| Article Access Statistics|
| Viewed||3607 |
| Printed||79 |
| Emailed||0 |
| PDF Downloaded||98 |
| Comments ||[Add] |
Click on image for details.
|LETTER TO EDITOR
|Year : 2001 | Volume
| Issue : 3 | Page : 221
Keratinous micro cysts in viral interstitial pneumonitis.
Source of Support: None, Conflict of Interest: None
Keywords: Abnormalities, Multiple, Case Report, Fatal Outcome, Human, Infant, Keratin, ultrastructure,Lung Diseases, Interstitial, pathology,Male, Metaplasia,
|How to cite this article:|
Vaideeswar P. Keratinous micro cysts in viral interstitial pneumonitis. J Postgrad Med 2001;47:221
Epithelial metaplasia is a well recognized phenomenon occurring in the healing phase of interstitial pneumonitis, viral or otherwise. Squamous metaplasia that occurs is usually assumed to be of the non-keratinising type, as is always depicted in the standard textbooks. We came across a case at autopsy where the lungs were studded with multiple foci of keratinising squamous metaplasia, largely of the alveolar lining.
A 11-month-old male child, diagnosed as a case of cardiofacial syndrome and perimembranous ventricular septal defect, used to have repeated episodes of lower respiratory tract infection. During the present admission, with clinical and radiological diagnosis of bronchopneumonia, he was given broad-spectrum antibiotics for 14 days, but ultimately succumbed. At autopsy, the lungs felt a little nodular with foci of congestion and consolidation. Histologically, there were characteristic features of giant cell interstitial pneumonitis with widened and inflammed septa, syncytial giant cells and balls of fibrin within spaces. At places, there was septal fibrosis and cuboidal or goblet cell metaplasia. What interested us were many areas of squamous metaplasia with extensive keratinisation, almost simulating a well differentiated squamous cell carcinoma [Figure]. Occasional bronchioles showed similar change. Viral inclusions were not seen. Other findings were perimembranous ventricular septal defect, associated mild vascular changes of pulmonary hypertension, abnormal tricuspid valve, left persistent superior vena cava and nonbacterial thrombotic endocarditis of the mitral valve leaflets.
When we went back to the gross specimen and examined the cut surface with a magnifying glass, we could make out a fine white mottling against the congested background. On slight pressure, some of these exuded white material (keratin), akin to comedocarcinoma of the breast. Such extensive keratinising metaplasia are unlikely to reverse and had the infant survived, this would set up a vicious circle of further infection, followed by subsequent parenchymal damage.
| :: References|| |
Colby TV, Churg AC. Patterns of pulmonary fibrosis. Pathol Annu 1986;21:277-309.
[Figure - 1]