ABSTRACT
Cancer patients frequently present with anaemia that may result from the direct or indirect effects of the tumor or its treatment. Anaemia is an independent adverse prognostic factor that exerts negative influence on quality of life and survival of cancer patients. Anaemia in malignant disorders often arises from an interplay of multiple aetiological and pathophysiologic mechanisms. Understanding these mechanisms will help the oncologist identify and treat specific causes of the anaemia thereby minimizing the use of blood transfusion, which is associated with many adverse effects. This paper reviewed the various aetiological and pathophysiologic mechanisms of anaemia in cancer patients including direct and indirect tumour effects that lead to reduced red cell production or increased red cell destruction via a myriad of mechanisms ranging from marrow infiltration and cancer-associated acute myelonecrosis to chronic inflammation, blood loss, iron, folate, vitamin B12 and other nutrients deficiencies, malignancy related renal injury, pure red cell aplasia, hypersplenism, haemophagocytic syndrome, red cell autoantibody production, non-immune red cell fragmentation and cytotoxic therapy-induced erythroid cell apoptosis and eryptosis. Hence anaemia in cancer patients is attributable to a wide spectrum of aetiological factors with multiple and sometimes overlapping pathophysiologic mechanisms. It is therefore necessary for the oncologists to thoroughly investigate all cases of anaemia with the aim of identifying the actual causative factors in order to offer more sustainable cause-specific treatment modalities that will minimize the use of blood transfusion with its attendant adverse effects
ABSTRACT
The role of disease severity in the development of opiate dependence was investigated by studying the pattern of steady state haematological parameters and vaso-occlusive crises in Sickle Cell Disease patients with and without opiate dependence as seen in Maiduguri, Nigeria. The patients were followed up for a 1-year period during which the levels of haematological parameters [including haematocrit, reticulocyte count, irreversibly sickled cells and foetal haemoglobin] and number of vaso-occlusive crises were studied and documented. Patients with opiate dependence had significantly [p < 0.05] lower mean haematocrit of [0.23 L/L], higher mean reticulocyte count [14%] and higher mean level of irreversibly sickled cells [6%] as compared to patients without opiate dependence who had higher mean haematocrit of 0.27 L/L, a lower mean reticulocyte count of 8.4% and lower mean level of irreversibly sickled cells of 3%. However, there was no statistically significant difference in the levels of foetal haemoglobin [Hb F] of 57c and 5.4% [p > 0.05] found among patients with opiate dependence and those without opiate dependence respectively. The number of episodes of vaso-occlusive crises per patient during the period of study was 5.5 among patients who were opiate dependent and was significantly higher than the figure of 1.9 [p < 0.05] seen among patients without opiate dependence. This data is interpreted to suggest that opiate dependent patients had higher rate of haemolysis and vaso-occlusive crises, and by implication greater disease severity, which leads to more vaso-occlusive crises that result in greater exposure to opiate analgesics to which they develop dependence in the course of time during clinical management. Therefore, disease severity is an important risk factor for the development of opiate dependence in sickle cell disease