Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027947 (neutropenia)
 17,527 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six common clinical situations in infants and children are discussed from the point of view of standard therapeutic regimens: neonatal sepsis and meningitis; febrile episodes in neutropenia; bacterial meningitis; acute pulmonary exacerbations of cystic fibrosis; pneumonia, bone and joint infections, and cellulitis in patients less than four years of age; and intra-abdominal sepsis. Potential or actual problems with these therapeutic regimens and newer therapeutic options are outlined.
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PMID:Current needs for new beta-lactam antibiotics in pediatrics. 407 87

Thirty-four infants and children ranging in age from 2.5 to 180 months (mean, 40 months) were treated with parenteral moxalactam (150 mg/kg per day) for suspected or proved bacterial infections outside the central nervous system. Six patients infected with Haemophilus influenzae b, nine infected with Staphylococcus aureus, three infected with Streptococcus pneumoniae, one infected with Streptococcus pyogenes, one infected with Enterobacter aerogenes, one infected with Fusobacterium nucleotum, and one infected with Staphylococcus epidermidis, microaerophilic streptococcus, and Propionibacterium sp. were clinically and bacteriologically cured. One patient with polymicrobial pansinusitis did not respond to moxalactam. No patients developed meningitis. All of the isolates tested were inhibited by less than or equal to 5 micrograms of moxalactam per ml, except for one Staphylococcus epidermidis isolate which was resistant to greater than 20 micrograms/ml. Five patients had transient neutropenia which resolved after the drug was discontinued. The mean peak serum level was 106 micrograms/ml at 15 min after a 50-mg/kg dose. The mean elimination half-life was 91.2 min. These data indicate that this dosage of moxalactam is a safe and effective treatment for bacterial infections outside the central nervous system.
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PMID:Clinical and pharmacokinetic evaluation of parenteral moxalactam in infants and children. 621 10

Prior to the introduction of new beta-lactam antibiotics, such as ureidopenicillins and some third generation cephalosporins, the choice of antibiotics for the treatment of meningitis caused by Ps. aeruginosa was limited, and even now, this infection remains of poor prognosis. Five patients with meningitis, aged from 18 to 75 years, were treated with azlocillin. The strains of Ps. aeruginosa isolated were all sensitive to azlocillin, the zones of inhibition being greater than 20 mm in diameter with bacteriostatic concentrations. Azlocillin was administered 8-hourly by intravenous injection in doses of 30 g/day in 3 cases and 15 g/day in 2 cases. The mean duration of treatment was 33 days (range 23-50 days). In addition to azlocillin 4 patients received an aminoglycoside (tobramycin or amikacin) parenterally and, in one case, intrathecally. Four patients underwent a surgical operation on the focus of infection between the 9th and 13th days of treatment. In 3 of these 4 patients surgery was necessary to obtain apyrexia, but in all cases the CSF was already sterile when it was performed. The outcome was favourable in all 5 cases. One patient relapsed on 4 occasions due to persistent petrous bone fistula; each time, the azlocillin treatment was reinstituted and brought about clinical and bacteriological cure. The germ was eradicated in CSF on the 3rd day of treatment in 3 patients and on the 7th day in one. One patient developed transient eosinophilia and another, transient neutropenia after 30 days. It is concluded that azlocillin, associated with an aminoglycoside, is an active and effective antibiotic for the treatment of Ps. aeruginosa meningitis.
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PMID:[Pseudomonas aeruginosa meningitis treated with azlocillin. 5 cases]. 623 4

A prospective study was done to determine the incidence of neutrophil storage pool (NSP) depletion in clinically septic neonates with peripheral neutropenia (less than 1500/mm3). Infants with NSP depletion were then randomized in a controlled study of polymorphonuclear leukocyte transfusions. Bone marrow examinations were done in 13 patients, and NSP depletion was noted in 3 (23%) patients. All patients with no NSP depletion had peripheral neutrophil recovery and 8 of 10 survived. Complications of meningitis contributed to both deaths. Two of the three patients with NSP depletion died. Neither the initial severity of illness nor the degree of peripheral neutropenia were predictive either of NSP depletion or of mortality. Most neonates with severe peripheral neutropenia and clinical sepsis had peripheral neutrophil recovery and survived with conservative management. Those at high risk could be identified only by examination of the NSP. Only those patients with NSP depletion should be considered for controlled studies of polymorphonuclear leukocyte transfusions.
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PMID:Neutrophil storage pool depletion in septic, neutropenic neonates. 649 11

Seventy infants with suspected bacterial infection in the first 48 hours of life were treated either with piperacillin and flucloxacillin or with penicillin and gentamicin. Infection was confirmed and successfully eradicated in 6 of the 35 infants receiving piperacillin and flucloxacillin. Four infants treated with penicillin and gentamicin had confirmed infection and one deteriorated initially but then recovered when treated with piperacillin. Serum piperacillin concentrations above 100 mg/l and cerebrospinal fluid piperacillin concentrations of 2.6-6 mg/l were noted for up to four hours and 7 hours respectively, even in the absence of inflamed meninges, after administration of piperacillin 100 mg/kg body weight intravenously. Median half life of piperacillin was 6.5 hours and was prolonged in renal impairment. Piperacillin is considered to be a safe and effective first line single agent treatment for early neonatal infection but because some Escherichia coli are resistant to it we recommend that a second agent be used in critically ill infants with neutropenia or meningitis.
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PMID:Piperacillin in early neonatal infection. 655 60

Thirty-four children with Haemophilus influenzae type b meningitis were given prospectively either moxalactam (200 mg/kg/day) or ampicillin (400 mg/kg/day) plus chloramphenicol (75 mg/kg/day). One patient in each group died. The mean duration of fever, clinical response, sequential cerebrospinal fluid findings, and incidence of neurologic sequelae were similar between groups. Moxalactam cerebrospinal fluid bioactivity was significantly greater than that of ampicillin or chloramphenicol throughout therapy. Neutropenia, liver enzyme abnormalities, and diarrhea were not significantly different. In eight of 11 patients given moxalactam (versus one of 14 controls) there was complete elimination of gram-negative aerobic flora in the stools by day 10 (P = 0.002); however, none acquired Clostridium difficile. Moxalactam in effective therapy for H. influenzae type b meningitis.
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PMID:Moxalactam therapy of Haemophilus influenzae type b meningitis in children. 660 81

We conducted a prospective, randomized evaluation of oral chloramphenicol administration for completion of therapy of Haemophilus influenza type b meningitis in 44 children: 21 received drug by this route after the second day of therapy, the remainder continued to receive the drug intravenously. Resolution of clinical manifestations and cerebrospinal fluid indicators of meningitis was equivalent with both routes in 43 patients. One infant failed to achieve efficacious serum concentrations by either route of administration. Paired analysis of the area under the serum concentration versus time curve in 13 patients after oral and intravenous administration indicated equivalent bioavailability. Neutropenia was the only observed drug-related toxicity and correlated with the highest observed serum concentration. We conclude that: (1) chloramphenicol can be used by the oral route to complete treatment of H. influenzae type b meningitis; (2) a dose of 75 mg/kg/day is effective and less likely than higher doses to cause neutropenia; and (3) the measurement of serum chloramphenicol concentrations is important, regardless of route of administration.
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PMID:Oral chloramphenicol in the treatment of Haemophilus influenzae meningitis. 697 11

Thirty-two infants and children ranging in age from 3 to 151 months (mean, 26 months) were treated with parenteral cefoxitin (150 mg/kg per day). Ten patients with isolates of Haemophilus influenzae (six with cellulitis, two with arthritis, and two with mastoiditis), four with Staphylococcus aureus (one with lymphadenitis, one with septicemia, and two with abscess), and three patients with Streptococcus pneumoniae (one each with cellulitis, abscess, and arthritis), were clinically and bacteriologically cured by therapy. Two additional patients with septic arthritis and facial cellulitis developed meningitis with H. influenzae type b and S. pneumoniae, respectively. Minimal inhibitory and bactericidal concentrations were </=5 mug/ml for 15 isolates. Minimal bactericidal concentrations were >20 mug/ml for one strain of S. aureus and one of H. influenzae type b. The mean peak serum levels were 81.9 and 68.5 mug/ml 15 min after intravenous or intramuscular doses, respectively. The mean elimination half-lives were 42.4 and 40.1 min after intravenous or intramuscular doses, respectively. The mean volumes of distribution were 5,540 and 4,760 ml after intravenous and intramuscular doses, respectively. Mean plasma clearance was 242 and 257 ml/min per m(2) after intravenous and intramuscular doses, respectively. Therapy was discontinued in one patient because of neutropenia, which resolved after cefoxitin was stopped. Eosinophilia and transiently elevated liver function tests occurred in eight and six patients, respectively. These data indicate that cefoxitin may be an effective treatment for infections due to susceptible bacteria in the dosage tested, but its use may be limited because of the occurrence of meningitis during therapy in some patients.
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PMID:Clinical and pharmacokinetic evaluation of parental cefoxitin in infants and children. 739 56

The Candida species account for approximately three-fourths of fungal infections in patients with cancer. Although Candida albicans is the most frequent cause, C. tropicalis is increasingly implicated as an important pathogen. Over a 12 year period 19 children treated for leukemia at our institution developed C. tropicalis infections. We describe their clinical presentation, extent of fungal infection, treatment, and outcome. Fungemia without meningitis in 11 children was treated successfully, whereas C. tropicalis meningitis in 7 children was uniformly fatal. An additional patient had unsuspected, widespread infection detected at autopsy. Multiple sites, including the cerebrospinal fluid yielded C. tropicalis. Previously reported risk factors including neutropenia, broad-spectrum antibiotic usage, corticosteroid therapy, and total parenteral nutrition were observed in our cases. A high index of suspicion and the early use of aggressive antifungal therapy are critical to the successful management of C. tropicalis infections in children with leukemia.
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PMID:Candida tropicalis infections in children with leukemia. 822 Jan 36

The range of oral antifungal therapy has been expanded recently by the introduction of itraconazole, and terbinafine. These agents have a broader spectrum of activity than griseofulvin and flucytosine, and induce less liver toxicity than ketoconazole. Treatment with these agents may be optimised by application of pharmacokinetic principles. Griseofulvin, ketoconazole and itraconazole should be administered with food to ensure adequate absorption. Maximal absorption of griseofulvin is achieved by administration of the drug as a solid solution in polyethylene glycol. Absorption of azole antifungal agents is impaired by high gastric pH, which is observed in some patients with acquired immunodeficiency syndrome. It is also impaired by frequent vomiting, which commonly occurs in patients with neutropenia. Furthermore, antacids, H2-antagonists and sucralfate interfere with absorption of ketoconazole. The newer oral antifungals are more slowly eliminated and associated with less pronounced drug interactions than ketoconazole. As with ketoconazole, itraconazole and fluconazole influence cyclosporin metabolism. These effects are of clinical relevance and necessitate cyclosporin dosage reduction. However, the cyclosporin dosage reduction required during coadministration of itraconazole and fluconazole (50 to 55%) is less than that required when ketoconazole is concomitantly administered (85%). Monitoring of cyclosporin concentrations during coadministration with these agents is necessary to avoid nephrotoxicity. Drug monitoring is also advisable when phenytoin, carbamazepine or rifampicin (rifampin) are administered concomitantly with azoles, due to a mutual influence on drug metabolism. The antifungal activity of itraconazole is not related exclusively to free drug concentrations. Therefore, the low protein binding of fluconazole does not place this agent at an advantage over itraconazole in the treatment of fungal meningitis. However, terbinafine may be superior to itraconazole for the treatment of tinea unguium, another recalcitrant fungal disease, because terbinafine more rapidly penetrates the nail plate. During repeated use, itraconazole concentrations increase slowly in the nail plate. Steady-state concentrations are reached in the stratum corneum only after several weeks' administration. Following cessation of treatment, terbinafine, itraconazole and ketoconazole concentrations in keratinised tissues decline slowly. This allows a short duration of drug treatment. Some clinical trials suggest that low concentrations of flucytosine, griseofulvin and itraconazole are associated with treatment failure. Flucytosine-induced myelotoxicity also appears to be concentration dependent. This adverse reaction may be caused by fluorouracil (which is produced by metabolism of flucytosine by enterobacillary flora in the gut) rather than by the parent compound.
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PMID:Pharmacokinetic optimisation of oral antifungal therapy. 826 15


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