Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pentamidine isethionate is a trypanocidal drug used for the treatment of Pneumocystis carinii pneumonitis. Hematological complications have occasionally been reported and include anemia, leukopenia, and thrombocytopenia. We report here several qualitative abnormalities of in vitro platelet function and coagulation that have not been described previously. Platelets were exposed in vitro to concentrations of pentamidine isethionate ranging from 0.5 to 100 mug/ml of platelet-rich plasma. Clot retraction, platelet adhesiveness to glass beads, and platelet aggregation (adenosine 5'-diphosphate [ADP], thrombin, epinephrine, collagen, and ristocetin) were inhibited in a dose-dependent fashion. The addition of pentamidine isethionate after aggregation had been initiated with ADP reversed both primary and, to a lesser degree, secondary aggregation. Platelet factor 3 availability and serotonin uptake and release (using collagen as the releasing agent) were not inhibited. Serotonin release with 10(-4) M ADP was slightly inhibited. Pentamidine isethionate prolonged the thrombin time of plasma at concentrations of 5 mug/ml and greater. The prothrombin time was prolonged at concentrations greater than 10 mug/ml of plasma. The inhibition of aggregation was reversed by washing and resuspension in plasma or by the addition of calcium or magnesium ions.
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PMID:In vitro inhibition of platelet function and coagulation by pentamidine isethionate. 92 Dec 38

This study was performed to evaluate bronchopulmonary lavage and chelation therapy as a treatment method to prevent the development of radiation pneumonitis after inhalation of a radioactive aerosol. Twelve beagle dogs were exposed to an aerosol of cerium-144 in fused clay particles resulting in initial lung burdens from 47 to 64 muCi of 144-Ce per kg of body weight. Eight of the dogs were treated with a series of 10 bronchopulmonary lavages and 10 intravenous injections of calcium diethylenetriamine pentaacetate acid during the first 56 days after exposure to remove the deposited 144-Ce; the remaing 4 exposed dogs receiged no treatment. An additional 4 dogs were exposed to stable cerium and were given the course of treatment as an additional control group. Three of the 4 untreated dogs and 2 of the 8 treated dogs died 171 to 246 days after exposure with radiation pneumonitis or pulmonary fibrosis, or both. All but one of the remaining dogs were alive and apparently in good clincial health 550 dyas after exposure; the one dog had radiographic indications of pulmonary fibrosis by 365 days after exposure. The relative distribution of 144-Ce in the lungs and other major organs was similar in the treated and untreated dogs that died.
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PMID:Prevention of radiation pneumonitis from inhaled cerium-144 by lung lavage in beagle dogs. 113 48

42 episodes of verified or clinically suspected cytomegalovirus (CMV) infection in 40 bone marrow transplant (BMT) recipients were treated with foscarnet (trisodium phosphonophormate hexahydrate). CMV infection was verified in 31/42 treatment episodes. Symptoms treated were pneumonia (n = 17), pancytopenia with or without fever (n = 12), enteritis (n = 5), fever (n = 4), encephalitis (n = 2), retinitis (n = 1) and hepatitis (n = 1). Foscarnet was given as a continuous intravenous infusion. Side-effects observed were increase in serum creatinine (38%), decrease in serum calcium (19%), increase in serum bilirubin (12%), decrease in hemoglobin concentration (7%), increase in serum calcium (5%), increase in serum transaminase (5%), hypophosphatemia (2%) and tremor (2%). CMV was eradicated from blood and/or urine in 11/25 (44%) of assessable treatment episodes with infection verified by isolation. Overall clinical improvements including eradication of CMV, afebrility and/or improvements in laboratory abnormalities were seen in 14/31 (45%) episodes of verified infection. All 15 patients with CMV interstitial pneumonia (CMV IP) died. We conclude that foscarnet is nephrotoxic but otherwise well tolerated with moderate clinical and virostatic effects on CMV infection. The effect on CMV IP is discouraging.
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PMID:Foscarnet for treatment of cytomegalovirus infections in bone marrow transplant recipients. 132 57

Forty-eight dogs were separated into four groups of six males and six females. Acrolein (0.1% aqueous) was administered in gelatin capsules to three of these groups at dosing levels of 0.1, 0.5 and 1.5 mg kg-1 day-1 based on results of a range-finding study. After 4 weeks, the high dose was increased to 2 mg kg-1 day-1. The fourth group received deionized water in the same number of gelatin capsules as the high-dose group. Dosing was 7 days per week for 53 weeks. Blood and biochemical measurements were made pretest and at 3-month intervals thereafter. At termination, all dogs were subjected to full necropsy and histological examination. The major test effect noted was frequent vomiting after dosing. This was observed to be dose-dependent and the frequency decreased with time, indicating an adaptive effect. One mid-dose female died during the test and was diagnosed as having died of severe bronchial pneumonia, probably a result of vomitus aspiration. Serum albumin, calcium and total protein values were depressed in high-dose animals throughout the study. Some variability in red blood cell parameters and coagulation times were noted but the significance of these effects was not obvious.
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PMID:One-year toxicity of orally administered acrolein to the beagle dog. 144 75

Pneumocystis carinii is the most common cause of life-threatening pneumonia in immunocompromised patients. In the current study, surfactant protein A (SP-A), the major nonserum protein constituent of pulmonary surfactant, is demonstrated to bind P. carinii in a specific and saturable manner. SP-A is surface bound and does not appear to be internalized or degraded by the P. carinii organism. Furthermore, SP-A binding to P. carinii is time- and calcium-dependent and is competitively inhibited by mannosyl albumin. In the absence of calcium or the presence of excess mannosyl albumin, SP-A binding to P. carinii is reduced by 95 and 71%, respectively. SP-A avidly binds P. carinii with a Kd of 8 x 10(-9) M and an estimated 8.4 x 10(6) SP-A binding sites per P. carinii organism, as determined from Scatchard plots. SP-A is shown to bind P. carinii in vivo, and a putative binding site for SP-A on P. carinii is demonstrated to be the mannoserich surface membrane glycoprotein gp120. These findings suggest that P. carinii can interact with the phospholipid-rich material in the alveolar spaces by specifically binding a major protein constituent of pulmonary surfactant.
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PMID:120-kD surface glycoprotein of Pneumocystis carinii is a ligand for surfactant protein A. 153 Aug 50

We present a new patient with vitamin D dependent rickets type II. A 20-month-old Arabian boy whose parents are first cousins showed florid rickets, myelofibrosis and recurrent septicaemia. In addition to absent specific binding for 1,25-dihydroxyvitamin D3 (1,25(OH)2D3). 25-Hydroxyvitamin D3-24-hydroxylase activity could not be induced in cultured fibroblasts. The patient did not respond to 99 micrograms 1,25(OH)2D3 per day, but skeletal and haematological abnormalities improved with daily infusion of 100 mg/kg calcium, as serum parathyroid hormone levels fell to normal values. At the age of 7 years, he died from pneumonia. The improvement of haematological abnormalities with calcium infusions but not with 1.25(OH)2D3 suggests a pathogenetic relationship of myelofibrosis and hyperparathyroidism. Having anti-lipid A IgM antibody titres up to 1:10.000 after Gram negative septicaemias, the patient never produced corresponding IgG antibodies. His neutrophil chemotaxis was persistently reduced to 57% +/- 3% of age-matched controls (P less than 0.028). The patient showed two pathological immune functions considered to contribute to the well-known susceptibility to infection in rickets.
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PMID:Vitamin D dependent rickets type II with myelofibrosis and immune dysfunction. 165 62

A 46-year-old man was admitted to Oita Medical College Hospital on October 16, 1987, because of cough and sputum. Chest X-ray and chest CT films showed diffuse reticulonodular shadow. The specimens obtained by transbronchial lung biopsy revealed cysts of pneumocystis carinii. Abnormal lymphocytes with lobulated nuclei were found 2-7% of peripheral leucocytes. The anti HTLV-I antibody was positive. According to these data, we diagnosed the patient as smoldering adult T cell leukemia with pneumocystis carinii pneumonia. The abnormal shadow on chest X-ray disappeared after SMX-TMP and pentamidine treatment. After about 1 year, he was again admitted for high fever. Chest X-ray showed infiltration with cavity in right upper lobe. Streptococcus pneumoniae was isolated from the sputum. The infiltration shadow on chest X-ray disappeared after antibiotics treatment. However, multiple nodular shadow appeared on the chest X-ray and ATL cell infiltration was found in the specimens of transbronchial lung biopsy. ATL cells in peripheral blood also increased and serum LDH and Calcium levels were markedly high. According to these data, we diagnosed the patient as having a ATL crisis. Although chemotherapy for ATL was started, the ATL, cell infiltration shadow on the chest X-ray enlarged, and bilateral diffuse patchy shadows was appeared on the chest X-ray. He died of respiratory failure on April 26, 1989. Cytomegalovirus pneumonia and ATL cell infiltration were revealed by necropsy.
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PMID:[A case of smoldering adult T-cell leukemia complicated by various pulmonary infections]. 166 67

Pulmonary toxicity may complicate the treatment of non-Hodgkin's lymphoma (NHL). The possible drug-related cause of pulmonary toxicity was investigated retrospectively in 207 NHL patients treated between 1981 and 1988 with three regimens containing cyclophosphamide with and without methotrexate or bleomycin: methotrexate, calcium, leucovorin, bleomycin, doxorubicin, cyclophosphamide, vincristine, and dexamethasone (m-BACOD) (n = 134); methotrexate, calcium, leucovorin, doxorubicin, cyclophosphamide, vincristine, and dexamethasone (m-ACOD) (n = 43); or cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) (n = 30) chemotherapy. These regimens contained the same drugs and were administered in the same schedule; the regimens differed primarily in the addition of bleomycin or methotrexate. Pulmonary toxicity occurred in 24 of 134 (18%) m-BACOD-treated and in six of 43 (14%) m-ACOD-treated patients (P = 0.65). Chest radiography revealed diffuse pulmonary infiltrates in 16 (67%) and six (100%) of the m-BACOD-treated and m-ACOD-treated patients with pulmonary toxicity, respectively. None of the CHOP-treated patients had pulmonary toxicity. The clinical features of pulmonary toxicity and the amount of chemotherapy administered before it occurred did not differ in patients treated with m-BACOD or m-ACOD, although the toxicity tended to be more severe in the m-BACOD group. Open lung or transbronchial biopsies done in six (38%) of the m-BACOD-treated and three (50%) of the m-ACOD-treated patients with pulmonary infiltrates revealed nonspecific pneumonitis compatible with drug-related toxicity. In summary, these results showed that pulmonary toxicity during m-BACOD and m-ACOD therapy occurred with similar frequency and clinicopathologic features. This suggested that bleomycin was not responsible uniquely for the pulmonary toxicity in m-BACOD-treated patients. That pulmonary toxicity was not observed in patients treated with CHOP suggested that methotrexate may play an important role in the pathogenesis of the pulmonary toxicity.
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PMID:Drug-related pulmonary toxicity in non-Hodgkin's lymphoma. Comparative results with three different treatment regimens. 171 21

A 73-year-old man was admitted to our hospital with chief complaint of macrohematuria. Computerized tomography revealed enlargement of right kidney, tumor thrombi and lymph nodal involvement. Distant metastases were found in liver, lung and pelvis. We performed conservative therapy including right renal embolization. However, serum calcium levels continued to increase. Patient died from renal failure and pneumonia after 2 months, and autopsy was performed. Histological examination revealed infiltrative transitional cell carcinoma of the right kidney. PTH like peptide was measured 1 ng/gram wet tissue from the primary tumor and 16.6 ng/gram wet tissue from the metastatic liver tumor.
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PMID:[A case of infiltrative transitional cell carcinoma of the kidney with hypercalcemia]. 192 77

46-year-old male patient was born in Niigata Prefecture and thereafter lived in Tokyo. In late January 1985, he noticed swelling of the bilateral inguinal lymph-nodes followed by fever and lumbago. In February, he consulted a local doctor and hepatosplenomegaly, marked leukocytosis and renal dysfunction were pointed out and he was referred to our hospital on February 22nd. The clinical laboratory data on admission were as follows; WBC 23,200/microliter, serum-Ca 18.4 mg/dl, BUN 85.3 mg/dl, creatinine 5.4 mg/dl, antibody to ATLV x160. ATL was diagnosed by biopsy of lymph nodes and examinations of peripheral blood and bone marrow hemogram. Remission was achieved in March by the treatment with adriacin. Renal failure and hypercalcemia also improved. However his respiratory dysfunction gradually worsened. The chest radiographies++ showed pulmonary edema, although there was no clinical evidence of heart failure. When his condition became stable, TBLB was performed and revealed extensive deposition of calcium along alveolar septae, suggesting that pulmonary edema was induced by the metastatic calcification of the lung. After the second treatment for ATL, he died of pneumonia. The autopsy showed calcium deposition not only in the lung but in pyramids of the kidney and in sub-serous layer of the small intestine. There was no tumor cell invasion into the bone or parathyroid gland. High urinary c-AMP together with normal levels of PTH suggested that the hypercalcemia in this case was induced by PTH-related protein. It was concluded that careful treatment for hypercalcemia is important as regards the occurrence of pulmonary edema.
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PMID:[An autopsy case of adult T-cell leukemia complicated with metastatic calcification of the lung]. 204 Dec 50


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