Cystic Fibrosis is a condition which is genetic and tends to appear in the subject's infancy. Symptoms with include a host of pulmonary and bronchial deficiencies manifesting in a chronic cough, a shortness of breath, a stunted physical growth, low display of energy, a salty residue on the skin and a notable and debilitating over-abundance of phlegm. (MP, 1) The condition is considered to significantly increase mortality rates for its sufferers, who are not expected to live out a full or healthy adulthood. Further, in the past, it was generally understood that the sufferer of cystic fibrosis was unlikely to live through infancy or early childhood, though treatment improvements have exceeded this expectation.
The essential danger represented to its sufferers by cystic fibrosis is the enhanced exposure thereto of infection and pneumonia. Accordingly, Medline Plus reports that under the conditions produced by the disease, "the mucus clogs the lungs, causing breathing problems and making it easy for bacteria to grow. This can lead to problems such as repeated lung infections and lung damage." (MP, 1) The heightened susceptibility to these conditions can wear on the subject's immunity and already limited stamina, making cystic fibrosis sufferers particularly vulnerable to the chronic resurgence of lung airway conditions that worsen bronchial and respiratory symptoms and experiences.
Today though, treatment options are revolving on an ever-improving understanding of the condition's cause. The inborn nature of cystic fibrosis is tied to its status as a genetic disease in which the proper reactions do not occur within the body to properly dispose of excess mucous and, as a result, to generate energy or growth from nutrition or to engage in taxing physical activity. This is the outcome of a genetic mutation which the text by Karem et al. (1989) connects in the majority of patients to the absence of specific gene pairs. As the study denotes, "approximately 70% of the mutations in cystic fibrosis patients correspond to a specific deletion of three base pairs, which results in the loss of a phenylalanine residue at amino acid position 508 of the putative product of the cystic fibrosis gene." (Karem et al., 1073)
With an increased focus today on the genetic implications of the condition, enhanced abilities to understand the behaviors of human DNA are opening the door to a more perceptive response to the condition in question. As the text by Davis (1993) indicates, "as mutational analysis and patient data continue to be compiled, patient genotyping should prove useful in both prognosticating and providing a framework for evaluating treatments. Furthermore, whether the heterozygous state of CF mutations predisposes to abnormalities such as chronic bronchial hypersecretion, airway hyperreactivity or infertility can now be more thoroughly addressed." (Davis, 17)
These factors are not just improving our understanding of what may cause cystic fibrosis, but it has also allowed us to pinpoint some strategies for controlling a condition that only 25 years ago, was seen as a pre-adulthood death sentence. As the table included in Appendix A demonstrates, the average life expectancy of one suffering from cystic fibrosis has more than doubled to 36.8 in 2006 from 18 in 1980. This change has been largely due to the improvement of treatment methods which has been achieved in recent years.
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