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)

Patients with cancer frequently develop pneumonitis for which no cause is documented ante mortem. Noninvasive diagnostic techniques, such as sputum induction, are generally inadequate, especially in myelosuppressed patients. To avoid pulmonary contamination with organisms colonizing the oronasopharynx and to obtain uncontaminated speciemens, 38 patients underwent bronchial brushing utilizing a transtracheal approach after sputum induction and transtracheal aspiration failed to establish the etiology. Patients with thrombocytopenia were brushed after platelet transfusion. Eleven patients were not clinically considered to be infected; seven proved to have pulmonary metastases, of which one case was diagnosed by this technique; and four patients in whom no diagnosis was obtained by brushing subsequently proved to have interstitial fibrosis (three cases) or a collapsed lobe (one case). Twenty-seven patients were clinically presumed to be infected. Ultimately, 17 of these 27 patients were proven to have pulmonary infection, and 14 of these 17 were etiologically documented by brushing. In ten of the 27 patients presumed to be infected, no etiology could be established by any method. Seven of these ten patients were receiving broad-spectrum antibiotic therapy at the time. Significant but nonfatal complications, including hemoptysis, pneumothorax, and cervical cellulitis, occurred in seven patients; however, this procedure is a relatively safe and useful method to include in the orderly evaluation of myelosuppressed cancer patients with suspected pulmonary infections.
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PMID:Transtracheal selective bronchial brushing for pulmonary infiltrates in patients with cancer. 97 5

Two cases of adult respiratory distress syndrome due to diffuse pulmonary haemorrhage are reported. The first patient was treated with azathioprine, prednisolone, cyclosporine and ranitidine for haemorrhagic rectocolitis; the second has untreated primary biliary cirrhosis. Haemoptysis only occurred in the latter. Both had severe isolated hypoxaemia. Chest X-rays revealed bilateral alveolar infiltrates. Bronchoscopies showed a diffusely bleeding bronchial tree. Both patients recovered after having been mechanically ventilated with positive end-expiratory pressure for six and eight days respectively. The cause of the diffuse pulmonary haemorrhage was, in the first case, severe thrombocytopaenia (17,000 G.1-1) of central origin, and, in the other patient, an unspecified vasculitis. Diffuse pulmonary haemorrhage should be added to the list of possible causes of the adult respiratory distress syndrome.
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PMID:[Acute respiratory insufficiency caused by diffuse pulmonary hemorrhage]. 150 95

Post-transfusion purpura is characterized by the occurrence of acute immune thrombocytopenia 5 to 10 days after transfusion of platelet-containing blood products in subjects who had been alloimmunized to specific platelet antigens. Four cases are reported here. Three of these 4 patients, who had a rare PLA1 platelet phenotype, had developed, during a previous sensitization (pregnancy n = 2, transfusion n = 1), an allo antibody directed against PLA1 antigen. The fourth patient presented a specific anti-PLA2 antibody. Thrombocytopenia (platelet count between 4 and 40 x 10(9)/1) appeared 1 to 12 days after the responsible transfusion and showed as haematomas (n = 3) or haemoptysis (n = 1). One patient was asymptomatic and remained untreated. The remaining 3 patients received corticosteroids orally associated, in one case, with infusions of human immunoglobulin concentrates. Thrombocytopenia was corrected within 5 to 13 days. In such cases, whenever another blood transfusion is necessary, a preventive treatment with perfectly platelet-free blood products is mandatory. Platelet depletion by freezing-thawing of red cell concentrates is probably not always sufficient, since recurrence was observed with such a product in one of our patients. The exact cause of immune destruction of autologous platelet remains a mystery.
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PMID:[Post-transfusion purpura. An unknown cause of acute immune thrombocytopenia. 4 new cases]. 214 98

A 56-year-old man had dyspnea, weight loss, hemoptysis, and a generalized bleeding diathesis. Physical examination disclosed hepatosplenomegaly, congestive heart failure, and multiple sites of bleeding. Severe anemia, thrombocytopenia, rouleaux formation, and a leukocytosis with circulating immature plasma cells were observed, along with azotemia, hyperuricemia, and marked elevation of total proteins with a monoclonal IgG kappa spike. The finding of increased serum viscosity confirmed the clinical impression of the hyperviscosity syndrome. Emergency plasma exchange produced marked improvement in the clinical manifestations of hyperviscosity syndrome. Systemic chemotherapy resulted in a partial remission of the disease, but the patient ultimately died of complications of treatment. In this review, we discuss the diagnosis and management of the hyperviscosity syndrome.
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PMID:Plasma cell leukemia and hyperviscosity syndrome. 219 91

Trimetrexate glucuronate (TMTX) is a methotrexate (MTX) analog that is active against transport-deficient MTX-resistant tumor cells. We performed a phase I study of TMTX administered by daily bolus for 9 consecutive days since this schedule is one of the most active in experimental murine tumor models. The drug was administered in this fashion every 4 weeks for at least two cycles. Fifteen patients with refractory metastatic cancers were studied and all had received prior chemotherapy. The dose-limiting toxicity was a rapidly reversible thrombocytopenia first seen at a daily dose of 4.0 mg/m2 which occurred 7 days after the end of TMTX administration. There was great inter- and intrapatient variability in the platelet nadirs observed in the six patients treated at 4.0 mg/m2. One patient died of massive hemoptysis during a platelet nadir at that dose level. Granulocyte counts never dropped below 1500/mm3. Only one patient had significant non-hematological toxicity: a radiation recall skin toxicity along with a self-limited maculopapular rash. One patient with melanoma and lung metastases treated at 4.0 mg/m2 had a partial response. TMTX plasma levels were measured by HPLC every 3 days prior to daily dosing in patients receiving 4 mg/m2 to determine whether drug accumulation occurred during this prolonged administration schedule. Nadir drug levels varied from less than 0.02 to 0.35 microM and did not seem to increase during the 9-day schedule in individual patients. By comparison with other phase I trials, the hematologic toxicity of TMTX seems to be schedule-dependent, with less drug being tolerated and more severe thrombocytopenia observed with more protracted treatment protocols. A firm phase II starting dose for daily bolus X 9 schedules is difficult to recommend in view of the variable toxicity observed in the patients treated at 4.0 mg/m2 daily, who, in addition, had all been extensively pretreated. A reasonable starting dose might be 3.0 mg/m2 daily with built-in dosage increases or decreases.
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PMID:A phase I study of trimetrexate, an analog of methotrexate, administered monthly in the form of nine consecutive daily bolus injections. 295 89

Eight cases of pulmonary involvement were observed in 17 severe cases of ictero-haemorrhagic leptospirosis. Haemoptysis (7 cases) occurred on the 4th day of the infectious syndrome and was associated with other haemorrhagic manifestations in 4 cases. Cough, pain and polypnoea were not constant. Chest X-ray showed diffuse, non-specific changes, such as nodular opacities or infiltrates. Septicaemia was confirmed in all cases with acute renal failure in 7 cases and meningitis in 6 cases. Severe thrombocytopenia was demonstrated in 2 cases. Six patients recovered quickly with regression of the lung changes within 12 days. Two patients died, one of a fulminant haemoptysis related to a disseminated intravascular coagulation syndrome, and the other of acute respiratory failure. All cases were confirmed serologically. Although lung changes in leptospirosis are usually benign and mild, haemoptysis and polypnoea with diffuse radiological changes are poor prognostic factors. The pathological changes were similar to those of haemorrhagic alveolitis. These changes may be either due to the liberation of toxins or to an immunological phenomenon.
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PMID:[Pulmonary manifestations in severe ictero-hemorrhagic leptospirosis]. 363 26

Rats infected with Trypanosoma brucei rhodesiense developed anemia, thrombocytopenia, and hypocomplementemia. Anemia, thrombocytopenia, and sharp reductions in parasitemia were associated with elevated titers of cold-active hemagglutinin, antibody to fibrinogen/fibrin-related products, and immunoconglutinin. Depletion of lytic complement, prolonged partial thromboplastin times, and presence of fibrin monomers in the blood occurred at the time anemia and significant elevations in precipitable immune complexes were observed. Terminally, consumption of immunologic factors coincided with accelerated partial thromboplastin times. At death, convulsions and hemoptysis with labored breathing suggested that the animals died of respiratory failure and that disseminated intravascular coagulation may have occurred. It is suggested that microthrombiosis might have resulted from the immunologic interaction of complex-coated blood cells with immunoconglutinin and contributed to the terminal disease signs.
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PMID:Immunologic reactions associated with anemia, thrombocytopenia, and coagulopathy in experimental African trypanosomiasis. 736 36

A patient with drug-induced thrombocytopenia who died because of massive pulmonary hemorrhage is described. The patient had a clinical picture of acute respiratory distress resembling pulmonary edema, but there was no hemoptysis. Chest x-ray films showed granular density in the pulmonary fields, and the electrocardiograms revealed a pattern of acute biatrial enlargement. The diagnosis was confirmed at autopsy.
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PMID:Lethal occult pulmonary hemorrhage in drug-induced thrombocytopenia. 747 71

A retrospective study on a consecutive series of 116 patients affected by acute leukaemia with documented pulmonary filamentous mycosis (FM) admitted between 1987 and 1992 to 14 tertiary-care hospitals in Italy was made in order to evaluate the characteristics of those patients who developed fatal massive haemoptysis. In 59/116 cases of pulmonary FM the infection was the principal cause of death and in 12 of these patients a massive haemoptysis was responsible for death. The diagnosis of FM infection was made ante-mortem in only four out of these 12 patients. The autopsy was performed in 11/12 patients and documented a FM infection. The mycetes isolated were: Hyphomycetes spp. (three patients), Mucorales spp. (two patients), Aspergillus spp. (seven patients). At the time of the massive haemoptysis the mean neutrophil count was 7.2 x 10(9)/l, and no patient had relevant thrombocytopenia (mean 184 x 10(9)/l, range 28-350) or coagulative abnormalities. The mean time which elapsed between resolution of chemotherapy-induced neutropenia (WBC < 10(9)/l) and occurrence of haemoptysis was 7 d. No signs or symptoms predictive of this fatal complication were identified. Massive haemoptysis can be the cause of death in patients with acute leukaemia and pulmonary FM which in the majority of patients was not diagnosed in vivo. This complication occurs most frequently shortly after the recovery from chemotherapy-induced aplasia. The mechanism of lesion is unknown, but it may involve the vascular tropism of FM and the release of leucocyte enzymes. Better preventive and therapeutic antifungal treatments are needed to avoid this serious, albeit rare, complication.
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PMID:Fatal haemoptysis in pulmonary filamentous mycosis: an underevaluated cause of death in patients with acute leukaemia in haematological complete remission. A retrospective study and review of the literature. Gimema Infection Program (Gruppo Italiano Malattie Ematologiche dell'Adulto) 875 37

We present preliminary results of a study undertaken in previously untreated patients with non-small cell lung cancer to determine the maximum tolerated dose of paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) when administered as a 3-hour intravenous infusion in combination with cisplatin every 3 weeks; to evaluate the nature, frequency, severity, and duration of adverse events associated with this drug combination; and to evaluate the combination's antitumor efficacy. Thus far, we have treated 10 patients with cisplatin (100 mg/m2) and increasing doses of paclitaxel (135, 170, and 200 mg/m2). Among nine evaluable patients, four partial responses have been obtained, disease in three patients progressed after three courses, and no changes were seen in one patient. One patient had two cardiac arrests within 8 days of the onset of therapy, from which he recovered; he died 1 month later of massive hemoptysis. Thrombocytopenia was not seen in these patients, and neutropenia (< 1,000 granulocytes/microL) was seen in only three patients. Infections were seen in these patients and were manageable in all cases. Other toxicities consisted mainly of World Health Organization grades II and III alopecia and nausea and/or vomiting. No grade III nephrotoxicity, neurotoxicity, hypersensitivity, mucositis, or infection was seen in this series after one to three courses of chemotherapy; one patient presented with grade IV cardiotoxicity 6 days after the onset of therapy. So far, the maximum tolerated dose of the cisplatin/paclitaxel combination has not been reached; however, definitive conclusions await the full treatment of additional patients. Moreover, the possibility of cumulative and delayed toxicity must be evaluated after a sufficient duration of follow-up in adequate numbers of patients.
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PMID:Dose-finding study of paclitaxel (Taxol) plus cisplatin in patients with non-small cell lung cancer. 793 62


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