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|Title: ||Drug-induced pulmonary fibrosis|
|Authors: ||Daba, Mohammed H.|
El-Tahir, Kamal E.
Al-Arifi, Mohammed N.
Gubara, Othman A.
|Issue Date: ||2004 |
|Publisher: ||Medical Services Department Saudi Arabian Armed forces|
|Citation: ||Saudi Medical Journal: 25(6); 700-706|
|Abstract: ||Pulmonary fibrosis is characterized by the accumulation of excessive connective tissue in the lungs. Its causes include
chronic administration of some drugs for example bleomycin, cyclophosphamide, amiodarone, procainamide,
penicillamine, gold and nitrofurantoin; exposure to certain environmental factors such as gases, asbestos and silica and
bacterial or fungal infections. Some systemic diseases also predispose to the disease for example rheumatoid arthritis
and systemic lupus erythematosus. The disease is associated with release of oxygen radicals and some mediators such
as tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta), PDGF, IGF-I, ET-I and
interleukins 1, 4, 8 and 13. The symptoms of the disease include dyspnea, non-productive cough, fever and damage to
the lung cells. It is diagnosed with the aid of chest radiography, high resolution computed tomographic scanning and
the result of pulmonary function tests. Drug-induced pulmonary fibrosis may involve release of free oxygen radicals
and various cytokines for example IL-Ibeta and TNF-alpha via activation of nuclear transcription factor (NF-beta) as in
the case of bleomycin and mitomycin or via release of TGF-beta as in case of tamoxifen or via inhibition of
macrophages’ and lymphocytes’ phospholipases as in the case of amiodarone with the resultant accumulation of
phospholipids and reduction of the immune system.|
|Description: ||From the Department of Clinical Pharmacy (Daba, Al-Arifi, Gubara), Department of Pharmacology (El-Tahir), College of Pharmacy, King Saud
University, Riyadh, Kingdom of Saudi Arabia|
|Appears in Collections:||College of Pharmacy|
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