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)

Fifty-seven patients with biopsy-proven sarcoidosis causing limb neuropathy were reviewed in order to delineate the characteristic symptoms, impairments, disability, course, outcome and response to corticosteroid treatment of limb sarcoid neuropathy. Typically the neuropathy had a definite date of symptomatic onset. Prominent were positive neuropathic sensory symptoms (P-NSS), especially pain, overshadowing weakness and sensory loss. P-NSS were the main cause of disability. Almost always the pattern was asymmetric and not length-dependent (unlike distal polyneuropathy). We inferred (from kind and distribution of symptoms, signs and electrophysiologic and other test results) that the pathologic process was focal or multifocal, involving most classes of nerve fibers and variable levels of proximal to distal levels of roots and peripheral nerves. Additional features aiding in diagnosis were: systemic symptoms such as fatigue, malaise, arthralgia, fever and weight loss; involvement of multiple tissues (i.e. skin, lymph nodes and eye); the patterns of neuropathy; MRI features; and ultimately tissue diagnosis. Axonal degeneration predominated, although an acquired demyelinating process was observed in 3 patients. For most cases, the disease had a chronic, monophasic course. MRI studies done in later years of affected neural structures were helpful in identifying leptomeningeal thickening, hilar adenopathy; and enlargement and T2 enhancement of nerve roots, plexuses, and limb nerves. Corticosteroid treatment appeared to ameliorate symptoms more than impairments. Several variables were associated with neuropathic improvement: CSF pleocytosis, short duration between symptom onset and treatment, and a higher grade of disability at first evaluation-a possible rationale for future earlier diagnosis and treatment.
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PMID:The natural history and long-term outcome of 57 limb sarcoidosis neuropathy cases. 1652 95

Celiac disease is a gastrointestinal disorder characterized by inflammation, leading to injury to the mucosal lining of the small intestine. The inflammation occurs when gliadin, a protein found in such gluten-containing foods as wheat, rye, and barley, is ingested by genetically susceptible individuals. The mucosal damage and subsequent malabsorption of nutrients leads to various complications. Researchers estimate that more than 2 million people in the United States have celiac disease-a prevalence that is greater than was previously believed. Approximately 60,000 Americans are diagnosed annually with celiac disease. Until recently, diagnosis has been complicated by the fact that the indicators of celiac disease are nonspecific. However, because of the development of new, easy-to-administer serology tests, diagnosis has become much less complicated. After conducting a review of the literature, the authors recommend a serologic testing sequence for diagnosis of celiac disease and urge that adults and children with an assortment of symptoms be tested for this disease. Common signs and symptoms of celiac disease include anemia, arthralgia, fatigue, infertility, neuropathy, and weight loss, in addition to such gastrointestinal symptomatology as abdominal pain, anorexia, bloating, constipation, and diarrhea. The only treatment for patients with celiac disease remains a gluten-free diet.
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PMID:New strategies for diagnosis and management of celiac disease. 1658 82

Anemia is more common in patients with diabetes than without diabetes, and the problem is magnified in patients with renal impairment. Diabetic patients with anemia may be at increased risk of adverse outcomes from diabetic retinopathy, nephropathy, neuropathy, and cardiovascular disease. The etiology of anemia in diabetes is multifactorial and includes inflammation, nutritional deficiencies, concomitant autoimmune diseases, drugs, and hormonal changes in addition to kidney disease. Anemia that is associated with erythropoietin deficiency may have prognostic significance for persons with nephropathy or heart failure. In early diabetic nephropathy, damage to the peritubular fibroblasts can occur and lead to erythropoietin deficiency and anemia prior to the loss of filtration. Correction of the anemia not only leads to less fatigue, greater exercise tolerance, and an improved quality of life but also to a reduction in mortality and hospital admissions for congestive heart failure (CHF). Data are accumulating that suggest that treatment of anemia will slow the progression of microvascular and macrovascular complications, including postural hypotension from autonomic neuropathy, retinopathy, and loss of renal function from diabetic nephropathy. Promptly diagnosing and treating anemia in patients with diabetes may result in an improved quality of life and decreased morbidity and mortality.
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PMID:Anemia and the role of erythropoietin in diabetes. 1679 79

Ixabepilone is a new class of non-taxane microtubule-stabilizing agents. These agents bind tubulin, stabilize microtubules and, thus, block mitosis and result in cell death (1-8). In phase I studies, neutropenia was the only grade 4 toxicity while fatigue, anorexia and mucositis occurred as grade 3 toxicities. Neuropathy, myalgia, arthralgia, alopecia and gastro-intestginal toxicities also occurred at grades 1 and 2. No dermatological effects have been documented to date. Here, a case is reported of a 62-year-old woman with stage 4 breast cancer being treated with Ixabepilone (40 mg/m2) who developed a dermatological reaction not previously described as a toxicity from Ixabepilone therapy.
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PMID:Dermatological toxicity of ixabepilone. 1682 2

Patients with chronic renal failure (CRF) often have signs and symptoms related to fluid and electrolyte disturbances, anemia, malnutrition, bone disease, and gastrointestinal problems. Vascular and neurologic impairment in particular remain an important source of morbidity and mortality in this vulnerable patient population. Sagliker syndrome is a novel syndrome that was recently described in 2004 in patients with CRF and severe and late secondary hyperparathyroidism who suffered from severe skull and facial bone changes, particularly from uglifying human face appearances and neuropsychiatric disorders. The goal of this study was to assess neuropsychiatric manifestations occurring in CRF patients with Sagliker syndrome. Four female and 8 male patients with CRF on regular dialysis at the hemodialysis units of the Internal Medicine Departments around southern Turkey participated in the study. All patients underwent a clinical neurologic examination performed by the same neurologist. Neuropsychiatric signs and symptoms were found in all cases. The results showed that the most frequent neurologic manifestations in CRF patients with Sagliker syndrome were headache, polyneuropathy, cranial neuropathy, fatigue, and psychiatric disorders.
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PMID:Neurologic manifestations in Sagliker syndrome: uglifying human face appearance in severe and late secondary hyperparathyroidism in chronic renal failure patients. 1682 26

Postural control is a common mechanism to compensate for unexpected displacements of the body. In the older population, a slip or fall due to a failure of postural control is a common cause of morbidity and mortality. The ability of postural control decreases with aging or neuropathy. In this study, 2 groups, diabetics and non-diabetics in the older population, were compared to determine how patterns of postural sway during quiet standing were related to the detection of perturbation. The SLIP-FALLS system was applied to the measurement of sway and detection of perturbation. In phase 1 of the development of the predictive model, neural network algorithms were applied to find determinant variables for perturbation detection. In phase 2, a fuzzy logic inference system was developed to investigate the relationship between sway and perturbation detection. Results of this study may be applied to the design of floor mats or shoe insoles for preventing fatigue in workplaces.
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PMID:Effects of diabetic neuropathy on body sway and slip perturbation detection in older population. 1698 84

There is no treatment for Charcot-Marie-Tooth disease 1A (CMT1A), but ascorbic acid (AA) is efficacious in the transgenic mouse model. Thus, a clinical trial of AA in CMT1A is warranted. The CMT-TRIAAL is a phase III randomized, double-blind, placebo-controlled study involving 222 CMT1A adults from eight Italian centers. Eligible for the study are symptomatic adults with genetically confirmed CMT1A. Treatment consists of 2-year oral AA (1500mg/day) or placebo. The primary trial endpoint is an improvement in CMT Neuropathy Score. Secondary efficacy endpoints are changes in distal arm and leg maximum voluntary isometric contraction; 10m timed walking; 9-hole-peg test; overall neuropathy limitations scale; pain and fatigue visual analog scales; health-related quality of life (SF-36); and electrophysiology. Clinical-electrophysiological assessments are performed at baseline and every 6 months thereafter. In consenting patients from three centers, skin biopsy is performed to evaluate PMP22 expression. The study will last 34 months, starting from March 2006.
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PMID:A multicenter, randomized, double-blind, placebo-controlled trial of long-term ascorbic acid treatment in Charcot-Marie-Tooth disease type 1A (CMT-TRIAAL): the study protocol [EudraCT no.: 2006-000032-27]. 1702 75

Extrahepatic manifestations of liver diseases especially the hepatitis B virus (HBV)-infection and hepatitis C virus (HCV)-infection may occur during acute and/or chronic viral hepatitis. Besides a serum like illness with fever, arthralgia and urticaria, haematological disorders with transient bone marrow suppression and cryoglobulinemia have been described. Vasculitis is a rare complication of viral hepatitis. However, HCV can trigger a cryoglobulinemic vasculitis and may clinically present with purpura, arthritis, neuropathy, glomerulonephritis and fatigue. Panarteritis nodosa is frequently associated with HBV infection, which is caused by deposits of immune complexes in the arterial wall. Therapy of both types of vasculitis depends on the severity of disease and may include immunosuppressive agents as well as antivirals.
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PMID:[Vasculitis and liver disease]. 1704 14

Numerous clinical forms of CIDP have been described, but pain is generally considered a rare or secondary sign. We describe here the clinical, electrophysiological and neuropathological characteristics of five patients with CIDP and pain as the main presenting symptom, and their course with treatment. Between January 2003 and December 2004, we selected five patients with prominent or isolated pain among 27 patients diagnosed with CIDP. All patients were subjected to clinical and electrophysiological examinations, and had a complete laboratory work up to exclude other causes of neuropathy. In view of the atypical clinical presentation, all five patients underwent nerve biopsy. There were two men and three women. The mean age at onset of neuropathy was 70+/-7.39 years. All patients initially presented with pain in the lower limbs associated with modest motor impairment (1 case), distal paresthesia (4 cases), cramps (1 case) and fatigue (2 cases). CSF was normal in three cases. On electrophysiological examination, three patients had nerve conduction abnormalities with subtle or clear signs of demyelination: three (case 1, 2 and 4) fulfilled the criteria of Rotta et al. and two (case 2 and 4) the criteria of both Nicolas et al and the INCAT group. Patients were all given symptomatic treatment and four patients received an immunomodulatory treatment, which was constantly effective. Pain may be a major and disabling symptom in patients with CIDP, so this diagnosis has to be considered in patients referred for a painful polyneuropathy. Moreover, immunomodulatory treatment has to be considered in such patients as symptomatic therapy may be ineffective.
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PMID:Pain as the presenting symptom of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). 1728 85

There is insufficient evidence to support the use of exercise in the management of chronic disablement in people with inflammatory peripheral neuropathy. Therefore, our study aimed to determine the feasibility and effectiveness of a physiotherapist prescribed community based exercise programme for reducing chronic disablement in patients with stable motor neuropathy. We assessed the effects of a 12 week unsupervised, community based strengthening, aerobic and functional exercise programme on activity limitation and other measures of functioning in 16 people with stable motor neuropathy and 10 healthy control subjects. Fourteen of 16 patients and 8 out of 10 healthy control subjects completed the study and exercised safely in the community with no adverse events. Significant improvements were seen in all measures of activity limitation and in wider measures of health including anxiety, depression and fatigue in the patient group. Improvements were sustained at six months after completion of the exercise programme, except for depression. Ten patients continued to exercise regularly at six months. These findings demonstrate that individually prescribed community based exercise is feasible and acceptable for people with stable motor neuropathy and participation in exercise may be successful in reducing chronic disablement. Future randomised controlled trials are needed to examine the efficacy of this complex community based intervention.
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PMID:A prospective study of physiotherapist prescribed community based exercise in inflammatory peripheral neuropathy. 1733 56


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