Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Goodpasture's syndrome has characteristically been described as being mediated by IgG antibodies. We have recently seen a 55-year-old man who developed renal failure and hemoptysis; a renal biopsy showed linear deposits of IgA and C3 involving glomerular and tubular basement membrane. Serologic tests for detecting (IgG) antiglomerular basement membrane antibodies were negative. Elution studies of kidney and lung showed the presence of an IgA antibasement membrane antibody only. The patient's serum contained IgA, but not IgG, antibodies reactive with glomerular and tubular basement membrane of normal human kidney and alveolar basement membrane of normal human lung. Attempts to transfer disease with the patient's IgA antibody to a monkey and to Lewis and Brown-Norway rats were unsuccessful. Immunoglobulin A antibasement membrane antibody must be considered in the design of immunoserologic procedures for the diagnosis of Goodpasture's syndrome.
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PMID:IgA antibasement membrane nephritis with pulmonary hemorrhage. 11 92

This is a very rare case report of Goodpasture's syndrome with IgA antibasement membrane antibody. A 43-year old male was admitted because of severe dyspnea with slight hemoptysis. Chest X-ray demonstrated extensive bilateral infiltrates with air bronchogram, predominantly in the right lung. Laboratory data on admission showed severe anemia and moderate renal impairment. The pulmonary infiltrates resolved spontaneously within 10 days. Goodpasture's syndrome or collagen vascular disease was suspected and he underwent a percutaneous renal and transbronchial lung biopsy. The renal biopsy showed crescent formation affecting 70-80% of glomeruli. Linear IgA deposits, but not IgG, were demonstrated along the glomerular basement membrane by the direct immunofluorescence procedure. The lung biopsy contained many hemosiderin-laden macrophages in the lumen of the alveoli and showed mild thickening of alveolar walls. However, linear immunoglobulin deposits on the alveolar capillary basement membrane were not demonstrated by direct immunofluorescence. The diagnosis of Goodpasture's syndrome with IgA antibasement membrane antibody was made. His serum was negative for antibasement antibody by indirect immunofluorescence. He was treated with prednisone, 30 mg daily. His pulmonary symptoms and anemia improved markedly, but his renal function did not change. Thirteen months after his first admission, he suffered from severe bacterial pneumonia, which was complicated by disseminated intravascular coagulation. He died of respiratory failure. Autopsy was rejected.
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PMID:[A case of Goodpasture's syndrome with IgA antibasement membrane antibody]. 221 6

A 64-year-old woman with a monoclonal gammopathy was admitted to Nagoya National Hospital with the complaint of occasional hemoptysis. On examination, there was no hepatosplenomegaly or no lymphadenopathy. The hemoglobin was 10.1 g/dl; platelets 22.5 X 10(4)/microliters; white blood cells 4.9 X 10(3)/microliters, with 4% of atypical lymphocytes. Immunoglobulin analysis of the serum by immunodiffusion revealed an IgG of 1,459 mg/dl, an IgA of 219 mg/dl, and an IgM of 5,091 mg/dl. Serum viscosity was 4.9. Serum immunoelectrophoresis demonstrated atypical precipitant arcs reacting with mu and kappa antisera. Urine immunoelectrophoresis showed a positive reaction against kappa antiserum. Radiologic studies of the bones revealed generalized osteoporosis with multiple punched out lesions of the skull. Thirty percent of bone marrow nucleated cells was atypical plasma cells, the presence of which was verified by electron microscopy. Although they were positive mainly for cytoplasmic mu and kappa chains by immunoperoxidase studies, cells positive for gamma, alpha, or lambda chains were occasionally found, indicating that normal immunoglobulin synthesis was not suppressed in this case of IgM myeloma.
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PMID:[IgM myeloma without depression in serum IgG and IgA--a case report]. 250 75

A patient is described with an asymptomatic exacerbation of allergic bronchopulmonary aspergillosis (ABPA), clinically characterized by pulmonary infiltrates, with absence of obstructive reactions and a short period of hemoptysis 2 weeks before hospitalization. Cell counts and antibody concentrations were measured in serum, and bronchoalveolar fluid (BAF) samples and values were compared with data from previous periods of symptomatic exacerbations. During the asymptomatic exacerbation, concentrations of antibody to Aspergillus fumigatus, total IgE, and precipitating antibodies were elevated in peripheral blood. No quantitative differences in specific antibody concentrations (IgE, IgG, IgA, and IgM) against A. fumigatus were found between sera from symptomatic and asymptomatic periods of ABPA. In contrast to observations in the serum, protein concentrations in BAL fluid were normal during the asymptomatic period, whereas high concentrations were found during the symptomatic phases. Local antibody concentrations (in BAF) were characterized by high levels of IgA antibodies against A. fumigatus. During asymptomatic and symptomatic phases, eosinophils were elevated in peripheral blood, in sputum, in BAF, and highly elevated in tissue biopsy specimens. Activated eosinophils were found, as indicated by the presence of light-density cells in the circulation and monoclonal antieosinophil cationic protein binding to bronchoalveolar lavage eosinophils. In contrast to the symptomatic phase of ABPA in 1980, demonstrating aspecific airway reactivity to several pharmacologically active substances, no such hyperreactivity was found during the asymptomatic phase of ABPA in 1986. It is proposed that the asymptomatic infiltrative phase of ABPA is an intermediate stage that can develop into a symptomatic phase after prolonged and intensified infiltration of eosinophils. Mediators from the inflammatory cells may be involved in the induction of bronchial hyperresponsiveness. After induction of this hyperreactive stage of the airways, additional liberation of mediators from either eosinophils and/or mast cells will lead to a symptomatic (obstructive) phase of ABPA.
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PMID:Cellular and humoral observations in a patient with allergic bronchopulmonary aspergillosis during a nonasthmatic exacerbation. 270 43

A 54-year-old man is described, suffering from adult linear IgA bullous dermatosis with involvement of the bronchial mucosa. The main respiratory symptoms were recurring haemoptysis, episodic narrowing of the airways and persistent non-specific bronchial hyperreactivity. On CT scan the trachea had a saber-sheath shape with tracheal ring calcification. Endoscopically the tracheo-bronchial mucosa was diffusely purpuric and hyperaemic and also showed pale elevated plaques, bullous lesions and ulceration. Histological examination of biopsies of skin and nasal and tracheo-bronchial mucosa showed subepithelial blister formation associated with an accumulation of polymorphonuclear cells at the epithelial-subepithelial junction, and linear IgA deposits on direct immunofluorescence.
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PMID:Adult linear IgA bullous dermatosis with bronchial involvement. 355 99

A young woman presented with arthralgia, a rash and dramatic haemoptysis, and renal involvement was indicated by proteinuria, haematuria and a rising serum creatinine. A systemic vasculitic disorder was suspected initially, but the diagnosis of Henoch-Schonlein purpura was established by the finding of mesangial IgA deposits on renal biopsy. Immunofluorescent study of renal biopsy material is vital to diagnosis where the clinical features of Henoch-Schonlein purpura and those of the systemic vasculitides with renal involvement prove to be indistinguishable.
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PMID:Henoch Schonlein purpura presenting with pulmonary haemorrhage. 356 74

The immunological and clinical features of 90 Javanese patients with smear -positive pulmonary tuberculosis were investigated. Many of the patients had advanced disease at the time of diagnosis and haemoptysis was common, especially in patients with cavitating lesions. Most patients had a significant elevation of one or more non-specific indicators of inflammation (erythrocyte sedimentation rate, third complement component, factor B and C-reactive protein). Rheumatoid factor was detected in 21% of the patients and was significantly associated with high levels of antibodies to M. tuberculosis in the IgM class. Five distinct responses were elicited by tuberculin testing; the most marked occurred at 24 hours. The degree of reaction at 6-8 hours correlated significantly with the levels of specific antibodies in the IgG and IgA classes and the 48 hour response correlated, although less markedly, with specific antibodies in the IgG class. Neither the degree of skin test reactivity nor the level of specific antimycobacterial antibodies correlated with the extent of disease as assessed radiologically. Nine per cent of the patients were skin-test negative at 48 hours but did not differ clinically, as a group, from tuberculin positive patients. It was not possible to place the cases in a spectrum of immunological responses similar to that occurring in leprosy and it is postulated that this is due to differences in the relevance to protection of the various immunological mechanisms in the two diseases. The need to establish more rigorous criteria for assessing the immune responses in tuberculosis and for studying the interactions between the protective and non-protective reactions is stressed.
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PMID:Immunological and clinical features of smear-positive pulmonary tuberculosis in East Java. 679 56

Extramedullary plasmacytoma is a rare form of plasma cell tumor that frequently involves the upper respiratory tract. Primary pulmonary plasmacytoma is even more rare. The usual presentation of primary pulmonary plasmacytoma is a solitary pulmonary nodule. We describe the case of a 58-year-old woman who presented with the chief complaints of progressive dyspnea on exertion, cough, and subsequently, hemoptysis. The main finding on chest imaging studies, including plain radiography, sonography, computed tomography, and magnetic resonance imaging, was consolidation of the right middle lobe. Percutaneous transthoracic lung biopsy of the right middle lobe demonstrated sheets of atypical plasma cells. Immunohistochemical study showed IgA lambda monoclonality. A bone marrow study and whole body bone scan showed normal findings. To the best of our knowledge, this is the first reported case of primary pulmonary plasmacytoma presenting with lobar consolidation of the lung but without a well-defined tumor mass.
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PMID:Primary pulmonary plasmacytoma with lobar consolidation: an unusual presentation. 970 Feb 50

A 19-year-old man presented to the emergency department with a chief complaint of generalized body rash for two weeks. The rash began shortly after he initiated penicillin therapy for a sore throat diagnosed one week previously. He also complained of having dark urine and abdominal discomfort. His urinalysis revealed proteinuria and hematuria, and he was admitted for further evaluation and management. While in the hospital, he had an episode of hemoptysis. A renal biopsy was performed and revealed IgA deposition. In light of his systemic symptoms including rash and abdominal pain, he was diagnosed with Henoch-Schonlein purpura (HSP).
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PMID:A 19-year-old man presenting with a generalized body rash. 1287 99

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


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