Biomedical subjects
R M Pitkin
Publications and source records attributed to R M Pitkin.
Response on the need for flexibility in academic obstetric-gynecologic residencies.
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Pregnancy in a patient with a history of myocardial infarction and coronary artery bypass grafting.
A 37-year-old woman conceived after experiencing a myocardial infarction and undergoing three-vessel aortocoronary artery bypass grafting. Pregnancy was complicated by angina, which was successfully treated with propranolol and bed rest. At term the patient underwent vaginal delivery, without evidence of intrapartum myocardial ischemia or failure.
Preinduction cervical ripening with prostaglandin E2 intracervical gel.
A double-blind, placebo-controlled, dose-ranging study was undertaken to evaluate the efficacy of two doses of intracervical prostaglandin E2 gel in patients with unfavorable Bishop scores. Mean change in Bishop score, success of softening, time to labor, and time to delivery were all significantly different in the two treatment groups as compared with the placebo group. Twenty-three of 30 treated patients had uterine contractions lasting greater than four hours and eight patients delivered during the observation period. Moreover, one case of uterine hyperactivity and five cases of severe fetal heart rate decelerations were noted in the treatment groups. Although efficacious for cervical ripening, caution is warranted when using this technique in patients at risk for placental insufficiency.
Calcium metabolism in pregnancy and the perinatal period: a review.
Calcium homeostasis is a complex process involving calcium, other involved ions, and three calcitropic hormones, parathyroid hormone, calcitonin, and 1,25-dihydroxyvitamin D3. The principal maternal adjustment during pregnancy is an increasing parathyroid hormone secretion which maintains the serum calcium concentration in the face of a falling albumin level, an expanding extracellular fluid volume, an increasing renal excretion, and placental calcium transfer. The placenta transports calcium ions actively, making the fetus hypercalcemic relative to its mother, which in turn stimulates calcitonin release and perhaps suppresses parathyroid hormone secretion by the fetus. A unique extrarenal system for 1 alpha-hydroxylation of 25-hydroxyvitamin D3 exists in the placenta and/or decidua, providing a source of 1,25-dihydroxyvitamin D3 for the fetus. With the abrupt cessation of the placental source of calcium at birth, the neonate's serum calcium level falls for 24 to 48 hours, then stabilizes and rises slightly. Hyperparathyroidism during pregnancy causes complications in both mother and infant and should usually be treated surgically as soon as diagnosed. Maternal hypoparathyroidism can be treated satisfactorily with high doses of supplemental calcium and vitamin D. Osteopenia accompanying long-term heparin administration may respond to 1,25-dihydroxyvitamin D3 (calcitriol) therapy. Diabetes in pregnancy is associated with disturbed neonatal calcium homeostasis, perhaps due to chronic hypomagnesemia. A possible etiologic role of calcium deficiency in pregnancy-related hypertension has been suggested. Dietary deficiency of calcium and/or vitamin D during gestation may lead to several adverse effects in the newborn infant.
Endometriosis: approaches to diagnosis and treatment.
Conservative or radical surgical treatment, steroidal hormones to produce pseudopregnancy, and danazol are all being used to relieve the symptoms of endometriosis or to treat the infertility that frequently accompanies it. The choice of therapy should be determined by the patient's desires and the extent of her disease. Our approach to treating this condition is as follows: Young patients with symptoms who wish to delay childbearing: Treat with danazol 400 mg to 600 mg per day for 6 months to induce regression of the disease and relieve symptoms. Once that is achieved, encourage use of low-dose oral contraceptive or the minipill to minimize progression of the disease. Delay surgical therapy, if needed, until the patient wishes to conceive . Infertile patients with mild endometriosis: Treat medically with danazol, 400 to 600 mg per day for 6 months. Then encourage attempts to conceive for 9 to 12 months. Patients who fail to become pregnant should have repeat laparoscopy to assess further the need for conservative surgical treatment. Infertile patients with moderate or greater disease: Treat with conservative operation. If conservative operation is not done at the same time as the diagnostic laparoscopy, give danazol for 2 to 3 months preoperatively to decrease the number and the size of the endometriotic areas, minimize the extent of operation, and avoid traumatizing the corpus luteum. Patients who remain infertile after conservative surgical treatment: Treat with danazol for approximately 6 months and then try for conception. A second conservative operation will have a modest chance (less than 30 percent) of success. If severe symptoms persist, perform definitive operation. Patients who are not desirous of further childbearing: Treat with definitive surgical treatment if symptoms are severe and the quality of life is impaired. Patients who want to postpone or avoid a major operation may benefit from a course of danazol. Patients with endometriosis involving the organs outside the pelvis: Advise total abdominal hysterectomy and bilateral salpingo-oophorectomy. For patients who desire further childbearing, danazol treatment has been reported to be successful in pulmonary, intestinal, and ureteral involvement. Endometriosis is a poorly understood, ubiquitous, and progressive disease with inconsistent clinical presentation and poorly standardized therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
Calcium metabolism in the hypertensive mother, fetus, and newborn infant.
Calcium metabolism in otherwise uncomplicated term pregnancies associated with essential hypertension is characterized by significantly reduced levels of parathyroid hormone and ionized calcium, as well as significantly increased levels of phosphorus in both the mother and fetus. It is not possible at this time to delineate with certainty the precise pathophysiology of these changes.
Calcium metabolism in diabetic mother, fetus, and newborn infant.
Peripheral blood levels of the minerals and hormones involved in calcium homeostasis were measured in insulin-dependent diabetic patients at delivery, and in umbilical arterial and venous blood. The minerals were also measured in neonatal blood at 24 hours of age. Insulin-dependent diabetic patients at delivery have depressed serum levels of parathyroid hormone, although serum total and ionized calcium levels are not different from those of nondiabetic patients. Fetuses of diabetic mothers are hypocalcemic and have reduced parathyroid hormone levels. Infants of diabetic mothers demonstrate early neonatal hypocalcemia. No differences between diabetic and control patients could be demonstrated in terms of calcitonin or phosphorus levels, in either mother, fetus, or neonate.
Polyarteritis nodosa.
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Endocrine regulation of calcium homeostasis during pregnancy.
The principal maternal physiologic adjustment with respect to calcium metabolism is increasing PTH secretion, which maintains the serum ionic calcium level within its characteristically narrow physiologic limits in the face of an expanding extracellular fluid volume, increased urinary excretion, and calcium transfer to the fetus. Additionally, PTH promotes increased renal synthesis of 1,25-(OH)2D3, which acts in concert with PTH to meet the calcium demands of gestation. Whether or not calcitonin secretion increases as well is not clear; if so, this effect may be important in protecting the maternal skeleton. The primary characteristic of perinatal calcium metabolism is the active placental transport of calcium ions from mother to fetus, making the fetus relatively hypercalcemic. Since none of the calcitropic hormones cross the placenta, hypercalcemia apparently suppresses either secretion or activity of PTH by the fetus and stimulates fetal calcitonin release, creating an environment (high calcium, low PTH, high calcitonin) favorable to skeletal growth. With birth, the transplacental calcium source terminates abruptly and the serum calcium level declines for 24 to 48 hours, after which it stabilizes and then rises slightly. Neonatal calcium homeostasis probably reflects multiple influences, including the respective calcitropic hormones and other involved ions such as magnesium and phosphate. The physiologic mechanisms regulating calcium homeostasis during pregnancy and the perinatal period generally operate very effectively. Thus, aberrations leading to clinically evident disease states are relatively infrequent. Maternal hyperparathyroidism causes several complications, notably hypocalcemic tetany in the newborn, and maternal hypoparathyroidism may be associated with perinatal hyperparathyroidism. Diabetic pregnancy leads to altered calcium metabolism in mother, fetus, and newborn; the primary feature may be chronic hypomagnesemia, which leads to hypoparathyroidism to mother and fetus. There is some suggestion of an etiologic role for calcium in hypertensive disorders, and, in any event, magnesium sulfate therapy influences calcium homeostasis. Finally, leg cramps in the pregnant woman may reflect alterations in calcium metabolism.
Breast milk magnesium and calcium concentrations following magnesium sulfate treatment.
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Maternal and cord blood background mercury levels: a longitudinal surveillance.
Fifty-seven prenatal patients with no known exposure to the element mercury, or any of its compounds, were observed for change in whole blood total mercury concentration from the initial prenatal clinic examination through delivery and postpartum hospitalization. On hospital admission for labor and delivery, whole blood total mercury averaged 1.15 parts per billion (ppb), compared to 0.79 ppb from the first prenatal clinic visit; these levels represent a 46% increase and significant difference in maternal concentration of a substance previously recognized for its peculiar ease at crossing the placental barrier. Previous stillbirths, as well as history of birth defects, exhibited significant positive correlation with background mercury levels. Search of the literature of the last 5 years revealed no other report of cohort heavy metal surveillance throughout pregnancy.
Calcitropic hormone responsiveness during pregnancy.
Release of the calcitropic hormones parathyroid hormone (PTH) and calcitonin (CT) in-response to provocative stimuli was assessed in pregnant rhesus monkeys tested three times during gestation (corresponding to the end of each trimester) and again 6 weeks post partum. In the case of PTH, although basal levels were higher during pregnancy than post partum and tended to increase with advancing gestation, similar to observations in human subjects, the incremental response of the hormone to a hypocalcemic stimulus was diminished in pregnant animals and tended to lessen with advancing gestation. Basal CT levels were also increased during pregnancy but, in contrast to PTH, the incremental CT response to a provocative stimulus was generally greater during pregnancy than post partum and tended to increase with advancing gestation. The explanation of these findings may lie in differing degrees of hormone storage. These adjustments in maternal endocrine physiology regulating calcium metabolism would have the net effect of tending to preserve the maternal skeleton by protecting it from excessive resorption at times of hypocalcemia and promoting increased calcium storage during episodes of hypercalcemia.
Placental transfer of taurine in the rhesus monkey.
Maternal to fetal transfer of taurine was examined in 10 pregnant monkeys infused with taurine. In four animals infused at 15 mg/kg body weight, maternal plasma taurine concentration increased from preinfusion values of 8.82 +/- 2.61 to 28.0 +/- 6.00 mumol/dl (mean +/- SD) by the end of the 2-h infusion period. Mean (+/- SD) fetal plasma taurine concentration increased concomitantly, rising from preinfusion values of 13.3 +/- 2.61 to 36.6 +/- 17.8 mumol/dl at the end of the infusion, maintaining the normal fetal to maternal plasma ratio of 1.3 to 1.5. Maternal infusion of larger quantities of taurine increased both maternal and fetal plasma taurine levels; however, the placenta was unable to maintain the normal fetal to maternal gradient. In four monkeys infused with taurine at 25 mg/kg body weight over a 2-h period, mean (+/- SD) maternal plasma taurine concentration increased from 10.0 +/- 1.33 to 43.5 +/- 11.0 mumol/dl. Fetal plasma concentration increased from 13.6 +/- 1.05 to 34.9 +/- 5.89 mumol/dl. However, the maternal to fetal plasma taurine ratio fell from 1.36 to 0.80. Similar results were noted in single animals infused with taurine at 50 and 250 mg/kg body weight. Maternal and fetal plasma concentrations of most other amino acids were not affected by taurine infusion. Fetal, but not maternal, plasma alanine concentration increased after taurine infusion. These data indicate that taurine is efficiently concentrated to the fetal circulation at postprandial maternal plasma taurine concentrations.
Assessment of nutritional status of mother, fetus, and newborn.
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William C. Keettel, M.D. 1911-1981.
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Urinary magnesium, calcium, and phosphate excretion during magnesium sulfate infusion.
Urinary excretion of magnesium, calcium, and phosphate was measured in 20 preeclamptic pregnant women treated with intravenous magnesium sulfate. Blood levels of these substances, as well as of parathyroid hormone and calcitonin, were also measured. Urinary magnesium excretion increased 20-fold during magnesium sulfate infusion. Seventy-five percent of the infused magnesium was excreted during the infusion, and 90% within 24 hours after treatment. Urinary calcium concentration increased 4.5-fold during magnesium sulfate infusion, and the urinary calcium excretion rate was 3 times that observed in controls. Urinary phosphate concentration and excretion rate were the same in treated and control subjects. During treatment, maternal serum total calcium fell 25%, ionized calcium fell 12%, and parathyroid hormone rose 26%. Magnesium sulfate therapy depresses maternal calcium levels by increasing urinary calcium loss, and increased parathyroid hormone output prevents more marked hypocalcemia.
Calcium-regulating hormones and ions in amniotic fluid.
Concentrations of the hormones and ions involved in calcium homeostasis were analyzed in simultaneous samples of amniotic fluid and maternal blood obtained from normal pregnant women between 14 weeks' gestation and term. Amniotic fluid total calcium, magnesium, and phosphorus levels fell progressively and markedly despite constant or only declining maternal serum levels. Ionized calcium was constant in both amniotic fluid (mean 2.22 mEq/L) and maternal serum (mean 2.33 mEq/L) throughout gestation. Parathyroid hormone levels in amniotic fluid declined after 20 weeks' gestation, despite rising maternal serum levels, consistent with suppressed fetal parathyroid activity secondary to the relative hypercalcemia of late fetal life. Calcitonin levels in both amniotic fluid and maternal serum were unchanged throughout gestation, with amniotic fluid levels being significantly lower than those in maternal serum.