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Abdominal pain and discomfort is a symptom that is commonly associated with CLL and is often experienced by patients. Such pain and discomfort is caused by the enlargement of the affected organs compressing onto other nearby organs and tissues. For instance, due to the enlargement of the spleen it may compress the stomach to the extent that the individual may experience the sensation of satiety or fullness. Consequently, this causes various levels of discomfort and may contribute to subtle weight loss over a duration of time.
In addition to, enlarged lymph nodes may prevent the urinary and/or gastrointestinal tracts to function properly (OncoLink, 2018). Several of the listed complications in the provided table above share a direct relationship with one another. For instance, lymphocytosis may cause autoimmunity in some patients which may lead to decreased levels of blood count. A decreased level of blood count in the body may result in low levels of red blood cells, otherwise known as anemia. Similarly, a low blood count may also cause decreased levels: neutrophils; platelets; and immunoglobulin (LLS).
How it works
There is no precise known cause for CLL. However recent research suggests significant differences between normal B lymphocytes and abnormal B lymphocytes associated with CLL. Typically the body’s cells mature and function according to the information present in each cell’s chromosomes. Chromosomes are long thread-like structures of DNA that are solely responsible for carrying genetic information. Further, a chromosome’s genetic coding is expressed in the form of genes. An individual’s genes not only influence physical appearance, but may also substantially affect the body’s ability to properly proliferate or divide cells (American Cancer Society, 2018). The process of cell proliferation is complex and many possibilities of genetic mutation may occur within the DNA.
There are 23 pairs of chromosomes existing in each human cell. Additionally, individuals who suffer from CLL contain an acquired mutation from at least one of their 46 chromosomes. The various following mutations may occur during any period of the development of B lymphocytes (Zhang and Kipps, 2013). In most confirmed cases of chronic lymphocytic leukemia there may be a deletion of chromosomes 11, 13 and 17. The partial loss of chromosome 13 remains the most commonly deleted in such cases (American Cancer Society, 2018). Abnormal structural changes may also occur in chromosomes 14 and/or 6. Very rarely an addition of chromosome 12, also known as trisomy 12, may genetically mutate an individual’s DNA (Zhang & Kipps, 2013).
In other words, the genetic expression of an immature stem cell present in the bone marrow becomes partially or wholly damaged. This mutated stem cell then develops into a leukemic cell and begins to proliferate rapidly in the body’s proliferation centers, or otherwise known as pseudo follicles (Zhang & Kipps, 2013). Thus, resulting in the production of CLL cells (LLS). Studies prove that CLL is derived from mature lymphocytes residing in the germinal center of bone marrow and other lymphoid tissues located within the body (Darawshy, Ben-Yehuda, Atlan & Rund). Researchers and scientists are also highly aware that such chromosomal mutations are clear indications of CLL; although it remains unclear as to which particular genes are directly involved and how they attribute to the body’s development of leukemia.
Moreover, B lymphocytes are part of the adaptive immune system and function on a cellular level to produce antibodies that attack antigens. Antigens may be characterized as any foreign substance entering or existing within the body. B lymphocytes are predominantly produced within the bone marrow. However, these particular cells may migrate to the spleen and other lymphoid tissue to begin maturation and become immunocompetent (OncoLink, 2018). Biologically speaking, a substantial amount of research currently suggests that the initial development of CLL may be caused when B lymphocytes continue to proliferate uncontrollably shortly following it’s reaction to an antigen (Zhang & Kipps, 2013). But, as mentioned previously the genetic and biological causes of CLL remains unknown.
CLL cannot be treated, however it can be properly managed through various medical treatments that are dependent upon the patient’s individual factors. These various factors may include, but are not limited to the following: age; physical fitness level; the presence of secondary chronic diseases; and the deletion of chromosome 17. Due to such factors it is difficult for healthcare professionals to effectively provide individuals who suffer from CLL with a universal treatment method. However, in order to provide CLL patients with proper treatment plans and prescribed management courses healthcare professionals attempt to subdivide these patients into several different groups (Cramer, Langerbeins, Eichhorst & Hallek, 2016; Rai & Jain, 2015).
The first subdivision of CLL patients consists of elderly individuals who are physically fit either with or without secondary diseases or conditions. These patients are typically treated using the standard methods for management of CLL. This particular method is primarily used to further the patient’s life expectancy and provide a long term remission period. Though there is no universal treatment method chemo-immunotherapy in addition to cyclophosphamide, fludarabine, and rituximab (FCR) is often used as a first-line defense for those that qualify (Cramer, Langerbeins, Eichhorst & Hallek, 2016). Although this particular method has shown an increase in progression-free survival and response rates it may cause neutropenia and increase risk of infection (Union for International Cancer Control, 2014). However, there is a poor prognosis rate associated with the deletion and/or mutation of chromosome 17 due to its high resistance to chemo-immunotherapy (Cramer, Langerbeins, Eichhorst & Hallek, 2016). Additionally, one of the components of chemo-immunotherapy called Rituximab is known to trigger mild allergic reactions when taken without certain pre-medications (Union for International Cancer Control, 2014).
Further, patients with secondary conditions or diseases that have a decreased life expectancy due to such circumstances are typically given a reduced dosage or a modified treatment method for disease management. More specifically, the suggested method of treatment for this particular type of patient would be a chlorambucil-based chemo-immunotherapy plan. Due to the fact that this is a dosage-reduced method it works best for the patient because it is a viable alternative to the original FCR chemo-immunotherapy and is chemically less toxic on a cellular level (Cramer, Langerbeins, Eichhorst, Hallek & 2016).
Lastly, patients with a significantly lower life expectancy with several secondary diseases or conditions are to be treated with the best supportive care possible. A common complication known as hypogammaglobulinemia may arise in patients who cannot participate in all other treatment options. This condition may occur when there are significantly low levels of Immunoglobulin G (IgG) and recurrent infections. Stem cell transplantations are often offered for patients of this subgroup. Such stem cell therapy or blood transfusion procedures are shown to temporarily improve the patients quality of life (Union for International Cancer Control, 2014; Mayo Clinic). The second and last treatment methods prescribed to patients with CLL are chiefly aimed to control and manage the disease as well as the associated symptoms (Cramer, Langerbeins, Eichhorst & Hallek, 2016).
All patients who suffer from Chronic Lymphocytic Leukemia are given the opportunity to participate in clinical trials with the approval of their physician (Rai & Jain, 2015). As mentioned previously, there is no definite cure for CLL. However, over the course of several decades recent medical discoveries and new treatment management methods have substantially increased the rate of survival for CLL patients (Lenartova, Johannesen, and Tjènnfjord, 2016).
There are currently several different clinical trials and pharmaceutical drugs undergoing extensive research to improve the treatments course for Chronic Lymphocytic Leukemia. In particular, CAR T-cell therapy is one of the most forefront experiments to potentially offer a legitimate treatment for CLL patients. CAR or Chimeric Antigen Receptor T-cell therapy offers the body an alternative technique to identify and terminate CLL cells in the body. In order to do so, the patient must consent to provide and surrender a sample of their own T cells. Upon the extraction of the patient’s T cells, the cells will be sent to a biomedical lab to be reprogrammed and then cultivated. After this process has been completed in the lab the patient will receive a transfusion of the newly programmed T cells in hopes to destroy the CLL cells present in the body (American Cancer Society, 2018; Rai & Jain, 2015).
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