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Bronchiectasis without CF is known as non-CF bronchiectasis. Historically, about half of all cases of non-CF bronchiectasis were found to be idiopathic, or without a known cause. [25] However, more recent studies with a more thorough diagnostic work-up have found an etiology in 60 to 90% of patients. [24] [26] [27]
Furthermore, Takeda et al. showed that the 1, 2, 3, and 5-year hemostatic rates of bronchiectasis (without nontuberculous mycobacteriosis or pulmonary aspergillosis) were 91.3, 84.2, 81.5, and 78.9%, respectively. [15] This paper is valuable for its long-term results of 5 years.
Bronchiolitis obliterans is a common complication in lung transplants because transplanted lungs are at greater risk of alloimmunization as compared to healthy lungs. The disease is often termed bronchiolitis obliterans syndrome (BOS) in the setting of post lung transplantation and hematopoietic stem cell transplant (HSCT). [6]
It is generally characterized by inflamed and easily collapsible airways, obstruction to airflow, problems exhaling, and frequent medical clinic visits and hospitalizations. Types of obstructive lung disease include asthma, bronchiectasis, bronchitis and chronic obstructive pulmonary disease (COPD).
It is often a complication of an existing chronic inflammatory disease such as rheumatoid arthritis, dermatomyositis, or it can be a side effect of certain medications such as amiodarone. COP was first described by Gary Epler in 1985. [5] The clinical features and radiological imaging resemble infectious pneumonia.
An acute exacerbation of chronic obstructive pulmonary disease, or acute exacerbations of chronic bronchitis (AECB), is a sudden worsening of chronic obstructive pulmonary disease (COPD) symptoms including shortness of breath, quantity and color of phlegm that typically lasts for several days.
In 1976, the first report of the occurrence of familial bronchiectasis in siblings was published, and it supported the theory that WCS was congenital, based on the uniformity of the cartilaginous defect. [13] [9] [10] It may have been the result of an autosomal recessive mutation, but the specific gene has not yet been identified. [3]
In addition to pneumonia, the stenosis may cause bronchiectasis, in which bronchi are dilated, to develop. [22] Even after an airway with a stricture is restored to normal, the resulting loss of lung function may be permanent. [22] Complications may also occur with treatment; for example, a granuloma can form at the suture site. [2]