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)

Toxicosis was induced in pregnant Holstein-Friesian heifers by giving polybrominated biphenyls a in gelatin capsules at the rate of 25 g/day. Initially, this dosage was approximately 67 mg/kg of body weight. Clinical signs were anorexia, excessive lacrimation and salivation, diarrhea, emaciation, dehydration, depression, and abortion. Fever was not evident during the experiment. Values for serum glutamic-oxalacetic transaminase, lactic dehydrogenase, blood urea nitrogen, and bilirubin were increased. Changes in packed cell volume, hemoglobin content, total erythrocyte and leukocyte counts, and differential leukocyte counts were minimal and reflected dehydration and secondary infection. The principal urine changes were decreased specific gravity and moderate proteinuria. Gross necropsy findings included dehydration; subcutaneous emphysema and hemorrhage; atrophy of the thymus; fetal death with concomitant necrosis of cotyledons; kidneys that were enlarged, pale tan to gray; thickened wall of the gallbladder; inspissated bile; edema of abomasal folds; mucoid enteritis; linear hemorrhage and edema of the rectal mucosa; and secondary pneumonia. Microscopic changes were most marked in the kidneys, gallbladder, and eyelid. In the kidney, the principal changes were extreme dilatation of collecting ducts and convoluted tubules, with epithelial degenerative changes of cloudy swelling, hydropic degeneration, and separation from the basement membrane. Common changes in the gallbladder were moderate to marked hyperplasia and cystic dilatation of the mucous glands in the lamina propria. The changes in the eyelids were characterized by hyperkeratosis, with accumulations of keratin in hair follicles of the epidermis and squamous metaplasia with keratin cysts in the tarsal glands. Clinical signs and lesions of toxicosis did not develop in heifers given the polybrominated biphenyls at the rate of 0.25 mg and 250 mg/day for 60 days. Initially these rates were approximately 0.00065 mg/kg and 0.65 mg/kg of body weight, respectively.
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PMID:Pathology of experimentally induced polybrominated biphenyl toxicosis in pregnant heifers. 18 92

To determine the sensitivity of serum KL-6 and serum lactate dehydrogenase for detecting the contraction of radiation pneumonitis, 15 patients with lung cancer who had radiation therapy were monitored. Six of the patients contracted radiation pneumonitis (pneumonitis group) and the other patients did not (control group). Serum levels of KL-6 were significantly (p less than 0.05) elevated according to the complication of radiation pneumonitis in all patients of the pneumonitis group. In the control group, however, one-sided changes of KL-6 level were not observed. In the pneumonitis group, serum LDH levels were not significantly changed. However, there was a strong correlation between the altered levels of KL-6 and those of LDH (r = 0.992). These observations indicate that the same cytopathologic changes may cause the elevation of serum KL-6 level and the elevated activity of serum LDH in the patients with radiation pneumonitis, and that KL-6 is much more sensitive than LDH for detecting radiation pneumonitis.
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PMID:Circulating antigen KL-6 and lactate dehydrogenase for monitoring irradiated patients with lung cancer. 132 May 62

It has been previously demonstrated that serum lactate dehydrogenase is elevated among HIV patients with pneumocystis carinii pneumonia (PCP). To evaluate the clinical utility of this test we analyzed the admission LDH levels of patients hospitalized for the first time due to the secondary complications of AIDS. Among 76 patients without a prior history of PCP, 41 (54%) had PCP diagnosed during their hospitalization while 35 (46%) did not have PCP. Serum LDH was significantly higher among PCP patients than in patients without PCP (mean = 423 IU/L vs 234 IU/L). Receiver operating characteristic curve analysis demonstrated that at an optimal cutoff point of LDH greater than or equal to 240 IU/L, the test sensitivity and specificity were 0.78 and 0.74 respectively among all hospitalized patients. However, when only patients with dyspnea were considered, the optimal test sensitivity and specificity improved to 0.94 and 0.78 at a cutoff point of LDH greater than or equal to 220 IU/L. Comparing the areas under fitted ROC curves, serum LDH was a significantly better discriminator among patients with dyspnea than among those who were not short of breath. We conclude that while serum LDH is strongly associated with the presence of PCP among AIDS patients, it is a poor screening test for PCP when applied to all hospitalized AIDS patients with and without respiratory complaints. Serum LDH is no substitute for appropriate microbiological studies. However, with further evaluation, it may prove to be a useful test in guiding the clinical management of dyspneic patients in whom sputum or bronchial examinations are negative or not immediately available.
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PMID:The clinical utility of serum lactate dehydrogenase in diagnosing pneumocystis carinii pneumonia among hospitalized AIDS patients. 151 88

Serum marker KL-6 antigen has been reported to be a valuable indicator of the disease activity of interstitial pneumonia. It is not clear how sensitive the serum KL-6 antigen level is in reflecting histologic changes in lung tissues. We report here the results of serial measurements of serum KL-6 antigen in a 76-year-old male patient with radiation pneumonia. Serum KL-6 antigen levels were more sensitive than lactate dehydrogenase and procollagen type III N-terminal peptide. The level of serum KL-6 antigen appears to reflect the histologic changes of the lung more sensitively than does C-reactive protein.
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PMID:Monitoring of serum KL-6 antigen in a patient with radiation pneumonia. 154 Nov 62

In the United States, approximately one million patients each year develop a pleural effusion. Pleural effusions have classically been divided into transudative and exudative pleural effusions. A transudative pleural effusion occurs when the systemic factors influencing pleural fluid formation and reabsorption are altered so that pleural fluid accumulates; an exudative pleural effusion occurs when the local factors influencing pleural fluid formation and reabsorption are altered, allowing accumulation of pleural fluid. The leading causes of transudative pleural effusions are left ventricular failure and cirrhosis with ascites. The leading causes of exudative pleural effusions are pneumonia, malignancy, and pulmonary embolization. Transudative pleural effusions can be differentiated from exudative pleural effusions by measurement of the pleural fluid protein and lactic dehydrogenase (LDH) levels. The ratio of the pleural fluid protein to the serum protein is less than 0.5, the ratio of the pleural fluid LDH to the serum LDH is less than 0.6, and the absolute value of the pleural fluid LDH level is less than two thirds of the upper normal limit for serum with transudative pleural effusions while at least one of these criteria is not met with exudative effusions. Most patients who have a pleural effusion with congestive heart failure have left ventricular failure. It is believed that the transudation of the pulmonary interstitial fluid across the visceral pleura overwhelms the capacity of the lymphatics to remove the fluid. Most patients with cirrhosis who have a pleural effusion also have ascites. It is also believed that the pleural effusions form when fluid moves directly from the peritoneal cavity into the pleural cavity through pores in the diaphragm. Approximately 40% of patients with pneumonia will have a pleural effusion. If these patients have a significant amount of pleural fluid, a diagnostic thoracentesis should be performed. Chest tubes should be inserted if the pleural fluid is gross pus, if the Gram stain of the pleural fluid is positive, if the pleural fluid glucose level is below 40 mg/dl, or if the pleural fluid pH level is less than 7.00. If drainage with the chest tubes is unsatisfactory, either streptokinase or urokinase should be injected intrapleurally. If drainage is still unsatisfactory, a decortication should be considered. The three leading malignancies that have an associated pleural effusion are breast carcinoma, lung carcinoma, lymphomas and leukemias. The diagnosis of pleural malignancy is made most commonly with pleural fluid cytology; in recent years immunohistochemical tests have proved invaluable in differentiating benign from malignant pleural effusions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pleural diseases. 157 32

Total Lactate Dehydrogenase (LD, EC 1.1.1.27) activity in serum and LD isoenzymes were quantified in 161 children (51 with pneumonia at the time of diagnosis, 60 hospitalized for asthma in acute period and 50 healthy subjects) to ascertain the relationship of these markers with injury of lung tissue. No statistical variations, between different groups in total activity, were found. Significantly decreased proportions of LD1 (p less than 0.000001) and of LD2 (p less than 0.000001) with simultaneous increase of LD4 (p less than 0.000001) and LD5 (p less than 0.000001) resulted in children with pneumonia, as to asthmatic or healthy subjects. Investigators conclude that LD should be determined in every patient with pneumonia because of the presence of a specific LD isoenzyme pattern.
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PMID:[Lactate dehydrogenase and its isoenzymes in respiratory diseases in children]. 158 97

Four out of eleven patients--none of them HIV positive--who received treatment for non-Hodgkin lymphoma by the MACOP-B protocol between June 1989 and February 1990 were taken ill during or shortly after the conclusion of the course with fulminant pneumonia necessitating artificial ventilation. In three cases Pneumocystis carinii was identified as the pathogen, and in one patient the diagnosis of pneumocystosis seemed probable. The mean cumulative doses given before the outbreak of pneumonia were as follows: cyclophosphamide 2753 +/- 1161 mg, methotrexate 1590 +/- 667 mg, bleomycin 36 +/- 16.8 mg and prednisone 4378 +/- 1734 mg. The mean haemoglobin concentration was 10.7 +/- 0.5 g/dl, leucocyte count 5250 +/- 2100/microliters, lymphocyte count 1300 +/- 300/microliters and lactate dehydrogenase 227 +/- 34 U/l. The cumulative doses and laboratory findings in the seven patients not affected by pneumocytosis were not significantly different. The patients with pneumonia were supported by mechanical ventilation for 6-26 days and treated with large doses of corticosteroids and co-trimoxazole. One patient died after 17 days' ventilation. Three patients were successfully weaned from the ventilator. Chemotherapy protocols such as MACOP-B predispose to acute Pneumocystis pneumonia. The risk of infection is independent of the cumulative doses of the drugs employed. For this reason, prophylaxis with co-trimoxazole is normally mandatory.
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PMID:[Acute pneumocystosis during polychemotherapy following the MACOP-B protocol]. 169 17

A total of 92 patients with previously untreated intermediate- or high-grade non-Hodgkin's lymphoma attending the University Department of Medicine, Queen Mary Hospital, Hong Kong, were treated with the m-BACOD chemotherapy regimen (methotrexate, bleomycin, doxorubicin, cyclophosphamide, vincristine and dexamethasone). Additional involved-field radiotherapy was given to 32 (35%) patients. Myelosuppression was the major toxicity, and 5 (5%) treatment-related deaths occurred due to pneumonia, bleomycin sensitivity, doxorubicin cardiotoxicity and reactivation of hepatitis B infection. The overall complete response (CR) rate was 65/92 (71%) and the relapse rate was 22/65 (34%). The disease-free survival of the 65 CR patients at 2 years was 52% and the overall survival of all 92 patients at 3 years was 56%. The CR rate of stage I and II patients was significantly better than that of those with stage III and IV disease (87% vs 59%; P = 0.01), and the CR rate of stage III patients was superior to that of those with stage IV disease (86% vs 50%; P = 0.05). The overall survival of stage III and IV patients was significantly worse than that of subjects with stage I and II disease (31% vs 73%; P = 0.02). Multivariate analysis revealed that the independent prognostic variables significantly determining the CR rate and survival included the clinical stage and the serum lactate dehydrogenase level. From this study, the results of treatment with the m-BACOD regimen in patients with advance disease appeared to be similar to those obtained using the conventional CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone).
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PMID:m-BACOD chemotherapy for intermediate- and high-grade non-Hodgkin's lymphoma. 171 34

Pneumonia caused by common pyogenic bacteria occurs frequently in HIV-infected patients. Its clinical presentation has been described as being similar to that seen in non-immunosuppressed hosts but clearly different to that of opportunistic pneumonias. An atypical presentation has rarely been seen. In a 10-month period, we saw 12 HIV-infected patients who presented with Haemophilus influenzae pneumonia which was clinically and radiologically indistinguishable from Pneumocystis carinii pneumonia. Ten of the patients were intravenous drug users and were in different stages of HIV disease. The clinical picture was characterized by a prolonged course (median 4 weeks), non-productive cough, dyspnoea, and absence of findings usually present in bacterial pneumonia. Laboratory data frequently showed absence of leukocytosis, increased lactate dehydrogenase levels, hypoxaemia, and decreased CD4+ cell counts. All presented with interstitial or mixed bilateral infiltrates. Resistance to ampicillin and trimethoprim-sulphamethoxazole were each found in seven cases. Eleven patients were cured with antibiotic therapy, although five relapsed. H. influenzae pneumonia should be considered in HIV-infected patients who present with pulmonary symptoms and bilateral infiltrates of subacute or chronic onset. Clinical resolution of pneumonia is the usual outcome, but recurrences of infection are frequent.
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PMID:Latent Haemophilus influenzae pneumonia in patients infected with HIV. 177 77

The clinical presentation of 60 consecutive Pneumocystis carinii pneumonias in 58 HIV-infected patients (48 men, 10 women, mean age 34 [22-53] years) was prospectively evaluated from April to August 1989 and compared with 60 consecutive P. carinii pneumonias in 59 HIV-infected patients (55 men, 4 women, mean age 37.5 [22-60] years) between 1981-88. Mortality rates within 14 days after diagnosis of P. carinii pneumonia were 50% (8 of 16 patients) until 1985, 20.5% (9 of 44) between 1986 and August 1988, and 1.7% (one of 60) in 1989. The degree of severity of the pneumonias at time of diagnosis was markedly lower in 1989, as shown by following parameters (averages of 1989, compared with averages of 1981-88): lactate dehydrogenase 540 (250-1419) U/l versus 680 (235-1920) U/l (not significant); alveolo-arterial difference of partial oxygen tension (pA-aO2) 22.9 (0.5-73.5) mmHg versus 39.7 (19-70) mmHg (P less than 0.001); score of radiological findings 1.4 (0-3) versus 2.7 (0-4) (P less than 0.001). In 1989, mainly clinical symptoms (dry cough: 57 of 60 cases, dyspnea: 44 of 60 cases, fever: 43 of 60 cases) initiated the diagnostic procedure: chest radiographs, lactate dehydrogenase and pA-aO2 were normal in 13, 25 and 33 episodes, respectively. The lower mortality rate of P. carinii pneumonia could not primarily be explained by therapeutical progress since the treatment of choice did not change fundamentally since 1981. Above all, early diagnosis fundamentally determined the probability of survival.
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PMID:[Pneumocystis carinii pneumonia in HIV infection: better prognosis because of early diagnosis]. 222 63


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