Lipoid Pneumonia Causes
Exogenous lipoid pneumonia
Most patients with exogenous lipoid pneumonia are elderly, usually in the late sixth or seventh decade of life. However, infants and mentally ......ed persons are also prone to this condition. The factors that predispose a person to contracting this disease are an impaired swallowing mechanism caused by neurological and esophageal disorders, and the consistent use of the various kinds of oils mineral, animal, and less commonly, the vegetable oils found in laxatives, nasal drops, mouth spray, oral lubricants, insecticides or traditional folk remedies. Lipid pneumonia also happens to be an occupational fire hazard of fire eaters. The irritation causing agent enters the lungs through aspiration, inhalation or during procedures which involve the use of iodized vegetable oils used as a radiopaque medium, such as lymphangiography, bronchography, hysterosalpingography, myelography or uterography.
Even though vegetable oils are mostly expectorated, residual elements often get blended in and can lead to exogenous lipoid pneumonia. Composed of liquid petroleum or paraffin, mineral oil is a mixture of long chain saturated hydrocarbons. It irritates the lung tissue and causes a diffuse parenchymal reaction or the development of localized masses called paraffinomas. Of all these substances animal fats are the most harmful to lung tissue. This is so because they are hydrolyzed by lipase in the pulmonary cells and broken down into free fatty acids, which could cause a severe inflammatory reaction and tissue necrosis. This process has been observed in infants and children with exogenous lipoid pneumonia to be a result of force feeding of animal fat (ghee), a cultural practice in Saudi Arabia.
When oil enters the lung, there are 3stages in the pathologic process that leads to the development of exogenous lipoid pneumonia. The first stage consists of a toxic agitation of capillary endothelium with plasma exuding into the alveoli. In the next stage, alveolar and interstitial macrophages get activated then phagocytose and degrade the oil.In the final stage, fibrointerstitial and granulomatous reactions develop. Depending on the quality and quantity of oil present, these stages vary in severity. With the inhalation of animal fat, the high lipid content represses phagocytosis, leaving the pulmonary lymphocytes as the main cells responsible for the removal of the inhaled fat. In such cases, fat-laden macrophages and prominent pleural lymphocytes can be observed on histologic examination and which could easily lead to the mistaken diagnosis of lymphatic carcinomatosis.
Endogenous lipoid pneumonia
Also called cholesterol pneumonitis, endogenous lipoid pneumonia is caused by the collection of intrinsic lipids in the lungs. It is generally observed in persons with chronic bronchial obstruction similar to tumors or foreign bodies. Other risk factors include fat embolism, pulmonary alveolar proteinosis, lipid storage diseases such as Gaucher's disease and Niemann-Pick disease and disseminated lipogranulomatosis.
Endogenous lipoid pneumonia has also been observed in patients with Hodgkins disease. A 5 year old child with a serious neurodevelopmental disorder reportedly developed a combination of endogenous and exogenous lipoid pneumonia and pulmonary alveolar proteinosis. Endogenous lipoid pneumonia has also been linked to lung cancer. In one research conducted, endogenous lipoid pneumonia was diagnosed in the resected lungs of 33 of 147 patients with lung cancer. It was found in 16 out of 89 (18%) of patients with adenocarcinoma and in 17 of 55 (31%) patients with squamous cell carcinoma. In 23 cases, it was observed that endogenous lipoid pneumonia was localized to lung parenchyma distal to the airway obstructed by the tumor, and of these 16 were patients with squamous cell carcinoma. Out of 5 patients with adenocarcinoma, 4 had endogenous lipoid pneumonia present distal to the tumor and having spread to isolated segments. These results indicate that transbronchial dissemination of the breakdown products of adenocarcinoma cells, including mucin, could contribute to the spread of the nonobstructive component of endogenous lipoid pneumonia.
A histopathologic examination of lung tissue of patients with nonsmall cell lung cancer has revealed changes similar to those observed in endogenous lipoid pneumonia, along with pulmonary alveolar proteinosis, located near the nonsmall cell lung cancer. One study described coexisting changes similar to those seen in endogenous lipoid pneumonia in the vicinity of primary lung tumors, particularly in samples of tissue from patients with squamous cell and large cell carcinoma.
When normal lung tissue is chemically analysed, it shows a total fat content of 8.63 per 100 g of dry tissue, of which 19% is cholesterol; although this percentage shows a marked increase in smokers. When the breakdown of these cells takes place, it results in the lipid gaining access to lung parenchyma and it is phagocytosed by the pulmonary macrophages. The absence of lysosomes in these macrophages impairs their ability to resist bacterial infections, and renders the patient more susceptible to opportunistic infections.If the macrophage nucleus displays morphologic evidence of an extreme increase in activity parachromatic clearing, chromatin clumping and hyperchromatic prominent nucleoli - a diagnosis of lung carcinoma is possible.
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