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Biomedical subjects

J W Larsen

Publications and source records attributed to J W Larsen.

At least 55 records · Page 3Linked to original sources
PubMed1986

The sonographic evaluation of fetal anomalies in oligohydramnios between 16 and 30 weeks gestation.

The sonograms of all patients with oligohydramnios between 16 and 30 weeks gestation seen over a 4-year period were reviewed to determine (1) whether sonographically detectable fetal anomalies were present, and (2) when these anomalies were present, how this information was used in maternal fetal management. Cases of ruptured membranes and fetal demise were excluded from the study. Sixteen patients with severe oligohydramnios were identified. On postmortem examination, nine had urinary tract anomalies, one had evidence of a chronic intrauterine infection, and four had no anomalies. There were only two neonatal survivors: one had no anomalies while the other had posterior urethral valves. These findings confirm that second trimester oligohydramnios has a poor prognosis and is often associated with anomalies of the urinary tract. Sonography aids in the clinical management of such patients.

Amniotic Fluid↗
PubMed1986

Comparison of cefoxitin and clindamycin-gentamicin for pelvic infections.

Cefoxitin and clindamycin-gentamicin were compared in a randomized study of antibiotic therapy for infections of the pelvis in 91 women. Clinical diagnoses included pelvic inflammatory disease (53), endomyometritis after cesarean section (24), and cellulitis following gynecological surgery (14). Treatment failures occurred in four (10%) of the 41 patients treated with cefoxitin compared with eight (16%) of the 50 patients treated with the clindamycin-gentamicin combination. Single-drug therapy with cefoxitin was shown to be as effective as the combination of clindamycin and gentamicin.

Adolescent↗
PubMed1985

Plasma and red blood cell beta-endorphin immunoreactivity in normal and complicated pregnancies: gestational age variation.

Recent observations suggest that there may be two pools of beta-endorphin-like immunoreactivity in mammalian circulation. One of these pools is present in plasma and the other is detected in association with erythrocytes. Elucidation of an erythrocyte-associated pool may explain some of the wide variability of plasma beta-endorphin levels reported in the literature. We measured beta-endorphin immunoreactivity levels in 85 normal and 33 complicated pregnancies to delineate a possible correlation between gestational age and beta-endorphin immunoreactivity levels in plasma and in erythrocytes. Our results indicate that beta-endorphin immunoreactivity levels in both plasma and erythrocytes vary systematically throughout the gestational period, reaching a peak at 31 to 32 weeks of gestation. Amniotic fluids at midgestation were also analyzed and no correlation was observed between the levels of beta-endorphin immunoreactivity and fetal sex. Compared to normal patients, diabetic patients had significantly lower levels of beta-endorphin immunoreactivity in plasma and higher levels in erythrocytes although the total beta-endorphin immunoreactivity was not statistically different from that in normal subjects. We conclude that (1) the total beta-endorphin immunoreactivity level in whole blood is much higher than that reported in plasma, (2) both plasma- and erythrocyte-associated beta-endorphin immunoreactivity levels vary with gestational age, with a peak level at 24 to 32 weeks of gestation, (3) amniotic fluid beta-endorphin immunoreactivity levels are unrelated to fetal sex, and (4) diabetic patients may have a different distribution of beta-endorphin immunoreactivity pools than normal individuals.

Amniotic Fluid↗
PubMed1985

Pharmacologic suppression of the fetal adrenal gland in utero. Attempted prevention of abnormal external genital masculinization in suspected congenital adrenal hyperplasia.

21-Hydroxylase deficiency results in congenital adrenal hyperplasia and leads to masculinization of the external genitalia of affected females. This complication could be avoided if fetal adrenal gland function were suppressed. A woman with mild 21-hydroxylase deficiency whose previous female child had classic congenital adrenal hyperplasia with masculinization was given dexamethasone beginning at the tenth week of gestation. Maternal estriol and cortisol values indicated rapid and sustained fetal and maternal adrenal gland suppression. At 39 weeks' gestation, the patient was spontaneously delivered of a female neonate with normal external genitalia. Postnatal tests indicated the infant was a single heterozygote for 21-hydroxylase deficiency. This study demonstrates prolonged suppression of the fetal adrenal gland with dexamethasone and suggests it might prevent abnormal masculinization in fetuses with severe congenital adrenal hyperplasia.

Adrenal Cortex↗
PubMed1985

First trimester prenatal diagnosis of adrenoleukodystrophy by determination of very long chain fatty acid levels and by linkage analysis to a DNA probe.

A first trimester prenatal diagnosis of adrenoleukodystrophy has been done on chorionic villi biopsy in the pregnancy of a carrier woman. Two different approaches allowed one to determine that the male fetus was affected: the linkage analysis of DNA from chorionic villi using the highly polymorphic probe St 14 and the determination of very long chain fatty acid levels in cultured chorionic villi.

Adrenoleukodystrophy↗
PubMed1984

Balanced rearrangement of chromosomes 2, 5, and 13 in a family with duplication 5q and fetal loss.

We have studied a family in which a mother and daughter (the proposita) had the karyotype 46,XX,ins(2;5),t(5;13). The mother had four spontaneous abortions, a mentally retarded son with duplication (5q), and a daughter who died at 3 months. The proposita had a phenotypically abnormal abortus. Rearrangements involving several chromosomes are very rare. Observations on this family are consistent with the predicted high likelihood of reproductive loss.

Abnormalities, Multiple↗
PubMed1983

Antibody to type III group B Streptococcus in the rhesus monkey.

Susceptibility to infection due to intra-amniotic type III group B streptococcal infection was studied in 27 rhesus monkeys. Sera from mothers and their offspring were tested to determine the concentration of antibody to the native type III group B Streptococcus antigen. Among 17 controls there was a statistically significant association between the concentration of maternal antibody prior to infection and both the neonatal survival rate and survival time (P less than 0.05). Neonatal survival was decreased to less than or equal to 6 hours (P = 0.005) if the maternal antibody concentration was less than 0.5 micrograms/ml. Modified immune serum globulin was given intravenously to the mothers prior to intra-amniotic infection with (five animals) or without (five animals) neonatal modified immune serum globulin. Neither of the modified immune serum globulin groups demonstrated a significant reduction in the neonatal mortality rate; however, the addition of the modified immune serum globulin provided protection against rapid neonatal death among those animals born to mothers which had low or no detectable antibody. All maternal groups developed a significant increase in the concentration of antibody in postpartum sera. These results indicate that both naturally acquired and passive (modified immune serum globulin) antibodies to type III group B Streptococcus antigen are partially protective against intra-amniotic infection.

Animals↗
PubMed1981

Penicillin treatment for group B streptococcal meningitis in the rhesus monkey.

Penicillin therapy for experimentally produced neonatal meningitis due to intracerebral inoculation of group B streptococci (GBS) was studied in 25 rhesus monkeys. Penicillin was administered either therapeutically to the newborns 3 hours after GBS inoculation or prophylactically as a bolus to the pregnant females 2 hours before delivery. The neonatal mortality in the newborn treatment groups was 40% (6 of 15) compared to 100% (5 of 5) in the maternal prophylaxis group, and 0% (0 of 5) among uninfected and untreated controls. It was concluded that although penicillin can be used successfully to treat neonates with meningitis after intracerebral inoculation of GBS, penicillin given antepartum as bolus prophylaxis to the mother monkey was ineffective.

Animals↗
PubMed1981

Intraamniotic infection due to group G streptococcus: treatment and antibody response.

Penicillin treatment and antibody response were studied using a rhesus monkey model for intraamniotic infection with type III group B streptococci (T3GBS). Acute and convalescent phase sera from mothers and their offspring were tested with a radioactive antigen-binding assay to determine the concentration of antibody to the capsular T3GBS antigen. The frequency of placentitis was significantly lower in penicillin-treated animals (3 of 8) than in controls (10 of 10; P less than .01). The penicillin group also had a significantly lower neonatal mortality (1 of 9) than controls (6 of 10; P less than .05). Both groups of rhesus mothers developed a significant increase in concentration of antibody to T3GBS, but the antibody response was of lesser magnitude in the penicillin-treated group. This experimental model appears to be useful for studying both therapy for intraamniotic infection and the humoral immune response to infection with T3GBS.

Amnion↗
PubMed1980

Stability of standard curves prepared for EMIT homogeneous enzyme immunoassay kits stored at room temperature after reconstitution.

We examined the stability of standard curves obtained with use of homogeneous enzyme immunoassay reagents (EMIT; Syva Corp., Palo Alto, CA) for assay of lidocaine, procainamide, N-acetylprocainamide, gentamicin, and theophylline, when stored at room temperature (23-24 degrees C) after reconstitution of the lyophilized materials. Standards were run and curves obtained for as long as 16 days after reconstitution. All standard curves were acceptable, according to the criteria specified in Syva product literature. Absorbance changes for all calibrators, including the zero calibrator, increased gradually with time. Increases of non-zero calibrators were largely offset by a parallel increase in the zero calibrator, such that the quantity delta A--delta A0 was very nearly constant with time. Standard curves based on the quantity delta A--delta A0 can be used for longer than curves based only on delta A.

Acecainide↗
PubMed1980

Prenatal diagnosis of congenital adrenal hyperplasia.

In patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency, the concentrations of the cortisol precursor 17-alpha hydroxyprogesterone (17-OHP) and its metabolite delta 4-androstenedione (delta 4 A) are increased. CAH was diagnosed in twins by measurement of 17-OHP and delta 4 A concentrations in amniotic fluid obtained by amniocentesis from both amniotic cavities at 17 weeks' gestation. Both prenatal karyotypes were 46,XX. Spontaneous labor and delivery of 2 nonviable fetuses with genital masculinization occurred at 26 weeks' gestation. It is concluded that delta 4 A measurement, like 17-OHP quantitation, is valuable in the prenatal diagnosis of CAH; that both methods appear useful in prediction of CAH in twin fetuses; and that abnormal adrenal-mediated masculinization in female CAH is well established before the end of the second trimester.

Adrenal Hyperplasia, Congenital↗