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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Idiopathic pulmonary hemosiderosis gives rise to anemia, due to repeated intra-alveolar hemorrhage, the reabsorption of which leads to hemosiderin deposits in the lung parenchyma. The authors report a case in a young woman aged 24 years whose illness started with anemia, then two months later, with hemoptysis and a broncho-pulmonary syndrome with a low grade fever. On the 6th month, there occurred a hazy infiltrate of both lung bases which was fleeting, mobile and recurrent. In the light of this triad of anemia, hemoptysis and infiltrates, the diagnosis of idiopathic pulmonary hemosiderosis was made and confirmed by three examinations:--Lung biopsy: siderophages were found in the sub-mucosa,--Radio-isotope examination, using Fe 59 which revealed iron deposits in the lung,--A surgical lung biopsy which showed a congestive area and a fibrous area. The congestive area was the site of recent hemorrhage, the alveolar limits were filled with siderophages. The fibrous area was the site of chronic repair of older hemorrhage. It was mutilating. The course was complicated by massive bleeding which led to acute recovering respiratory failure. The patient is at present stabilised by corticosteroids. Three hundred cases of idiopathic pulmonary hemosiderosis have been reported in the world literature. Although the main characteristic is intra-alveolar hemorrhage, its course has not yet been determined. It seems however, to be due to an immunologic process as shown by the relationship between this curious disease and Goodpasture's syndrome.
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PMID:[Idiopathic pulmonary hemosiderosis. Apropos of 1 case]. 18 18

Two brothers, aged 3 and 6 years, respectively, had their pulmonary conditions diagnosed as idiopathic pulmonary hemosiderosis (IPH). Both boys had severe iron-deficiency anemia, chronic cough, hemoptysis, and exertional dyspnea, and one had recurrent epistaxis. The results of light microscopic lung histopathologic studies in both patients showed numerous hemosiderinladen macrophages and chronic interstitial pneumonitis. No specific patterns of immunofluorescence of the alveolar capillary basement membranes were found. The results of electron microscopic examinations showed intact alveolar and capillary basement membranes and no evidence of electron-dense deposits. The lack of clinical or biochemical evidence for renal disease as well as the absence of serum antinuclear and antibasement membrane antibodies excluded associated autoimmune disorders. Evaluation for milk-protein allergy was negative and neither child demonstrated a clinical response to a milk-free diet. Sequential pulmonary function studies performed over four years showed episodes of acute obstructive airway disease that correlated with pulmonary hemorrhage and mild persistent restrictive lung disease. The results of this family study suggested that some cases of IPH may have a genetic basis.
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PMID:Familial idiopathic pulmonary hemosiderosis. 37 18

A male forestry worker presented with chest pain followed by severe continuing haemoptysis and an extensive bilateral nodular pulmonary infiltrate. A needle biopsy of lung demonstrated micronodular deposits of malignant tissue. The patient died from respiratory failure. Necropsy showed a disseminated haemangiosarcoma arising in the right atrium. Haemoglobin and serum iron levels were normal. Electron microscopy of the lung biopsy showed a close relationship between tumour cells and basement membrane and suggested that haemorrhage occurred directly from the tumour nodules. The ultrastructure of alveoli adjacent to tumour deposits was normal. This case provides further indirect evidence that the clinical and histological features of idiopathic pulmonary haemosiderosis cannot be explained by the mere occurrence of alveolar haemorrhage.
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PMID:Pulmonary haemorrhage in disseminated cardiac haemangiosarcoma. 55 87

Two patients, a mother and her son, had idiopathic pulmonary hemosiderosis. In the son, the onset was acute and he died of massive hemoptysis. The mother's disorder developed less acutely and the condition improved after temporary respiratory support and massive corticosteroid therapy. This is the first reported instance of idiopathic pulmonary hemosiderosis occurring in more than one member of the same family. The diagnosis of idiopathic pulmonary hemosiderosis depends on compatible clinical and pathologic data and on exclusion of secondary causes of intrapulmonary hemorrhage.
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PMID:Idiopathic pulmonary hemosiderosis: two cases in a family. 62 56

Anatomic and clinical observations of 28 cases, including 23 previously unpublished, of pulmonary lymphangiomyomatosis are recorded and discussed. This brings the total reported to 57. All patients were women in the reproductive age group with the major complaint of breathlessness. This was usually progressive, and death from pulmonary insufficiency resulted within 10 years. Functional changes were obstructive or restrictive, or both. Pneumothorax, chylous effusions and hemoptysis were frequent complications. Radiographically the lesions initially appear as fine, linear and nodular, predominantly basal densities, and progress to a pattern of bullous change, or honeycombing, involving all portions of the lungs not sparing the region of the costophrenic sinuses as is typical of eosinophilic granuloma. There may be associated pleural effusions. A progressively increasing lung volume is characteristic. The lesions consist of an irregular, nodular or laminar "irrational" proliferation of smooth muscle within all portions of the lung, with loss of parenchyma leading to honeycombing. Proliferated muscle can obstruct bronchioles (with air trapping and formation of bullae often complicated by pneumothorax), venules (with pulmonary hemorrhage and hemosiderosis accompanied clinically by hemoptysis) and lymphatics (with chylothorax or chyloperitoneum). Both thoracic and abdominal lymph nodes and the thoracic duct can also be involved in the myoproliferative process with formation of subsidiary minute channels and obstruction. Renal or perirenal angiomyolipomas can also occur, as exemplified by 2 patients in the present series. Identical pulmonary lesions occasionally occur in tuberous sclerosis. Especially since these patients usually have no neurologic disturbances and are almost women, the possibility of a relationship between tuberous sclerosis and lymphangiomyomatosis must be considered. One feature of note in pulmonary lesions of tuberous sclerosis is the presence of adenomatoid proliferations of epithelium. Such changes were also observed in 2 patients of the present series, and it is remarkable that both of these women had "retarded"children. At present the question of whether by lymphangiomyomatosis is a forme fruste of tuberous sclerosis must be considered as unresolved. It may yield to further investigation, possibility including chromosomal studies.
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PMID:Pulmonary lymphangiomyomatosis. A review. 114 65

The paper is concerned with observations over 3 patients in whom unusual vasculitis lay at the basis of the clinicopathological manifestations. All the patients were men of the young age. The disease debut was marked by fever, weakness, dyspnea, palpitation, cough, hemoptysis, the articulation syndrome. In two cases, there was hemorrhagic rash on the leg skin. All the patients manifested liver and spleen enlargement, two patients had lymphoadenopathy. The leading clinical symptoms included dilated cardiomyopathy, complete blockade of the inferior peduncle of His bundle and reduction of myocardial contractility. Anemia belonged to iron deficient one. The clinical examples provided indicate that immunocomplex vasculitis with evident lesions of the lungs and myocardium, not going into criteria for the known diseases, is not likely to be a casuistic rarity. Those syndromes may be associated with more or less pronounced hemosiderosis of the lungs (and, probably, of the lymph nodes, spleen and liver), with transitory or steady derangements of myocardial conduction, which attests to diffuse lesions of the myocardium possibly with both immune complexes and hemosiderin. The pathology requires further studies.
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PMID:[Generalized immune-complex vasculitis combined with pulmonary hemosiderosis and dilated cardiomyopathy]. 214 20

The case of idiopathic pulmonary hemosiderosis in a 20 year old male is presented. Iron deficiency anemia, recurrent hemoptysis and micronodular infiltrate in lower lung areas were the most important signs observed. The transbronchial biopsy showed alveolar and interstitial hemorrhage and hemosiderin in the pulmonary macrophages. Treatment was started with prednisone, but the addition of immunosuppressive drugs (cyclophosphamide) was needed, followed by a clinical remission.
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PMID:[Idiopathic pulmonary hemosiderosis in the adult: a case report]. 229 62

Alveolar hemorrhage (AH) is the result of diffuse bleeding into the acinar portion of the lung. Cardinal symptoms of AH include hemoptysis, dyspnea, alveolar filling opacities on chest roentgenogram, anemia and hypoxemia. However, AH is often misdiagnosed as pneumonia or pulmonary edema at the time of initial presentation. Isolated AH may occur but is more often seen in diffuse connective tissue diseases or in rapidly progressive glomerulonephritis. - At the Medical Clinic of the University Hospital of Zurich we have diagnosed AH in 18 patients (13 males, 5 females) over the last ten years (1978-1988). In 2 patients AH occurred as an isolated symptom: once due to occupational inhalation of fumes containing trimellitic anhydride, and once as so-called idiopathic pulmonary hemosiderosis. In 16 patients AH was associated with kidney disease, including the following disorders: vasculitis and collagen vascular disorders (9), rapidly progressive glomerulonephritis (4) and Goodpasture's syndrome (3). In 5 patients the presenting symptom was AH. 9 patients presented initially with renal symptoms and in 2 patients renal and pulmonary features occurred simultaneously. 7 patients died of the underlying disease or its complications. Both patients with isolated AH have survived. In the remaining 9 patients 1 required dialysis temporarily and 4 permanently. All patients except the one with AH due to inhalation of trimellitic anhydride were treated with immunosuppressive agents. - Since the pulmonary features are similar in each of the AH syndromes, diagnosis of the underlying disorder is heavily dependent upon pathologic evaluation of diseased extrapulmonary organs. Moreover, immunologic studies are essential. Failure to diagnose or treat AH syndromes in the early stages may have lethal consequences.
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PMID:[Alveolar hemorrhage]. 268 52

A 24-year-old male with recurrent hemoptysis due to idiopathic pulmonary hemosiderosis and celiac sprue developed infranodal heart block necessitating implantation of a pacemaker. A possible common underlying mechanism is discussed.
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PMID:Idiopathic pulmonary hemosiderosis, complete heart block and celiac disease. 273 Oct 63

The diagnosis of pulmonary hemorrhage syndromes (PHS) rests on a body of clinical and paraclinical evidence found in all etiologic forms. Usually, the combination of hemoptysis, iron deficiency anemia, and roentgenologic infiltrates is easy to recognize; in more atypical cases, alveolar bleeding can be demonstrated by determination of the Golde score on bronchoalveolar lavage specimens. Whereas clinical features are nearly invariable, etiologies cover a broad spectrum including some glomerular diseases, idiopathic pulmonary hemosiderosis, connective tissue disorders, pulmonary conditions related to compromised immunity, airborne pulmonary aggressions, and some apparently primary vascular disorders. Regardless of the severity of clinical features at presentation, pulmonary hemorrhage syndromes are always a diagnostic and therapeutic emergency.
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PMID:[Pulmonary hemorrhagic syndromes. Clinical and diagnostic approach]. 281 96


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