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

A 31 year-old inhabitant of French Guiana was prescribed mercuric iodide per os for two and a half months. Shortly before the end of the treatment he developed fasciculations in the trunk and particularly the lower limb muscles, distal painful paresthesias with vasomotor disorders, episodes of excessive perspiration and palmoplantar erythema, moderate fluctuating hypertension, progressive loss of weight and irritability with insomnia. Clinical and electrical signs of neuropathy were lacking. The clinical picture was that of Morvan's fibrillary chorea with acrodynia, the conditions of onset strongly suggesting a mercurial intoxication. Blood and particularly urine mercury levels were elevated. Administration of dimercaprol (BAL) considerably increased urinary excretion of mercury and there was progressive improvement and finally recovery after two months of BAL treatment. This case exemplifies the possible co-existence of fibrillary chorea and acrodynia. Whereas in many cases of fibrillary chorea a precise etiology cannot be determined, the affection can be induced by mercury as by gold administration. The fact that cases of fibrillary chorea due to mercury poisoning are rarely reported may be the result of individual patient hypersensitivity or particular metabolic absorption and excretion features of mercury. This case cannot be included within the continuous activity syndrome of muscle fibers described by Isaacs, since muscle contractures were absent and there was associated acrodynia. Moreover, there was no latent polyneuropathy, in spite of the intense fasciculations. It must be concluded, therefore, that in spite of its rarity fibrillary chorea should keep its semiologic autonomy.
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PMID:[Morvan's fibrillary chorea and acrodynic syndrome following mercury treatment]. 652 13

A case of severe mercuric chloride poisoning with clinical signs of mucosal damage of the gastrointestinal tract and anuric renal failure, is presented. The initial whole blood mercury concentration was 14,300 micrograms l-1. This concentration is supposed to be associated with fatal outcome due to multiple organ failure. Because of anuric renal failure, haemodialysis was necessary. Kidney function returned to normal within 10 days. Haemodialysis proved to be ineffective with regard to total mercury elimination. Treatment with DMPS was started because of very severe poisoning, anuric renal failure and optimistic reports on the "new" chelating agent 2,3-dimercapto-1 propanesulphonic acid (DMPS) in mercury poisoning. DMPS was administered by parenteral route initially and was continued thereafter by oral route, until whole blood and urine mercury concentrations had decreased below a level considered as toxic. Except for a temporary pruritic erythema of the skin, no side effects of DMPS treatment were observed. The clinical course was mild, despite continuing high whole blood mercury concentrations. Recovery was uneventful and complete. DMPS treatment, administered by intravenous and oral route, was shown to be an effective alternative for BAL in life-threatening mercuric chloride intoxication. The pharmacokinetic data presented in this case report suggest that non-renal mercury clearance may considerably exceed renal mercury clearance.
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PMID:Mercury kinetics in a case of severe mercuric chloride poisoning treated with dimercapto-1-propane sulphonate (DMPS). 819 24

The aim of this study was to investigate the cellular and biochemical events associated with repeated exposures to ozone. Twenty-three healthy subjects underwent single exposures to 200 ppb ozone and to filtered air (FA), as well as repeated exposures to 200 ppb ozone on 4 consecutive days, each for 4 h of intermittent exercise. Bronchoalveolar lavage was performed and mucosal biopsies were taken 20 h after the single or the last of the repeated exposures. As compared with FA, the single exposure to ozone caused a decrease in FEV(1), an increase in the percentages of neutrophils and lymphocytes, the concentrations of total protein, IL-6, IL-8, reduced glutathione, urate, and ortho-tyrosine in BAL fluid (BALF), but no changes in the cellular composition of biopsy. After the repeated exposure, the effect on lung function was abolished and differential cell counts in BALF were not significantly different from those after FA. However, the concentrations of total protein, IL-6, IL-8, reduced glutathione, and ortho-tyrosine were still increased. IL-10 could only be detected in BALF after repeated ozone exposures. Furthermore, macroscopic scores for bronchitis, erythema, and hypervulnerability of airway mucosa were increased, as well as numbers of neutrophils in bronchial mucosal biopsies. Our data demonstrate that airway inflammation persists after repeated ozone exposure, despite attenuation of some inflammatory markers in BALF and adaptation of lung function.
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PMID:The effect of repeated ozone exposures on inflammatory markers in bronchoalveolar lavage fluid and mucosal biopsies. 1085 57

We identified the etiological agents responsible for two fatal cases of rhinocerebral mucormycosis with the classical risk factor for uncontrolled type II diabetes mellitus. Their initial symptoms did not point immediately to the suspicion of mucormycosis. Case 1, caused by Rhizopus microsporus var. oligosporus, was a 52-year-old man who presented with a painful pimple on his nose, which evolved with swelling, erythema, and a central pustule on his right hemiface suspected to be cellulitis. After 7 days of antibiotic treatment, the patient worsened with signs of sepsis and the lesion evolved to necrosis involving all his right face. Case 2, caused by Rhizopus microsporus var. rhizopodiformis, was a 57-year-old woman placed on continuous therapy with azathioprine and corticoids after a renal transplant due to chronic arterial hypertension and uncontrolled type II diabetes mellitus. Because she was suspected to have sepsis, the patient was treated with broad-spectrum antibiotics and mechanical ventilation, yet she deteriorated. Because Candida spp. were isolated from urine and a BAL, she was treated with fluconazole for 10 days, then substituted by caspofungin. Two weeks later, she presented with exophthalmus of the left eye that was surrounded by a large inflammatory and necrotic area. Both patients were the diagnosed with mucormycosis via direct microscopy of necrotic material prior to their death.
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PMID:Mucormycosis in Mato Grosso, Brazil: a case reports, caused by Rhizopus microsporus var. oligosporus and Rhizopus microsporus var. rhizopodiformis. 2195 35