renal transplant patient. 1239 40


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