Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine if urine pentamidine was reflective of lung pentamidine, we compared levels of the drug in bronchoalveolar lavage fluid and simultaneously obtained urine. Thirty-one patients who were receiving aerosolized pentamidine either as treatment or as prophylaxis underwent BAL and submitted urine samples for pentamidine analysis. Pentamidine was analyzed in both phases of BAL fluid (supernatant and cell pellet) and in urine using high performance liquid chromatography. Urine results were normalized for creatinine. Patients were categorized as prophylaxis failures (active Pneumocystis carinii pneumonia on prophylaxis), electives (free from PCP on prophylaxis), treatment (daily AP in treatment doses for active PCP, or miscellaneous (single dose of AP). Levels in BAL fluid and urine varied widely over several orders of magnitude. However, for all patients, we found a highly significant relationship between BAL supernatant and urine (r = 0.97, p less than 0.0001). No statistical differences were found when comparing levels of pentamidine between failures and electives; however, the number of failures was small. We conclude that urine pentamidine is related to lung pentamidine and can be used as a clinical indicator in patients receiving aerosolized therapy.
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PMID:Urine pentamidine as an indicator of lung pentamidine in patients receiving aerosol therapy. 193 74

1 Rats received a total of 18 mg/kg cis-dichlorodiammineplatinum (II) (CDDP) intravenously and were treated concomitantly with calcium-disodium ethylenediaminetetraacetic acid (CaNa2EDTA), 2,3-dimercaptopropanol (BAL), deferoxamine, 2,3-dimercaptosuccinic acid (DMS) or vehicle. In comparison to controls, renal platinum concentration was significantly reduced in the DMS and deferoxamine-treated groups. However, significant deterioration occurred in the deferoxamine-treated group. The hepatic platinum concentration was unaffected by the chelating agents. 2 Following a dose of 6 mg/kg CDDP intravenously, eight days of treatment with DMS, 50 mg/kg daily, had no effect on renal platinum excretion, while treatment with 100 or 200 mg/kg daily reduced renal platinum concentration by 50%. 3 In order to determine whether DMS could prevent the nephrotoxicity of CDDP, rats were given 6 mg/kg CDDP intravenously, followed by a four day course of DMS treatment at doses of 0, 50, 100 or 200 mg/kg daily begun 3 h after the CDDP dose. DMS failed to prevent renal toxicity as indicated by weight loss, serum creatinine concentration, renal histology, and the urinary excretion of N-acetyl-beta-glucosaminidase, a renal tubular enzyme.
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PMID:The effect of heavy metal chelators on the renal accumulation of platinum after cis-dichlorodiammineplatinum II administration to the rat. 626 16

One hundred thirty children aged 1 to 8 years with blood lead levels greater than 50 micrograms/100 ml of whole blood (WB) and free erythrocyte protoporphyrin (FEP) concentration greater than 250 micrograms/100 ml of WB received 207 chelation treatments for plumbism. All chelation treatments consisted of CaNa2 ethylenediaminetetraacetic acid (EDTA) 25 mg/kg per dose every 12 hours and 2,3-dimercapto-1-propanol (BAL) 3 mg/kg per dose every four hours for five days. Seventeen children demonstrated transient doubling of pre-chelation treatment serum creatinine (less than or equal to 2.0 mg/100 ml) during or following chelation treatment; 5/17 also had mild proteinuria. Four children developed severe oliguric (greater than 250 ml/sq m/day) acute renal failure. Serum creatinine levels were elevated six to seven days after chelation treatment was started and reached maximal values of 3.9 to 8.4 mg/100 ml, three to six days later. Renal function returned to pre-chelation treatment values during the subsequent six to 18 days. In the 21 nephrotoxic patients and the 109 nontoxic patients there were no significant differences in age (3.8 +/- 0.6 vs 3.2 +/- 0.2 years), sex (61% vs 53% males), percent who received multiple chelation treatments (38% vs 30%), blood lead levels (85 +/- 5 vs 79 +/- 1 microgram/100 ml of WB), FEP (380 +/- 30 vs 382 +/- 18 micrograms/100 ml of WB), hemoglobin (11.5 +/- 0.4 vs 11.1 +/- 0.2 gm/100 ml, and pre-chelation treatment serum creatinine (0.46 +/- 0.06 vs 0.58 +/- 0.03 mg/100 ml). It was concluded that 13% of children with plumbism who received chelation treatments developed mild transient biochemical evidence of nephrotoxicity and another 3% developed acute renal failure characterized by oliguria four to eight days after chelation treatment was discontinued.
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PMID:Reversible nephrotoxic reactions to a combined 2,3-dimercapto-1-propanol and calcium disodium ethylenediaminetetraacetic acid regimen in asymptomatic children with elevated blood lead levels. 709 93

Sepsis is still a major cause of the high mortality rate in the intensive care unit. Many studies have been published about the severity of sepsis, but the cause of mortality in sepsis and multiorgan failure is still obscure. This study investigated the effects of caffeic acid phenethyl ester (CAPE) particularly on the inflammatory and related histopathological changes in the lung, liver and kidney in an experimental sepsis model. Forty Sprague Dawley rats were used in this study, and were divided into four groups of ten rats each, as follows: Group I was given intraperitoneal saline infusion treatment. Group II was given intraperitoneal CAPE infusion treatment. Sepsis was induced in the animals in Group III (sepsis with saline infusion), while Group IV rats underwent induced sepsis plus CAPE infusion treatment (sepsis with CAPE infusion). Sampling was performed 48 h after treatment. The induction of sepsis resulted in a significant increase in serum glucose, leukocytes, urea, creatinine, LDH levels in BAL, plasma MDA, AST and ALT levels in the sepsis + saline group. The use of CAPE significantly decreased these parameters. Histopathological examination revealed less congestion, portal inflammation, and focal necrosis of the liver, and less congestion, edema, and emphysematous and inflammatory changes in the lung in the sepsis + CAPE group than in the other groups. These results support that CAPE may be used for the treatment of organ failure during sepsis.
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PMID:Effects of caffeic acid phenethyl ester (CAPE) on sepsis in rats. 1860 6