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

Invasive pulmonary aspergillosis is an important cause of morbidity and mortality in granulocytopenic patients. The purpose of this article is to review the current understanding of the microbiology, hospital epidemiology, clinical manifestations, diagnosis, prevention, and treatment of invasive pulmonary aspergillosis. Aspergillus conidia (spores) are inhaled from environmental sources into the paranasal sinuses and lower respiratory tract. Persistent fever, pulmonary infiltrates, and pleuritic pain in granulocytopenic patients receiving antibacterial antibiotics is a common manifestation of invasive pulmonary aspergillosis. Computerized tomographic scans of the chest often reveal characteristic peripheral nodules that also may progress to characteristic cavitary lesions. Hemoptysis may develop due either to hemorrhagic infarction during granulocytopenia or to the rupture of mycotic aneurysms during recovery from granulocytopenia. Aspergillus organisms may extend locally from the lung to involve other thoracic structures, including the heart and chest wall, and may disseminate to extrapulmonary sites, such as the brain, where focal neurological deficits ensue. Early diagnosis of invasive pulmonary aspergillosis may be difficult. Isolation of Aspergillus organisms from respiratory secretions of a persistently febrile granulocytopenic patient is usually indicative of invasive pulmonary aspergillosis and should not be dismissed as a contaminant or saprophyte. Amphotericin B is the treatment of choice; however, high dosages (1.0 to 1.5 mg/kg/day) are often necessary. Aspergillosis may develop in granulocytopenic patients who are already receiving empirical amphotericin B in lower doses (0.5 to 0.6 mg/kg/day). It is hoped that further investigation directed toward an understanding of pathogenesis, improving diagnostic methodology, and developing new therapeutic and preventive strategies will improve the outcome of this life-threatening infection.
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PMID:Invasive pulmonary aspergillosis in patients with neoplastic diseases. 224 6

Immediately after induction therapy for acute lymphoblastic leukemia, a 2 1/2-year-old child developed invasive pulmonary aspergillosis revealed by pneumothorax, an unusual manifestation. Despite treatment with amphotericin B, status epilepticus occurred; this manifestation was related to diffuse ischemic cerebral lesions probably caused by cerebral aspergillosis. Outcome was fatal. Early invasive pulmonary aspergillosis is responsible for non-specific pneumonia. Thoracic CT scan and fiberoptic bronchoscopy are informative investigations. At recovery of bone marrow aplasia, the occurrence of hemoptysis and the discovery of excavated lesions on roentgenograms are suggestive of the diagnosis. Cerebral aspergillosis should be routinely considered whenever neurologic symptoms develop in a patient with agranulocytosis, fever, and pneumonia. The prognosis of invasive aspergillosis depends above all on the promptness of treatment; amphotericin B should be given intravenously whenever broad spectrum antimicrobial therapy fails to induce apyrexia in a patient with agranulocytosis.
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PMID:[Fatal cerebral and pulmonary aspergillosis in acute leukemia in a child]. 226 96

Pulmonary fungal infections complicating hematological malignancies are difficult to diagnose antemortem because clinical findings are actually considered to be not specific. From December 1984 to June 1986 we documented the clinical findings in sixteen patients, 9 with ANLL, 6 with ALL and 1 with CML + BC; all patients were diagnosed as pulmonary fungal infection and treated for this complication. Pulmonary infiltrates occurred after severe aplasia (range 5-90 days) or during bone marrow relapse. We studied pulmonary signs and symptoms (pleuritic pain, cough, hemoptysis, shortness of breath, rales, rub, bronchial murmur) both at the beginning and during the management of this infectious complication and we related them to chest x-ray findings, the duration of granulocytopenia, and fever. Our purpose was to identify clinical characteristics for these episodes and establish roentgenological criteria for prognosis. These findings should improve the possibilities for an early diagnosis and prompt treatment.
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PMID:[Pulmonary mycosis as a complication of acute leukemia in the adult. Diagnostic study]. 274 May 98

The recognition of aspergillus in all its clinical disguises remains a challenge to clinicians in all fields of medicine. Fortunately, aspergillus has low pathogenicity for humans and requires very heavy inoculum of spores (aspergillary pneumonitis) in order to infect those whose pulmonary defense mechanisms, inherent structure, and physiology are intact. Patients with problems from aspergillus may be seen in either inpatient or outpatient clinical practice. The patient with fibrotic or cavitary lung disease finds himself at risk to be colonized and develop an aspergilloma (fungus ball). Conservative therapy (that is, antibiotics, pulmonary hygiene) or simple observation is often all that is required. With significant hemoptysis, surgical removal could be definitive treatment; but these patients often have such compromised pulmonary function that alternative therapies like infusion of antifungal agents locally are tempting. Part of the problem of the patient with asthma or COPD may actually be secondary to hypersensitivity to aspergillus (ABPA), which exacerbates bronchospasm and adds "pulmonary infiltrates" to the underlying disease. The recognition of this entity and then the judicious use of corticosteroids to control the symptoms will stabilize the clinical course of the disease. The immunocompromised patient may be relatively free of pulmonary disease.; but aspergillus, waiting until cytotoxic agents, corticosteroids, granulocytopenia, broad-spectrum antibiotics, and previous pneumonias destroy the local lung defense mechanisms, will then attack with a vengeance. The resultant invasive pulmonary aspergillosis requires treatment with amphotericin B, along with its own inherent toxicity.
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PMID:The many faces of pulmonary aspergillosis. 389 65

The influence of bone marrow recovery on the clinical and radiographic course of invasive pulmonary aspergillosis in patients with acute leukemia has not been well characterized. We studied 26 patients with acute leukemia and invasive pulmonary aspergillosis, comparing those who recovered from chemotherapy-induced granulocytopenia (Group 1, 15 patients) with those who did not (Group 2, 11 patients). Radiographic evidence of pulmonary cavitation was not seen in any Group 2 patient, but developed in 11 of 15 (73%) Group 1 patients (p less than 0.005). In these patients, cavitation always occurred after marrow recovery, an average of 2.0 days (range: 0 to 6 days) after the granulocyte count exceeded 500/mm3. Eight patients in Group 1 and 2 in Group 2 experienced a total of 38 episodes of hemoptysis. Four of the 26 patients, all in Group 1, developed massive hemoptysis (greater than 150 ml of blood per episode), leading to 1 death. In 3 of these 4 patients, cavitation preceded the episode of massive hemoptysis. At the time of massive bleeding, the granulocyte count was greater than 500/mm3, the platelet count greater than 38,000/mm3, and the other coagulation parameters were normal in all 4 patients. Our findings demonstrate that in patients with acute leukemia undergoing chemotherapy, bone marrow recovery markedly influences the clinical and radiographic course of invasive pulmonary aspergillosis. Development of a granulocyte count greater than 500/mm3 is associated with pulmonary cavitation, and on occasion with massive hemoptysis.
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PMID:Pulmonary cavitation and massive hemoptysis in invasive pulmonary aspergillosis. Influence of bone marrow recovery in patients with acute leukemia. 396 97

This case describes a 42-year-old female with longstanding history of rheumatoid arthritis (RA) and Felty syndrome (FS). She presented with acute renal kidney failure, skin rash and hemoptysis. A clinical suspicion of small vessel vasculitis (SVV) was thought, serology was also positive for various markers of SVV. However, these serology markers could be false-positive in a patient of rheumatoid arthritis. A renal biopsy was performed that led to the final diagnosis of cryoglobulinemic vasculitis. Patient was managed according to the standard guidelines for therapy (plasmafiltration and immunosuppression). It is challenging to manage a patient of RA, in the presence of Felty syndrome-related granulocytopenia and thrombocytopenia. Patient initially showed signs of improvement, but finally succumbed to complications of therapy. The case provides insight into the diagnosis and management of such cases.
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PMID:Female with rash, acute kidney failure and rheumatoid arthritis. 2302 60