ABSTRACT
The frequency of drug-induced damage to the lung in inpatients is estimated to be about 10%. Pathoanatomically, varying damage patterns result, ranging from acute pulmonary edema via inflammatory reactions to pulmonary fibrosis. The ATS/ERS 2001 classification, which is based on the suggestions made by Liebow 1969, is an accepted system for classifying findings according to recurring patterns. Generally, there are no specific morphological findings which allow safe conclusions on possible administered drugs. Clinical information is mandatory. Differentiation from pulmonary alterations due to the underlying disease is often difficult. In daily routine diagnostics, it is important to consider iatrogenic causal factors in cases of "undetermined pulmonary disease".
Subject(s)
Drug-Related Side Effects and Adverse Reactions , Lung/pathology , Diagnosis, Differential , Humans , Inpatients , Lung/drug effects , Pulmonary Edema/chemically induced , Pulmonary Edema/etiology , Pulmonary Edema/pathologyABSTRACT
Aspects of histogenesis and nomenclature of so called "sclerosing hemangioma" of the lung (WHO 1999) are discussed and compared with immunohistochemical findings in eight examined operation specimen. The lesion is characterised by the presence of typical surface cells, which can be related to type II pneumocytes. Progesterone-receptor positive stromal cells may derive from primitive mesenchymal cells. Endothelial proveniance of tumor cells could not be confirmed by immunohistochemistry. Therefore, this rare usually benign pulmonary neoplasm should be entitled "pneumocytoma" analogous to the suggestion of several other authors.
Subject(s)
Lung Neoplasms/pathology , Pulmonary Sclerosing Hemangioma/pathology , Female , Humans , Lung Neoplasms/classification , Lung Neoplasms/epidemiology , Lung Neoplasms/genetics , Male , Pulmonary Sclerosing Hemangioma/classification , Pulmonary Sclerosing Hemangioma/epidemiology , Pulmonary Sclerosing Hemangioma/genetics , Terminology as TopicABSTRACT
We report on three autopsy cases with clinical and morphological evidence of pulmonary hypertension and concurrent myeloproliferative disorders. Massive accumulations of pleomorphic, atypical megakaryocytes and thrombotic material are found within the pulmonary capillary beds. Morphometrical studies allowed us to identify on average 1,293.4 (1,145.8-1,401) megakaryocytes per one square centimetre lung tissue (standard value: 25 megakaryocytes/cm(2) lung tissue). The lungs of the controls with unaffected parenchyma show smaller numbers of megakaryocytes. It seems highly unlikely that these haematopoietic cells originate in lung capillaries in the absence of morphological correlates. Recurrent chronic microemboli consisting of megakaryocytes and thrombocytes could be held responsible for the development of secondary chronic pulmonary hypertension. Our observations suggest that pulmonary hypertension associated with chronic myeloproliferative disorders should be classified into the fourth group of the EVIAN-classification of pulmonary hypertension.
