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

Pulmonary hemosiderosis (PH) has been described in association with a variety of immunological and non-immunological diseases. It is characterised by iron-deficiency anaemia, hemoptysis and diffuse pulmonary infiltrates based on recurrent intraalveolar hemorrhages. We present the case of a child with pulmonary hemosiderosis and a pathological gastroesophageal reflux activity. The child suffered from recurrent anaemic episodes the age of three months (hemoglobin level up to 5.4 g/dl). The symptoms decreased after removal of the gastroesophageal reflux and accompanying steroid therapy. There has been one relapse of pulmonary hemorrhage seven months later (hemoglobin level 6.1 g/dl). Since then the patient has been in good general condition and the steroid was slowly reduced. No more anaemic episodes occurred. We discuss a possible association of pathological gastroesophageal reflux activity in pulmonary hemosiderosis.
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PMID:[Pulmonary hemosiderosis and gastroesophageal reflux in an infant]. 973 94

Idiopathic pulmonary haemosiderosis (IPH) is a rare clinical entity characterized by recurrent episodes of diffuse alveolar haemorrhage, often presenting with haemoptysis. Many patients have iron deficiency anaemia due to deposition of haemosiderin iron in the alveoli, and eventually develop moderate pulmonary fibrosis. Typically, intensive search for an aetiology ends up negative. There is no evidence of pulmonary vasculitis or capillaritis. The aetiology is obscure, but may be an immunological or toxic mechanism causing a defect in the basement membrane of the pulmonary capillary. IPH affects both children and adults. During an acute episode, a chest X-ray demonstrates bilateral, alveolar infiltrates. Sputum examination discloses haemosiderin-laden alveolar macrophages. Diagnosis is established by lung biopsy (fiber-optic or thoracoscopic), showing large numbers of haemosiderin-laden macrophages in the alveoli and without evidence of capillaritis or deposition of immunoglobulins. Corticosteroids and/or immunosuppressive drugs may be effective during an acute bleeding episode, and may in some patients improve symptoms and prognosis on the long-term, but the response to treatment displays great interindividual variation.
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PMID:Idiopathic pulmonary haemosiderosis. Epidemiology, pathogenic aspects and diagnosis. 1007 May 62

Idiopathic pulmonary hemosiderosis (IPH) is a rare disease of unknown etiology characterized by hemoptysis, diffuse pulmonary infiltrates and iron-deficiency anemia. It is typically found in children and young adults. Finding that the concentration of siderophages exceeds 20% in bronchoalveolar lavage indicates a diagnosis of IPH. We report the case of a 72-year-old man with repeated diagnoses of respiratory infection, bronchiectasis and melena. Because such a clinical picture is rare for IPH, the final diagnosis was obtained by open lung biopsy.
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PMID:[Idiopathic pulmonary hemosiderosis in a patient of advanced age]. 1100 93

Idiopathic pulmonary hemosiderosis is a rare condition manifested by recurrent pulmonary hemorrhage of unknown cause, diffuse radiologic abnormalities, cough, hemoptysis and moderate to severe hypochromic anemia. Diagnosis can be confirmed by iron stains of the sputum or lung aspiration or by biopsy. Prolonged spontaneous remission may occur without the use of corticosteroid therapy. Studies here reported indicated that the anemia is hypochromic and microcytic anemia of blood loss and iron deficiency, in spite of the presence of large amounts of iron in the pulmonary tissue. Correction of the anemia by intensive iron therapy and transfusion is considered an important part of therapy.
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PMID:Idiopathic pulmonary hemosiderosis. 1378 18

Heiner syndrome (HS) is a food hypersensitivity pulmonary disease that affects primarily infants, and is mostly caused by cow's milk (CM). Only a few reports have been published, which may be due to its misdiagnosis. We review here a series of eight cases. When first diagnosed they were 4-29 months of age. They were fed CM from birth and their chronic respiratory symptoms began at age 1-9 months. The symptoms were in the form of cough in seven, wheezing in three, hemoptysis in two, nasal congestion in three, dyspnea in one, recurrent otitis media (OM) in three, recurrent fever in four, anorexia, vomiting, colic or diarrhea in five, hematochezia in one, and failure to thrive (FTT) in two. All had radiologic evidence of pulmonary infiltrates. High titers of precipitating antibodies to CM proteins were demonstrated in six of six and milk-specific immunoglobulin E (IgE) was positive in one of two. Pulmonary hemosiderosis (PH) was confirmed in one patient who showed iron-laden macrophages (ILM) in the bronchoalveolar lavage (BAL), gastric washing, and open lung biopsy. Additional findings, in a descending frequency, were eosinophilia, anemia, and elevated level of total IgM, IgE or IgA. Milk elimination resulted in remarkable improvement in symptoms within days and clearing of the pulmonary infiltrate within weeks. Parents consented to milk challenge in only three cases, all of whom developed recurrence of symptoms. After 2 yr of milk avoidance in one patient, milk challenge was tolerated for 2 months, and then the patient developed symptoms, serum milk precipitins, pulmonary infiltrate, and ILM. The HS should be suspected in young children with chronic pulmonary disease of obscure cause. The diagnosis is supported with a positive milk precipitin test and improvement on a trial of milk elimination. Severe cases may be complicated with PH, which should be suspected in the presence of anemia or hemoptysis and be confirmed with the demonstration of ILM.
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PMID:Milk-induced pulmonary disease in infants (Heiner syndrome). 1617 5

Restless leg syndrome (RLS) and periodic limb movement disorder (PLMD) are considered to be a continuum of a neurological sleep disorder associated with abnormal iron metabolism or deficiency. I describe a case of RLS and PLMD in a cystic fibrosis patient with iron deficiency from chronic hemoptysis. This is the first case that reports RLS and PLMD manifesting from iron deficiency caused by chronic hemoptysis in advanced cystic fibrosis lung disease.
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PMID:Restless leg syndrome manifested by iron deficiency from chronic hemoptysis in cystic fibrosis. 1698 19

We report a case of hemorrhagic pulmonary oxalosis secondary to a noninvasive Aspergillus niger fungus ball. A patient with cavitary lung disease and hemoptysis developed progressive lung infiltrates and intractable metabolic acidosis leading to death. At autopsy, aspergillomas were identified in both the right upper and middle lobes surrounded by a large rim of necrotic and hemorrhagic parenchyma. Microscopic examination showed extensive crystal deposition and vascular thrombosis. Fungal growth was limited to the intraluminal mycelia, and no tissue or blood vessel invasion was present. Remote crystal deposits were also localized in the absence of fungal organisms to the contralateral lung and to the tubules of both kidneys. The crystals were birefringent in polarized light and stained with colloidal iron. X-ray powder diffractometry and electron impact ionization mass spectrometry identified the crystals as calcium oxalate monohydrate. Furthermore, non-necrotizing granulomatous lesions were identified in the lungs, liver, and spleen, consistent with sarcoidosis, and may have predisposed this patient to developing pulmonary aspergillomas.
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PMID:Hemorrhagic pulmonary oxalosis secondary to a noninvasive Aspergillus niger fungus ball. 1778 71

The significance of severe pulmonary intra-alveolar hemosiderosis in sudden infant death is controversial in forensic pathology. We report a previously healthy 9-month-old female infant who died suddenly and unexpectedly after being placed and then found prone in her crib. Her gestation and delivery were uncomplicated, and she had no history of anemia, hemoptysis, chest trauma, or chronic lung disease. Autopsy revealed diffuse severe pulmonary congestion and severe multifocal intra-alvedar hemorrhage. Metabolic and toxicological screening, microbiologic cultures, and vitreous chemistry were noncontributory. A diagnosis of SIDS had been made by the medical examiner. Subsequent semiquantitative assessment of the severity of pulmonary intra-alveolar hemosiderosis prompted consideration of other disorders, including a heretofore undescribed lethal infantile variant of idiopathic pulmonary hemosiderosis, but none could be confirmed. Therefore, we assigned a study diagnosis of unclassified sudden infant death. We recommend that a diagnosis of SIDS not be made in cases with unexplained large numbers of intra-alveolar PS. We also recommend that quantitative assessment of lung sections stained for iron be undertaken in cases with numerous intra-alveolar macrophages in order to accumulate data that might allow diagnostic correlations with the circumstances of death and autopsy findings.
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PMID:Unclassified sudden infant death associated with pulmonary intra-alveolar hemosiderosis and hemorrhage. 1796 71

Pulmonary thromboembolism is a life-threatening condition resulting mostly from lower extremity deep-vein or pelvic-vein thrombosis. A 46-year-old woman was admitted to hospital with pain on the right side of the chest and hemoptysis. On laboratory analysis, D-dimer level was elevated. Computed tomographic pulmonary angiography revealed intravascular filling defects due to thrombi in right lower lobe pulmonary segmental arteries. Screening for thrombophilic states was normal except for heterozygous mutations of both prothrombin and methylene tetrahydrofolate reductase (MTHFR 677) genes. Homocysteine level was high, and vitamin B12 level and serum ferritin level were reduced. Serum antiparietal antibody was positive, and therefore, pernicious anemia was diagnosed along with iron-deficiency anemia. After the diagnoses were established, enoxaparin followed by warfarin was started in addition to oral vitamin B12, pyridoxine, thiamine, folic acid, and ferroglycine sulfate supplementation. At the end of 8 weeks of the replacement therapy, vitamin B12, folate, and homocysteine levels and red cell volume were found to be normal, with complete resolution of the thrombus confirmed by repeat computed tomographic pulmonary angiography. We conclude that hyperhomocysteinemia due to vitamin B12 deficiency associated with pernicious anemia might have decreased the threshold for thrombosis. In addition, the presence of heterozygous prothrombin and methylene tetrahydrofolate reductase mutations might serve as synergistic cofactors triggering pulmonary thromboembolism.
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PMID:Hyperhomocysteinemia due to pernicious anemia leading to pulmonary thromboembolism in a heterozygous mutation carrier. 1858 84

Idiopathic pulmonary hemosiderosis (IPH) is a rare disorder (triad of iron-deficiency anemia, hemoptysis, and alveolar infiltrates). A 3-year-old male presented with mild fever, breathlessness, dry cough, and bluish nail discoloration for 8 days. He had required five blood transfusions in the past 1 year (last transfusion was given 4 months ago). He had a respiratory rate of 58/min with respiratory distress, cyanosis, and grade III clubbing. Respiratory system examination was normal. Several previous reports of hemoglobin were as low as 3.6 g/dl with hypochromic and microcytic anemia. There were transient increases in the hemoglobin and normalization of red cell morphology with blood transfusions. Serum iron, G6PD enzyme assay, hemoglobin electrophoresis, the sickling test, Coomb's test, stool and urine analysis, and a Meckel's scan were normal. HIV antibody and dsDNA were negative. The chest radiograph revealed symmetrical patchy infiltrates sparing lung apices (confirmed on high-resolution computed tomography). Lung biopsy diagnosed pulmonary hemosiderosis (interstitial lung disease with hemosiderin-laden macrophages scattered in the alveoli and areas of fibrosis in the alveolar septa). The patient showed marked clinical improvement in 10 days of therapy with prednisolone. IPH should be listed in the differential diagnosis of a child presenting with unexplained hypochromic, microcytic anemia and respiratory symptoms.
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PMID:Idiopathic pulmonary hemosiderosis: alveoli are an answer to anemia. 2120 22


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