Cancer patients are often at risk of developing anaemia in the course of the disease, treatment and particularly during chemotherapy. A majority of those who undergo chemotherapy develop anaemia in the course of their treatment (Kitano, et al., 2007). The prevalence of the condition has reported variedly, with records of 30% to 83% (Barrett-Lee, Ludwig, Birgegard, Bokemeyer, & Kosmidis, 2006).Anaemia is defined as a haemoglobin level of less 12.0 g/dL. Anaemia often exacerbates symptoms such as weakness, dyspnoea, and fatigue and as a result causing a further decline in the quality of life, and as a result, affect the prognosis in the patients.
Bone marrow stem cells have the ability to self-renew and also have the capacity to supply normal haemoglobin levels through an individual’s life. Erythropoiesis is a complex process that maintains the number of erythrocytes circulating in an individual’s physiological conditions. Erythrocytes are obtained from committed stem cells that undergo differentiation and multiplication through the various erythroblastic stages (Dicato, 2003). Human cells exhibit an inverse relationship between the events of proliferation potential and differentiation. Both differentiation and proliferation are regulated by cytokines, and erythropoietin is of great significance once the erythroid pathway is initiated. Erythropoietin binds to specific receptors n erythrocyte progenitors and produces a signal that initiates proliferation and differentiation and also an antiapoptotic effect. An alternative antiapoptotic pathway is the production of nuclear factor kappa-light-chain-enhancer of activated B cells (NF – KB) which occurs as a response to inflammatory events in the body. Digicaylioglu and Lipton (2001), linked NF – KB production with a possibility of cross-association with erythropoietin antiapoptosis mechanism in the central nervous system. In summary, erythropoietin as the primary growth factor interacts with specific receptors on erythroid progenitor cells and contributes to mitogenesis in the marrow (Rim, 2012). Agents used for chemotherapy interfere with erythropoiesis, and as a result, increases the incidence of anaemia among cancer patients.
Anaemia in Cancer
In anaemic cancer just like in anaemia of chronic conditions, several mechanisms interfere with the normal process of erythrocyte production. Most probable inhibitory mechanisms include the cytokines interferon gamma, transforming growth factor-beta, interleukin (IL)-1, IL-6, and tumour necrosis factor-alpha (TNF-?) (Dicato, 2003). Papadaki, Kritikos, and Valatas (2002) agree with the observation made y Dicato (2003), by claiming that the network of the above-mentioned cytokines play a role in the modulation of iron metabolism, and the erythropoeitin effect is diluted by TNF-? among others.
Anaemia of cancer impairs almost all body tissues and organs and also leads to several disturbances in normal physiological functions, with the potential to decrease the capacity of mental and physical performance. Fatigue is the primary expression of organ disturbance. Fatigue ranks first among patent complaints (Curt, Breitbart, & Cella, 2005), and it parallels haemoglobin level (Littlewood, Bajetta, & Nortier, 2009). Averagely, one out of every three patients develops anaemia after three cycles of chemotherapy (Glaspy, Degos, & Dicato, 2002).
Pathophysiology of Chemotherapy-Induced Anaemia
Chemotherapy-induced anaemia results from an interruption in the process of erythropoiesis among cancer patients and this has been linked to various factors which include; patient related factors such as thalassemia and haemoglobinopathies, disease related factors that include bone marrow infiltration, diminished nutritional state and hypersplenism, and lastly, therapy related factors such as hypoplasia of bone marrow-bearing areas following radiotherapy, and renal and bone marrow toxicity as a result of chemotherapy (Dicato, 2003).
Cancer treatment-related anaemia is quite common, mainly attributed to the poor capacity of stem cells to repair radiation damage. Chemotherapy is likely to cause both transient and sustained anaemia. Agents used for chemotherapy interfere with erythropoiesis, and as a result, increases the incidence of anaemia among cancer patients. The mechanisms of chemotherapy-induced anaemia in cancer patients include the delaying or blockage of haematopoietic factors, immune-mediated haematopoietic cell destruction, stem cell death, long-term myelodysplasia, microangiopathy, plasma volume expansion with dilutional anaemia, oxidant damage to mature haematopoietic cells, and immune-mediated haematopoietic cell destruction (Mercadante, Gebbia, Marrazzo, & Filosto, 2000).
Among agents used for chemotherapy, nitrosoureas, alkylating agents, and antitumor antibiotics have been demonstrated to cause damage to both dividing and resting cells, and also causes myelosuppressive effects of much greater intensity compared to cell-cycle-specific agents (Rim, 2012). According to Barrett-Lee, Ludwig, Birgegard, Bokemeyer, and Kosmidis, (2006, those patients on chemotherapy using platinum based chemotherapy have a heightened risk of developing anaemia compared to those on non-platinum based chemotherapy.
Apart from the type of chemotherapy drug used, other risk factors that increase the incidence for chemotherapy induced anaemia include tumour type, low baseline haemoglobin, and concurrent treatment with chemotherapy/radiation therapy (Rim, 2012). As attested by Barrett-Lee, Ludwig, Birgegard, Bokemeyer, and Kosmidis, (2006), cancer patients exhibitng low baseline levels of haemoglobin (<= 13.4 dL in males and <= 12.9 g/dL in females) have a heightened risk of developing anaemia following chemotherapy. With regard to the type of tumour, those with tumour types such as gynecologic cancer or lung cancer have a threefold increased chance of developing anaemia compared to those with colorectal/gastrointestinal cancer (Rim, 2012). On concurrent treatment, cancer patients on concurrent chemotherapy have a higher risk for chemotherapy induced anaemia. This is supported by evidence from a 2004 study by European Cancer Anaemia Survey (ECAS) which demonstrated that fifty percent of those with lung cancer on concomitant therapy had evidenced more severe anaemia, compared to those who received radiation therapy or chemotherapy separately, at 39% each (Kosmidis & Krzakowski, 2005).
Chemotherapy induced anaemia is a common problem in cancer patients receiving chemotherapy. This form of therapy is responsible for increased fatigue, poor prognosis, negative effect on quality of life, and a decline in functional and psychological wellbeing in cancer patients. Compared to cell-cycle agents, a higher incidence of anaemia in patients receiving have been reported among those on treatment using nitroureas, alkylating agents, and antitumor antibiotics. These agents interfere with erythropoiesis, and as a result, increase the incidence of anaemia among cancer patients. Some of the mechanisms that lead to chemotherapy-induced anaemia include the delaying or blockage of haematopoietic factors, immune-mediated haematopoietic cell destruction, stem cell death, and long-term myelodysplasia.
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