Market Research Report
Cystic Fibrosis - Epidemiology Forecast - 2030
|Published by||DelveInsight Business Research LLP||Product code||955316|
|Published||Pre-Order||Content info||100 Pages
Delivery time: 10 business days
|Cystic Fibrosis - Epidemiology Forecast - 2030|
|Published: Pre-Order||Content info: 100 Pages||
DelveInsight's 'Cystic Fibrosis - Epidemiology Forecast - 2030' report delivers an in-depth understanding of the Cystic Fibrosis (CF), historical and forecasted epidemiology in the United States, and EU5 (Germany, Spain, Italy, France, and the United Kingdom).
Cystic Fibrosis (CF) Disease Understanding
First identified nearly 80 years ago, cystic fibrosis (CF) is an autosomal recessive genetic disorder that causes damage to the lungs and the digestive system with the highest prevalence in Europe, North America, and Australia. A genetic mutation causes this disease in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The CFTR protein is a chloride-conducting trans-membrane conductance regulator belonging to the ABC transporter class. It helps in the transportation of chloride ions, thereby maintaining the electrochemical gradient as well as osmotic and fluid balance in the passageways.
A defect in CFTR protein due to an autosomal recessive mutation in the gene can have a wide range of debilitating consequences. The most common defect is highly viscous mucus that obstructs airway tracts which leads to difficulty in breathing. Moreover, it serves as a breeding ground for a huge range of bacterial infections like Staphylococcus aureus, Haemophilus influenza, and Pseudomonas aeruginosa. CFTR is present in other parts of the body as well; therefore, other consequences of such a mutation include malabsorption, pancreatic dysfunction, infertility, bowel obstruction, among many others.
The Cystic Fibrosis (CF) epidemiology division provides insights about the historical and current patient pool along with the forecasted trend for every seven major countries. It helps recognize the causes of current and forecasted trends by exploring numerous studies and views of key opinion leaders. This part of the report also provides the diagnosed patient pool and their trends along with assumptions undertaken.
The total prevalent cases of Cystic Fibrosis (CF) patients are increasing in 6MM during the study period, i.e. 2017-2030.
The disease epidemiology covered in the report provides historical as well as forecasted Cystic Fibrosis (CF) symptoms epidemiology segmented as the Total Prevalent cases of Cystic Fibrosis (CF), Gender-specific cases of Cystic Fibrosis (CF), Age-specific cases of Cystic Fibrosis (CF), Type-specific cases of Cystic Fibrosis (CF). The report includes the prevalent scenario of Cystic Fibrosis (CF) symptoms in 6MM covering the United States and EU5 countries (Germany, France, Italy, Spain, and the United Kingdom) from 2017 to 2030.
The epidemiology segment also provides the Cystic Fibrosis (CF) epidemiology data and findings across the United States, and EU5 (Germany, France, Italy, Spain, and the United Kingdom).
The total prevalent cases of Cystic Fibrosis (CF) associated in 6MM countries was 61,306 in 2017.
We interview, KOLs and SME's opinion through primary research to fill the data gaps and validate our secondary research. The opinion helps understand the total patient population and current treatment pattern. This will support the clients in potential upcoming novel treatment by identifying the overall scenario of the indications.
Key Questions Answered
The Cystic Fibrosis (CF) Epidemiology report will allow the user to -
Study Period: 2017-2030
Cloning of CF Transmembrane conductance Regulator (CFTR) gene has provided a breakthrough in the understanding of the molecular basis of this disease. There are over 1,800 mutations of CFTR identified so far, wherein 23 variants account for the majority of CF-causing mutations. The CF-causing mutations of CFTR can be grouped into classes depending on the physiological effect. Some mutations cause little or no protein to be made (Class I and IV), others create a defective protein that does not make it to the cell membrane (Class II), and others cannot be effectively regulated or conduct chloride (Class III and IV).
Classification of the mutations allows the development of specialized drugs to overcome the specific gene mutation. The most common CF mutation, F508del, is primarily considered to be a processing mutation. The F508del mutation removes a single amino acid from the CFTR protein. Without this building block, the CFTR protein cannot stay in the correct 3-D shape. The cell recognizes that the protein is not the right shape and disposes of it.
Approximately 44% of CF patients are homozygous for the F508del mutation (i.e., F508del/F508del), while around 41% are compound heterozygotes (i.e., F508del/other CF causing CFTR mutation), and about 15% have two non-F508del CF-causing CFTR mutations.