Biomedical subjects

D I Hoffman

Publications and source records attributed to D I Hoffman.

22 records · Page 2Linked to original sources

PubMed1984

The prevalence and significance of elevated dehydroepiandrosterone sulfate levels in anovulatory women.

One hundred nineteen euprolactinemic anovulatory infertility patients who were being evaluated for induction of ovulation with clomiphene citrate were studied to determine the prevalence of increased adrenal androgen (AA) secretion in this group. Fifty percent of these patients exhibited increased AA secretion, as evidenced by an elevated serum dehydroepiandrosterone sulfate (DHEA-S) level. Seventy-seven percent of these women with elevated levels of DHEA-S were nonhirsute . Twenty-six patients with elevated serum DHEA-S levels underwent adrenocorticotropic hormone (ACTH) stimulation tests in order to determine a possible mechanism(s) for the increase in DHEA-S. Plasma ACTH, as well as total, low-density lipoprotein, and high-density lipoprotein cholesterol were also measured. These levels were normal and did not correlate with the elevated levels of DHEA-S. Seven of 16 patients (34%) had exaggerated responses of serum DHEA-S and of 17-OH pregnenolone to ACTH stimulation. In six of these seven patients, our data suggested the occurrence of a mild deficiency of 3 beta-ol dehydrogenase-isomerase. All of these six patients were considered to have polycystic ovary syndrome. While these data do not explain the increased AA secretion in the majority of patients with elevated levels of DHEA-S, we suggest that serum DHEA-S is frequently elevated in anovulatory infertile patients.

17-alpha-Hydroxypregnenolone↗

PubMed1984

Chlamydia trachomatis is not an important cause of abnormal postcoital tests in ovulating patients.

To examine the role of Chlamydia trachomatis infections of the cervix and abnormal postcoital tests (PCT) in a general infertility clinic, 63 consecutive patients undergoing a midcycle PCT during a routine infertility workup underwent endocervical curettage, and a 10-ml blood sample was obtained. The endocervical tissue was cultured for C. trachomatis; the serum sample was analyzed for chlamydial IgG and IgM antibodies using an indirect microimmunofluorescence assay. A negative titer was considered to be less than or equal to 1:8 dilution for IgG antibodies and less than or equal to 1:32 dilution for IgM antibodies. A good PCT was defined as greater than or equal to 5 motile sperm per high power field (HPF). A poor PCT was defined as less than 2 motile sperm/HPF, and a fair PCT was defined as 2 to 4 motile sperm/HPF. Of the 63 PCTs done, 27 (42.9%) were good, 14 (22.2%) were fair, and 22 (34.9%) were poor. All endocervical tissue cultures for C. trachomatis obtained during PCTs were negative. All IgM chlamydial antibody titers were negative (less than or equal to 1:32 dilution), 55 (87.3%) of the patients having a zero titer. Eleven (17.5%) of the patients had negative IgG chlamydial antibody titers (less than or equal to 1:8 dilution), none of the patients had a 1:16 dilution, and 52 (82.5%) had positive IgG chlamydial antibody titers (greater than or equal to 1:32 dilution). Thus, chlamydial infections of the endocervix are rare and not commonly associated with poor PCTs in this patient population.

Adult↗

PubMed1983

Effects of induction of general and regional anesthesia for cesarean section on maternal plasma beta-endorphin levels.

Plasma beta-endorphin was measured in 40 healthy pregnant women undergoing cesarean section. Group 1 patients (N = 14) received general anesthesia by rapid-sequence induction and endotracheal intubation with curare, thiopental, and succinylcholine. Anesthesia was maintained with nitrous oxide, oxygen, and muscle relaxant until delivery. Group 2 patients (N = 26) received regional anesthesia (spinal, 14, and epidural, 12). Maternal blood samples were drawn from indwelling venous catheters prior to and after induction of either general or regional anesthesia. Plasma beta-endorphin was determined by radioimmunoassay following silicic acid extraction and gel chromatography. In the 14 patients who underwent general anesthesia, the mean (+/- SEM) plasma beta-endorphin increased significantly (p less than 0.025) from 46 +/- 7.4 to 111.6 +/- 8.9 fmol/ml. There was no significant change in plasma beta-endorphin level of the 26 patients who underwent regional anesthesia; beta-endorphin levels averaged 44.5 +/- 5.1 and 47.6 +/- 4.8 fmol/ml prior to and after induction of anesthesia, respectively. These data demonstrate that plasma beta-endorphin concentrations are elevated following induction of general anesthesia but not with induction of regional anesthesia, which suggests that less stress is associated with regional than with general anesthesia induction in patients undergoing cesarean section.

Anesthesia, Epidural↗

PubMed1982

beta-Endorphin and beta-lipotropin concentrations in umbilical cord blood.

Antisera suitable for human beta-endorphin and beta-lipotropin radioimmunoassay were developed, and radioimmunoassays were established to measure these peptides in umbilical cord plasma, with silicic acid extraction and gel chromatography used to separate the beta-endorphin from the beta-lipotropin fraction. These two peptides were determined in umbilical venous plasma from 64 newborn infants. Umbilical vein beta-endorphin and beta-lipotropin concentrations averaged 38.5 +/- 3.2 and 50.4 +/- 4.1 (+/- SE) fmoles/ml in the 54 newborn infants without and 115 +/- 18 and 110 +/- 25 fmoles/ml in the 10 newborn infants with apparent fetal distress. Neither the presence or absence of labor nor the route or mode of delivery was found to affect umbilical vein beta-endorphin or beta-lipotropin concentrations. However, cord plasma levels of both peptides were significantly elevated in conjunction with fetal distress, as evidenced by prolonged bradycardia, late and prolonged variable fetal heart rate decelerations, or fetal acidosis. In 18 of 22 pairs of simultaneously measured umbilical venous and arterial beta-endorphin and beta-lipotropin concentrations in newborn infants without apparent intrapartum distress, the venous beta-endorphin concentrations, which averaged 40.4 +/- 3.5 fmoles/ml, were significantly higher than the arterial beta-endorphin levels, with a mean of 28.5 +/- 4.2 fmoles/ml. No significant umbilical arteriovenous concentration difference could be observed for beta-lipotropin. This suggests that at least a portion of the coad plasma beta-endorphin is derived from the placenta. The ratio of umbilical arterial to venous beta-endorphin concentrations rose as the absolute cord plasma beta-endorphin levels increased. Furthermore, both the molar umbilical venous and arterial beta-lipotropin to beta-endorphin ratios decreased significantly in association with intrapartum fetal distress. These data indicate tat the stress-related increase in umbilical plasma beta-endorphin exceeds that of beta-lipotropin and may be, at least in part, of fetal origin. Umbilical venous beta-endorphin and beta-lipotropin levels of neonates whose mothers did not receive meperidine or other narcotics agents did not differ from those of neonates whose mothers were given meperidine or other narcotics during labor. Our data, in conjunction with those of others, are consistent with the hypothesis that fetal hypoxia causes the release of neurotransmitters such as beta-endorphin, which may modulate the regulation of fetal heart rate patterns.

Chromatography, Gel↗