Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prospective randomized study compared the use of moxalactam disodium vs clindamycin phosphate and tobramycin sulfate for treatment of 190 patients with penetrating abdominal trauma. Twenty-seven patients were disqualified because of early death or failure to follow the protocol. The patients in each group were comparable regarding the cause and severity of injury. No significant difference was seen in the incidence of intra-abdominal infection between the moxalactam-treated group (13%) and the clindamycin- and tobramycin-treated group (9%). The intra-abdominal infection rate in patients with colon injuries (21%) was significantly increased when compared with the patients without colon injuries (6%), but the antibiotic regimen did not significantly change the infection rate. No evidence of bleeding problems from moxalactam were noted. Changes in prothrombin and partial thromboplastin times appeared to be related to shock rather than the use of moxalactam. The most severe coagulopathies occurred prior to moxalactam therapy and were seen only in those patients who had shock requiring 10 or more units of blood. Moxalactam is as effective as combination (clindamycin and tobramycin) antimicrobial therapy in patients with penetrating abdominal trauma.
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PMID:Single-antibiotic use for penetrating abdominal trauma. 394 16

A bleeding diathesis characterized by in-vitro platelet dysfunction and prolongation of the template bleeding time (TBT) has been reported in patients receiving latamoxef ('moxalactam'), but not cefotaxime or cefoperazone. Hypoprothrombinaemia has been associated with the use of both latamoxef and cefoperazone in seriously ill and malnourished patients. We administered either latamoxef, cefotaxime or cefoperazone intravenously, at dosages within the range recommended by each manufacturer, to 14 normal volunteers. Latamoxef caused a dose and time dependent defect in platelet function characterized in vitro by abnormalities in aggregation to adenosine diphosphate and in vivo by prolongation of the template bleeding time. In two out of two subjects, a single 4 g dose of latamoxef caused neither prolongation of template bleeding times nor aggregation abnormalities. Two out of two subjects receiving latamoxef 6 g/day for six days had progressive prolongation of bleeding times to 12 and 15 min. Two additional subjects receiving latamoxef 12 g/day for four days had prolongation of template bleeding times to greater than 20 min. Of four subjects receiving cefotaxime 12 g/day for seven days, none had prolongation of template bleeding times or abnormalities in platelet aggregations. Of four subjects receiving cefoperazone 6 g/day, none had significant prolongation of template bleeding times and one had abnormalities in aggregation attributed to inadvertent salicylate ingestion. Prolongation of the prothrombin time or activated partial thromboplastin time did not occur in any of the 14 volunteers. Latamoxef is more likely to interfere with platelet function than either cefotaxime or cefoperazone.
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PMID:The effects of latamoxef, cefotaxime, and cefoperazone on platelet function and coagulation in normal volunteers. 404 67

Sixty-seven patients were treated with moxalactam in a noncomparative trial of hospitalized patients; 32 had endometritis or chorioamnionitis, 12 had skin and soft tissue infections, 5 had osteomyelitis, 5 had pneumonia, 5 had urinary tract infections, 4 had arthritis, 2 had sepsis from an unknown source, 1 had endocarditis, and 1 had peritonitis. Bacteremia was present in 12 of these patients. Patients were given 3 to 12 g of moxalactam per day (mean, 6.24 g/day) in divided doses every 6 to 8 h. Seven patients were given intramuscular treatment for 3 to 20 days for part or all of their therapy. The rest were given intravenous treatment exclusively. Treatment was continued for 2 to 42 days (mean, 10 days). The dose and the duration of therapy were determined by the type of infection and the response of each patient. There were four treatment failures and one enterococcal-clostridial superinfection. Moxalactam was well tolerated. Allergic reactions led to the discontinuation of the antibiotic in three patients. Prolonged prothrombin and partial thromboplastin times were observed in 2 of 11 patients tested; in both instances in patients had severe underlying diseases, including malnutrition and alcoholism. Pain on intramuscular injection was noted in two patients receiving 1,500 mg, but not in five receiving a lower dose; in one case the pain forced the use of intravenous therapy after one dose, and in the other case the pain was mild and the patient was treated for 20 days. We concluded that moxalactam was effective in the treatment of the types of infections included in this study and produced few adverse reactions.
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PMID:Moxalactam in the therapy of serious infections. 621 Nov 40

Moxalactam penetrates cerebral spinal fluid (CSF) and subdural fluid well enough to be a promising antimicrobial for enteric bacterial meningitis in neonates and infants. Clinical trials in adults and children have found few adverse effects. Prolongation of prothrombin time (PT) and partial thromboplastin time (PTT) with or without bleeding was reported in adults. This paper reports this complication in two infants occurring at a time of clinical improvement following addition of Moxalactam to other antibiotics to which the meningitis had failed to respond. It is not certain if this complication was related to the underlying meningitis, the use of Moxalactam together with other antibiotics, or a combination of many factors. Further observation, close hemostatic monitoring, and timely vitamin K administration during its use are warranted.
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PMID:Hemorrhagic tendency as a complication of Moxalactam therapy in bacterial meningitis. 663 97