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One important side effect from alpha interferon is depression of bone marrow function and studies have shown that patients with carcinoid tumours treated with alpha interferon suffers from fatigue and impaired physical functions. The aim of this pilot study was to investigate if treatment with erythropoietin (EPO) could have a positive effect on self-rated quality of life (QoL). Eighteen patients with midgut carcinoid treated with alpha interferon were included in the study. There were statistical significant increases in haemoglobin (Hb) levels between baseline and 4 months, between baseline and 8 months as well as between baseline and 2-year follow-up. No EPO related side effects were reported. There were improvements of more than 10 points in self-rated QoL-issues related to anaemia. Even though the analysis did not reveal any statistically significant relation between the observed increase in Hb levels and self-rated QoL, this pilot study has increased the knowledge about benefits, doses and frequency of EPO treatment in patients with midgut carcinoid suffering from interferon related anaemia.
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PMID:Anemia in patients with midgut carcinoid, treated with alpha interferon: effects by erythropoietin treatment on the perceived quality of life. 1830 58

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

Darbepoetin alpha (DA), a long-acting erythropoietin derivative stimulating erythropoiesis, can, by antiapoptotic effects, mitigate myocardial I/R injury. We tested the hypothesis that DA treatment improves left ventricular function (LV) in LPS evoked cardiomyopathy and alters gene expression of apoptosis-regulating proteins (Bcl-XL, Bcl-2, Bax, and Bcl-Xs) and TNF-alpha. In a prospective, controlled, randomized study in Lewis rats (n = 56; 8 groups), myocardial depression was evoked by LPS administration (serotype O127:B8; 10 mg/kg, i.p.). Darbepoetin alpha or vehicle was injected either 24 h before (pretreatment) or 2 h after LPS injection (treatment). Hearts were isolated 8 h after LPS injection, perfused (Krebs-Henseleit solution) in a Langendorff apparatus, and LV developed pressure and its derivatives were measured. For gene expression analysis, real-time polymerase chain reaction of LV specimen was performed. LPS decreased LV developed pressure (-64.6 +/- 7.9 mmHg) and its derivates by more than 60% in comparison to vehicle (P < 0,01), but this effect was not attenuated by DA pretreatment or DA treatment. LPS administration increased gene expression of Bcl-Xs, Bax, and TNF-alpha, but this was not altered by DA pretreatment. Furthermore, there was no effect on Bcl-Xl and Bcl-2 expression by DA alone. Whereas proapoptotic genes of the myocardium are up-regulated in LPS-induced cardiomyopathy, neither DA pretreatment nor treatment has significant effects on LV function or gene expression. This may suggest cardiac resistance to darbepoetin in LPS-mediated sepsis.
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PMID:Darbepoetin alpha, a long-acting erythropoeitin derivate, does not alter LPS evoked myocardial depression and gene expression of Bax, Bcl-Xs, Bcl-XL, Bcl-2, and TNF-alpha. 1849 5

An 11-year-old female Dachshund was presented with depression, diarrhea, weight loss, and radiographic evidence of masses involving the liver, spleen, and cranial lobe of the right lung. Results of a CBC included severe nonregenerative anemia (HCT 14.2%, hemoglobin, 4.3 g/dL, reticulocytes 66,000/microL) with marked metarubricytosis (nucleated RBCs 6.39 x 10(3)/microL). Examination of the peripheral blood smear revealed marked erythroid dysplasia, including marked anisocytosis with a prevalence of macrocytes, Howell-Jolly bodies, diffuse basophilic stippling, and multinucleated and atypical nucleated RBCs. Neutrophil hypersegmentation and giant forms were also noted. Numerous erythrocytes, particularly polychromatophilic cells, contained inclusions consistent with Cabot rings, which appeared as delicate red-purple ellipsoid or figure 8 structures. Rarely, Cabot rings were observed extracellularly. The dog was treated symptomatically with blood transfusions, prednisone, erythropoietin, and vitamin supplementation, but the anemia progressively worsened. The dog was euthanized 2 months after presentation. Bone marrow aspirate and core biopsy specimens obtained at the time of euthanasia revealed marked dysplastic changes in all cell lines, especially dyserythropoiesis, along with infiltrating carcinoma cells. A necropsy was performed, and histologic examination revealed poorly differentiated adenocarcinoma of the lung with multiple metastases to the marrow, spleen, and liver. The final diagnosis was marked myelodysplasia secondary to metastatic adenocarcinoma. Cabot rings are found rarely in humans with myelodysplasia, but have not been described previously in dogs. Based on the findings in this case, Cabot rings may occur rarely in dogs with severe dyserythropoiesis.
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PMID:Cabot rings as a result of severe dyserythropoiesis in a dog. 1853 17

Fatigue is a debilitating symptom or side effect experienced by many patients on long-term dialysis therapy. Fatigue has a considerable effect on patient health-related quality of life and is viewed as being more important than survival by some patients. Renal providers face many challenges when attempting to reduce fatigue in dialysis patients. The lack of a reliable, valid, and sensitive fatigue scale complicates the accurate identification of this symptom. Symptoms of daytime sleepiness and depression overlap with fatigue, making it difficult to target specific therapies. Moreover, many chronic health conditions common in the long-term dialysis population may lead to the development of fatigue and contribute to the day-to-day and diurnal variation in fatigue in patients. Key to improving the assessment and treatment of fatigue is improving our understanding of potential mediators, as well as potential therapies. Cytokines have emerged as an important mediator of fatigue and have been studied extensively in patients with cancer-related fatigue. In addition, although erythropoietin-stimulating agents have been shown to mitigate fatigue, the recent controversy regarding erythropoietin-stimulating agent dosing in patients with chronic kidney disease suggests that erythropoietin-stimulating agent therapy may not serve as the sole therapy to improve fatigue in this population. In conclusion, fatigue is an important and often underrecognized symptom in the dialysis population. Possible interventions for minimizing fatigue in patients on long-term dialysis therapy should aim at improving health care provider awareness, developing improved methods of measurement, understanding the pathogenesis better, and managing known contributing factors.
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PMID:Fatigue in patients receiving maintenance dialysis: a review of definitions, measures, and contributing factors. 1857 90

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

Anemia is common in congestive heart failure (CHF) and is associated with an increased mortality and morbidity. The most likely causes of anemia are chronic kidney disease (CKD) and excessive cytokine production, both of which can cause depression of erythropoietin (EPO) production and bone marrow activity. The cytokines also induce iron deficiency by both reducing gastrointestinal iron absorption and iron release from iron stores located in the macrophages and hepatocytes. Iron deficiency can cause thrombocytosis which might also contribute to cardiovascular complications in both CHF and CKD and is partially reversible with iron treatment. Thus attempts to control this anemia will have to consider both the use of erythropoiesis-stimulating agents (ESA), such as EPO, as well as oral and, probably more importantly, intravenous (IV) iron. The many studies on anemia in CHF patients treated with ESA and oral or IV iron, and even with IV iron without ESA have up to now shown a quite consistent positive effect on hospitalization, fatigue, shortness of breath, quality of life, exercise capacity, and beta-natriuretic peptide reduction, in the absence of increased cardiovascular damage related to the therapy. Adequately powered long-term placebo-controlled studies of ESA and/or IV iron are currently being carried out and their results are eagerly awaited.
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PMID:The anemia of heart failure. 1990 48

We tested the hypotheses that chronic human urinary obstruction impairs the renal regulation of the red blood cell (RBC) production and compared the chronic outcome of relief of obstruction between parenchyma-saving surgery and extracorporeal lithotripsy (SWL). We measured RBC count and serum erythropoietin (Epo) concentration before and 3 months after relief of urinary obstruction in 60 patients treated with pyelolithotomy, ureterolithotomy or ureteroscopy and in 62 patients treated with SWL. Compared with 333 healthy controls, at baseline, patients scheduled for parenchyma-saving surgery had lowered RBC count [9.9% (6.9-13.1); 95% confidence interval] in case of males and 17.7% (14.2-21.4) in case of females; minor depression in RBC count was also observed in female patients scheduled for SWL. Epo serum levels were mildly reduced in SWL patients and halved in parenchyma-saving surgery group. At 3 months following relief of obstruction in 50 operated patients without recurrent or residual stone, Epo levels almost doubled, becoming normal, while RBC count and haemoglobin concentration increased for 6.1% (3.8-8.8) and 8.8% (6.1-10.6). In contrast, in 49 SWL patients only minor, bidirectional responses to treatment were observed. We conclude that obstructive uropathy is associated with clinically relevant effects on erythropoiesis, which is reversed after relief of obstruction by parenchyma-saving surgery that saves the renal parenchyma.
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PMID:Urinary obstruction depresses erythropoiesis which recovers after parenchyma-saving surgery but not SWL. 1994 83

Severe malarial anemia is the most common syndrome of severe malaria in endemic areas. The pathophysiology of chronic malaria is characterised by a striking degree of abnormal development of erythroid precursors (dyserythropoiesis) and an inadequate erythropoietic response in spite of elevated levels of erythropoietin. The cause of dyserythropoiesis is unclear although it has been suggested that bone-marrow macrophages release cytokines, chemokines or lipo-peroxides after exposure to hemozoin, a crystalloid form of undigested heme moieties from malarial infected erythrocytes, and so inhibit erythropoiesis. However, we have previously shown that hemozoin may directly inhibit erythroid development in vitro and the levels of hemozoin in plasma from patients with malarial anemia and hemozoin within the bone marrow was associated with reduced reticulocyte response. We hypothesized that macrophages may reduce, not enhance, the inhibitory effect of hemozoin on erythropoiesis. In an in vitro model of erythropoiesis, we now show that inhibition of erythroid cell development by hemozoin isolated from P. falciparum is characterised by delayed expression of the erythroid markers and increased apoptosis of progenitor cells. Crucially, macrophages appear to protect erythroid cells from hemozoin, consistent with a direct contribution of hemozoin to the depression of reticulocyte output from the bone marrow in children with malarial anemia. Moreover, hemozoin isolated from P. falciparum in vitro inhibits erythroid development independently of inflammatory mediators by inducing apoptotic pathways that not only involve activation of caspase 8 and cleavage of caspase 3 but also loss of mitochondrial potential. Taken together these data are consistent with a direct effect of hemozoin in inducing apoptosis in developing erythroid cells in malarial anemia. Accumulation of hemozoin in the bone marrow could therefore result in inadequate reticulocytosis in children that have adequate levels of circulating erythropoietin.
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PMID:Hemozoin (malarial pigment) directly promotes apoptosis of erythroid precursors. 2004 Nov 81

Fatigue is one of the most common and debilitating symptoms experienced by HIV-infected people. We report the results of our longitudinal analysis of physiological and psychosocial factors that were thought to predict changes in HIV-related fatigue in 128 participants over a 1-year period, in an effort to sort out the complex interplay among a comprehensive set of physiological and psychosocial variables. Physiological measures included hepatic function (aspartate aminotransferase, alanine aminotransferase, gamma glutamyl transpeptidase, alkaline phosphatase, total bilirubin, hepatitis C status), thyroid function (thyroid stimulating hormone, thyroxine), HIV viral load, immunologic function (CD4, CD8, CD4/CD8 ratio, CD16, CD8CD38), gonadal function (testosterone, dehydroepiandrosterone), hematologic function (hemoglobin, hematocrit, serum erythropoietin), and cellular injury (lactic acid). Psychosocial measures included childhood and adult trauma, anxiety, depression, social support, stressful life events, and post-traumatic stress disorder (PTSD). Unemployment, not being on antiretroviral therapy, having fewer years since HIV diagnosis, more childhood trauma, more stressful life events, less social support, and more psychological distress (e.g., PTSD, anxiety and depression) put HIV-infected persons at risk for greater fatigue intensity and fatigue-related impairment in functioning during 1-year follow-up. Physiological variables did not predict greater fatigue. Stressful life events had both direct and indirect effects on fatigue.
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PMID:Physiological and psychosocial factors that predict HIV-related fatigue. 2035 17


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