Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.27 (lactate dehydrogenase)
 29,211 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stimulated by a patient with dyspnea, thrombocytopenia, and leukopenia after sodium morrhuate sclerotherapy, we studied the effect of this agent on the plasma coagulation and complement systems, the formed elements of the blood, and cultured human endothelial cells. The addition of sodium morrhuate to citrated plasma did not cause clotting or shorten the prothrombin time or partial thromboplastin time. Incubation of a 1:100 dilution of the clinical sodium morrhuate preparation in heparinized plasma led to a modest rise in [C3a]. The addition of the drug (dilutions 1:50 to 1:300) to granulocytes caused prompt aggregation (and, at the higher concentrations, granulocyte cytotoxicity [trypan blue exclusion; lactate dehydrogenase release]), but the same dilutions failed to aggregate platelets. However, 0.05% morrhuate added to washed red blood cells caused a prompt 84.0% (+/- 0.8% SEM) hemolysis, rendering the supernatant buffer a potent platelet aggregant. Not only was this sclerosing agent toxic to granulocytes and red cells, but a 1:1000 dilution of the drug also caused the destruction of 35.5% (+/- 6.6%) of cultured endothelial cells as measured by chromium 51 release. Three other agents in current use (ethanolamine oleate, sodium tetradecyl sulfate, and polidocanol) were studied and found to cause effects qualitatively similar to those of sodium morrhuate. We conclude that these drugs cause phlebosclerosis not primarily through induction of plasma coagulation, but by directly damaging endothelium and red cells, triggering platelets, and aggregating granulocytes at the venous wall endothelium. These effects likely derive from the surfactant properties of sodium morrhuate as well as its high arachidonate content.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sodium morrhuate stimulates granulocytes and damages erythrocytes and endothelial cells: probable mechanism of an adverse reaction during sclerotherapy. 405 66

A railroad accident in Somerville, Massachusetts, led to spillage of phosphorus trichloride liquid. Attempted clean-up with water led to the liberation of phosphorus trichloride, phosphoric acid, hydrochloric acid, and phosphorus oxides. Seventeen people exposed to this mixture were studied. Patients experienced eye irritation, lacrimination, nausea, vomiting, and dyspnea. Six patients had transient elevation of lactic dehydrogenase. Although all patients had normal chest roentgenographic findings, pulmonary function tests showed statistically significant decreases in vital capacity (p = 0.02), maximal breathing capacity (p = 0.02), forced expiratory volume in one second (p = 0.02), and maximal expiratory flow rate at 25 percent of vital capacity (p = 0.05) in those closest to the accident site. Further, patients exposed for less than one and a half hours had significantly greater maximal expiratory flow rates at 25 percent of vital capacity when compared with patients who had been exposed longer (p = 0.02). In seven patients, repeated pulmonary function tests one month later showed improvement, suggesting strongly that the acute effects may have been due to phosphorus trichloride toxicity.
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PMID:Phosphorus trichloride toxicity. Preliminary report. 650 58

A 71-year-old woman with psoriasis-associated rheumatoid arthritis had for 15 months been treated with methotrexate (5 mg/week orally). Four weeks before admission she had developed dyspnoea and cough. On admission her axillary temperature was 38.2 degrees C, the white cell count was normal. Erythrocyte sedimentation rate (50/90 mm), lactate dehydrogenase activity (449 U/l) and the creatinine level (1.33 mg/dl) were all elevated. Blood gas analysis revealed partial respiratory impairment (pO2 52 mm Hg), and the chest X-ray demonstrated bilateral interstitial-alveolar changes. Despite antibiotics the temperature continued to rise, and on the 11th day a blood eosinophilia of 4% was noted. The bronchial mucosa was normal on bronchoscopy, and transbronchial biopsy showed only minor interstitial fibrosis, occasional macrophages and lymphocytes. Cultures of the lavage-fluid were negative. As methotrexate pneumonitis was suspected the drug was discontinued and prednisolone administered (50 mg daily for 3 days, gradually reducing over 7 days). The symptoms quickly improved, and blood gas analysis and the X-rays became normal. The patient was discharged symptom-free after 30 days.
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PMID:[Severe pneumonitis as a complication of low-dose methotrexate therapy in psoriasis-associated polyarthritis]. 773 58

A 51-year-old man, known to have chronic-aggressive hepatitis B, HIV infection and exertional dyspnoea, was hospitalized because of acute physical deterioration, cough with whitish exudate and dyspnoea at rest. Despite a CD4/CD8 ratio of 0.16 no prophylactic measures against Pneumocystis carinii had been taken. On examination the lungs were unremarkable, but the liver was enlarged and there were petechiae over all parts of the body. Laboratory tests showed impaired liver functions and a rise in lactate dehydrogenase activity (538 U/l). Chest radiogram demonstrated small to very small infiltrates in the lung. As Pneumocystis carinii pneumonia was suspected but bronchoscopy was too risky, he was at first treated with trimethoprim/sulphamethoxazole (four times 320/1600 mg/24 h intravenously). When this failed, he received pentamidine (4 mg/kg, after 4 days 2 mg/kg intravenously), and finally cefotiam (twice 2 g daily), tobramycin (three times 40 mg daily) and corticoids (100 mg). Despite this treatment he died after 10 days from respiratory failure. Autopsy revealed interstitial pneumonia throughout the lung as well as focal mucor infiltrations in the wall of middle-calibre lung veins. Mucor is a ubiquitous, facultatively pathogenic mold fungus.
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PMID:[Pulmonary mucormycosis in an HIV-infected patient]. 783 42

The authors present the results of a ten year retrospective analysis about amiodarone-induced pulmonary toxicity. Only cases without any etiology (after complete explorations made in hospital), and judged probably imputable to amiodarone treatment were kept. This work finds all characteristics usually described with amiodarone pulmonary toxicity: dyspnea, cough, weight loss, restrictive lung disease and interstitial infiltration in the chest roentgenogram. It shows three another points: pulmonary disease is more frequent during first and fourth years of amiodarone treatment, pneumopathy occurs more rapidly in patients with a previous history of pulmonary disease, and patients with amiodarone lung toxicity may have elevation in lactate dehydrogenase activity.
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PMID:[Amiodarone-induced pleuropneumopathies: experience 1983-1993 in a drug vigilance Regional Center]. 785 56

A crude, whole-body extract of female or male heartworms was injected IV into 28 dogs with and 22 dogs without heartworm (HW) infection. The female HW extract caused shock in 22 of 24 dogs with and 12 of 20 dogs without HW infection. The male HW extract induced shock in 4 of 4 dogs with and 1 of 2 dogs without HW infection. Prevalence of shock caused by female HW extract was significantly (P < 0.05) higher in dogs with than without HW infection; shock developed 5 to 30 minutes after HW injection. These signs were observed: marked decrease in blood pressure; collapse (initial collapse); paleness of mucous membranes; weak heart sounds; dyspnea; skin coldness; intestinal hyperperistalsis, and defecation; increases in RBC count, serum total protein concentration, serum osmolality, serum Na and blood glucose concentrations; and decreases in neutrophil, eosinophil, and platelet counts. Alanine transaminase, alkaline phosphatase, and lactate dehydrogenase activities increased substantially from the time of initial collapse to 24 hours after HW injection. Of 39 dogs with shock, 29 recovered from initial collapse, but 5 of the 29 subsequently collapsed again (secondary collapse), with bloody diarrhea followed by death. Of these 39 dogs, 6 died during initial collapse without bloody diarrhea, and 4 were euthanatized during initial collapse. It was confirmed that HW extract had, in fact, induced shock. These clinical, hematologic, and biochemical findings were fundamentally similar to those associated with shock resulting from administration of drugs, such as diethylcarbamazine and milbemycin D, in microfilaremic dogs with HW infection.
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PMID:Clinical, hematologic, and biochemical findings in dogs after induction of shock by injection of heartworm extract. 787 76

Two dogs were seen at the University Veterinary Teaching Hospital, Nairobi, Kenya, both having histories of dyspnoea, progressively enlarging abdomens, anasarca, ascites, pleural and pericardial effusion, and pulmonary oedema. One of the dogs had a mild neutrophilic leucocytosis, elevated levels of alkaline phosphatase, alanine aminotransferase, lactate dehydrogenase and proteinuria. Histopathological examination of the myocardium revealed some damage to myocytes and a mononuclear cellular infiltration involving the myocardium, liver and kidneys. The two dogs had a fondness for avocado fruits and, as the presenting syndrome is identical to that seen in goats, sheep and horses poisoned by avocados, a comparison is made and the probable manifestation of this poisoning presented.
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PMID:Putative avocado toxicity in two dogs. 789 92

A 69-year-old man with coronary heart disease complained of pain in his right flank. He had dyspnoea, cough and fever up to 38.8 degrees C. In addition to various positive indicators of inflammatory disease he had a creatinine concentration of 1.8 mg/dl and an increased activity of lactate dehydrogenase (1655 U/l). The chest radiograph demonstrated pneumonia and computed tomography showed an infarct in the right kidney. The ECG indicated atrial fibrillation with an irregular ventricular rate and left bundle branch block. Echocardiography demonstrated dilatation of the left ventricle and a thrombus adherent to the wall. Transoesophageal echocardiography additionally recorded spontaneous type I echo-contrast, which disappeared after therapeutic heparinization. Cerebral infarctions were shown by computed tomography, undertaken because of neurological symptoms. There were also signs of silent myocardial ischaemia. As a coronary artery bypass operation was contraindicated, percutaneous transluminal balloon angioplasty was attempted but dissection occurred, causing irreversible cardiogenic shock of which the patient died.
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PMID:[Spontaneous echo contrast in the left ventricle as an indicator for an increased risk of thromboembolism]. 792 30

We report two cases of idiopathic interstitial pneumonia (IIP) with acute deterioration after bronchoalveolar lavage (BAL). Case 1 was a 54-year-old woman, and case 2 was a 75-year-old man. Both were diagnosed as having IIP, and hospitalized with complaints of high fever and dyspnea. After BAL, the degree of dyspnea increased. White blood cell count and lactate dehydrogenase were elevated, and PaO2 was decreased. Chest X-ray revealed consolidation of the upper lung fields and reticulo-granular shadows spreading through both lungs. BAL fluid examination showed an elevated neutrophil fraction (case 1: 6.5%, case 2: 35.2%), suggesting respiratory tract infection although bacteria could not be detected. Case 1 died of respiratory failure despite corticosteroid therapy. Autopsy revealed diffuse alveolar damage with focal pneumonia in the right S6 corresponding to the upper lobe consolidation. Case 2 improved after antibiotic therapy. These findings suggest that aspiration of infected fluid during BAL can cause acute exacerbation of IIP. It is important to recognize that the BAL procedure can induce an acute exacerbation of IIP.
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PMID:[Acute exacerbation following bronchoalveolar lavage in idiopathic interstitial pneumonia]. 812 Nov 1

A 41-year-old man infected with HIV-1 developed fever up to 39.8 degrees C together with nonproductive cough and dyspnoea. Lactate dehydrogenase concentration rose from a level of 998 U/l to 6307 U/l. As pneumocystis carinii pneumonia was at first suspected he was treated with co-trimoxazole (1600 mg sulfamethoxazole and 320 mg trimethoprim, four times daily). But the symptoms did not abate. Bone-marrow puncture revealed numerous macrophages containing ovoid inclusions typical of Histoplasma capsulatum varietas capsulatum. The diagnosis of disseminated histoplasmosis was confirmed by culture and serologically by an increase in Histoplasma polysaccharide antigen. On treatment with amphotericin B (at first 10 mg, then 50 mg daily for 4 weeks) the symptoms regressed within a few days. After the concentrations of lactate dehydrogenase and Histoplasma antigen had become normal again, maintenance treatment was changed to itraconazole (200 mg twice daily), after a total amphotericin B dose of 1150 mg. The patient has remained free of recurrence.
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PMID:[Disseminated histoplasmosis in AIDS]. 818 12


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