Old drug, new use: article of manufacture claims. Should you try this new type of claim?
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Biomedical subjects
Publications and source records attributed to P D Kelly.
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The West Virginia Health Care Surrogate Act of 1993 became effective July 1, 1993. This law establishes a process for making health care decisions for adults who lack decision-making capacity and who have not completed a medical power of attorney that does not require judicial involvement. The law describes how a health care surrogate is to be selected by the physician, and it provides immunity to the physician and surrogate who make health care decisions according to its provisions. This article presents a case in which the application of the new law is demonstrated.
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To determine the value of prenatal cultures in defining maternal colonization status at delivery, 5,586 pregnant women were screened at prenatal visits for vaginal and rectal carriage of group B streptococci (GBS). GBS were isolated from 1,272 (22.8%). At delivery, semiquantitative cultures were obtained from 393 prenatal carriers, of whom 264 (67.2%) retained carriage at delivery. Seventeen (8.5%) of 200 women with negative prenatal cultures acquired carriage. The predictive value of a positive prenatal culture was highest (72.5%) in women with prenatal vaginal and rectal colonization and lowest (59.7%) in women with only rectal colonization. The predictive value varied inversely with the interval between prenatal sampling and delivery. In mothers with prenatal carriage, density of colonization at parturition was not predicted by the sites of prenatal colonization. Density of colonization, however, strongly influenced rates of vertical transmission to neonates and rates of heavy infant colonization. Ten infants born to prenatally cultured mothers developed group B streptococcal early-onset disease; the mothers of eight (80%) of the 10 had prenatal colonization with the homologous GBS serotype.
The effect of intrapartum ampicillin treatment on vertical transmission of group B streptococci (GBS) was examined in 575 prenatally colonized parturient women and their 580 newborn infants. Eighty women (43 receiving ampicillin) with premature labor and/or prolonged rupture of amniotic membranes were randomized. The other 495 were stratified into groups of 358 (31 receiving ampicillin) with no perinatal risk factors; 119 (28 receiving ampicillin) with premature labor and/or prolonged membrane rupture; and 23 (18 receiving ampicillin) with intrapartum fever. Ampicillin virtually eliminated vertical transmission in the treatment group with no risk factors and in both treatment groups with premature labor and/or prolonged membrane rupture. GBS colonization of neonates was detected only in women with intrapartum fever or brief (less than 1 hr) duration of treatment prior to delivery. Ampicillin treatment was associated with a highly significant reduction in maternal postpartum vaginal colonization by GBS. There were six group B streptococcal early-onset infections in infants of untreated subjects and no cases in treated subjects.
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The protective value of pooled human gamma globulin (GG) and a group B streptococcal immune globulin (GBSIG) was studiedf in a chick embryo and a murine model of group B streptococcal (GBS) infection. Chick embryos were protected by the IV administration of 0.4 to 0.8 mg of GG from three manufacturers against IV challenge with type Ia GBS. Two of three GG preparations at doses of 0.4 to 1.65 mg protected chick embryos against type III, but 1.65 mg of all three preparations failed to protect against GBS types Ib and II. MIce were protected from lethal IP challenges with types Ia and Ib by the prior IM inoculation of three and two of the three GG preparations at doses of 0.5 to 1.0 mg, respectively. Administration IM of 1 mg of GG failed to protect mice against types II and III. The IV administration of 0.2 mg of GBSIG protected chick embryos against IV inoculation with GBS types Ia, Ib, II, and III. Administration IM of 0.5 mg of GBSIG protected mice against IP challenges with types Ia, Ib, and II, but not with type III. The IP administration of 0.25 mg of GBSIG simultaneously with type III GBS protected mice, whereas GG was not protective. GBSIG should undergo clinical trials for the prevention of GBS infections and their recurrences and as a possible adjunct to antibiotic and supportive therapy of severe GBS infections.
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