Campbell had suggested that the cause of chronic bronchitis was due to toxic substances, and recommended pure air, simple food, and exercise to remove them from the body.A joint research programme was undertaken in Chicago and London from 1951 to 1953 in which the clinical features of one thousand cases of chronic bronchitis were detailed. The findings were published in the Lancet in 1953. It was stated that since its introduction by Badham, chronic bronchitis had become an increasingly popular diagnosis. The study had looked at various associations such as the weather, conditions at home, and at work, age of onset, childhood illnesses, smoking habits, and breathlessness. It was concluded that chronic bronchitis invariably led to emphysema, particularly when the bronchitis had persisted for a long time.In 1957 it was noted that at the time there were many investigations being carried out into chronic bronchitis and emphysema in general, and among industrial workers exposed to dust. Excerpts were published dating from 1864 in which Charles Parsons had noted the occurring consequence of the development of emphysema from bronchitis. This was seen to be not always applicable. His findings were in association with his studies on chronic bronchitis among pottery workers.A CIBA (now Novartis) meeting in 1959, and a meeting of the American Thoracic Society in 1962, defined chronic bronchitis as a component of COPD, in the terms that have not changed.
People who have been treated with fludarabine will usually be asked to take co-trimoxazole or to use monthly nebulised pentamidine to prevent Pneumocystis jiroveci pneumonia. The profound lymphopenia caused by fludarabine renders patients susceptible to transfusion-associated graft versus host disease, an oftentimes fatal complication of blood transfusion. For this reason, all patients who have ever received fludarabine should only be given irradiated blood components. Fludarabine causes anemia, thrombocytopenia and neutropenia, requiring regular blood count monitoring. Some patients require blood and platelet transfusion, or G-CSF injections to boost neutrophil counts. Fludarabine is associated with the development of severe autoimmune hemolytic anemia in a proportion of patients.Difficulties are often encountered when harvesting peripheral blood stem cells from patients previously treated with fludarabine. Pharmacology
Fludarabine is a purine analog, and can be given both orally and intravenously. Fludarabine inhibits DNA synthesis by interfering with ribonucleotide reductase and DNA polymerase. It is active against both dividing and resting cells. Being phosphorylated, fludarabine is ionized at physiologic pH and is effectually trapped in blood. This provides some level of specificity for blood cells, both cancerous and healthy. History
Fludarabine was produced by John Montgomery and Kathleen Hewson of the Southern Research Institute in 1968. Names
Fludarabine is generally administered as its 5-O-phosphorylated form known as fludarabine phosphate, which is rapidly dephosphorylated to fludarabine in the plasma. References
External links
"Fludarabine". Drug Information Portal. U.S. National Library of Medicine.