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Biomedical subjects

S Kivinen

Publications and source records attributed to S Kivinen.

At least 55 records · Page 3Linked to original sources
PubMed1982

Sulpiride improves inadequate lactation.

Twenty-eight newly delivered mothers with inadequate lactation volunteered for a placebo-controlled double-blind trial of sulpiride 50 mg thrice daily for four weeks. Treatment was allocated at random, and serum prolactin concentrations and breast-milk yields were measured before and serially during the trial. Of the 26 women who completed the trial, 14 had taken sulpiride and 12 the placebo. In the sulpiride-treatment group the mean maternal serum prolactin concentration rose from 49.0 +/- SE 3.6 micrograms/l to a maximum of 402.1 +/0 43.2 micrograms/l at two weeks; in the placebo-treated group, however, the concentration fell during the trial (from 84.7 +/- 24.0 micrograms/l to 47.8 +/- 8.6 micrograms/l). Mean breast-milk yields also increased in the sulpiride-treatment group (by an average of 212-265 ml) and fell in the women given placebo. Of the 14 infants in the sulpiride-treatment group, four did not need supplementary feeds during the trial; in the control group, however, all infants continued to require such feeds. Infants in the sulpiride-treatment group gained significantly more weight than did the controls (p less than 0.05). Three women taking sulpiride complained of mild side effects, but none occurred in the infants. These findings suggest that sulpiride is an effective treatment for inadequate lactation in the puerperium.

Clinical Trials as Topic↗
PubMed1982

Smooth muscle antibodies in pre-eclampsia of pregnancy.

Sera from 176 patients with hypertensive disorders of pregnancy, intrahepatic cholestasis of pregnancy, and oedema of pregnancy, and from 51 normal pregnant control subjects were tested for smooth muscle antibodies (SMA) by indirect immunofluorescence. An increased incidence of SMA positivity was found in cases of pre-eclampsia and in superimposed pre-eclampsia of pregnancy, oedema of pregnancy and intrahepatic cholestasis of pregnancy combined with oedema of pregnancy. In the pre-eclampsia group, SMA positivity occurred only in cases of pre-eclampsia levis and was often accompanied by mild proteinuria. This indicates that SMA are a result rather than a cause of an (immuno)pathological process, the short duration of which in severe forms is not enough for the development of the antibodies. The increased incidence of positive SMA titres in oedematous pregnant patients may be a sign of imminent pre-eclampsia, although oedema is often regarded as being a feature of otherwise normal pregnancies.

Antibodies↗
PubMed1981

Postmenopausal hormone replacement therapy with estrogen periodically supplemented with antiestrogen.

To inhibit endometrial stimulation during postmenopausal estrogen therapy, 25 women with climacteric symptoms were treated with a daily dose of 1.25 mg of conjugated estrogens for 7 weeks followed by a period of 10 days with clomiphene citrate administration (50 mg per day). This combination was repeated three times during the 6-month trial. The marked relief of climacteric symptoms with estrogen was slightly less during clomiphene treatment. Uterine bleeding occurred five times during estrogen treatment periods but never during or after clomiphene supplementation. Histologic examination revealed endometrial atrophy in 41% of the samples after the first estrogen treatment, whereas after the first and third clomiphene periods this was increased to 77% and 73%, respectively. The first clomiphene treatment significantly decreased the concentrations of cytosol estrogen and progestin receptors in endometrium, as compared with the levels recorded at the end of the preceding estrogen therapy. The depression in the cytosol estrogen receptor concentration was persistent, whereas cytosol progestin receptor concentration tended to increase during the subsequent estrogen-plus-clomiphene treatment. Estrogen declined serum concentration of follicle-stimulating hormone (FSH), whereas the concentration of luteinizing hormone (LH) and prolactin remained unchanged. Clomiphene did not change the levels of these hormones from those observed during the estrogen treatment. The concentration of free fatty acids in serum was increased during the estrogen and clomiphene treatments, whereas the levels of cholesterol and high-density lipoprotein--cholesterol did not change. Our results suggest that this treatment regimen relieves climacteric symptoms without endometrial stimulation or other adverse effects. Thus, clomiphene appears to be a practical alternative to progestin for interruption of the postmenopausal endometrial effect of estrogen.

Clomiphene↗
PubMed1981

A dose response relation between improved lactation and metoclopramide.

In a placebo-controlled, cross-over study, thirty-seven puerperal women with inadequate production of breast-milk were treated with 5, 10, or 15 mg of metoclopramide three times a day for 2 weeks. Doses of 10 or 15 mg significantly raised maternal serum prolactin; they also increased breast-milk secretion by 42.5 +/- 34.7 (SD) ml and 50.0 + 35.9 ml per feed, respectively. This effect was unrelated to the phase of the puerperium during which treatment was started. The increase in milk secretion was associated with a decreased need for supplementary feeds, and 33% of the infants of these mothers needed no supplementary feeds during treatment. 5 mg doses did not stimulate prolactin milk secretion. Although placebo had no objective effect on the milk yield, 24% of the women judged its effect to be good, and 89% of women on metoclopramide reported a good effect. Seven women on metoclopramide and three women on the placebo complained of slight side-effects. No adverse effects upon the infants were observed. Metoclopramide therapy may be useful for improving poor lactation.

Clinical Trials as Topic↗
PubMed1981

Pregnancy and delivery at the age of forty and over.

One hundred and eighty-six deliveries from mothers of age 40 and over at Oulu University Central Hospital during 1975-77 are summarized. The commonest maternal complications were pre-eclampsia (25.8%) and pathological glucose tolerance (7.0%). The cesarean section rate of the whole group was 126.7%, and for the primiparas, 47%. Placental complications were slightly but not significantly more common among parturients over 40 compared with our general obstetric population. The pregnancies did not adversely affect the mothers' health despite commonly occurring maternal diseases. The commonest pathological findings among the newborns were hyperbilirubinemia (7.9%), neonatal infections (4.2%), clavicular fractures (3.2%) and postpartum asphyxia (2.6%). Congenital anomalies occurred in 2.6% of the children and were the main cause of the perinatal mortality, which was 5/189 (2.6%). Prematurity and low birth weight were not increased.

Adult↗
PubMed1981

Metoclopramide increases prolactin release and milk secretion in puerperium without stimulating the secretion of thyrotropin and thyroid hormones.

To explore the effect of metoclopramide (MC) on the secretion of PRL, TSH, and thyroid hormones (T3 and T4) and on defective lactation, 17 mothers with poor lactation were treated with oral MC (10 mg. three times daily) for 3 weeks starting 18-141 days post partum. After a pause of 1 week, the medication was given for a further 2 weeks. The breast milk yield was monitored objectively before and during the trial. Furthermore, iv stimulation tests with MC (10 mg) and TRH (200 microgram) were done before and at the end of oral MC therapies. Oral MC increased the mean (+/-SEM) plasma PRL level from 36.6 +/- 9.2 to 90.6 +/- 7.5 ng/ml (P less than 0.001) after 1 week, and the PRL level remained elevated for as long as MC was administered. During the pause, the PRL level decreased to 19.5 +/- 7.5 ng/ml, but increased once again during the second MC treatment to 85.5 +/- 16.0 ng/ml (P less than 0.01). Plasma TSH, T3, and T4 did not change. The PRL level rose significantly after TRH and MC injections before and during oral treatments with MC, whereas the TSH concentrations were elevated only after TRH stimulation. The PRL response to iv MC or TRH and the TSH response to iv TRH were not affected by oral MC treatment. The mean daily milk volume increased from 433 +/- 55 to 626 +/- 75 ml (P less than 0.001) during the first treatment and from 390 +/- 73 to 606 +/- 56 ml (P less than 0.01) during the second oral MC treatment. Correspondingly, the volume of daily supplemental alimentation decreased from 348 +/- 61 to 280 +/- 59 ml (P less than 0.05) and from 526 +/- 68 to 363 +/- 66 ml (P less than 0.01), respectively. MC caused no significant side effects.

Adult↗
PubMed1981

Experimental hyperprolactinemia and hypoprolactinemia and human chorionic gonadotropin during early pregnancy.

The effect of experimental hyperprolactinemia and hypoprolactinemia on human chorionic gonadotropin (hCG) concentration was studied in 34 healthy volunteers between weeks 6 and 11 of normal pregnancy. Hyperprolactinemia was induced in 12 women with 150 mg of sulpiride daily for 2 weeks; treatment led to a mean plasma prolactin (PRL) rise from 14.6 to 84.1 microgram/liter after 1 week and to 83.0 microgram/liter after 2 weeks. Hypoprolactinemia was effected in 11 women wit 5.0 to 7.5 mg of bromocriptine, daily for 2 weeks; treatment decreased the mean plasma prolactin from 19.2 to 6.0 microgram/liter after 1 week and to 5.2 microgram/liter after 2 weeks. These PRL changes were significant (P less than .001) in comparison with the plasma PRL concentrations in the 11 control women. Hyperprolactinemia induced by the sulpiride treatment was accompanied by a significant decrease in hCG concentration, whereas no difference in hCG was seen between hypoprolactinemia and control groups. This may suggest a synergistic action of hCG and PRL, or a direct effect of sulpiride on hCG, but the final mechanism and biologic importance of the phenomenon remain to be investigated.

Adult↗
PubMed1981

Therapeutic, clinical and histological factors related to the survival of patients with advanced ovarian carcinoma.

Retrospective evaluation of 137 patients with advanced ovarian carcinoma was attempted 4-12 years after therapy. The operation was radical or almost radical in 56 cases (40.8%). Postoperative treatment consisted of single-drug (N = 53) or multi-drug cytotoxic chemotherapy (N = 53) and irradiation alone (N = 8) or together with cytotoxic chemotherapy (N = 53). Postoperative therapy of any kind was impossible in 23 cases. Nine patients were alive 5 years after therapy. Eight of them had had a clinical stage III (survival rate 7.7%) and one clinical stage IV malignancy (survival rate 3.0%). The extent of the operation was of major importance, 8 out of 9 survivors having undergone a radical operation, which also prolonged the life of the non-survivors. Single drug chemotherapy and combination chemotherapy yielded similar results, 4 and 5 survivors, and 21.1 and 19.6 months as the mean length of survival respectively. None of the patients on postoperative radiotherapy survived. Their mean survival period was 16.6 months. Radiotherapy as an additional measure did not produce any benefit. The prognosis was most favourable for patients with serous cystadenocarcinoma. A poor prognosis was typical of nulliparous women, suggesting that hormones may contribute to the clinical behaviour of this illness.

Adenocarcinoma↗
PubMed1980

Bromocriptine suppresses the thyrotrophin response to thyrotrophin releasing hormone during human pregnancy.

Thyrotrophin (TSH) responses to 200 microgram of intravenous thyrotrophin releasing hormone (TRH) were measured in fifteen healthy women in normal early pregnancy before and at the end of a bromocriptine treatment of 5.0-7.5 mg daily for 1-2 weeks. Bromocriptine did not change the basal levels of TSH, triiodothyronine (T3) and thyroxine (T4) during pregnancy. Before the start of bromocriptine, TRH caused a significant TSH elevation from 12.8 +/- 0.5 muu/ml (mean +/- SE) to 21.2 +/- 1.9 muu/ml after 20 min. During bromocriptine intake, TRH caused a TSH elevation from 11.9 +/- 0.4 muu/ml to only 15.5 +/- 1.1 muu/ml which is significantly less (P less than 0.001) than before bromocriptine. Similarly, the mean maximal TSH increment of 8.4 +/- 1.5 muu/ml before bromocriptine was greater (P less than 0.001) than that of 3.8 +/- 60 muu/ml during bromocriptine intake. When women were retested with TRH before and during bromocriptine after legal abortion, bromocriptine did not change the basal levels of TSH, T3 and T4 or the TSH response to TRH. Therefore, the TSH inhibition caused by bromocriptine is specifically related to the pregnancy itself, but the mechanism for this inhibition remains unknown.

Adolescent↗
PubMed1980

Does bromocriptine block thyrotropin-releasing hormone-induced prolactin release during pregnancy?

PRL responses to 200 microgram of iv TRH were measured in 16 healthy women with normal early pregnancy before and at the endo of bromocriptine treatment of 5.0--7.5 mg daily for 1--2 weeks. Before the start of bromocriptine, TRH caused a PRL elevation from 19.1 +/- 2.2 to 95.2 +/- 12.6 ng/ml (mean +/- SE) after 20 min, with a mean maximal PRL increment of 71.7 +/- 11.6 ng/ml. Bromocriptine suppressed basal plasma PRL level to 3.6 +/- 0.8 ng/ml (P less than 0.001). TRH then caused a PRL rise to 18.8 +/- 1.8 ng/ml at 20 min, with a mean maximal PRL increment of 15.7 +/- 1.8 ng/ml. The absolute PRL response was significantly smaller (P less than 0.001) during bromocriptine intake than before, whereas the mean percent increments in PRL levels after TRH administration were similar in the presence and absence of bromocriptine. Fifteen of these women were restudied with TRH stimulation 4--6 weeks after legal abortion, and the PRL responses to TRH were normal. When 7 of these women were once again treated with bromocriptine and retested with TRH, no absolute or relative PRL response to TRH emerged. These results release differs between the pregnant and nonpregnant states.

Abortion, Induced↗
PubMed1980

Sulpiride treatment during early human pregnancy: effect on the levels of prolactin, six steroids, and placental lactogen.

To study the role of PRL in the regulation of the production of 17 beta-estradiol, progesterone, testosterone, and human placental lactogen (hPL), 11 healthy women were given 150 mg sulpiride daily for 14 days, beginning between weeks 6--9 of normal gestation. Plasma PRL, estradiol, progesterone, testosterone, and hPL were measured before and 1 and 2 weeks after the start of sulpiride treatment, and the results were compared with those from 16 control women who were followed similarly but without sulpiride treatment. Sulpiride treatment induced significant (P less than 0.001) elevations of plasma PRL at 1 week [84.1 +/- 4.9 vs. 23.7 +/- 2.8 ng/ml (mean +/- SE)] and 2 weeks (83.0 +/- 4.1 vs. 31.9 +/- 4.1 ng/ml). No differences were observed in the concentrations of estradiol, progesterone, testosterone, or hPL. Two women treated with sulpiride reported mild uterine contractions, but no spontaneous abortion occurred in either group. It is evident that hyperprolactinemia or sulpiride treatment do not change the circulating concentrations of sex steroids and hPL between 6--11 of normal gestation.

Estradiol↗
PubMed1980

Oral administration of TRH in puerperal women: effect on insufficient lactation, thyroid hormones and on the responses of TSH and prolactin to intravenous TRH.

Thirteen puerperal women with insufficient lactation were treated with thyrotrophin releasing hormone (TRH) 20 mg twice daily for two weeks. Intravenous (iv) TRH stimulation tests were done before the TRH therapy and within 3-5 h after the last dose of oral TRH. Plasma samples were assayed for prolactin (Prl), thyrotrophin (TSH), triiodothyronine (T3) and thyroxine (T4) by radioimmunoassays, and the lactational response was objectively monitored in 11 women. Oral TRH treatment was associated with significantly (P less than 0.05) depressed Prl levels (23.0 +/- 7.9 microgram/l vs. 61.4 +/- 26.2, mean +/- SEM), no change in TSH levels (3.7 +/- 0.4 IU/l vs. 4.0 +/- 0.4) but significantly (P less than 0.01) elevated T3 (2.17 +/- 1.14 nmol/l vs. 1.83 +/- 0.09) and T4 (131.6 +/- 7.9 nmol/l vs. 96.6 +/- 5.8) levels. Oral TRH entirely blocked the TSH response and significantly (P less than 0.01) blunted the Prl response to iv TRH stimulation. No improvement in lactation was observed.

Administration, Oral↗
PubMed1980

Bromocriptine treatment during early human pregnancy: effect on the levels of prolactin, sex steroids and placental lactogen.

To elucidate the role of prolactin (Prl) in the endocrinology of early human pregnancy, 28 healthy women were given 5.0-7.5 mg of bromocriptine daily for two weeks between weeks 6-9 of normal gestation. Plasma Prl, oestradiol-17 beta (Oe2), progesterone (P), testosterone (T) and human placental lactogen (hPL) were measured before, and one and two weeks after the start of bromocriptine, and they were compared with those in 22 control women who were followed similarly but without bromocriptine treatment. Bromocriptine treatment induced a significant Prl depression at one week (7.3 +/- 4.3 ng/ml vs 23.7 +/- 11.4 ng/ml) and two weeks (5.3 +/- 2.5 ng/ml vs 31.9 +/- 16.4 ng/ml). Oe2, P, T and hPL levels, however, showed no significant differences between the groups. Two women undergoing bromocriptine treatment (7.1%) and one control women (4.5%) experienced spontaneous incomplete abortion during the study period, but these three already had a low Oe2 level and a low/or undetectable hPL level at the beginning of the study. It is obvious that neither maternal 'hypoprolactinaemia' nor bromocriptine during early human pregnancy interfere with the normal progress of pregnancy or with the normal synthesis of sex steroids and hPL at this time.

Bromocriptine↗
PubMed1980

Twin pregnancy in woman with 45,X/47,XXX karyotype.

A successful twin pregnancy in a woman with a 45,X/47,XXX karyotype is described. This report demonstrates that in patients with a mosaic genotype with a 45,X/47,XXX chromosome constitution, somatic defects may be absent or milder than in those with a typical Turner's phenotype, and the women may even be fertile.

Adult↗
PubMed1979

Maternal serum prolactin and its response to TRH in normal and complicated early pregnancy.

Maternal serum prolactin levels (PRL) were measured by radioimmunoassay in thirty-four women with either normal or complicated early pregnancy. The basal PRL level (mean +/- S.D.) of 33.4 +/- 16.4 ng/ml in normal pregnancy (n = 15) was similar to the level of 32.7 +/- 18.8 ng/ml in threatened abortion (n = 11) and 32.8 +/- 16.9 ng/ml in hyperemesis gravidarum (n = 8). Two patients, one with blighted ovum and the other with subsequent spontaneous abortion, demonstrated PRL levels lower than the range of 20-63 ng/ml in the control group. The PRL response to 200 microgram of synthetic thyrotropin releasing hormone (TRH) administered intravenously was similar throughout the patient groups. The basal level of PRL in the whole series was more closely related to the level of serum oestradiol (r = 0.778, P less than 0.001) than to that of serum progesterone (r = 0.442, P less than 0.05). However the increments of PRL following TRH administration did not correlate with either oestradiol or progesterone.

Adult↗