Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic sciatic nerve constriction injury (CCI) induces Wallerian degeneration and exaggerated pain-like behaviors. These effects are mediated in large part by pro-inflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha). In this study, we demonstrate that systemically administered recombinant human erythropoietin (rhEpo) facilitates recovery from chronic neuropathic pain associated with CCI in rats. Because TNF-alpha has been implicated in the development of pain-related behaviors, we measured TNF-alpha mRNA at the nerve injury site. Systemically or locally administered rhEpo decreased TNF-alpha mRNA, compared with that observed in untreated animals. RhEpo also significantly (P < 0.05) decreased axonal degeneration. Immunohistochemistry of CCI nerve showed abundant TNF-alpha in Schwann cells, axoplasm and macrophages. In rhEpo-treated animals, TNF-alpha immunopositivity was decreased selectively in Schwann cells. These results suggest a model in which rhEpo counteracts the effects of TNF-alpha in CCI by blocking expression of TNF-alpha in Schwann cells. To further test this model, we studied primary Schwann cell cultures. RhEpo inhibited TNF-alpha expression in response to lipopolysaccharide, supporting the conclusions of our in vivo CCI experiments. In addition, rhEpo directly counteracted Schwann cell death induced by exogenously added TNF-alphain vitro. These results indicated that rhEpo regulates TNF-alpha by multiple mechanisms; rhEpo regulates TNF-alpha mRNA expression by Schwann cells but also may directly counteract TNF-alpha signaling pathways that lead to injury, chronic pain and/or death.
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PMID:Erythropoietin reduces Schwann cell TNF-alpha, Wallerian degeneration and pain-related behaviors after peripheral nerve injury. 1648 43

Cancer-related fatigue (CRF) is either a symptom or a syndrome depending on criteria for diagnosis. CRF is present in 20% to 30% of long-term cancer survivors and 80% to 90% during treatment and at the end of life. Assessment requires determining the presence, severity, and interference with daily activities. Different descriptors for fatigue (eg, tiredness, lack of vigor) measure different patient experiences. Associated factors such as depression, pain, insomnia, dyspnea, anemia, and deconditioning worsen CRF and should be treated if present. Associated factors that contribute to the severity of fatigue differ depending on the stage of cancer. Pharmacologic interventions include recombinant erythropoietin, psychostimulants, corticosteroid, anti-inflammatory drugs other than steroids, and L-carnitine. Advances in the management of CRF will require an understanding of the underlying mechanism before target-specific therapies can be developed.
Curr Pain Headache Rep 2006 Aug
PMID:Management of fatigue in cancer patients. 1683 40

Schwann cells provide trophic support and in some cases, insulation to axons. After injury, Schwann cells undergo phenotypic modulation, acquiring the capacity to proliferate, migrate, and secrete soluble mediators that control Wallerian degeneration and regeneration. Amongst the soluble mediators are pro-inflammatory cytokines that function as chemoattractants but also may sensitize nociceptors. At the same time, Schwann cells produce factors that counterbalance the pro-inflammatory cytokines, including, for example, interleukin-10 and erythropoietin (Epo). Epo and its receptor, EpoR, are up-regulated in Schwann cells after peripheral nerve injury. EpoR-dependent cell signaling may limit production of TNF-alpha by Schwann cells within the first five days after injury. In addition, EpoR-dependent cell signaling may reduce axonal degeneration and facilitate recovery from chronic pain states. Other novel factors that regulate Schwann cell phenotype in nerve injury have been recently identified, including the low-density lipoprotein receptor related protein (LRP-1). Our recent studies indicate that LRP-1 may be essential for Schwann cell survival after peripheral nerve injury. To analyze the function of specific Schwann cell gene products in nerve injury and sensory function, conditional gene deletion and expression experiments in mice have been executed using promoters that are selectively activated in myelinating or non-myelinating Schwann cells. Blocking ErbB receptor-initiated cell-signaling in either myelinating or non-myelinating Schwann cells results in unique sensory dysfunctions. Data obtained in gene-targeted animals suggest that sensory alterations can result from changes in Schwann cell physiology without profound myelin degeneration or axonopathy. Aberrations in Schwann cell biology may lie at the foundation of neuropathic pain and represent an exciting target for therapeutic intervention.
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PMID:Schwann cells: activated peripheral glia and their role in neuropathic pain. 1732 18

Systemic sclerosis (SSc) is frequently complicated by skin ulcers, often unresponsive to traditional treatments. A preliminary evaluation of the effects of recombinant human erythropoietin (rHuEPO) was carried out in 14 patients with SSc with nonhealing, severe cutaneous ulcers. Patients received rHuEPO subcutaneously at a dosage of 150 IU/kg 3 times weekly for 2 weeks, twice weekly for the next 2 weeks, and then once weekly for 1 month. At follow-up 3-6 months from the beginning of the treatment, six patients showed complete resolution of the skin ulcers, while a significant reduction (> 60%) in lesional areas was obtained in the other eight patients (mean +/- SD ulcer area reduced from 27.6 +/- 28 to 5.3 +/- 7.8 cm(2); P<0.005). Moreover, patients' quality of life significantly improved (pain, as measured on visual analogue scale reduced from 96 +/- 5 to 46 +/- 17 points; P=0.0001; disability as measured by the Health Assessment Questionnaire-Disability Index reduced from 1.6 +/- 0.5 to 0.9 +/- 0.4 points; P=0.0001). The rHuEPO may represent a novel treatment of nonhealing scleroderma skin ulcers, suggesting some important aetiopathological implications.
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PMID:Treatment of severe scleroderma skin ulcers with recombinant human erythropoietin. 1739 51

The nephrological department of Copenhagen University Hospital Herlev experienced an epidemic accumulation of patients developing nephrogenic systemic fibrosis in the period 2002-2006. Systematic studies of these patients revealed that they all had a gadodiamide-enhanced magnetic resonance examination prior to their symptoms, and that they all had severe renal insufficiency (chronic kidney disease stage 5) at the time of their exposure to gadodiamide. Besides exposure to gadodiamide, our analyses indicated that increasing cumulative gadodiamide exposure (i.e. repeated exposures), and higher serum concentrations of ionized calcium and phosphate were cofactors that raised the risk of developing nephrogenic systemic fibrosis. Higher cumulative gadodiamide exposure, higher prescribed erythropoietin dosage at exposure, and being hemodialysis patient were three factors associated with nephrogenic systemic fibrosis in its most severe form. Retrospective reviews of patients records and patient interviews revealed the large variability in symptoms and clinical course of nephrogenic systemic fibrosis, but also highlighted that the typical initial symptoms were symmetric swelling, discoloration and pain of lower legs, whereas the typical late symptoms of severely affected patients were skin thickening, stiffness, contractures, and debilitating disabilities. In conclusion, nephrogenic systemic fibrosis is a serious iatrogenic disease of patients with renal insufficiency caused by some Gd-containing contrast agents, in particular gadodiamide. Unfortunately, there is no proven curative treatment. It is therefore essential that future cases of nephrogenic systemic fibrosis are prevented.
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PMID:An epidemic outbreak of nephrogenic systemic fibrosis in a Danish hospital. 1832 59

The quality of life (QoL) of end stage renal disease (ESRD) patients is a frequently overlooked yet critical consideration when evaluating the overall medical care of patients. There are a variety of measures used to assess the QoL of ESRD patients. Some of the more frequently used tools include the single-question QoL questionnaire, the 36 Item Short Form Health Survey (SF-36), and the Kidney Disease Quality of Life (KDQoL) questionnaire. The best intervention to improve the QoL of ESRD patients is renal transplantation. The role of erythropoietin and intensification of dialysis dose in improving patients' QoL is undergoing review. We have previously shown relationships between patients' perception of quality of life and depressive affect, perception of burden of illness (IEQ), social support (MSP), pain and sleep disturbances. Further studies should focus on interventions that modify patients' perceptions of these psychosocial parameters with the goal of improving their QoL. Treatment of depression, pain and sleep disorders holds particular promise in this regard.
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PMID:Quality of life in patients with end-stage renal disease treated with hemodialysis: survival is not enough! 1844 33

Lung cancer is a bad prognostic illness with a limited survival and many side effects related to treatment used. Supportive care in cancer attends to enhance patient care among cancer and treatments suffering. Opioids are one of the most important treatments in the management of dyspnoea and pain. Every new drug in supportive care is tested to diminish side effects of treatment like erythropoietin against anemia or aprepitant against emesis. Many trials are developed to enhance this supportive care especially in lung cancer management.
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PMID:[Role of supportive care in lung cancer]. 1858 94

Neuropathic pain is a complex syndrome resulting from damage to the peripheral nervous system. Central neuroimmune activation contributes to the generation and maintenance of chronic pain after nerve injury. The current study determined the effects of recombinant human erythropoietin (rhEPO) on behavioral hyperalgesia and neuroimmune activation in a rat model of neuropathic pain induced by L5 spinal nerve transection. Animals were randomly assigned into 3 groups: sham-operation with saline; L5 spinal nerve transection with rhEPO (5000 units/kg); or L5 transection with saline. The rhEPO or saline was given ip on the day before surgery and continued daily to day 7 post-transection. The paw pressure threshold and paw withdrawal latencies were measured before surgery and on days 1, 3, and 7 post-operation. Glial activation markers such as macrophage antigen complex-1 (Mac-1, OX-42) and glial fibrillary acidic protein (GFAP), production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-10, as well as nuclear factor-kappa B (NF-kappaB) activation were determined in the lumbar spinal cord. Administration of rhEPO resulted in attenuation of mechanical and thermal hyperalgesia. Furthermore, rhEPO markedly inhibited neuroimmune activation characterized by glial activation, production of proinflammatory cytokines like TNF-alpha, IL-1beta, and NF-kappaB activation, but rhEPO enhanced the level of IL-10. These results support the significance of neuroinflammation and neuroimmune activation in the initiation and persistence of behavioral pain responses. The data indicate that rhEPO attenuates behavioral hyperalgesia and neuroimmune activation in neuropathic pain induced by L5 nerve transection.
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PMID:Recombinant human erythropoietin attenuates spinal neuroimmune activation of neuropathic pain in rats. 1920 47

The early diagnosis of the graft intolerance syndrome or a subclinical state of chronic inflammation due to a failed kidney allograft, is one of the goals that the nephrologists must fulfill to take a series of measures directed to solve this situation. Fever, haematuria, local pain and/or tenderness are the main clinical criteria to make a diagnosis. However, oftenly there are not any clinical symptoms and only the presence of parameters of chronic inflammation (elevated C-reactive protein, erythrocyte sedimentation rate, hypoalbuminemia and anemia resistant to erythropoietin therapy) are signs of this entity. Maintenance of immunosuppressive treatment is not advisable due to the risk of infections as well as the increase in cardiovascular risk (level evidence A). Transplantectomy is the best treatment if there are some associated complications such as allograft infection, neoplasia or high risk of graft rupture. However, surgical treatment is not exempt from risks and it is associated to a considerable rate of complications, with the consequent prolongation of the hospitalization stay. Therefore it is desirable to use less invasive procedures, such as embolization. This could be the first step unless the conditions enumerated in point 3 come up (Level evidence B). It is desirable to use prophylactic antibiotic before the embolization to avoid infectious complications (Level evidence B).
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PMID:[Managing a failed kidney graft. Nephrectomy versus embolisation]. 1967 63

These guidelines propose a treatment algorithm in which patients are evaluated regularly for fatigue using a brief screening instrument, and are treated as indicated by their fatigue level. The algorithm's goal is to identify and treat all patients with fatigue that causes distress or interferes with their daily activities or functioning. Management of fatigue begins with primary oncology team members who perform the initial screening and either provide basic education and counseling or expand the initial screening to a more focused evaluation for moderate or higher levels of fatigue. At this point the patient is assessed for current disease and treatment status, a review of body systems, and an in-depth fatigue evaluation. In addition, the patient is assessed for the presence of seven treatable factors known to contribute to fatigue: pain, emotional distress, sleep disturbance, anemia, alterations in nutrition, deconditioning, and comorbidities. If any of these conditions are present, they should be treated according to practice guidelines, with referral to other care professionals as appropriate, and the patient's fatigue should be reevaluated regularly. If none of the seven factors are present or the fatigue is unresolved, selection of appropriate fatigue management and treatment strategies is considered within the context of the patient's clinical status: receiving active cancer treatment, receiving disease-free long-term follow-up, or receiving care at the end of life. Management of fatigue is cause-specific when conditions known to cause fatigue can be identified and treated. When specific causes, such as infection, fluid and electrolyte imbalances, or cardiac dysfunction, cannot be identified and corrected, nonpharmacologic and pharmacologic treatment of the fatigue should be considered. Nonpharmacologic interventions may include a moderate exercise program to improve functional capacity and activity tolerance, psychosocial programs to manage stress and increase support, restorative therapies to decrease cognitive alterations and improve mood state, and nutritional and sleep interventions for patients with disturbances in eating or sleeping. Pharmacologic therapy may include drugs, such as antidepressants for depression or erythropoietin for anemia. A few clinical reports of the use of psychostimulants suggest the need for further research on these agents as potential treatment modalities in managing fatigue. Effective management of cancer-related fatigue involves an informed and supportive oncology care team that assesses patients' fatigue levels regularly and systematically, educates and counsels patients regarding strategies for coping with fatigue, and uses institutional fatigue management experts for referral of patients with unresolved fatigue.
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PMID:Cancer-related fatigue. Clinical practice guidelines in oncology. 1976 Oct 67


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