Cystic Fibrosis organisations in Australia provide support and services to people with Cystic Fibrosis (CF) and their carers and families. This is complemented by a commitment to research and a quality improvement program focussing on improved clinical care for people with CF.
Every four days a baby is born in Australia with cystic fibrosis (CF) and more than one million Australians are carriers of cystic fibrosis. Cystic Fibrosis Australia (CFA) is committed to improving clinical practice and patient outcomes through its quality improvement programmes and research with the aim of extending life expectancy from 47 to 55 years by 2025.
Cystic Fibrosis is a recessive genetic condition. It primarily affects the lungs and digestive system because of a malfunction in the exocrine system, responsible for producing saliva, sweat, tears and mucus.
In addition to working for a cure, Cystic Fibrosis Australia also provides support and advocacy to improve the lives of people with cystic fibrosis. Get involved by raising awareness about CF, participating in a fundraising event or volunteering.
Cystic Fibrosis Australia has established a consistent approach to advocacy across Australia and is now a subject matter expert for government, industry and the media.
The Australian Cystic Fibrosis Research Trust (ACFRT) is managed by Cystic Fibrosis Australia (CFA). Since 1989 it has funded more than 300 projects valued at over $6,000,000.
Visit the media room to browse through number of resources including media representatives, press releases and reports.
The pancreas is universally affected in people with cystic fibrosis (CF). The detection of an inflamed pancreas on the heel prick blood spot forms the foundation of newborn screening test for CF in Australia and many countries around the world.
The pancreas can be divided into the exocrine pancreas, which is responsible for producing digestive enzymes and large volumes of alkaline fluid for the small intestine required for normal digestive health, and the endocrine pancreas, which is responsible for sugar control.
People with CF either have pancreatic insufficiency (PI) or pancreatic sufficiency (PS). PI affects over 80% of the CF population, and is the result of severe blockages of the ducts in the pancreas and the subsequent scarring (fibrosis) and destruction of the exocrine pancreas.
Pancreatic insufficiency begins early in life for those who carry two severe CF mutations. People who are PI are unable to digest foods normally, which leads to malabsorption and malnutrition. Pancreatic enzyme replacement therapy is a prescription medicine for people with PI that helps improve digestion of foods.
People with CF who are PS do not typically have problems related to digestion of foods although this does not imply that their exocrine pancreas is unaffected. They are still at future risk of developing PI and therefore regular monitoring using a stool test (stool elastase) is recommended.
People with PS are also at risk of developing painful episodes of inflammation of the pancreas called “pancreatitis”. Pancreatitis can be extremely painful.
The endocrine pancreas when affected by CF, can lead to CF related diabetes (CFRD). Being PI and having severe inflammation of the exocrine pancreas at early life, increases the chances of later developing CFRD.
CFRD can affect nutrition and lung function. Diabetes is a crucial lifestyle obstacle for individuals who are living with CF because it affects so many areas of life simultaneously.
CF-related diabetes imposes further dietary restrictions and obligations whilst at the same time making healthy physical activity more difficult and taxing.
Tissue degeneration in major organ groups is also highly associated with CF-related diabetes and so is increased risk of anxiety and depression.
Fortunately CF-related diabetes has attracted a lot of research attention. New biotechnological improvements are becoming possible. These help to regulate blood sugar levels in the pancreas and monitor tissue damage.
CF and the Pancreas:
Pancreatitis and Pancreatic Cystosis: https://www.cysticfibrosisjournal.com/article/S1569-1993(17)30819-6/fulltext